Page last updated: 2024-11-04

thalidomide

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Description

Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID5426
CHEMBL ID468
CHEBI ID74947
CHEBI ID9513
SCHEMBL ID7581
SCHEMBL ID15197560
MeSH IDM0021267

Synonyms (365)

Synonym
AC-917
HMS3266F13
STL356025
AB00052362-11
AB00052362-13
AB00052362-12
BRD-A93255169-001-06-9
nsc527179
nsc-527179
1h-isoindole-1,3(2h)-dione, 2-(2,6-dioxo-3-piperidinyl)-
KBIO1_000051
DIVK1C_000051
NCI60_023904
smr000058524
MLS000069353
synovir
thaled
talizer
thalidomide celgene
thalidomide pharmion
thalomid
2-(2,6-dioxopiperidin-3-yl)-1h-isoindole-1,3(2h)-dione
pro-bam m
thalidomidum [inn-latin]
n-phthalyl-glutaminsaeure-imid [german]
neaufatin
talidomida [inn-spanish]
nsc 527179
talidomide [dcit]
enmd 0995
1h-isoindole-1,3(2h)-dione, 2-(2,6-dioxo-3-piperidinyl)-, (+-)-
ai3-50606
einecs 200-031-1
thalomide
brn 0030233
hsdb 3586
phthalimide, n-(2,6-dioxo-3-piperidyl)-
EU-0101224
(+/-)-thalidomide, >=98%, powder
valgis
pangul
tensival
e-217
shinnibrol
kevadon
isomin
glupan
predni-sediv
glutarimide, 2-phthalimido-
softenil
quietoplex
nsc-66847
kedavon
calmore
bonbrrin
slipro
asmadion
sedisperil
talismol
nibrol
sedin
thalomid (tn) (celgene)
softenon
k-17
ectiluran
1h-isoindole-1, 2-(2,6-dioxo-3-piperidinyl)-
distaval
asmaval
distaxal
wln: t56 bvnvj c- dt6vmvtj
neosedyn
yodomin
ulcerfen
sedoval
thalidomide (soluble form)
2,6-dioxo-3-phthalimidopiperidine
.alpha.-phthalimidoglutarimide
.alpha.-(n-phthalimido)glutarimide
glutanon
grippex
enterosediv
quetimid
thalin
imida-lab
thalinette
noxodyn
3-phthalimidoglutarimide
gastrinide
theophilcholine
hippuzon
calmorex
sandormin
bonbrain
nerosedyn
neurodyn
imidene
corronarobetin
telargean
profarmil
psycholiquid
n-phthalyl-glutaminsaeure-imid
telagan
valgraine
shin-naito s
pantosediv
neufatin
n-phthalylglutamic acid imide
sedimide
n-phthaloylglutamimide
pro-ban m
talimol
psychotablets
distoval
algosediv
nevrodyn
talargan
n-(2,6-dioxo-3-piperidyl)phthalimide
neurosedin
phthalimide,6-dioxo-3-piperidyl)-
sleepan
k 17
sedalis sedi-lab
contergan
imidan (peyta)
neurosedym
neosydyn
noctosediv
asidon 3
PRESTWICK2_000192
PRESTWICK_463
BIO2_000418
cas-50-35-1
BIO1_000876
BIO2_000898
BIO1_000387
BIO1_001365
CMAP_000022
phthalimide,6-dioxo-3-piperidyl)-, (+)-
phthalimide,6-dioxo-3-piperidyl)-, l-(-)-
nsc-91730
wln: t56 bvnvj c- dt6vmvtj -d
nsc91729
1h-isoindole-1, 2-(2,6-dioxo-3-piperidinyl)-, (r)-
nsc91730
phthalimide,6-dioxo-3-piperidyl)-, d-(+)-
phthalimide,6-dioxo-3-piperidyl)-, (-)-
wln: t56 bvnvj c- dt6vmvtj -l
1h-isoindole-1, 2-(2,6-dioxo-3-piperidinyl)-, (s)-
BSPBIO_001156
BSPBIO_003330
IDI1_000051
LOPAC0_001224
PRESTWICK3_000192
IDI1_002173
thalomid (tm)
.alpha.-n-phthalylglutaramide
2-(2,6-dioxo-3-piperidyl)isoindoline-1,3-dione
2-(2,6-dioxo-3-piperidinyl)-1h-isoindole-1,3(2h)-dione
nsc66847
UPCMLD-DP139:001
AB00052362
50-35-1
thalidomide
C07910
alpha-phthalimidoglutarimide
alpha-(n-phthalimido)glutarimide
alpha-n-phthalylglutaramide
(+/-)-n-(2,6-dioxo-3-piperidyl)phthalimide
UPCMLD-DP139
(+-)-thalidomide
(+-)-n-(2,6-dioxo-3-piperidyl)phthalimide
DB01041
1,3-dioxo-2-(2,6-dioxopiperidin-3-yl)isoindoline
thaled (tn)
D00754
thalidomide (jan/usp/inn)
thalomid (tn)
BPBIO1_000159
SPECTRUM5_001791
BSPBIO_000143
NCGC00024708-05
NCGC00024708-04
(+/-)-2-(2,6-dioxo-3-piperidinyl)-1h-isoindole-1,3(2h)-dione
NCGC00024708-08
NCGC00024708-03
(+/-)-thalidomide
NCGC00024708-07
KBIO2_004890
KBIO2_000496
KBIOSS_002324
KBIO3_000912
KBIO2_003064
KBIO3_002550
KBIO2_007458
KBIO2_005632
KBIOGR_000496
KBIO2_002322
KBIOGR_001474
KBIO3_000911
KBIOGR_002322
KBIOSS_000496
KBIO3_002802
PRESTWICK1_000192
SPECTRUM4_001087
NINDS_000051
SPECTRUM3_001715
SPECTRUM2_000707
NCIOPEN2_003188
SPBIO_000893
PRESTWICK0_000192
SPBIO_002064
SPECTRUM1503607
NCGC00024708-09
NCGC00024708-06
(?)-thalidomide
NCGC00024708-02
NCGC00015989-03
HMS2090O05
HMS2093G15
HMS1990J17
( inverted question mark)-2-(2,6-dioxo-3-piperidinyl)-1h-isoindole-1,3(2h)-dione
( inverted question mark)-thalidomide
NCGC00015989-13
neurosedyn
myrin
pharmion
celgene
CHEMBL468 ,
chebi:74947 ,
HMS500C13
HMS1362J17
HMS1792J17
HMS1568H05
HMS1922E12
bdbm50070114
2-(2,6-dioxo-piperidin-3-yl)-isoindole-1,3-dione
[(r,s)-2-(2,6-dioxo-3-piperidinyl)-1h-isoindole-1,3(2h)-dione
2-(2,6-dioxopiperidin-3-yl)isoindoline-1,3-dione
2-(2,6-dioxopiperidin-3-yl)isoindole-1,3-dione
NCGC00015989-09
NCGC00024708-11
NCGC00024708-10
HMS3263F10
HMS2095H05
HMS3259C22
tox21_300580
NCGC00254343-01
pharmakon1600-01503607
nsc758479
nsc-758479
tox21_110275
dtxcid402524
dtxsid9022524 ,
2-(2,6-dioxopiperidin-3-yl)-2,3-dihydro-1h-isoindole-1,3-dione
HMS2234C07
AKOS009529198
CCG-39878
NCGC00015989-07
NCGC00015989-05
NCGC00015989-06
NCGC00015989-10
NCGC00015989-12
NCGC00015989-14
NCGC00015989-08
NCGC00015989-04
NCGC00015989-11
thalidomine usp26
sedalis
n-phthalimidoglutamic acid imide
telargan
HY-14658
CS-1084
talidomide
ccris 8148
thalidomide [usan:usp:inn:ban:jan]
talidomida
thalidomidum
4z8r6ors6l ,
unii-4z8r6ors6l
FT-0600001
FT-0631211
FT-0602275
BRD-A93255169-001-24-2
NCGC00015989-16
LP01224
BBL023439
gtpl7327
2-(6-hydroxy-2-oxo-2,3,4,5-tetrahydropyridin-3-yl)-2,3-dihydro-1h-isoindole-1,3-dione
HMS3373E06
HMS3373G15
thalidomide [ema epar]
thalidomide [mart.]
thalidomide [inn]
thalidomide [usp monograph]
thalidomide [orange book]
1h-isoindole-1,3(2h)-dione, 2-(2,6-dioxo-3-piperidinyl)-, (+/-)-
thalidomide [usan]
thalidomide [jan]
thalidomide [usp-rs]
thalidomide [hsdb]
thalidomide [who-dd]
thalidomide [vandf]
thalidomide [mi]
NC00600
SCHEMBL7581
tox21_110275_1
NCGC00015989-17
NCGC00261909-01
tox21_501224
(y)-thalidomide
1012310-87-0
T2524
S1193
(.+/-.)-thalidomide
2-(2,6-dioxo-3-piperidinyl)-1h-isoindole-1,3(2h)-dione #
talinol
SCHEMBL15197560
W-105969
n-(2,6-dioxo-3-piperidinyl)phthalimide
HMS3403J17
(a+/-)-thalidomide
AB00052362_14
AB00052362_15
mfcd00153873
sr-01000076184
SR-01000076184-1
thalidomide, united states pharmacopeia (usp) reference standard
HMS3654A20
isopropyl (3,4-dichlorophenyl)carbamodithioate
SR-01000076184-5
SR-01000076184-3
SR-01000076184-8
SBI-0051191.P003
HMS3712H05
SW196678-4
BP-30256
FT-0675130
BCP19772
Z905162656
HMS3678F19
thalidomide,(s)
AS-12367
HMS3414F19
Q203174
BRD-A93255169-001-04-4
SDCCGSBI-0051191.P004
NCGC00015989-29
HMS3884I05
SY052614
thalidomide n-(2,6-dioxopiperidin-3-yl)phthalimide
BT164465
EN300-60005
talidomida (inn-spanish)
thalidomide (usan:usp:inn:ban:jan)
thalidomide (usp monograph)
thalidomide (mart.)
chebi:9513
2-((3rs)-2,6-dioxopiperidin-3-yl)isoindoline-1,3-dione
thalidomide (usp-rs)
2-phthalimidoglutarimide
thalidomidum (inn-latin)
l04ax02
sedoval k-17
2, 6-dioxo-3-phthalimidopiperidine
rac-2-(2,6-dioxopiperidin-3-yl)-1h-isoindole-1,3(2h)-dione

Research Excerpts

Overview

Thalidomide is an immunomodulatory drug and first choice in the treatment of erythema nodosum leprosum. The effects on the gut microbiota still remain unclear. Thalidmide surveillance is a public health challenge.

ExcerptReferenceRelevance
"Thalidomide is an immunomodulatory drug and first choice in the treatment of erythema nodosum leprosum. "( Etonogestrel-releasing contraceptive implant in a patient using thalidomide for the treatment of erythema nodosum leprosum: a case report.
Bahamondes, L; Baracat, EC; de Almeida, PG; Duarte, DC; Ferreira-Filho, ES; Guimarães, ALM; Soares-Júnior, JM; Sorpreso, ICE, 2022
)
2.4
"Thalidomide surveillance is a public health challenge."( Thalidomide control and use: are these appropriate to extend the use and mitigate the risk of teratogenicity in Brazil?
Campos, FT; Costa, JP; Pádua, CAM; Santos, RMMD, 2021
)
2.79
"Thalidomide is a medication that has been in existence for over half a century, and has proven to be useful and effective in severe dermatological conditions. "( The role of thalidomide in dermatology.
Hussain, K; Patel, P; Roberts, N, 2022
)
2.54
"Thalidomide is suggested to be a concomitant therapy with IFX for intestinal BS patients."( Predictors of infliximab refractory intestinal Behçet's syndrome: A retrospective cohort study from the Shanghai Behçet's syndrome database.
Bao, HF; Cai, JF; Guan, JL; Hou, CC; Luo, D; Shen, Y; Ye, B; Zou, J, 2023
)
1.63
"Thalidomide is a drug responsible to a spectrum of congenital anomalies known as Thalidomide Embryopathy (TE), which includes mainly limb and heart defects."( Genetic evaluation of HAND2 gene and its effects on thalidomide embryopathy.
Bremm, JM; do Amaral Gomes, J; Fraga, LR; Kowalski, TW; Rengel, BD; Schüler-Faccini, L; Vianna, FSL, 2022
)
1.69
"Thalidomide is an important immunomodulatory and antitumor drug and its effects on the gut microbiota still remain unclear."( A metagenome-wide association study of the gut microbiota in recurrent aphthous ulcer and regulation by thalidomide.
Duan, N; Hu, Q; Huang, F; Huang, J; Jiang, H; Lin, L; Liu, Q; Qian, Y; Ruan, H; Song, Y; Wang, W; Wang, X; Xiong, K; Yan, F; Ye, P; Zhao, M; Zheng, L; Zhu, Y, 2022
)
1.66
"Thalidomide is an immunomodulatory and anti-inflammatory drug currently used to treat this condition."( Evaluation of the influence of genetic variants in Cereblon gene on the response to the treatment of erythema nodosum leprosum with thalidomide.
Caldoncelli, DIO; Camargo, LMA; Costa, PDSS; Feira, MF; Fraga, LR; Kowalski, TW; Maciel-Fiuza, MF; Schuler-Faccini, L; Silveira, MIDS; Vianna, FSL, 2022
)
1.65
"The "Thalidomide tragedy" is a landmark in the history of the pharmaceutical industry. "( Thalidomide interaction with inflammation in idiopathic pulmonary fibrosis.
Alampady, V; Baby, K; Byregowda, BH; Dsouza, NN; Maity, S; Nayak, Y, 2023
)
2.87
"Thalidomide, which is an angiogenesis inhibitor and immunomodulator that reduces tumor necrosis factor-alpha, has regained value in the treatment of multiple myeloma. "( Thalidomide-induced bronchiolitis obliterans organizing pneumonia in a patient with multiple myeloma.
Beji, S; Cherif, J; El Ati, Z; Fatma, LB; Hamida, FB; Jbali, H; Khedher, R; Krid, M; Lamia, R; Mami, I; Smaoui, W; Zouaghi, MK,
)
3.02
"Thalidomide is an effective systemic agent in the management of ulcerative oromucosal conditions. "( Thalidomide use in the management of oromucosal disease: A 10-year review of safety and efficacy in 12 patients.
Harte, MC; Hodgson, TA; Saunsbury, TA, 2020
)
3.44
"Thalidomide is an anti- tumor necrosis factor alpha (TNF-a) drug used mainly in the management of moderate to severe form of Erythema Nodosum Leprosum (ENL). "( Rationale use of Thalidomide in erythema nodosum leprosum - A non-systematic critical analysis of published case reports.
Babu, S; Gurunthalingam, M; T, T; Thangaraju, P; Venkatesan, S, 2020
)
2.34
"Thalidomide is a medication with strong anti-inflammatory, immunomodulatory, antiangiogenic, and sedative properties."( Thalidomide as a potential adjuvant treatment for paraneoplastic pemphigus: A single-center experience.
Pan, M; Wang, J; Zhang, Y, 2020
)
2.72
"Thalidomide has proven to be a steroid-sparing agent and is useful in controlling the reactions."( Thalidomide in the treatment of erythema nodosum leprosum (ENL) in an outpatient setting: A five-year retrospective analysis from a leprosy referral centre in India.
Pallapati, MS; Srikantam, A; Tarwater, P; Upputuri, B, 2020
)
2.72
"Thalidomide is an effective drug in inflammatory bowel disease, which might be related to its multiple role in anti-inflammatory, immunoregulatory, and anti-angiogenesis."( Thalidomide Inhibits Angiogenesis via Downregulation of VEGF and Angiopoietin-2 in Crohn's Disease.
Huang, Y; Shi, J; Wang, L; Wang, S; Xue, A; Zheng, C, 2021
)
2.79
"Thalidomide is a second-line treatment for discoid lupus erythematosus (DLE). "( Clinical-therapeutic study on the efficacy and safety of thalidomide in the management of discoid lupus erythematosus. A single-centre, retrospective study.
Aguilar-Mena, C; Bonifaz, A; Hernández-Salgado, Y; Rodriguez-Mendoza, A; Tirado-Sánchez, A, 2021
)
2.31
"Thalidomide is an anti-inflammatory agent that has been used in the treatment of inflammatory disorders."( Thalidomide reduces glycerol-induced acute kidney injury by inhibition of NF-κB, NLRP3 inflammasome, COX-2 and inflammatory cytokines.
Amirshahrokhi, K, 2021
)
2.79
"Thalidomide is a drug that presents two enantiomers with markedly different pharmacological and toxicological activities. "( The structure of isolated thalidomide as reference for its chirality-dependent biological activity: a laser-ablation rotational study.
Blanco, S; López, JC; Macario, A, 2021
)
2.36
"Thalidomide is an old well-known drug firstly used as morning sickness relief in pregnant women and then withdrawn from the market due to its severe side effects on fetal normal development. "( Recent Advances in the Development of Thalidomide-Related Compounds as Anticancer Drugs.
Barbarossa, A; Carocci, A; Franchini, C; Iacopetta, D; Sinicropi, MS, 2022
)
2.44
"Thalidomide is a teratogen that affects many organs but primarily induces limb truncations like phocomelia. "( The Molecular Mechanisms of Thalidomide Teratogenicity and Implications for Modern Medicine.
Jungck, D; Knobloch, J; Koch, A, 2017
)
2.19
"Thalidomide is a drug with interesting therapeutic properties but also with severe side effects which require a careful and monitored use. "( A Mini-Review on Thalidomide: Chemistry, Mechanisms of Action, Therapeutic Potential and Anti-Angiogenic Properties in Multiple Myeloma.
Adriani, G; Carocci, A; Catalano, A; Cavalluzzi, MM; Corbo, F; Franchini, C; Lentini, G; Mercurio, A; Rao, L; Vacca, A, 2017
)
2.24
"Thalidomide is an anti-angiogenic compound that may offer a potential option for management of refractory LVAD-related GIB."( Novel use of low-dose thalidomide in refractory gastrointestinal bleeding in left ventricular assist device patients.
Chan, LL; Kerk, KL; Lim, CP; Seng, BJJ; Sim, DKL; Sivathasan, C; Soon, JL; Tan, TE; Teo, LLY, 2017
)
1.49
"Thalidomide appears to be a safe and effective option for management of refractory LVAD-related GIB. "( Novel use of low-dose thalidomide in refractory gastrointestinal bleeding in left ventricular assist device patients.
Chan, LL; Kerk, KL; Lim, CP; Seng, BJJ; Sim, DKL; Sivathasan, C; Soon, JL; Tan, TE; Teo, LLY, 2017
)
2.21
"Thalidomide is an effective therapy in children with inflammatory bowel disease refractory to standard treatments, but thalidomide-induced peripheral neuropathy (TiPN) limits its long-term use. "( Risk Factors and Outcomes of Thalidomide-induced Peripheral Neuropathy in a Pediatric Inflammatory Bowel Disease Cohort.
Arrigo, S; Barp, J; Bramuzzo, M; Calvi, A; Carrozzi, M; Chicco, A; Costa, S; Decorti, G; Di Chio, T; Fontana, M; Ghione, S; Lanteri, P; Lazzerini, M; Lionetti, P; Lucafò, M; Magazzù, G; Maggiore, G; Martelossi, S; Montico, M; Pellegrin, MC; Pellegrino, S; Stocco, G; Udina, C; Ventura, A; Zuin, G, 2017
)
2.19
"Thalidomide is a drug used worldwide for several indications, but the molecular mechanisms of its teratogenic property are not fully understood. "( Genetic susceptibility to thalidomide embryopathy in humans: Study of candidate development genes.
Fraga, LR; Gomes, JDA; Kowalski, TW; Sanseverino, MTV; Schuler-Faccini, L; Tovo-Rodrigues, L; Vianna, FSL, 2018
)
2.22
"Thalidomide is an effective and safe drug for remission of CD in pediatric patients who have been treated for tuberculosis."( Efficacy of thalidomide therapy in pediatric Crohn's disease with evidence of tuberculosis.
Hong, Y; Huang, Y; Leung, YK; Wang, L; Wu, J, 2017
)
2.28
"Thalidomide is a glutamic acid derivative, recently has been reconsidered for its clinical use due to elucidation of different clinical effects."( Thalidomide attenuates development of morphine dependence in mice by inhibiting PI3K/Akt and nitric oxide signaling pathways.
Dehpour, AR; Ejtemaei-Mehr, S; Jahanabadi, S; Khan, MI; Momeny, M; Ostadhadi, S; Sameem, B; Zarrinrad, G, 2018
)
2.64
"Thalidomide is an antipruritic and anti-inflammatory agent that has shown to be very effective in treating a variety of dermatologic conditions."( Thalidomide for the treatment of chronic refractory prurigo nodularis.
Aguh, C; He, A; Kwatra, SG; Okoye, GA, 2018
)
2.64
"Thalidomide is a teratogenic drug which is known to inhibit angiogenesis and effectively inhibit cancer metastasis, yet the specific cellular targets for its effect are not well known."( CUL5 is required for thalidomide-dependent inhibition of cellular proliferation.
Burnatowska-Hledin, MA; Dean, S; DeBruine, ZJ; Grossens, D; Hledin, MP; Kunkler, B; Madden, J; Marquez, GA; Ploch, C; Salamango, D; Schnell, A; Short, M, 2018
)
1.52
"Thalidomide is a drug that has been reported to inhibit angiogenesis and reduce VEGF production by downregulating VEGF expression."( Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.
Cai, DZ; Fang, H; Li, L; Song, JL, 2018
)
1.49
"Thalidomide, which is a specific VEGF inhibitor, significantly inhibited neointimal hyperplasia and vascular restenosis after balloon injury to the carotid artery in rats, thus potentially providing a novel method for the prevention and treatment of restenosis, especially in-stent restenosis."( Local delivery of thalidomide to inhibit neointima formation in rat model with artery injury.
Bai, F; Chang, P; Hu, H; Sun, S; Wang, Q; Wu, Q; Xu, G; Zhang, Q, 2018
)
2.26
"Thalidomide is a known sensory neurotoxin in adults."( Thalidomide and neurotrophism.
Bonar, SF; McCredie, J; O'Sullivan, DJ; Soper, JR; Willert, HG, 2019
)
2.68
"Thalidomide is a widely prescribed immunomodulatory drug (iMiD) for multiple myeloma, but causes reversible memory loss in humans. "( BK channel blocker paxilline attenuates thalidomide-caused synaptic and cognitive dysfunctions in mice.
Choi, SY; Choi, TY; Jo, Y; Kim, SJ; Lee, SH; Park, CS, 2018
)
2.19
"Thalidomide is an infamous teratogen and it is continuously being explored for its anticancer properties. "( Thalidomide and Its Analogs Differentially Target Fibroblast Growth Factor Receptors: Thalidomide Suppresses FGFR Gene Expression while Pomalidomide Dampens FGFR2 Activity.
Anishetty, S; Balaguru, UM; Chatterjee, S; Kasiviswanathan, D; Kumar, P; Manivannan, J; Sundaresan, L; Veeriah, V, 2019
)
3.4
"Thalidomide is a widely used anti-angiogenic and immunomodulatory drug with anticancer effects."( Synergistic effects of gefitinib and thalidomide treatment on EGFR-TKI-sensitive and -resistant NSCLC.
Guo, Z; Huang, C; Huang, H; Jiang, L; Liao, Y; Liu, J; Liu, Y; Wang, X; Xia, X; Zhang, F, 2019
)
1.51
"Thalidomide is a synthetic derivative acid with anti-inflammatory and anti-angiogenic properties."( Thalidomide ameliorates rosacea-like skin inflammation and suppresses NF-κB activation in keratinocytes.
Chen, M; Chen, Z; Deng, Z; Li, J; Liu, T; Peng, Q; Sha, K; Wang, B; Xiao, W; Xie, H; Xu, S; Zhang, Y, 2019
)
2.68
"Thalidomide is a sedative/hypnotic agent that is currently used to treat patients suffering from multiple myeloma, myelodysplastic syndromes and erythema nodosum leprosum. "( Involvement of the nitric oxide pathway in the anti-depressant-like effects of thalidomide in mice.
Dehpour, AR; Gharedaghi, A; Norouzi-Javidan, A; Rostamian, A, 2019
)
2.18
"Thalidomide is a tumor necrosis factor alpha (TNFα) inhibitor which has been found to have abilities against tumor growth, angiogenesis and inflammation. "( Long-term treatment of thalidomide ameliorates amyloid-like pathology through inhibition of β-secretase in a mouse model of Alzheimer's disease.
Cheng, X; He, P; Li, R; Shen, Y; Staufenbiel, M, 2013
)
2.14
"Thalidomide is a drug that is well known for its teratogenic properties in humans. "( Organizer formation in Hydra is disrupted by thalidomide treatment.
Bode, HR; Brooun, M; Manoukian, A; McNeill, H; Shimizu, H, 2013
)
2.09
"Thalidomide is a synthetic glutamic acid derivative first introduced in 1956 in Germany as an over the counter medications. "( [Current therapeutic indications of thalidomide and lenalidomide].
Cosiglio, FJ; Ordi-Ros, J, 2014
)
2.12
"Thalidomide (THD) is an immunomodulatory agent used to treat immune-mediated diseases. "( Thalidomide corrects impaired mesenchymal stem cell function in inducing tolerogenic DCs in patients with immune thrombocytopenia.
Guo, CS; He, WD; Hou, M; Hou, XY; Hou, Y; Li, H; Liu, XG; Ma, J; Min, YN; Ning, YN; Peng, J; Qin, P; Shao, LL; Shi, Y; Wang, N; Xu, M; Yu, YY; Zhou, H, 2013
)
3.28
"Thalidomide is an oral immunomodulatory and anti-inflammatory drug with antitumor necrosis factor-α (TNF-α) activity. "( Mucosal healing with thalidomide in refractory Crohn's disease patients intolerant of anti-TNF-α drugs: report of 3 cases and literature review.
Cantoro, L; Cosintino, R; Kohn, A; Marrollo, M; Scribano, ML, 2014
)
2.16
"Thalidomide is an old glutamic acid derivative which was initially used as a sedative medication but withdrawn from the market due to the high incidence of teratogenicity. "( Nitric oxide mediates the anticonvulsant effects of thalidomide on pentylenetetrazole-induced clonic seizures in mice.
Ahmadi-Dastgerdi, M; Amanlou, M; Aminizade, M; Bahremand, A; Berijani, S; Dehpour, AR; Dianati, V; Gholizadeh, R; Gooshe, M; Payandemehr, B; Rahimian, R; Sarreshte-Dari, A, 2014
)
2.1
"Thalidomide is an immunomodulatory and anti-inflammatory agent and is used for the treatment of various inflammatory diseases."( Thalidomide ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in an experimental model.
Amirshahrokhi, K; Khalili, AR, 2015
)
2.58
"Thalidomide is a sedative with unique pharmacological properties; studies on epilepsy and brain ischemia have shown intense neuroprotective effects. "( Neuroprotective effect of thalidomide on MPTP-induced toxicity.
Escamilla-Ramírez, A; Garcia, E; Osorio-Rico, L; Palencia, G; Sotelo, J; Trejo-Solís, C, 2015
)
2.16
"Thalidomide is a TNF-alpha inhibitor and has been administrated for erythema nodosum leprosum (ENL, Type II leprosy reaction) which is one of leprosy reactions and can cause serious illness to patients oflepromatous pole among the immune spectrum. "( [Effectiveness of thalidomide for erythema nodosum leprosum (ENL): retrospective study of 20 Japanese cases in National Sanatrium Oku-Komyoen].
Aoki, Y; Hatano, K; Ishida, Y; Kumano, K; Matsuki, T; Okano, Y, 2014
)
2.18
"Thalidomide is a species-specific developmental toxicant that causes severe limb malformations in humans but not in mice."( Thalidomide induced early gene expression perturbations indicative of human embryopathy in mouse embryonic stem cells.
Gao, X; Sprando, RL; Yourick, JJ, 2015
)
2.58
"Thalidomide is a known teratogen and it is estimated that more than ten thousand babies were affected by thalidomide embryopathy (TE), which is characterized mainly by limb defects, but can involve many organs and systems. "( Thalidomide embryopathy: Follow-up of cases born between 1959 and 2010.
Kowalski, TW; Sanseverino, MT; Schuler-Faccini, L; Vianna, FS, 2015
)
3.3
"Thalidomide seems to be a promising agent that might bring about beneficial changes to the disarrangements of peripheral, hepatic, splanchnic and collateral systems in cirrhosis."( Thalidomide Improves the Intestinal Mucosal Injury and Suppresses Mesenteric Angiogenesis and Vasodilatation by Down-Regulating Inflammasomes-Related Cascades in Cirrhotic Rats.
Alan, L; Hsieh, SL; Hsieh, YC; Huang, CC; Lee, KC; Lee, SD; Li, TH; Lin, HC; Tsai, CY; Yang, YY, 2016
)
2.6
"Thalidomide is an immunomodulatory and anti-angiogenic drug that has shown promise in patients with myeloma. "( Thalidomide-based Regimens for Elderly and/or Transplant Ineligible Patients with Multiple Myeloma: A Meta-analysis.
Ding, ZX; Li, BY; Lyu, WW; Song, DH; Wei, CM; Zhang, JJ; Zhao, QC, 2016
)
3.32
"Thalidomide is a teratogen in humans but not in rodents. "( Thalidomide-induced limb abnormalities in a humanized CYP3A mouse model.
Abe, S; Akita, M; Kamataki, T; Kazuki, K; Kazuki, Y; Kobayashi, K; Ohta, R; Osaki, M; Oshimura, M; Satoh, D; Takehara, S; Yamazaki, H, 2016
)
3.32
"Thalidomide is an immunomodulatory drug used in the experimental treatment of refractory Crohn disease and ulcerative colitis. "( Thalidomide for inflammatory bowel disease: Systematic review.
Bramuzzo, M; Lazzerini, M; Martelossi, S; Ventura, A, 2016
)
3.32
"Thalidomide is an effective treatment option in cases of recalcitrant PN; however, its most frequent adverse effect is neurotoxicity, which often results in its discontinuation."( Treatment of prurigo nodularis with lenalidomide.
Arjona-Aguilera, C; Jiménez-Gallo, D; Linares-Barrios, M; Ossorio-García, L; Rodríguez-Mateos, ME, 2017
)
1.18
"Thalidomide is an old glutamic acid derivative which recently reemerged because of its potential to counteract a number of disorders including neurodegenerative disorders."( Thalidomide attenuates the development and expression of antinociceptive tolerance to μ-opioid agonist morphine through l-arginine-iNOS and nitric oxide pathway.
Dehpour, AR; Ejtemaei-Mehr, S; Hassanipour, M; Khan, MI; Moghaddaskho, F; Momeny, M; Mumtaz, F; Ostadhadi, S, 2017
)
2.62
"Thalidomide is an immunomodulatory drug (IMiD) with proven therapeutic action in several autoimmune/inflammatory diseases; however, its inherent high toxicity has led to the development of more powerful and safer thalidomide analogs, including lenalidomide and pomalidomide. "( Therapeutic effect of the immunomodulatory drug lenalidomide, but not pomalidomide, in experimental models of rheumatoid arthritis and inflammatory bowel disease.
Criado, G; Delgado, M; Diaz de la Guardia, R; García-Herrero, CM; Gonzalez-Rey, E; Lavoie, JR; Lopez-Millan, B; Menendez, P; O'Valle, F; Roca-Ho, H; Rosu-Myles, M, 2017
)
1.9
"Thalidomide is a drug with pleiotropic effects."( Two cases of bacterial meningitis accompanied by thalidomide therapy in patients with multiple myeloma: is thalidomide associated with bacterial meningitis?
Altintas, A; Ayyildiz, O; Bayan, K; Cil, T; Danis, R; Pasa, S; Tuzun, Y; Urakci, Z; Ustun, C, 2009
)
1.33
"Thalidomide is considered to be a potent antiangiogenic and immunomodulatory drug for cancer therapy. "( The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma.
Mei, SC; Wu, RT, 2008
)
2
"Thalidomide is an effective agent for advanced refractory or relapsed multiple myeloma (MM), although dose-limiting toxicity (DLT) may limit its use. "( Combined bendamustine, prednisolone and thalidomide for refractory or relapsed multiple myeloma after autologous stem-cell transplantation or conventional chemotherapy: results of a Phase I clinical trial.
Boldt, T; Goldschmidt, H; Haas, A; Hoffmann, FA; Kreibich, U; Niederwieser, D; Pönisch, W; Ritter, U; Rohrberg, R; Rozanski, M; Schirmer, V; Schwalbe, E; Schwarzer, A; Uhlig, J; Zehrfeld, T, 2008
)
2.06
"Thalidomide is an important advance in the treatment of multiple myeloma. "( [Comparison of dissolution profile and plasma concentration-time profile of the thalidomide formulations made by Japanese, Mexican and British companies].
Aomori, T; Fujita, Y; Horiuchi, R; Murakami, H; Yamamoto, K, 2008
)
2.02
"Thalidomide is a potent teratogen that induces a range of birth defects, most commonly of the developing limbs. "( Thalidomide induces limb defects by preventing angiogenic outgrowth during early limb formation.
Erskine, L; Figg, WD; Gardner, ER; Therapontos, C; Vargesson, N, 2009
)
3.24
"Thalidomide is a very potent teratogen capable of causing severe systemic malformations if the fetus is exposed during the sensitive period. "( Thalidomide and misoprostol: Ophthalmologic manifestations and associations both expected and unexpected.
Miller, MT; Strömland, K; Ventura, L, 2009
)
3.24
"Thalidomide is an effective drug for chronic inflammatory diseases, but the mechanism underlying its immunomodulatory action remains uncertain. "( Thalidomide prevents formation of multinucleated giant cells (Langhans-type cells) from cultured monocytes: possible pharmaceutical applications for granulomatous disorders.
Kondo, Y; Manki, A; Morishima, T; Nagaoka, Y; Tsuge, M; Wada, T; Yashiro, M; Yasui, K,
)
3.02
"Thalidomide is an efficient anti-inflammatory and anti-angiogenic drug, but its therapeutic use is problematic due to a strong teratogenic activity. "( Thalidomide inhibits activation of caspase-1.
Beer, HD; Keller, M; Sollberger, G, 2009
)
3.24
"Thalidomide seems to be a good choice for patients with low-risk MM and for those who achieved less than very good partial remission after induction treatment."( Evolving role of novel agents for maintenance therapy in myeloma.
Magarotto, V; Palumbo, A,
)
0.85
"Thalidomide is an active anticancer agent and also shows wide pharmacological variation."( A pharmacogenetic study of docetaxel and thalidomide in patients with castration-resistant prostate cancer using the DMET genotyping platform.
Cormier, T; Dahut, WL; Deeken, JF; Figg, WD; Liewehr, DJ; Miao, X; Price, DK; Sissung, TM; Steinberg, SM; Tran, K, 2010
)
1.35
"Thalidomide based regimen is an effective and well tolerated therapy in multiple myeloma (MM) patients, however, there were a small number of studies written about the results of thalidomide therapy in non-transplant MM patients. "( Treatment outcome of thalidomide based regimens in newly diagnosed and relapsed/refractory non-transplant multiple myeloma patients: a single center experience from Thailand.
Atichartakarn, V; Aungchaisuksiri, P; Chuncharunee, S; Jootar, S; Niparuck, P; Puavilai, T; Sorakhunpipitkul, L; Ungkanont, A, 2010
)
2.12
"Thalidomide is an effective treatment for recurrent aphthosis but its effectiveness at low dose has been rarely assessed."( [Recurrent aphthosis: safety of low dose thalidomide].
Dupond, JL; Gil, H; Hafsaoui, C; Limat, S; Magy-Bertrand, N; Meaux-Ruault, N; Perrin, S, 2010
)
2.07
"Thalidomide is an effective second-line therapy for SRAS, but is suppressive rather than curative, and adverse events limit its use."( Use of thalidomide for severe recurrent aphthous stomatitis: a multicenter cohort analysis.
Barbarot, S; Bastuji-Garin, S; Chosidow, O; Hello, M; Revuz, J, 2010
)
1.54
"Thalidomide is a drug currently used in Brazil for treating erythema nodosum leprosum."( [Thalidomide used by patients with erythema nodosum leprosum].
Valente, Mdo S; Vieira, JL,
)
2.48
"Thalidomide is a drug with bad reputation from the 1960's as it appeared to be teratogenic by causing foetal anomalies. "( [Thalidomide in oncological and hematological diseases].
Anttila, P; Kivivuori, SM, 2010
)
2.71
"Thalidomide and analogues are a class of immunomodulatory drugs or IMiDS. "( Thalidomide and analogues: potential for immunomodulation of inflammatory and neoplastic dermatologic disorders.
Ladizinski, B; Levis, WR; Sanchez, MR; Shannon, EJ, 2010
)
3.25
"Thalidomide is a powerful treatment for inflammatory and cancer-based diseases. "( Apoptosis induction by thalidomide: critical for limb teratogenicity but therapeutic potential in idiopathic pulmonary fibrosis?
Jungck, D; Knobloch, J; Koch, A, 2011
)
2.12
"Thalidomide is a drug with pleiotropic effects: it appears to downregulate production of TNF-alpha and other proinflammatory cytokines."( Management of central nervous system tuberculosis in children: light and shade.
Buonsenso, D; Serranti, D; Valentini, P, 2010
)
1.08
"Thalidomide is a useful drug for pediatric refractory CD."( Treatment of pediatric refractory Crohn's disease with thalidomide.
Huang, Y; Leung, YK; Xu, JH; Zheng, CF, 2011
)
2.06
"Thalidomide is an anti-angiogenic agent with anti-TNF-α and anti-NF-κB activity."( t(11;18)(q21;q21) translocation as predictive marker for non-responsiveness to salvage thalidomide therapy in patients with marginal zone B-cell lymphoma with gastric involvement.
Chen, LT; Cheng, AL; Hsu, CH; Kuo, SH; Lin, CW; Tzeng, YS; Wu, MS; Yeh, KH, 2011
)
1.31
"Thalidomide is an effective salvage treatment for standard therapy-failure, t(11;18)(q21;q21) translocation-negative gastric MALT lymphoma and deserves further exploration."( t(11;18)(q21;q21) translocation as predictive marker for non-responsiveness to salvage thalidomide therapy in patients with marginal zone B-cell lymphoma with gastric involvement.
Chen, LT; Cheng, AL; Hsu, CH; Kuo, SH; Lin, CW; Tzeng, YS; Wu, MS; Yeh, KH, 2011
)
2.03
"Thalidomide is an immunomodulatory drug that has been associated with improved appetite in those with HIV infections and cancer."( A Phase II dose titration study of thalidomide for cancer-associated anorexia.
Bicanovsky, L; Davis, M; Lagman, R; Lasheen, W; Mahmoud, F; Walsh, D, 2012
)
1.38
"Thalidomide is a potentially effective rescue therapy for severe refractory CD in children who fail to respond to anti-TNF medications."( Thalidomide use and outcomes in pediatric patients with Crohn disease refractory to infliximab and adalimumab.
Felipez, LM; Gokhale, R; Kirschner, BS; Tierney, MP, 2012
)
3.26
"Thalidomide is an effective and relatively safe treatment for patients with refractory bleeding from gastrointestinal vascular malformations. "( Efficacy of thalidomide for refractory gastrointestinal bleeding from vascular malformation.
Chen, HM; Chen, HY; Fang, JY; Gao, YJ; Ge, ZZ; Liu, WZ; Tan, HH; Wei, W; Xiao, SD; Xu, CH, 2011
)
2.19
"Thalidomide is an effective and safe treatment agent for GIVM and its associated bleeding."( The role of HIF-1, angiopoietin-2, Dll4 and Notch1 in bleeding gastrointestinal vascular malformations and thalidomide-associated actions: a pilot in vivo study.
Chen, HM; Chen, HY; Fang, JY; Gao, YJ; Ge, ZZ; Liu, WZ; Tan, HH; Xiao, SD, 2011
)
1.3
"Thalidomide is an oral immunomodulatory agent with anti-TNF-α properties."( Thalidomide induces mucosal healing in Crohn's disease: case report.
Leite, MR; Lyra, AC; Mota, J; Santana, GO; Santos, SS, 2011
)
2.53
"Thalidomide is a drug that, since its development, has made history in the world of medicine--having been withdrawn and now has returned with a boom as an anticancer and immunomodulatory drug. "( Thalidomide: an old drug with new action.
Chhibber, S; Kumar, V, 2011
)
3.25
"thalidomide is an effective treatment in gastrointestinal bleeding due to angiodysplasia, but it was withdrawn due to side effects in 16% of the patients included in our study."( Thalidomide in refractory bleeding due to gastrointestinal angiodysplasias.
Bellido, F; Garrido, A; León, R; López, J; Márquez, JL; Sayago, M, 2012
)
3.26
"Thalidomide is an anti-inflammatory and anti-angiogenic drug currently used for the treatment of several diseases, including erythema nodosum leprosum, which occurs in patients with lepromatous leprosy. "( A framework to identify gene expression profiles in a model of inflammation induced by lipopolysaccharide after treatment with thalidomide.
de Carvalho, DS; Fulco, TO; Lopes, UG; Nobre, FF; Paiva, RT; Sales, Jde S; Saliba, AM; Sampaio, EP; Sarno, EN, 2012
)
2.03
"Thalidomide is an immunomodulatory and anti-inflammatory agent and is used in autoimmune disorders. "( Thalidomide attenuates multiple low-dose streptozotocin-induced diabetes in mice by inhibition of proinflammatory cytokines.
Amirshahrokhi, K; Ghazi-Khansari, M, 2012
)
3.26
"Thalidomide is a developmental toxicant in vivo and acts in a species-dependent manner."( Identification of thalidomide-specific transcriptomics and proteomics signatures during differentiation of human embryonic stem cells.
Gaspar, JA; Hescheler, J; Hildebrand, D; Jagtap, S; Lehmann, K; Meganathan, K; Sachinidis, A; Schlüter, H; Trusch, M; Wagh, V; Winkler, J, 2012
)
1.43
"Thalidomide is an infamous drug whose use by pregnant women in the middle of last century tragically resulted in serious birth defects. "( Revisiting thalidomide: fighting with caution against idiopathic pulmonary fibrosis.
Hallowell, RW; Horton, MR, 2012
)
2.21
"Thalidomide is a reasonably promising drug in treatment-resistant ankylosing spondylitis."( One-year open-label trial of thalidomide in ankylosing spondylitis.
Gu, J; Huang, F; Yu, DT; Zhang, J; Zhao, W; Zhu, J, 2002
)
2.05
"Thalidomide is a glutamic acid derivative initially introduced as a sedative hypnotic nearly forty years ago. "( Thalidomide as an anti-cancer agent.
Kumar, S; Rajkumar, SV; Witzig, TE,
)
3.02
"Thalidomide appears to be a safe and effective alternative for short-term healing in patients who develop infliximab-induced delayed hypersensitivity reaction and may be an alternative strategy for those at risk."( Thalidomide as "salvage" therapy for patients with delayed hypersensitivity response to infliximab: a case series.
Ehrenpreis, E; Kane, S; Stone, LJ, 2002
)
2.48
"Thalidomide is an effective treatment for patients with advanced myeloma, in particular, who have no poor-risk features. "( Thalidomide in patients with advanced multiple myeloma: a study of 83 patients--report of the Intergroupe Francophone du Myélome (IFM).
Attal, M; Bay, JO; Berthou, C; Dauriac, C; Delannoy, V; Dorvaux, V; Duguet, C; Duhamel, A; Dumontet, C; Facon, T; Grosbois, B; Harousseau, JL; Lamy, T; Monconduit, M; Moreau, P; Yakoub-Agha, I, 2002
)
3.2
"Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) in vitro. "( Polymorphisms of the tumor necrosis factor-alpha gene promoter predict for outcome after thalidomide therapy in relapsed and refractory multiple myeloma.
Goldschmidt, H; Ho, AD; Kraemer, A; Moehler, TM; Mytilineos, J; Neben, K; Opelz, G; Preiss, A, 2002
)
1.98
"Thalidomide is a drug that can enhance mitogen- and antigen-stimulated cells' ability to synthesize IL-2. "( Thalidomide can costimulate or suppress CD4+ cells' ability to incorporate [H3]-thymidine--dependence on the primary stimulant.
Sandoval, FG; Shannon, EJ, 2002
)
3.2
"Thalidomide is an immunomodulatory agent; although its mechanisms of action are not fully understood, many authors have described its anti-inflammatory and immunosuppressive properties. "( Thalidomide: focus on its employment in rheumatologic diseases.
Cassarà, EA; Ossandon, A; Priori, R; Valesini, G,
)
3.02
"Thalidomide is an effective agent to treat over 25 seemingly unrelated dermatological conditions that have an inflammatory or autoimmune basis. "( Thalidomide in dermatology.
Cooper, AJ; Wines, MP; Wines, NY, 2002
)
3.2
"Thalidomide is an anti-inflammatory agent and an immunomodulator that inhibits the production of tumor necrosis factor alpha. "( Low-dose thalidomide therapy for refractory cutaneous lesions of lupus erythematosus.
Fleischer, AB; Grummer, SE; Housman, TS; Jorizzo, JL; McCarty, MA; Sutej, PG, 2003
)
2.18
"Thalidomide is a potent inhibitor of angiogenesis. "( Thalidomide prevents donor corneal graft neovascularization in an alkali burn model of corneal angiogenesis.
Abbas, A; Feroze, AH; Hyman, GF; Khan, B, 2002
)
3.2
"Thalidomide is an effective inhibitor of corneal angiogenesis and prolongs graft survival as measured by graft clarity in donor corneas in eyes with previous neovascularization secondary to alkali injury."( Thalidomide prevents donor corneal graft neovascularization in an alkali burn model of corneal angiogenesis.
Abbas, A; Feroze, AH; Hyman, GF; Khan, B, 2002
)
3.2
"Thalidomide is an immunomodulatory and antiangiogenic drug. "( Thalidomide: from tragedy to promise.
Cerny, T; Gillessen, S; Stolz, R; von Moos, R, 2003
)
3.2
"Thalidomide is a promising agent, although many dose-related issues are still in question."( Thalidomide dosing in patients with relapsed or refractory multiple myeloma.
Hansen, LA; Thompson, JL, 2003
)
2.48
"Thalidomide is an effective therapy for multiple myeloma, although its mechanisms of action remain unclear. "( Tolerability and efficacy of thalidomide for the treatment of patients with light chain-associated (AL) amyloidosis.
Berk, JL; Choufani, EB; Dember, LM; Falk, RH; Fennessey, S; Finn, KT; O'Hara, C; Sanchorawala, V; Seldin, DC; Skinner, M; Wiesman, JF; Wright, DG, 2003
)
2.05
"Thalidomide is reported to be an anti-angiogenic agent, which is currently in phase II clinical trials for the treatment of advanced malignancies."( Effects of thalidomide on the expression of angiogenesis growth factors in human A549 lung adenocarcinoma cells.
Jiang, W; Li, QQ; Li, X; Liu, X; Liu, Y; Reed, E; Wang, J; Wang, Z; Zhang, Y, 2003
)
1.43
"Thalidomide is a hypnotic/sedative drug that was withdrawn from the market because of teratogenicity."( Structural development of synthetic retinoids and thalidomide-related molecules.
Hashimoto, Y, 2003
)
1.29
"Thalidomide is a new therapeutic option with promising results; however, it is associated with significant side effects including deep venous thrombosis and peripheral neuropathy."( Recent developments and future directions in the treatment of multiple myeloma.
Mehta, J; Pichardo, D; Rosen, S; Singhal, S, 2003
)
1.04
"Thalidomide is an antiangiogenic drug, but its mechanism of action is not well known and demands further studies. "( [Preliminary results of monotherapy with thalidomide in recurrent and treatment resistant cases of multiple myeloma].
Helbig, G; Hołowiecki, J; Kyrcz-Krzemień, S; Stella-Hołowiecka, B, 2003
)
2.03
"As thalidomide is an effective treatment for ENL, this study assessed the effect of this drug on these phenomena."( Thalidomide does not modify the ability of cells in leprosy patients to incorporate [3H]-thymidine when incubated with M. leprae antigens.
Sandoval, F; Shannon, EJ; Tadesse, A; Taye, E, 2003
)
2.28
"Thalidomide is a putative anti-angiogenesis agent that has significant anti-tumour activity in haematological malignancies with increased bone marrow angiogenesis, including multiple myeloma (MM) and myelodysplastic syndromes (MDS). "( Single agent thalidomide in patients with relapsed or refractory acute myeloid leukaemia.
Albitar, M; Cortes, J; Estey, E; Faderl, S; Giles, FJ; Kantarjian, H; Keating, M; O'Brien, S; Thomas, DA, 2003
)
2.13
"Thalidomide is an anti-inflammatory pharmacologic agent that has been utilized as a therapy for a number of dermatologic diseases. "( Thalidomide inhibits UVB-induced mouse keratinocyte apoptosis by both TNF-alpha-dependent and TNF-alpha-independent pathways.
Brenneman, S; Burns, R; Gaines, E; Gaspari, A; Haake, A; Lu, KQ; Vink, A, 2003
)
3.2
"Thalidomide is an effective treatment for several inflammatory and autoimmune disorders including erythema nodosum leprosum, Behcet's syndrome, discoid lupus erythematosus, and Crohn's disease. "( Thalidomide inhibits tumor necrosis factor-alpha production and antigen presentation by Langerhans cells.
Deng, L; Ding, W; Granstein, RD, 2003
)
3.2
"Thalidomide is a promising treatment for patients with active AS who are resistant to conventional therapies other than biologics."( Thalidomide for severe refractory ankylosing spondylitis: a 6-month open-label trial.
Chan, TW; Chou, CT; Huang, F; Lin, HS; Wei, JC, 2003
)
3.2
"Thalidomide seems to be an effective treatment of severe corticosteroid resistant and dependent or when systemic corticosteroids are contraindicated erosive oral lichen planus. "( [Treatment of erosive oral lichen planus with thalidomide].
Balguerie, X; Joly, P; Macario-Barrel, A, 2003
)
2.02
"Thalidomide is a promising therapy for multiple myeloma. "( Thalidomide neuropathy: clinical, electrophysiological and neuroradiological features.
Barbero, P; Bergamasco, B; Bergui, M; Bertola, A; Boccadoro, M; Ciaramitaro, P; Cocito, D; Durelli, L; Isoardo, G; Palumbo, A, 2004
)
3.21
"Thalidomide is an anti-angiogenic and immunomodulatory drug with a wide spectrum of activities, which are not clearly understood."( Thalidomide for the treatment of idiopathic myelofibrosis.
Gattermann, N; Germing, U; Haas, R; Kündgen, A; Mödder, U; Scherer, A; Strupp, C, 2004
)
2.49
"Thalidomide appears to be a safe drug in the post-transplant setting, perhaps adding to the response achieved post-transplant without major toxicity. "( Thalidomide effects in the post-transplantation setting in patients with multiple myeloma.
Byrnes, JJ; Fernandez, HF; Goodman, M; Santos, ES, 2004
)
3.21
"Thalidomide is an oral agent with significant activity in one-third of patients with refractory myeloma. "( Pulsed cyclophosphamide, thalidomide and dexamethasone: an oral regimen for previously treated patients with multiple myeloma.
Anagnostopoulos, A; Anagnostopoulos, N; Dimopoulos, MA; Efstathiou, E; Gika, D; Grigoraki, V; Hamilos, G; Poziopoulos, C; Xilouri, I; Zomas, A; Zorzou, MP, 2004
)
2.07
"Thalidomide is a selective inhibitor of tumor necrosis factor-alpha (TNF-alpha), a cytokine involved in mycobacterial death mechanisms. "( Experimental murine mycobacteriosis: evaluation of the functional activity of alveolar macrophages in thalidomide- treated mice.
Arruda, MS; Oliveira, SM; Richini, VB; Vilani-Moreno, FR, 2004
)
1.98
"Thalidomide is a racemic glutamic acid derivative approved in the US for erythema nodosum leprosum, a complication of leprosy. "( Clinical pharmacokinetics of thalidomide.
Colburn, WA; Jaworsky, MS; Kook, KA; Laskin, OL; Scheffler, MA; Stirling, DI; Teo, SK; Thomas, SD; Tracewell, WG, 2004
)
2.06
"Thalidomide is an anti-angiogenic drug that has shown promise in multiple hematological diseases, and myeloma and other cancers."( The effect of thalidomide on non-small cell lung cancer (NSCLC) cell lines: possible involvement in the PPARgamma pathway.
Andreola, F; De Luca, LM; DeCicco, KL; Tanaka, T, 2004
)
1.41
"Thalidomide is an antiangiogenic drug that produces a response rate ranging from 32 to 64% in patients with refractory/relapsed multiple myeloma (MM). "( Extramedullary multiple myeloma escapes the effect of thalidomide.
Aymerich, M; Bladé, J; Cibeira, MT; Cid, MC; Esteve, J; Filella, X; Montserrat, E; Rosiñol, L; Rozman, M; Segarra, M, 2004
)
2.01
"Thalidomide is an anti-inflammatory and immunomodulatory agent with proven efficacy in several refractory inflammatory skin conditions including photoexacerbated skin diseases. "( Photoprotection by thalidomide in patients with chronic cutaneous and systemic lupus erythematosus: discordant effects on minimal erythema dose and sunburn cell formation.
Cummins, DL; Gaspari, AA, 2004
)
2.09
"Thalidomide is an immunodulatory and antiangiogenic drug; the most pronounced effect of this drug is the inhibition of tumor necrosis factor-alpha (TNF-alpha ) production."( [Anti-cytokine therapy: present status and future perspectives in nephrology].
Panichi, V; Paoletti, S,
)
0.85
"Thalidomide is an effective agent for patients with refractory multiple myeloma (MM) with a response rate of 30-40% at doses of 200-800 mg but with considerable side effects. "( Combined thalidomide and cyclophosphamide treatment for refractory or relapsed multiple myeloma patients: a prospective phase II study.
Daenen, SM; de Wolf, JT; Hovenga, S; Kluin-Nelemans, HC; Sluiter, WJ; van Imhoff, GW; Vellenga, E, 2005
)
2.19
"Thalidomide is an effective drug for the treatment of erythema nodosum leprosum (ENL). "( Effects of thalidomide on intracellular Mycobacterium leprae in normal and activated macrophages.
Shannon, EJ; Tadesse, A, 2005
)
2.16
"Thalidomide is an immunomodulatory drug with numerous properties that has proven effective in relapsed multiple myeloma and, to a lesser extent, in other hematologic diseases."( Single-agent thalidomide induces response in T-cell lymphoma.
Bilger, K; Bouabdallah, R; Damaj, G; Gastaut, JA; Mohty, M; Vey, N, 2005
)
1.42
"Thalidomide is an immunomodulator agent of inflammatory cytokines including TNF-alpha."( A case of disseminated Langerhans' cell histiocytosis treated with thalidomide.
Castoldi, G; Fraulini, C; Galeotti, R; Mauro, E; Rigolin, GM; Spanedda, R, 2005
)
1.29
"Thalidomide, which is an inhibitor of TNF-alpha synthesis, may represent a novel and rational approach to the treatment of cancer cachexia."( Thalidomide in the treatment of cancer cachexia: a randomised placebo controlled trial.
Duncan, HD; Ellis, RD; Goggin, PM; Gordon, JN; Johns, T; Trebble, TM, 2005
)
2.49
"Thalidomide is a rediscovered old drug with anti-angiogenic, immunomodulatory and anti-inflammatory properties."( Successful management of cryoglobulinemia-induced leukocytoclastic vasculitis with thalidomide in a patient with multiple myeloma.
Cem Ar, M; Hatemi, G; Salihoglu, A; Soysal, T; Ulku, B; Yazici, H, 2005
)
1.27
"Thalidomide is an inhibitor of tumour necrosis factor-alpha (TNFalpha) that has been proven effective for the treatment of experimental sepsis by Escherichia coli. "( Immunomodulatory intervention in sepsis by multidrug-resistant Pseudomonas aeruginosa with thalidomide: an experimental study.
Bolanos, N; Giamarellos-Bourboulis, EJ; Giamarellou, H; Karayannacos, PE; Koussoulas, V; Laoutaris, G; Papadakis, V; Perrea, D, 2005
)
1.99
"Thalidomide is an antiangiogenic drug and is clinically useful in a number of cancers. "( Thalidomide inhibits growth of tumors through COX-2 degradation independent of antiangiogenesis.
Du, GJ; Lin, HH; Wang, MW; Xu, QT, 2005
)
3.21
"Thalidomide is a first-generation immuno-modulating agent that down-regulates TNF-alpha and VEGF."( Results of a phase 1 clinical trial of thalidomide in combination with fludarabine as initial therapy for patients with treatment-requiring chronic lymphocytic leukemia (CLL).
Berger, C; Bernstein, ZP; Chanan-Khan, A; Czuczman, MS; Donohue, K; Klippenstein, D; Koryzna, A; Miller, KC; Mohr, A; Takeshita, K; Wallace, P; Zeldis, JB, 2005
)
1.32
"Thalidomide is an immunomodulatory drug with strong antimyeloma activity. "( Oral melphalan, prednisone, and thalidomide for newly diagnosed patients with myeloma.
Bertola, A; Boccadoro, M; Callea, V; Cangialosi, C; Caravita, T; Falco, P; Grasso, M; Musto, P; Nunzi, M; Palumbo, A, 2005
)
2.05
"Thalidomide is an interesting maintenance therapy."( The future role of thalidomide in multiple myeloma.
Attal, M; Blade, J; Boccadoro, M; Palumbo, A, 2005
)
1.38
"Thalidomide is a racemate with potentially different pharmacokinetics and pharmacodynamics of the component (+)-(R)- and (-)-(S)-thalidomide enantiomers. "( Thalidomide enantiomers: determination in biological samples by HPLC and vancomycin-CSP.
Boyle, F; Gu, XQ; Mather, LE; Murphy-Poulton, SF, 2006
)
3.22
"Thalidomide is an effective therapy for some LR patients with LCH, but showed no significant responses in HR patients. "( A phase II trial using thalidomide for Langerhans cell histiocytosis.
Kozinetz, CA; McClain, KL, 2007
)
2.09
"Thalidomide is a putative antiangiogenesis agent with activity in several hematologic malignancies."( Thalidomide therapy for myelofibrosis with myeloid metaplasia.
Albitar, M; Cortes, JE; Faderl, S; Garcia-Manero, G; Giles, FJ; Kantarjian, HM; Keating, MJ; O'Brien, SM; Pierce, S; Thomas, DA; Verstovsek, S; Zeldis, J, 2006
)
3.22
"Thalidomide is an immunomodulatory agent, which arrests angiogenesis. "( Thalidomide attenuates nitric oxide mediated angiogenesis by blocking migration of endothelial cells.
Chatterjee, S; Indhumathy, M; Kolluru, GK; Rajaram, M; Saranya, R; Tamilarasan, KP, 2006
)
3.22
"Thalidomide treatment is an adequate therapeutic measure in adult Langerhans cell histiocytosis, which is rare and difficult to treat. "( [Thalidomide in adult multisystem Langerhans cell histiocytosis: a case report].
Alioua, Z; Frikh, R; Ghfir, M; Hjira, N; Oumakhir, S; Rimani, M; Sedrati, O, 2006
)
2.69
"Thalidomide is a relatively safe and efficacious form of therapy in the treatment of advanced, refractory multiple myeloma. "( Thalidomide-induced severe hepatotoxicity.
Hanje, AJ; Meis, GM; Shamp, JL; Thomas, FB, 2006
)
3.22
"Thalidomide is an anti-angiogenesis agent that has shown activity in some solid tumors. "( Safety and efficacy of thalidomide in recurrent epithelial ovarian and peritoneal carcinoma.
Chan, JK; Cheung, MK; Ciaravino, G; Husain, A; Manuel, MR; Teng, NN, 2006
)
2.09
"Thalidomide is a drug with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that were found to inhibit the production of TNF-alpha in vitro, stimulate reactive oxygen species production, and inhibit VEGFR in acute leukemias. "( Ex vivo activity of thalidomide in childhood acute leukemia.
Czyzewski, K; Styczynski, J; Wysocki, M, 2006
)
2.1
"Thalidomide is an effective maintenance therapy in patients with multiple myeloma."( Maintenance therapy with thalidomide improves survival in patients with multiple myeloma.
Attal, M; Avet-Loiseau, H; Benboubker, L; Berthou, C; Bourhis, JH; Caillot, D; Doyen, C; Dumontet, C; Facon, T; Garderet, L; Grobois, B; Harousseau, JL; Hulin, C; Leyvraz, S; Marit, G; Monconduit, M; Moreau, P; Pegourie, B; Renaud, M; Voillat, L; Yakoub Agha, I, 2006
)
1.36
"Thalidomide is an anti-angiogenic agent currently used to treat patients with malignant cachexia or multiple myeloma. "( Toxicity profile of the immunomodulatory thalidomide analogue, lenalidomide: phase I clinical trial of three dosing schedules in patients with solid malignancies.
Daines, CA; Dalgleish, AG; Knight, RD; O'Byrne, KJ; Sharma, RA; Steward, WP, 2006
)
2.04
"Thalidomide is an effective treatment for ENL but not RR."( Effect of thalidomide on the expression of TNF-alpha m-RNA and synthesis of TNF-alpha in cells from leprosy patients with reversal reaction.
Abebe, M; Aseffa, A; Bizuneh, E; Mulugeta, W; Shannon, EJ; Tadesse, A, 2006
)
1.46
"Thalidomide is an immunomodulatory, anti-inflammatory and anti-angiogenic drug. "( [Thalidomide in treatment of connective diseases and vasculities].
Cantatore, FP; Maruotti, N; Ribatti, D,
)
2.48
"Thalidomide is a derivative of glutamic acid with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that was found to inhibit the production of tumor necrosis factor alpha in vitro, stimulate reactive oxygen species production, and inhibit vascular endothelial growth factor receptor in acute leukemias. "( Thalidomide increases in vitro sensitivity of childhood acute lymphoblastic leukemia cells to prednisolone and cytarabine.
Czyzewski, K; Styczyński, J; Zaborowska, A,
)
3.02
"Thalidomide was intended to be a sup-pressor of capillary proliferation, and STI571, which is known to be a tyrosine kinase receptor inhibitor, was used for preventing mesangial proliferation."( Postinflammatory glomerular recanalization is established under the accommodation of transformed mesangial cells.
Aoyagi, D; Chowdury, R; Otani, M; Shigematsu, H; Zhang, L,
)
0.85
"Thalidomide is a potent inhibitor of angiogenesis in experimental models."( Macroscopic appearance of intestinal angiodysplasias under antiangiogenic treatment with thalidomide.
Bauditz, J; Lochs, H; Voderholzer, W, 2006
)
1.28
"Thalidomide is a potent anti-myeloma drug which can produce up to a 30-50% overall response rate (ORR) in pre-treated, chemorefractory multiple myeloma. "( Thalidomide plus monthly high-dose dexamethasone in chemorefractory myeloma. Results of a phase II clinical study.
Bernardeschi, P; Dentico, P; Fiorentini, G; Giustarini, G; Montenora, I; Rossi, S; Turano, E; Turrisi, G,
)
3.02
"Thalidomide is a racemate with known pharmacologic and pharmacokinetic enantioselectivity."( Enantioselectivity of thalidomide serum and tissue concentrations in a rat glioma model and effects of combination treatment with cisplatin and BCNU.
Boyle, FM; Davey, RA; Gu, XQ; Mather, LE; Murphy, S, 2007
)
1.38
"Thalidomide is an effective short- to medium-term treatment in selected patients with refractory luminal and fistulizing Crohn's disease. "( Thalidomide in luminal and fistulizing Crohn's disease resistant to standard therapies.
Kamm, MA; Ng, SC; Plamondon, S, 2007
)
3.23
"Thalidomide is a beneficial agent for treating a variety of refractory dermatologic disorders including erythema nodosom leprosum, lupus erythematosus, prurigo nodularis, actinic prurigo, pyoderma gangrenosum and aphthous stomatitis. "( Thalidomide and its dermatologic uses.
Paghdal, KV; Schwartz, R, 2007
)
3.23
"Thalidomide is an antiangiogenic agent with activity in refractory multiple myeloma."( Multi-centre phase II trial of Thalidomide in the treatment of unresectable hepatocellular carcinoma.
Boyer, M; Chuah, B; Clarke, S; Goh, BC; Kong, HL; Lim, R; Millward, M; Ong, AB; Wong, SW, 2007
)
1.35
"Thalidomide is an anti-inflammatory agent that potentiates the anti-tumour activity of DMXAA but decreases induction of TNF in plasma."( Consequences of increased vascular permeability induced by treatment of mice with 5,6-dimethylxanthenone-4-acetic acid (DMXAA) and thalidomide.
Baguley, BC; Ching, LM; Chung, F; Liu, J, 2008
)
1.27
"Thalidomide is an antiangiogenic drug used in cancer therapy."( Arterial thrombosis and thalidomide.
Cakir, O; Eren, MN; Goz, M, 2008
)
1.37
"Thalidomide is a potent anticancer therapeutic drug whose mechanism of action has not yet been elucidated. "( Characterization of thalidomide using Raman spectroscopy.
Cipriani, P; Smith, CY, 2008
)
2.11
"Thalidomide is an immunomodulatory, antiangiogenic drug. "( Combination of thalidomide and cisplatin in an head and neck squamous cell carcinomas model results in an enhanced antiangiogenic activity in vitro and in vivo.
Beckhove, P; Dyckhoff, G; Helmke, BM; Herold-Mende, CC; Kashfi, F; Lemke, B; Lohr, J; Plinkert, PK; Schirrmacher, V; Vasvari, GP, 2007
)
2.14
"Thalidomide is a promising agent that may exert a therapeutic benefit in HS."( Thalidomide for the treatment of histiocytic sarcoma after hematopoietic stem cell transplant.
Abidi, MH; Ibrahim, RB; Maria, D; Peres, E; Tove, I, 2007
)
2.5
"Thalidomide+IFN is a safe and tolerable palliative treatment for previously treated stage IV melanoma."( A pilot study of low-dose thalidomide and interferon alpha-2b in patients with metastatic melanoma who failed prior treatment.
Berd, D; Mastrangelo, MJ; Sato, T; Solti, M, 2007
)
1.36
"Thalidomide is an immunomodulating agent which reverses many of the cytokine disturbances seen in systemic onset juvenile idiopathic arthritis (SoJIA) with inadequate response to other treatments. "( Efficacy of thalidomide in systemic onset juvenile rheumatoid arthritis.
Escárcega, RO; Escobar, LE; Fuentes-Alexandro, S; García-Carrasco, M; Rojas-Rodriguez, J, 2007
)
2.16
"Thalidomide is an immunomodulatory agent that acts to inhibit production of tumor-necrosis factor-alpha (TNF-alpha), an important mediator in CNS inflammation, by enhancing TNF-alpha mRNA degradation. "( Thalidomide for acute treatment of neurosarcoidosis.
Hammond, ER; Kaplin, AI; Kerr, DA, 2007
)
3.23
"Thalidomide is an immunomodulatory drug used in the treatment of relapsed or refractory multiple myeloma (MM). "( Monotherapy with low-dose thalidomide for relapsed or refractory multiple myeloma: better response rate with earlier treatment.
Bláha, V; Büchler, T; Hájek, R; Maisnar, V; Malý, J; Radocha, J, 2007
)
2.08
"Thalidomide is shown to be an effective treatment for mucocutaneous symptoms of Behcet's disease (BD). "( Thalidomide has both anti-inflammatory and regulatory effects in Behcet's disease.
Direskeneli, H; Eksioglu-Demiralp, E; Ergun, T; Hamuryudan, V; Yavuz, S, 2008
)
3.23
"Thalidomide is an antiangiogenic agent with immune modulating potential. "( A prospective randomized trial of thalidomide with topotecan compared with topotecan alone in women with recurrent epithelial ovarian carcinoma.
Abu-Ghazaleh, SZ; Argenta, PA; Bliss, RL; Boente, MP; Carson, LF; Chen, MD; Downs, LS; Geller, MA; Ghebre, R; Judson, PL; Nahhas, WA, 2008
)
2.07
"Thalidomide is an anti-neoplastic agent with anti-angiogenic and other mechanisms of action."( Efficacy and tolerability of low-dose thalidomide as first-line systemic treatment of patients with advanced hepatocellular carcinoma.
Chan, P; Cheung, TT; Chok, SH; Epstein, RJ; Fan, ST; Lam, V; Ng, KK; Poon, RT; Wong, H; Yau, T, 2007
)
1.33
"Thalidomide is an oral immunomodulatory agent with antiangiogenic properties and activity in ovarian cancer. "( Thalidomide-induced reversible interstitial pneumonitis in a patient with recurrent ovarian cancer.
Buttin, BM; Moore, MJ, 2008
)
3.23
"Thalidomide is an immunomodulatory agent with demonstrated activity in multiple myeloma, mantle cell lymphoma and lymphoplasmacytic lymphoma. "( Thalidomide has limited single-agent activity in relapsed or refractory indolent non-Hodgkin lymphomas: a phase II trial of the Cancer and Leukemia Group B.
Bartlett, NL; Cheson, BD; Grinblatt, D; Johnson, JL; Niedzwiecki, D; Rizzieri, D; Smith, SM, 2008
)
3.23
"Thalidomide seems to be an active drug in advanced SM."( Thalidomide in advanced mastocytosis.
Bernit, E; Canioni, D; Claisse, JF; Damaj, G; Ghez, D; Harlé, JR; Hermine, O; Schleinitz, N, 2008
)
2.51
"Thalidomide is a well-known anti-angiogenic drug."( The effect of thalidomide on neovascularization in a mouse model of retinopathy of prematurity.
Katz, G; Pri-Chen, S; Rabinowitz, R; Rosner, M; Spierer, A, 2008
)
1.43
"Thalidomide is a teratogenic/hypnotic/sedative agent which elicits a wide range of pharmaceutical/biological activities. "( Thalidomide as a multi-template for development of biologically active compounds.
Hashimoto, Y, 2008
)
3.23
"Thalidomide is an effective treatment for severe OGU."( Thalidomide in severe orogenital ulceration.
Allen, BR; Jenkins, JS; Littlewood, SM; Maurice, PD; Powell, RJ; Smith, NJ, 1984
)
2.43
"Thalidomide is a very effective drug in CDLE, but in most cases it exerts its effect only whilst treatment is continued."( Thalidomide in the treatment of sixty cases of chronic discoid lupus erythematosus.
Bonsmann, G; Happle, R; Knop, J; Ludolph, A; Macher, E; Matz, DR; Mifsud, EJ, 1983
)
2.43
"Thalidomide is an effective drug in the treatment of actinic prurigo but it must be used with adequate contraception in women of child-bearing age."( Thalidomide in actinic prurigo.
Calnan, CD; Hawk, JL; Lovell, CR; Magnus, IA, 1983
)
2.43
"Thalidomide is a potent teratogen causing dysmelia (stunted limb growth) in humans. "( Thalidomide is an inhibitor of angiogenesis.
D'Amato, RJ; Flynn, E; Folkman, J; Loughnan, MS, 1994
)
3.17
"Thalidomide is a safe and effective drug for the treatment of chronic GVHD in children and may avoid the use of long-term corticosteroid therapy."( Thalidomide in the management of chronic graft-versus-host disease in children following bone marrow transplantation.
Chan, KW; Cole, CH; Phillips, G; Pritchard, S; Rogers, PC, 1994
)
2.45
"Thalidomide is an effective immunomodulatory drug in man, but its mechanism of action remains unclear. "( The immunosuppressive drug thalidomide induces T helper cell type 2 (Th2) and concomitantly inhibits Th1 cytokine production in mitogen- and antigen-stimulated human peripheral blood mononuclear cell cultures.
Deighton, J; Ewan, PW; Lachmann, PJ; Lockwood, CM; McHugh, SM; Rifkin, IR; Wilson, AB, 1995
)
2.03
"Thalidomide is a teratogenic sedative-hypnotic drug that is structurally similar to phenytoin, which is thought to be bioactivated by prostaglandin H synthase (PHS) and other peroxidases to a teratogenic reactive intermediate. "( Inhibition of thalidomide teratogenicity by acetylsalicylic acid: evidence for prostaglandin H synthase-catalyzed bioactivation of thalidomide to a teratogenic reactive intermediate.
Arlen, RR; Wells, PG, 1996
)
2.1
"Thalidomide is a drug that is being used in several diseases with an immunological component, but the effects on the different immune functions have only been studied partially. "( Thalidomide and its metabolites have no effect on human lymphocyte proliferation.
Estrada-García, L; Estrada-Parra, S; Favila-Castillo, L; Labarrios, F; Oltra, A; Santos-Mendoza, T; Tamaríz, J, 1996
)
3.18
"Thalidomide is an immunomodulating agent shown to prolong graft survival in experimental skin, renal, cardiac and bone marrow transplantation. "( Moderate additive immunosuppressive effect of thalidomide combined with cyclosporin A in rat cardiac transplantation.
Ekberg, H; Gannedahl, G; Ostraat, O; Qi, Z; Tufveson, G, 1996
)
2
"Thalidomide is a sedative hypnotic that was widely used in the 1950s but was withdrawn due to its teratogenic properties. "( Thalidomide, a hypnotic with immune modulating properties, increases cataplexy in canine narcolepsy.
Dement, WC; Hishikawa, Y; Kanbayashi, T; Mignot, E; Nishino, S; Tafti, M, 1996
)
3.18
"Thalidomide is a useful addition to the therapeutic armamentarium for treatment-resistant dermatoses as long as proper vigilance for adverse effects is maintained."( Rediscovering thalidomide: a review of its mechanism of action, side effects, and potential uses.
Pak, G; Pomeranz, MK; Shupack, JL; Tseng, S; Washenik, K, 1996
)
1.38
"Thalidomide appears to be an effective and well-tolerated alternative to prednisone for the treatment of IEU."( A prospective trial of thalidomide for the treatment of HIV-associated idiopathic esophageal ulcers.
Alexander, LN; Wilcox, CM, 1997
)
1.33
"Thalidomide is a specific inhibitor of TNF-alpha production, and this effect has been shown to be useful for the treatment of various immunodiseases."( [Novel biological response modifiers: phthalimides with TNF-alpha production regulating activity].
Azuma, A; Hashimoto, Y; Miyachi, H, 1997
)
1.02
"Thalidomide is an effective treatment for aphthous ulceration of the mouth and oropharynx in patients with HIV infection."( Thalidomide for the treatment of oral aphthous ulcers in patients with human immunodeficiency virus infection. National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group.
Chernoff, M; Fahey, JL; Fox, L; Greenspan, JS; Jackson, JB; Jacobson, JM; Ketter, N; MacPhail, LA; Spritzler, J; Vasquez, GJ; Wohl, DA; Wu, AW, 1997
)
3.18
"Thalidomide is a potent inhibitor of TNF-alpha action."( Randomised comparison of thalidomide versus placebo in toxic epidermal necrolysis.
Bocquet, H; Boudeau, S; Brun-Buisson, C; Duguet, C; Latarjet, J; Maignan, M; Milpied, B; Pilorget, A; Revuz, J; Roujeau, JC; Schuhmacher, MH; Vaillant, L; Wolkenstein, P, 1998
)
1.32
"Thalidomide is a good alternative therapy to SLE patients with refractory cutaneous lesions and without any risk of pregnancy."( Long-term thalidomide use in refractory cutaneous lesions of systemic lupus erythematosus.
Andrade, LE; Assis, LS; Lourenzi, VP; Sato, EI,
)
1.98
"Thalidomide, (1), is a known inhibitor of TNF-alpha release in LPS stimulated human PBMC. "( Amino-substituted thalidomide analogs: potent inhibitors of TNF-alpha production.
Chen, R; Chen, Y; Corral, LG; Huang, SY; Kaplan, G; Muller, GW; Patterson, RT; Stirling, DI; Wong, LM, 1999
)
2.08
"Thalidomide is a teratogen with anti-angiogenic properties and causes stunted limb growth (dysmelia) during human embryogenesis. "( Thalidomide inhibits angiogenesis in embryoid bodies by the generation of hydroxyl radicals.
Günther, J; Hescheler, J; Sauer, H; Wartenberg, M, 2000
)
3.19
"Thalidomide is a generally well-tolerated drug that may have antitumor activity in a minority of patients with recurrent high-grade gliomas. "( Phase II trial of the antiangiogenic agent thalidomide in patients with recurrent high-grade gliomas.
Black, PM; Figg, WD; Fine, HA; Jaeckle, K; Kaplan, R; Kyritsis, AP; Levin, VA; Loeffler, JS; Pluda, JM; Wen, PY; Yung, WK, 2000
)
2.01
"Thalidomide is a potent anti-inflammatory drug in patients with SLE and cutaneous LE, possibly interacting with the recruitment of lymphocytes. "( Clinical and immunologic parameters during thalidomide treatment of lupus erythematosus.
Messer, G; Meurer, M; Plewig, G; Walchner, M, 2000
)
2.01
"Thalidomide is an active agent in the treatment of patients with advanced myeloma."( Thalidomide in the treatment of relapsed multiple myeloma.
Dispenzieri, A; Fonseca, R; Gertz, MA; Greipp, PR; Kyle, RA; Lacy, MQ; Lust, JA; Rajkumar, SV; Witzig, TE, 2000
)
3.19
"The thalidomide product is a racemic mixture of the L- and D-enantiomeric forms of a synthetic glutamic acid derivative that contains a phthalimide ring and a glutarimide ring. "( Thalidomide: a remarkable comeback.
Jacobson, JM, 2000
)
2.31
"Thalidomide is a potentially useful drug for several dermatological disorders."( Thalidomide usage in Wales: the need to follow guidelines.
Chave, TA; Finlay, AY; Knight, AG, 2001
)
3.2
"Thalidomide seems to be an effective and safe treatment in patients with refractory Crohn disease. "( Efficacy of long-term treatment with thalidomide in children and young adults with Crohn disease: preliminary results.
Candusso, M; Facchini, S; Liubich, M; Martelossi, S; Panfili, E; Ventura, A, 2001
)
2.03
"Thalidomide is an experimental drug currently used for oral aphthous ulcers and wasting syndrome, and is the same drug associated with severe fetal abnormalities in the 1960s."( Thalidomide shows benefit for microsporidial diarrhea.
Bartnof, HS, 1997
)
2.46
"Thalidomide is a drug associated with devastating side effects. "( Thalidomide's long and winding road.
Hanna, L, 1998
)
3.19
"Thalidomide is a potent teratogen that causes dysmelia in humans. "( A randomized phase II trial of thalidomide, an angiogenesis inhibitor, in patients with androgen-independent prostate cancer.
Chen, CC; Dahut, W; Dixon, S; Duray, P; Figg, WD; Floeter, MK; Gubish, E; Hamilton, M; Jones, E; Kohler, DR; Krüger, EA; Linehan, WM; Pluda, JM; Premkumar, A; Reed, E; Steinberg, SM; Tompkins, A, 2001
)
2.04
"Thalidomide is an immunomodulator, anti-angiogenic agent, anti-cytokine, and anti-integrin. "( Thalidomide: dual benefits in palliative medicine and oncology.
Davis, MP; Dickerson, ED,
)
3.02
"Thalidomide is an infamous molecule for its teratogenicity, yet it possesses potent immunomodulatory, anti-angiogeneic and, in higher concentrations, direct anti-myeloma-cell properties."( [Role of thalidomide in the treatment of multiple myeloma].
Jákó, J; Mikala, G; Vályi-Nagy, I, 2001
)
1.45
"Thalidomide is a synthetic derivative of glutamic acid with sedative-hypnotic activity, which caused devastating teratogenic effects in the 1960s. "( Thalidomide: an old sedative-hypnotic with anticancer activity?
Alberti, AM; Capaccetti, B; Gasparini, G; Gattuso, D; Magnani, E; Morabito, A, 2001
)
3.2
"Thalidomide (Thal) is a drug with anti-angiogenic properties. "( Response to thalidomide in progressive multiple myeloma is not mediated by inhibition of angiogenic cytokine secretion.
Benner, A; Egerer, G; Goldschmidt, H; Ho, AD; Kraemer, A; Moehler, T; Neben, K, 2001
)
2.13
"Thalidomide is an immunomodulatory agent that is approved for use in patients with cutaneous manifestations of erythema nodosum leprosum (ENL). "( Thalidomide: a novel template for anticancer drugs.
Stirling, D, 2001
)
3.2
"Thalidomide is a well-tolerated drug that may have some activity in the treatment of recurrent glioblastoma."( Phase II study of thalidomide in the treatment of recurrent glioblastoma multiforme.
Bell, DR; Biggs, M; Boyle, FM; Cook, R; Levi, JA; Little, N; Marx, GM; McCowatt, S; Pavlakis, N; Wheeler, HR, 2001
)
1.37
"Thalidomide is an anti-angiogenesis agent that currently is being evaluated in the treatment of various types of cancer. "( Thalidomide: when everything old is new again.
Nirenberg, A,
)
3.02
"Thalidomide is an effective treatment for relapsed multiple myeloma (MM), but is associated with a significant side effect profile at higher doses. "( Thalidomide in low doses is effective for the treatment of resistant or relapsed multiple myeloma and for plasma cell leukaemia.
Abdalla, SH; Johnston, RE, 2002
)
3.2
"Thalidomide appears to be an effective and relatively safe drug to maintain response to infliximab in chronically active and fistulizing refractory Crohn's disease."( An open-label study of thalidomide for maintenance therapy in responders to infliximab in chronically active and fistulizing refractory Crohn's disease.
Allez, M; Bonnet, J; Lemann, M; Modigliani, R; Sabate, JM; Villarejo, J, 2002
)
2.07
"Thalidomide thus appears to be a very effective drug in the treatment of severe type-2 lepra reaction and apart from its historically well-documented embryopathic effects, does not seem to have any other serious side effects in the patients under study."( Thalidomide in type-2 lepra reaction--a clinical experience.
Jadhav, VH; Mehta, JM; Patki, AH,
)
2.3
"Thalidomide appears to be an effective agent for the treatment of severe RAS unresponsive to traditional therapies."( Thalidomide: treatment of severe recurrent aphthous stomatitis in patients with AIDS.
Nicolau, DP; West, TE, 1990
)
2.44

Effects

Thalidomide was introduced as a sedative drug in the late 1950s. It has a number of approved and off-label uses in dermatologic, oncologic, infectious and gastrointestinal conditions. Thalidomid has a different toxicity profile than corticosteroids or immunosuppressives.

Thalidomide has been shown to antagonize basic fibroblast growth factor-induced angiogenesis in the rat corneal micropocket assay. The drug is very effective in alleviating erythema nodosum leprosum in leprosy patients and aphthous ulcers in AIDS patients. Thalidomides has been found to cause increases in body weight in patients with HIV and tuberculosis infections.

ExcerptReferenceRelevance
"Thalidomide has a protective effect on ALI induced by PQ poisoning in rats in a dose-dependent manner, the mechanism may be achieved by reducing the level of oxygen free radicals, reducing the inflammatory factor and inhibiting the IκB-α/NF-κB signal pathway activation."( [Protective effect of thalidomide on ALI induced by paraquat poisoning in rats and its mechanism].
Liu, T; Xie, Y; Xu, M; Zheng, F, 2017
)
2.21
"Thalidomide has a rapid action but its use is limited due the teratogenicity and neurotoxicity."( Erythema Nodosum Leprosum: Update and challenges on the treatment of a neglected condition.
Costa, PDSS; Daxbacher, ELR; Fraga, LR; Kowalski, TW; Schuler-Faccini, L; Vianna, FSL, 2018
)
1.2
"Thalidomide (THD) has a therapeutic effect on fibrotic and inflammatory disorders."( Thalidomide (THD) alleviates radiation induced lung fibrosis (RILF) via down-regulation of TGF-β/Smad3 signaling pathway in an Nrf2-dependent manner.
Bian, C; Chen, J; Qin, WJ; Wang, YY; Zhang, CY; Zhao, R; Zhe, H; Zhu, YZ; Zou, GL, 2018
)
2.64
"Thalidomide has a strong potential to improve response and survival measures in patients with standard risk MM."( 10 years of experience with thalidomide in multiple myeloma patients: report of the Czech Myeloma Group.
Adam, Z; Adamova, D; Bacovsky, J; Gregora, E; Gumulec, J; Hajek, R; Jarkovsky, J; Maisnar, V; Melicharova, H; Minarik, J; Pavlicek, P; Pika, T; Plonkova, H; Pour, L; Radocha, J; Sandecka, V; Scudla, V; Spicka, I; Starostka, D; Straub, J; Walterova, L; Wrobel, M, 2013
)
1.41
"Thalidomide has a favorable safety profile compared with other alternatives and could be considered a feasible therapeutic option for this type of condition in selected patients."( Chronic Recurrent Multifocal Osteomyelitis and Thalidomide in Chronic Granulomatous Disease.
Barber, I; Fernández-Polo, A; Fontecha, CG; Martín-Nalda, A; Martinez-Gallo, M; Roca, I; Soler-Palacin, P, 2016
)
1.41
"Thalidomide has a broad spectrum of anti-cancer activity. "( Immunomodulatory properties of thalidomide analogs: pomalidomide and lenalidomide, experimental and therapeutic applications.
Bodera, P; Stankiewicz, W, 2011
)
2.1
"Thalidomide has a significant anti-inflammatory effect by inhibiting TNF-α, which plays role in Aβ neurotoxicity."( Thalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in rats.
Alan, S; Elçioğlu, H; Kabasakal, L; Karan, M; Salva, E; Tufan, F, 2013
)
2.55
"Thalidomide has a significant therapeutic effect in myelodysplastic syndrome (MDS) by improving cytopenia and achieving independence of transfusion therapy in a subset of patients."( Antiangiogenic therapy in hematologic malignancies.
Goldschmidt, H; Hillengass, J; Ho, AD; Moehler, TM, 2004
)
1.04
"Thalidomide has a variety of biological effects that vary considerably according to the species tested. "( Thalidomide pharmacokinetics and metabolite formation in mice, rabbits, and multiple myeloma patients.
Baguley, BC; Browett, P; Ching, LM; Chung, F; Kestell, P; Lu, J; Palmer, BD; Tingle, M, 2004
)
3.21
"Thalidomide has a different toxicity profile than corticosteroids or immunosuppressives."( Newer therapies for cutaneous sarcoidosis: the role of thalidomide and other agents.
Baughman, RP; Lower, EE, 2004
)
1.29
"Thalidomide has a potent immunomodulatory property and has now a number of approved and off-label uses in dermatologic, oncologic, infectious and gastrointestinal conditions."( New cases of thalidomide embryopathy in Brazil.
Castilla, EE; de Sousa, AC; Luna, E; Maximino, C; Schuler-Faccini, L; Schwartz, IV; Soares, RC; Waldman, C, 2007
)
1.43
"Thalidomide, which has a long history of tragedy because of its ability to cause severe birth defects, is very effective in alleviating erythema nodosum leprosum in leprosy patients and aphthous ulcers in AIDS patients. "( Immunomodulatory assays to study structure-activity relationships of thalidomide.
Morales, MJ; Sandoval, F; Shannon, EJ, 1997
)
1.97
"Thalidomide has a significant antiangiogenic effect against VEGF-induced neovasclar growth. "( Thalidomide inhibits corneal angiogenesis induced by vascular endothelial growth factor.
Becker, MD; Joussen, AM; Kruse, FE; Rohrschneider, K; Völcker, HE, 1998
)
3.19
"Thalidomide has a chiral centre, and the racemate of (R)- and (S)-thalidomide was introduced as a sedative drug in the late 1950s. "( Clinical pharmacology of thalidomide.
Björkman, S; Eriksson, T; Höglund, P, 2001
)
2.06
"Thalidomide has a role to play in the management of chronic GVHD and further studies are needed."( Thalidomide treatment for chronic graft-versus-host disease.
Bailey, CC; Barnard, DL; Heney, D; Lewis, IJ; Norfolk, DR; Wheeldon, J, 1991
)
2.45
"Thalidomide has a beneficial effect on type II Lepra reaction especially chronic and recurrent reaction. "( Thalidomide in leprosy--study of 94 cases.
Ganapati, R; Parikh, DA; Revankar, CR,
)
3.02
"Thalidomide has been shown to be an effective systemic drug in the treatment of RAS, but the value of undertaking a trial to evaluate various maintenance doses was warranted."( A Randomized controlled clinical trial on dose optimization of thalidomide in maintenance treatment for recurrent aphthous stomatitis.
Deng, Y; Du, G; Pan, L; Tang, G; Wang, Y; Wei, W; Yao, H, 2022
)
1.68
"Thalidomide (THD) has been found to synergize with cisplatin (DDP) in certain types of cancers; however, their combined use in the treatment of cervical cancer has not been reported to date, at least to the best of our knowledge. "( Synergistic effects of thalidomide and cisplatin are mediated via the PI3K/AKT and JAK1/STAT3 signaling pathways in cervical cancer.
Feng, H; Li, S; Liu, C; Song, L; Wu, Y; Yang, L, 2022
)
2.47
"Thalidomide (TAL) has shown potential therapeutic effects in neurological diseases like epilepsy. "( Thalidomide Attenuates Epileptogenesis and Seizures by Decreasing Brain Inflammation in Lithium Pilocarpine Rat Model.
Cumbres-Vargas, IM; Pichardo-Macías, LA; Ramírez-San Juan, E; Zamudio, SR, 2023
)
3.8
"Thalidomide has emerged as an effective immunomodulator in the treatment of pediatric patients with inflammatory bowel disease (IBD) refractory to standard therapies. "( Gene expression profiling in white blood cells reveals new insights into the molecular mechanisms of thalidomide in children with inflammatory bowel disease.
Bidoli, C; Bramuzzo, M; Brumatti, LV; Celsi, F; Curci, D; Decorti, G; Edomi, P; Gerdol, M; Lega, S; Licastro, D; Lionetti, P; Lucafò, M; Maestro, A; Nonnis, M; Paci, M; Pallavicini, A; Pugnetti, L; Renzo, S; Stocco, G, 2023
)
2.57
"Thalidomide (THD) has anti-inflammatory, immunomodulatory, antiangiogenic, and antitumor properties, which have led to its use in various autoimmune diseases, hematological malignancies, solid tumors, and other disorders."( A case report of thalidomide in the treatment of camrelizumab-induced reactive cutaneous capillary hyperplasia.
Fu, S; Li, C; Wang, Z; Zhong, Y; Zhong, Z, 2023
)
1.97
"Thalidomide has been evaluated for the treatment of recurrent bleeding due to small-intestinal angiodysplasia (SIA), but confirmatory trials are lacking."( Thalidomide for Recurrent Bleeding Due to Small-Intestinal Angiodysplasia.
Chen, H; Dai, Z; Du, Y; Gao, Y; Ge, Z; Gong, S; Li, X; Li, Z; Liu, S; Lu, H; Lu, L; Shen, X; Shen, Y; Tang, M; Wu, S; Xiong, H; Xu, L; Xue, H; Yang, A; Yang, S; Zhang, Q; Zhao, R; Zhong, J; Zhong, L, 2023
)
3.07
"Thalidomide (Thal) has been shown to increase the anti-tumor effect of chemotherapy agents in solid tumors."( Tumor vasculature remolding by thalidomide increases delivery and efficacy of cisplatin.
Li, S; Liu, P; Shen, Y; Tian, Q; Wang, B; Wang, J; Wang, M; Wang, X; Yang, J, 2019
)
1.52
"Thalidomide has shown exceptional results in systemic/cutaneous lupus erythematosus(SLE/CLE). "( Thalidomide and Lenalidomide for Refractory Systemic/Cutaneous Lupus Erythematosus Treatment: A Narrative Review of Literature for Clinical Practice.
Aikawa, NE; Bonfa, E; Heise, CO; Pasoto, SG; Romiti, R; Silva, CA; Yuki, EFN, 2021
)
3.51
"Thalidomide has been shown to reactivate fetal hemoglobin (HbF) production and reduce the need for blood transfusions in β-thalassemia patients. "( The association of HBG2, BCL11A, and HBS1L-MYB polymorphisms to thalidomide response in Chinese β-thalassemia patients.
Ma, Y; Wu, Y; Xiao, J; Yang, K; Yin, X; Zhou, Y, 2020
)
2.24
"Thalidomide has been used successfully in a variety of chronic refractory inflammatory dermatological conditions with underlying autoimmune or infectious pathogenesis. "( Efficacy of Thalidomide in Discoid Lupus Erythematosus: Insights into the Molecular Mechanisms.
Cortés-Hernández, J; Domingo, S; Ferrer, B; Moliné, T; Ordi-Ros, J; Solé, C, 2020
)
2.38
"Thalidomide has proven to be a steroid-sparing agent and is useful in controlling the reactions."( Thalidomide in the treatment of erythema nodosum leprosum (ENL) in an outpatient setting: A five-year retrospective analysis from a leprosy referral centre in India.
Pallapati, MS; Srikantam, A; Tarwater, P; Upputuri, B, 2020
)
2.72
"Thalidomide has been used to treat ankylosing spondylitis (AS) patients, but the efficacy and safety of thalidomide on psychological symptoms and sleep disturbances in the patient with refractory AS has not been evaluated."( Efficacy and safety of thalidomide on psychological symptoms and sleep disturbances in the patient with refractory ankylosing spondylitis.
Chen, Z; Gao, F; He, J; Lin, D; Lin, H; Liu, J; Wu, Y; Zhang, S, 2021
)
2.37
"Thalidomide has been reported being able to inhibit the effects of fibroblast growth factor 2 and vascular endothelial growth factor (VEGF), and inhibit tumour necrosis factor-alpha synthesis, and suppress tumour necrosis factor-induced nuclear factor-kappa B activation in Jurkat cells, resulting in suppression of proliferation inflammation, angiogenesis, and the immune system, which are related to the pathogenesis of psoriasis."( Thalidomide Improves Psoriasis-like Lesions and Inhibits Cutaneous VEGF Expression without Alteration of Microvessel Density in Imiquimod- induced Psoriatic Mouse Model.
Gao, Q; Liu, JH; Luo, DQ; Wang, F; Wu, HH; Zhao, YK, 2018
)
2.64
"Thalidomide has shown excellent results for severe cutaneous lupus erythematosus (CLE), but its prescription is limited by potentially severe adverse events."( Efficacy and tolerance profile of thalidomide in cutaneous lupus erythematosus: A systematic review and meta-analysis.
Arnaud, L; Barbaud, A; Cesbron, E; Chasset, F; Francès, C; Tounsi, T, 2018
)
2.2
"Thalidomide has a protective effect on ALI induced by PQ poisoning in rats in a dose-dependent manner, the mechanism may be achieved by reducing the level of oxygen free radicals, reducing the inflammatory factor and inhibiting the IκB-α/NF-κB signal pathway activation."( [Protective effect of thalidomide on ALI induced by paraquat poisoning in rats and its mechanism].
Liu, T; Xie, Y; Xu, M; Zheng, F, 2017
)
2.21
"Thalidomide has a rapid action but its use is limited due the teratogenicity and neurotoxicity."( Erythema Nodosum Leprosum: Update and challenges on the treatment of a neglected condition.
Costa, PDSS; Daxbacher, ELR; Fraga, LR; Kowalski, TW; Schuler-Faccini, L; Vianna, FSL, 2018
)
1.2
"Thalidomide has been trialled in CNS TB due to its immunomodulatory and immune reconstitution effects through the inhibition of tumour necrosis factor alpha."( Clinical perspectives into the use of thalidomide for central nervous system tuberculosis.
Adams, A; Bharambe, V; Gnanapavan, S; Jayakumar, A; Keddie, S; Sanchez, V; Shah, A, 2018
)
1.47
"Thalidomide has been used as a therapeutic strategy for refractory epistaxis in hereditary haemorrhagic telangiectasia patients."( The use of thalidomide therapy for refractory epistaxis in hereditary haemorrhagic telangiectasia: systematic review.
Harrison, L; Jervis, P; Kundra, A, 2018
)
1.59
"Thalidomide (THD) has a therapeutic effect on fibrotic and inflammatory disorders."( Thalidomide (THD) alleviates radiation induced lung fibrosis (RILF) via down-regulation of TGF-β/Smad3 signaling pathway in an Nrf2-dependent manner.
Bian, C; Chen, J; Qin, WJ; Wang, YY; Zhang, CY; Zhao, R; Zhe, H; Zhu, YZ; Zou, GL, 2018
)
2.64
"Thalidomide has been used as an effective treatment for prurigo nodularis (PN) with a median dose of 200 mg, but the risk of peripheral neuropathy precludes long-term use. "( An observational analysis of low-dose thalidomide in recalcitrant prurigo nodularis.
Gupta, A; Sardana, K; Sinha, S, 2020
)
2.27
"Thalidomide has shown its efficacy in the treatment of epistaxis in hereditary hemorrhagic telangiectasia (HHT) patients. "( Pulmonary arteriovenous malformations etiologies in HHT patients and potential utility of thalidomide.
El Hajjam, M; Lacombe, P; Lacout, A; Marcy, PY, 2013
)
2.05
"Thalidomide has shown antiangiogenic activity, and we hypothesised that its use in the maintenance setting could improve outcomes."( Thalidomide versus active supportive care for maintenance in patients with malignant mesothelioma after first-line chemotherapy (NVALT 5): an open-label, multicentre, randomised phase 3 study.
Baas, P; Buikhuisen, WA; Burgers, JA; Custers, FL; Gans, SJ; Groen, HJ; Korse, CM; Nowak, AK; Pavlakis, N; Schouwink, JH; Schramel, FM; Strankinga, WF; van Klaveren, RJ; Vincent, AD, 2013
)
2.55
"Thalidomide has indications for the treatment of several immune-related, neoplastic, and inflammatory diseases, in both adults and children. "( Thalidomide affects the skeletal system of young rats.
Kaczmarczyk-Sedlak, I; Rymkiewicz, I; Sedlak, L,
)
3.02
"Thalidomide has been used in inflammatory and autoimmune disorders due to its anti-inflammatory activity. "( Anti-inflammatory effect of thalidomide in paraquat-induced pulmonary injury in mice.
Amirshahrokhi, K, 2013
)
2.13
"New thalidomide analogues have been developed but lack clinical experience."( [Current therapeutic indications of thalidomide and lenalidomide].
Cosiglio, FJ; Ordi-Ros, J, 2014
)
1.16
"Thalidomide has a strong potential to improve response and survival measures in patients with standard risk MM."( 10 years of experience with thalidomide in multiple myeloma patients: report of the Czech Myeloma Group.
Adam, Z; Adamova, D; Bacovsky, J; Gregora, E; Gumulec, J; Hajek, R; Jarkovsky, J; Maisnar, V; Melicharova, H; Minarik, J; Pavlicek, P; Pika, T; Plonkova, H; Pour, L; Radocha, J; Sandecka, V; Scudla, V; Spicka, I; Starostka, D; Straub, J; Walterova, L; Wrobel, M, 2013
)
1.41
"Thalidomide has been the medication of choice for the control of ENL episodes since 1965."( Prevention of repeated episodes of type 2 reaction of leprosy with the use of thalidomide 100 mg/day.
Lastória, JC; Padovani, CR; Putinatti, MS,
)
1.08
"Thalidomide has been utilized in the treatment of refractory bleeding because of gastrointestinal vascular malformations."( Treatment of left ventricular assist device-associated arteriovenous malformations with thalidomide.
Banerjee, D; Ha, R; Kale, PP; Ray, R,
)
1.07
"Thalidomide has immunomodulatory and anti-tumor necrosis factor-α effects as well as antiangiogenic properties, making it useful for a broad spectrum of inflammatory disorders."( Review of thalidomide use in the pediatric population.
Antaya, RJ; Kim, C; Yang, CS, 2015
)
1.54
"Thalidomide (Thal) has been used to treat multiple myeloma due to its inhibitory effects on IL-6-induced cell growth."( Thalidomide prevents cigarette smoke extract-induced lung damage in mice.
Nakamura, K; Nakano, T; Tabata, C; Tabata, R; Takahashi, Y, 2015
)
2.58
"Thalidomide has shown protective effects in different models of ischemia/reperfusion damage. "( Anti-apoptotic, anti-oxidant, and anti-inflammatory effects of thalidomide on cerebral ischemia/reperfusion injury in rats.
Farfán, DJ; Medrano, JÁN; Ortiz-Plata, A; Palencia, G; Sánchez, A; Sotelo, J; Trejo-Solís, C, 2015
)
2.1
"Thalidomide has anti-inflammatory and anti-angiogenetic activity that makes it suitable for treating inflammatory bowel diseases (IBD). "( The clinical implications of thalidomide in inflammatory bowel diseases.
Bracci, F; Capriati, T; Corsetti, T; Diamanti, A; Elia, D; Knafelz, D; Papadatou, B; Torre, G, 2015
)
2.15
"Thalidomide has anti-inflammatory, immunomodulatory, and anti-angiogenic properties. "( Anti-inflammatory effect of thalidomide dithiocarbamate and dithioate analogs.
Agwa, HS; El-Sayed, W; Gamal-Eldeen, AM; Moawia, S; Talaat, R; Zahran, MA, 2015
)
2.15
"Thalidomide has demonstrated clinical activity in various malignancies affecting immunomodulatory and angiogenic pathways. "( Anticancer Properties of a Novel Class of Tetrafluorinated Thalidomide Analogues.
Ambrozak, A; Barnett, S; Beedie, SL; Chau, CH; Figg, WD; Gardner, ER; Gütschow, M; Mahony, C; Peer, CJ; Pisle, S; Vargesson, N, 2015
)
2.1
"Thalidomide has emerged as a promising medical strategy in angiodysplasia-related bleeding."( Thalidomide in angiodysplasia-related bleeding.
Boey, JP; Hahn, U; McRae, SJ; Sagheer, S, 2015
)
2.58
"Thalidomide has been reported to cause numerous thromboembolic events. "( Myocardial infarction, symptomatic third degree atrioventricular block and pulmonary embolism caused by thalidomide: a case report.
Jin, X; Yang, J; Zhang, S, 2015
)
2.07
"Thalidomide has been used to treat several inflammatory manifestations in CGD patients with good clinical results."( Chronic Recurrent Multifocal Osteomyelitis and Thalidomide in Chronic Granulomatous Disease.
Barber, I; Fernández-Polo, A; Fontecha, CG; Martín-Nalda, A; Martinez-Gallo, M; Roca, I; Soler-Palacin, P, 2016
)
1.41
"Thalidomide has been successful use in patients with refractory Crohn disease (CD) in recent years."( Thalidomide induces mucosal healing in postoperative Crohn disease endoscopic recurrence: Case report and literature review.
Hu, H; Liu, S; Wang, X, 2016
)
3.32
"Thalidomide has been reported for treatment of various malignancies."( Anticancer effect of thalidomide in vitro on human osteosarcoma cells.
Guo, Q; Liu, S; Liu, Y; Wang, Y; Wu, Y; Xu, H; Yang, Y; Zhang, G; Zhu, J, 2016
)
1.47
"Thalidomide has antiangiogenic and immunomodulatory effects."( A phase II study of thalidomide in patients with brain metastases from malignant melanoma.
Bastholt, L; Larsen, S; Lindeløv, B; Vestermark, LW, 2008
)
1.39
"Both thalidomide and atenolol have been reported to cause bradycardia."( Syncope and sinus bradycardia from combined use of thalidomide and beta-blocker.
Yamaguchi, T, 2008
)
1.05
"Thalidomide has been shown to down-regulate the production of TNF-alpha."( Two cases of bacterial meningitis accompanied by thalidomide therapy in patients with multiple myeloma: is thalidomide associated with bacterial meningitis?
Altintas, A; Ayyildiz, O; Bayan, K; Cil, T; Danis, R; Pasa, S; Tuzun, Y; Urakci, Z; Ustun, C, 2009
)
1.33
"Thalidomide has been reported to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) that are involved in the down-regulation of hepatic cytochrome P450 (CYP) induced by endotoxin. "( Effect of thalidomide on endotoxin-induced decreases in activity and expression of hepatic cytochrome P450 3A2.
Abe, F; Hasegawa, T; Kanazawa, H; Kondo, T; Miyamoto, K; Nadai, M; Saito, H; Takagi, K; Ueyama, J; Wakusawa, S; Zhao, YL, 2008
)
2.19
"Thalidomide has been shown to have anti-angiogenic effects in pre-clinical models as well as a significant antitumor effect in hematologic tumors. "( Effects of thalidomide on DMBA-induced oral carcinogenesis in hamster with respect to angiogenesis.
Ge, JP; Yang, Y; Zhou, ZT, 2009
)
2.19
"Thalidomide has inhibitory effect against the malignant transformation of oral pre-cancerous lesion and angiogenesis during oral carcinogenesis. "( Effects of thalidomide on DMBA-induced oral carcinogenesis in hamster with respect to angiogenesis.
Ge, JP; Yang, Y; Zhou, ZT, 2009
)
2.19
"Thalidomide has been shown to exert its antitumor activity through the significant effects on microenvironment and immunomodulatory properties. "( Thalidomide inhibits leukemia cell invasion and migration by upregulation of early growth response gene 1.
Li, J; Liu, P; Lu, H; Xu, B, 2009
)
3.24
"Thalidomide has been reported to be effective for these patients; however, high-dose thalidomide has induced many adverse events, including in the nervous, gastrointestinal, and hematopoietic systems in approximately 20%-50% of patients."( A pharmacokinetic study evaluating the relationship between treatment efficacy and incidence of adverse events with thalidomide plasma concentrations in patients with refractory multiple myeloma.
Abe, M; Iida, S; Kodama, T; Miyata, A; Murakami, H; Ozaki, S; Sakai, A; Sawamura, M; Shimazaki, C; Wakayama, T, 2009
)
1.28
"Thalidomide has emerged as an effective agent for treating multiple myeloma, however the precise mechanism of action remains unknown. "( Differential activities of thalidomide and isoprenoid biosynthetic pathway inhibitors in multiple myeloma cells.
Hohl, RJ; Holstein, SA; Tong, H, 2010
)
2.1
"Thalidomide has been described as inhibitor of the fibroblast growth factor (FGF) and the vascular endothelial growth factor (VEGF)."( Phase I trial of metastatic renal cell carcinoma with oral capecitabine and thalidomide.
Brossart, P; Gorschlüter, M; Hauser, S; Kim, Y; Kraemer, A; Müller, SC; Schmidt-Wolf, IG, 2009
)
1.3
"Thalidomide has been shown to be anti-angiogenic via reduction of VEGF levels."( Intravitreal thalidomide reduces experimental preretinal neovascularisation without induction of retinal toxicity.
Erber, R; Hammes, HP; Jonas, JB; Kamppeter, BA; Vom Hagen, F, 2010
)
1.45
"Thalidomide has been reported to clinically improve chronic inflammatory granulomatous disorders."( Thalidomide prevents formation of multinucleated giant cells (Langhans-type cells) from cultured monocytes: possible pharmaceutical applications for granulomatous disorders.
Kondo, Y; Manki, A; Morishima, T; Nagaoka, Y; Tsuge, M; Wada, T; Yashiro, M; Yasui, K,
)
2.3
"Thalidomide has recently been shown to have significant antimyeloma activity."( Initial cytoreductive treatment with thalidomide plus bolus vincristine/doxorubicin and reduced dexamethasone followed by autologous stem cell transplantation for multiple myeloma.
Jang, G; Jo, JC; Kang, BW; Kim, S; Kim, SW; Lee, DH; Lee, JS; Lee, SS; Suh, C; Sym, SJ, 2011
)
1.36
"Thalidomide has changed the treatment paradigm of patients with MM."( Immunomodulatory compounds (IMiDs) in the treatment of multiple myeloma.
Hussein, M; Srkalovic, G, 2009
)
1.07
"Thalidomide has been used in the treatment of refractory Crohn's disease (CD), but the therapeutic mechanism is not defined."( Thalidomide inhibits inflammatory and angiogenic activation of human intestinal microvascular endothelial cells (HIMEC).
Binion, DG; Nelson, VM; Otterson, MF; Rafiee, P; Shaker, R; Stein, DJ, 2010
)
2.52
"Thalidomide has anti-angiogenic effect and also can inhibit cytokines, and therefore plays a certain role in the treatment of a subset of idiopathic myelofibrosis."( [Advances in thalidomide therapy for idiopathic myelofibrosis].
Chen, JL; Song, L, 2009
)
1.44
"Thalidomide has alternative mechanisms of action; it can be combined with dexamethasone or alkylating agents for the treatment of multiple myeloma (MM); however, the optimal doses and appropriate intervals of thalidomide continue to be debated."( Induction treatment with cyclophosphamide, thalidomide, and dexamethasone in newly diagnosed multiple myeloma: a phase II study.
Ahn, JS; Choi, YJ; Chung, JS; Joo, YD; Kim, HJ; Kim, YK; Lee, JH; Lee, JJ; Lee, JL; Lee, WS; Moon, JH; Shin, HJ; Sohn, SK; Yang, DH, 2010
)
2.07
"Thalidomide has received approval from the European Agency for the Evaluation of Medicinal Products for the treatment of newly diagnosed multiple myeloma (MM) patients older than 65 years or ineligible for transplant. "( Consensus guidelines for the optimal management of adverse events in newly diagnosed, transplant-ineligible patients receiving melphalan and prednisone in combination with thalidomide (MPT) for the treatment of multiple myeloma.
Bladé, J; Davies, F; Delforge, M; Facon, T; Garcia Sanz, R; Kropff, M; Leal da Costa, F; Moreau, P; Morgan, G; Palumbo, A; Schey, S, 2010
)
2
"Thalidomide analogues have been used as inhibitors of alpha glucosidase and could be potential drugs for diabetes treatment."( Pharmacological properties of thalidomide and its analogues.
Compagnone, R; De Sanctis, JB; Garmendia, J; Mijares, M; Moreno, D; Salazar-Bookaman, M; Suárez, A, 2010
)
1.37
"Thalidomide has been reported to have anti-angiogenic and antimetastatic effects. "( Effect of thalidomide dithiocarbamate analogs on the intercellular adhesion molecule-1 expression.
Abdou, BY; Agwa, HS; Guirgis, AA; Mohamed, AS; Talaat, RM; Zahran, MA, 2010
)
2.21
"Thalidomide has been shown to selectively inhibit TNF-α production."( Intraperitoneal injection of thalidomide attenuates bone cancer pain and decreases spinal tumor necrosis factor-α expression in a mouse model.
Gu, X; Ma, Z; Mei, F; Ren, B; Zhang, J; Zhang, R; Zheng, Y, 2010
)
1.37
"Thalidomide has been demonstrated to possess antitumor activity in patients with advanced hepatocellular carcinoma (HCC). "( Phase II study of concomitant thalidomide during radiotherapy for hepatocellular carcinoma.
Ch'ang, HJ; Chang, JS; Chang, YH; Chen, CH; Chen, LT; Hsu, C, 2012
)
2.11
"Thalidomide has shown modest activity in advanced hepatocellular carcinomas (HCCs). "( Activity of thalidomide and capecitabine in patients with advanced hepatocellular carcinoma.
Ang, SF; Choo, SP; Foo, KF; Ong, SY; Poon, DY; Tan, SH; Toh, HC, 2012
)
2.2
"Thalidomide has a broad spectrum of anti-cancer activity. "( Immunomodulatory properties of thalidomide analogs: pomalidomide and lenalidomide, experimental and therapeutic applications.
Bodera, P; Stankiewicz, W, 2011
)
2.1
"Thalidomide has reported efficacy in treating refractory idiopathic aphthous ulceration and aphthous ulceration in Behçet disease (BD). "( Refractory aphthous ulceration treated with thalidomide: a report of 10 years' clinical experience.
Cheng, S; Murphy, R, 2012
)
2.08
"Thalidomide maintenance has the potential to modulate residual multiple myeloma (MM) after an initial response. "( The role of maintenance thalidomide therapy in multiple myeloma: MRC Myeloma IX results and meta-analysis.
Bell, SE; Brown, JM; Child, JA; Cook, G; Coy, NN; Davies, FE; Drayson, MT; Gregory, WM; Jackson, GH; Morgan, GJ; Owen, RG; Roddie, H; Ross, FM; Rudin, C; Russell, NH; Szubert, AJ, 2012
)
2.13
"Thalidomide has potent antimyeloma activity, but no prospective, randomized controlled trial has evaluated thalidomide monotherapy in patients with relapsed/refractory multiple myeloma."( Thalidomide versus dexamethasone for the treatment of relapsed and/or refractory multiple myeloma: results from OPTIMUM, a randomized trial.
Avet-Loiseau, H; Baylon, HG; Bladé, J; Caravita, T; Facon, T; Glasmacher, A; Goranov, S; Hajek, R; Hillengass, J; Hulin, C; Kropff, M; Kueenburg, E; Liebisch, P; Lucy, L; Moehler, TM; Pattou, C; Robak, T; Zerbib, R, 2012
)
3.26
"Thalidomide also has some activity in lower-risk MDS without del5q, but its side effects limit its practical use in these patients."( Immunomodulating drugs in myelodysplastic syndromes.
Adès, L; Fenaux, P, 2011
)
1.09
"Thalidomide has been used to reduce liver inflammation and fibrosis in HCV-infected patients, but its impact on HCV replication remains unclear."( Inhibition of IκB kinase by thalidomide increases hepatitis C virus RNA replication.
Alfieri, C; Rance, E; Tanner, JE, 2012
)
1.39
"Thalidomide has been shown to have antitumor activity in some patients with advanced hepatocellular carcinoma (HCC). "( Efficacy, safety, and potential biomarkers of thalidomide plus metronomic chemotherapy for advanced hepatocellular carcinoma.
Cheng, AL; Hsiao, CH; Hsu, C; Hsu, CH; Huang, CC; Lee, KD; Lin, ZZ; Lu, YS; Shao, YY; Shen, YC, 2012
)
2.08
"Thalidomide has been proven to be helpful and averted the adverse effects from systemic corticosteroids and other immunosuppressive drugs in this patient."( Propylthiouracil-induced ANCA-positive erythema nodosum treated with thalidomide.
Hunasehally, RY; Shi, R; Wan, P; Zhao, X; Zheng, J, 2012
)
1.33
"Thalidomide has potent anti-inflammatory and anti-angiogenic properties. "( Analysis of circulating angiogenic biomarkers from patients in two phase III trials in lung cancer of chemotherapy alone or chemotherapy and thalidomide.
Brown, NJ; Jitlal, M; Lee, SM; Tin, AW; Woll, PJ; Young, RJ, 2012
)
2.02
"Thalidomide has proven to exert anti-inflammatory, anti-proliferative and anti-angiogenic activities in both neoplastic and non-neoplastic conditions. "( Thalidomide attenuates mammary cancer associated-inflammation, angiogenesis and tumor growth in mice.
Alves Neves Diniz Ferreira, M; Cândida Araújo E Silva, A; da Silva Vieira, T; Dantas Cassali, G; Fonseca de Carvalho, L; Maria de Souza, C; Passos Andrade, S; Teresa Paz Lopes, M, 2012
)
3.26
"Thalidomide has already been proven to differentially regulate immune responses and support anti-apoptosis in immunodeficiency syndromes."( Thalidomide has anti-inflammatory properties in neonatal immune cells.
Faust, K; Härtel, C; Puzik, A; Thiel, A, 2013
)
2.55
"Thalidomide has various effects, such as immune modulation, anti-angiogenicity, anti-inflammation and anti-proliferation. "( Attenuation of nephritis in lupus-prone mice by thalidomide.
Choi, KH; Kim, BS; Lee, SK; Lee, SW; Park, KH; Park, YB; Yang, J, 2012
)
2.08
"Thalidomide monotherapy has demonstrated consistent results in the treatment of advanced multiple myeloma. "( Predictive factors of survival after thalidomide therapy in advanced multiple myeloma: long-term follow-up of a prospective multicenter nonrandomized phase II study in 120 patients.
Attal, M; Bellissant, E; Decaux, O; Facon, T; Grosbois, B; Moreau, P; Pegourie, B; Renault, A; Sébille, V; Tiab, M; Voillat, L; Zerbib, R, 2012
)
2.09
"Thalidomide monotherapy has demonstrated consistent results in the treatment of advanced multiple myeloma."( Predictive factors of survival after thalidomide therapy in advanced multiple myeloma: long-term follow-up of a prospective multicenter nonrandomized phase II study in 120 patients.
Attal, M; Bellissant, E; Decaux, O; Facon, T; Grosbois, B; Moreau, P; Pegourie, B; Renault, A; Sébille, V; Tiab, M; Voillat, L; Zerbib, R, 2012
)
2.09
"Thalidomide has proven its efficacy in refractory cutaneous lupus disease, although it is not exempt from significant side effects and frequent relapses after withdrawal."( Efficacy and safety of lenalidomide for refractory cutaneous lupus erythematosus.
Ávila, G; Cortés-Hernández, J; Ordi-Ros, J; Vilardell-Tarrés, M, 2012
)
1.1
"Thalidomide has a significant anti-inflammatory effect by inhibiting TNF-α, which plays role in Aβ neurotoxicity."( Thalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in rats.
Alan, S; Elçioğlu, H; Kabasakal, L; Karan, M; Salva, E; Tufan, F, 2013
)
2.55
"Thalidomide has antiangiogenic and immunomodulatory properties and is an effective inhibitor of TNF-alpha."( Thalidomide in the treatment of multiple myeloma.
Rajkumar, SV, 2001
)
2.47
"Thalidomide therapy has been shown to modify granulomatous diseases, such as tuberculosis and leprosy. "( Thalidomide for chronic sarcoidosis.
Baughman, RP; Judson, MA; Lower, EE; Moller, DR; Teirstein, AS, 2002
)
3.2
"Thalidomide has proven activity in refractory multiple myeloma (MM), and although single-agent thalidomide has minimal prothrombogenic activity, its combination with cytotoxic chemotherapy is associated with a significantly increased risk of DVT."( Thrombogenic activity of doxorubicin in myeloma patients receiving thalidomide: implications for therapy.
Anaissie, E; Barlogie, B; Fassas, A; Fink, L; Morris, C; Saghafifar, F; Siegel, E; Tricot, G; Zangari, M, 2002
)
1.27
"Thalidomide has shown excellent results in the treatment of multiple myeloma probably due to its anti-angiogenic activity."( Thalidomide in the treatment of myelodysplastic syndrome with fibrosis.
Apostolidis, P; Dervenoulas, J; Kontopidou, F; Rontogianni, D; Tsirigotis, P; Venetis, E, 2002
)
2.48
"Thalidomide has been reported to yield anti-tumor activity in cancer. "( Phase II trial of thalidomide in renal-cell carcinoma.
Angevin, E; Couanet, D; Dupouy, N; Escudier, B; Garofano, A; Laplanche, A; Lassau, N; Leborgne, S; Leboulaire, C; Mesrati, F, 2002
)
2.09
"Thalidomide has various immunomodulatory effects."( [Thalidomide: new uses for an old drug].
Sonneveld, P; Wu, KL, 2002
)
1.95
"Thalidomide has antitumour activity in refractory multiple myeloma."( [Thalidomide in the treatment of refractory multiple myeloma: a Dutch study of 72 patients: an antitumor effect in 45%].
Lokhorst, HM; Schaafsma, MR; Sonneveld, P; van der Holt, B; Wijermans, PW; Wu, KL, 2002
)
2.67
"Thalidomide has been used to treat ENL since the 1960s."( Thalidomide in the treatment of leprosy.
Kook, KA; Resztak, KE; Scheffler, MA; Stirling, DI; Teo, S; Thomas, SD; Zeldis, JB, 2002
)
2.48
"Thalidomide has shown efficacy in relapsed or refractory patients of multiple myeloma (MM). "( The adverse effects of thalidomide in relapsed and refractory patients of multiple myeloma.
Grover, JK; Raina, V; Uppal, G, 2002
)
2.07
"Thalidomide has anti-inflammatory properties and selectively inhibits TNF."( Preclinical and clinical assessment of the safety and potential efficacy of thalidomide in heart failure.
Agoston, I; Bozkurt, B; Dibbs, ZI; Mann, DL; Muller, G; Wang, F; Zeldis, JB, 2002
)
1.27
"Thalidomide has been used in several diseases (i.e."( Thalidomide: focus on its employment in rheumatologic diseases.
Cassarà, EA; Ossandon, A; Priori, R; Valesini, G,
)
2.3
"Thalidomide has been shown to have both antiinflammatory and antiangiogenic effects in several diseases. "( Thalidomide suppresses the interleukin 1beta-induced NFkappaB signaling pathway in colon cancer cells.
Han, DS; Jin, SH; Kim, TI; Kim, WH; Shin, SK, 2002
)
3.2
"Thalidomide has no effect on tumor growth, but is also associated with increased VEGF and p53 expression."( Vascular endothelial growth factor monoclonal antibody inhibits growth of anaplastic thyroid cancer xenografts in nude mice.
Bauer, AJ; Doniparthi, NK; Francis, GL; Patel, A; Ringel, MD; Saji, M; Terrell, R; Tuttle, RM, 2002
)
1.04
"Thalidomide has been used in the treatment of many dermatological disorders. "( The potential efficacy of thalidomide in the treatment of recalcitrant alopecia areata.
Namazi, MR, 2003
)
2.06
"Thalidomide has been found to be effective for relapsed or refractory myeloma and, more recently, also as induction therapy."( Pharmacotherapy of multiple myeloma: an economic perspective.
Messori, A; Santarlasci, B; Trippoli, S, 2003
)
1.04
"Thalidomide has significant activity in early-stage myeloma and has the potential to delay progression to symptomatic disease."( Thalidomide as initial therapy for early-stage myeloma.
Dispenzieri, A; Fonseca, R; Gertz, MA; Geyer, SM; Greipp, PR; Iturria, N; Kumar, S; Kyle, RA; Lacy, MQ; Lust, JA; Rajkumar, SV; Witzig, TE, 2003
)
2.48
"Thalidomide (Thal) has been successfully used in such situations and it's use has also been expanded to the up-front therapy and as adjuvant to stem cell transplantation."( Advances in the treatment of multiple myeloma: the role of thalidomide.
Colleoni, GW; Ribas, C, 2003
)
1.28
"Thalidomide has recently shown considerable promise in the treatment of a number of conditions, such as leprosy and cancer. "( Immunological effects of thalidomide and its chemical and functional analogs.
Dalgleish, AG; Dredge, K; Marriott, JB, 2002
)
2.06
"Thalidomide has antiangiogenic properties and was found to be effective in patients with multiple myeloma (MM) when used in the setting of posttransplantation relapse. "( Thalidomide and deep vein thrombosis in multiple myeloma: risk factors and effect on survival.
Barlogie, B; Eddleman, P; Fassas, A; Fink, L; Jacobson, J; Lee, CK; Talamo, G; Thertulien, R; Tricot, G; Van Rhee, F; Zangari, M, 2003
)
3.2
"Thalidomide has hypnosedative, antiangiogenic, antiinflammatory, and immunomodulatory properties. "( Dermatologic and nondermatologic uses of thalidomide.
Cheigh, NH; Micali, G; Nasca, MR; West, DP; West, LE, 2003
)
2.03
"Thalidomide has anti-inflammatory, anti-tumour necrosis factor-alpha and anti-collagen activities. "( Thalidomide ameliorates carbon tetrachloride induced cirrhosis in the rat.
Fernández-Martínez, E; García, J; Lara-Ochoa, F; Muriel, P; Pérez-Alvarez, V; Ponce, S; Shibayama, M; Tsutsumi, V, 2003
)
3.2
"Thalidomide, (1), has made a remarkable comeback from its days of a sedative with teratogenic properties due to its ability to selectively inhibit TNF-alpha, a key pro-inflammatory cytokine and its clinical benefit in the treatment of cancer. "( Alpha-fluoro-substituted thalidomide analogues.
Corral, LG; Man, HW; Muller, GW; Stirling, DI, 2003
)
2.07
"Thalidomide has significant neurotoxicity and its efficacy was not confirmed in recent studies."( Renal cell carcinoma: novel treatments for advanced disease.
Heinzer, H; Huland, E, 2003
)
1.04
"Thalidomide has demonstrated significant activity in both resistant and previously untreated multiple myeloma. "( Thalidomide and its derivatives: new promise for multiple myeloma.
Weber, D,
)
3.02
"(2) Thalidomide has been granted temporary authorization in France for patients with multiple myeloma who have no other therapeutic option."( Thalidomide: new indication. A last resort in myeloma.
, 2003
)
2.24
"Thalidomide has previously been shown to have anti-angiogenic properties. "( Thalidomide is anti-angiogenic in a xenograft model of neuroblastoma.
Beck, L; Frischer, JS; Huang, J; Kadenhe-Chiweshe, A; Kaicker, S; Kandel, JJ; McCrudden, KW; New, T; Serur, A; Yamashiro, DJ; Yokoi, A, 2003
)
3.2
"Thalidomide has demonstrated significant activity in both resistant and previously untreated multiple myeloma. "( Treatment of plasma cell dyscrasias with thalidomide and its derivatives.
Anagnostopoulos, A; Dimopoulos, MA; Weber, D, 2003
)
2.03
"Thalidomide has recently shown significant antimyeloma activity."( Primary treatment of multiple myeloma with thalidomide, vincristine, liposomal doxorubicin and dexamethasone (T-VAD doxil): a phase II multicenter study.
Anagnostopoulos, A; Dimopoulos, MA; Hatzicharissi, E; Korantzis, J; Maniatis, A; Mitsouli, Ch; Panagiotidis, P; Papaioannou, M; Tzilianos, M; Zervas, K, 2004
)
1.31
"Thalidomide has several targets and mechanisms of action: a hypnosedative effect, several immunomodulatory properties with an effect on the production of TNF-alpha and the balance between the different lymphocyte subsets and an antiangiogenic action. "( Thalidomide: an old drug with new clinical applications.
Laffitte, E; Revuz, J, 2004
)
3.21
"Thalidomide recently has been proven to have an impact on plasma cell dyscrasia through multiple mechanisms. "( Thalidomide effects in the post-transplantation setting in patients with multiple myeloma.
Byrnes, JJ; Fernandez, HF; Goodman, M; Santos, ES, 2004
)
3.21
"Thalidomide has anti-inflammatory, immuno-modulating and antiangiogeneic properties but the mechanism of its action is not yet completely understood."( [Multiple myeloma: the role of angiogenesis and therapeutic application of thalidomide].
Jurczyszyn, A; Skotnicki, AB; Wolska-Smoleń, T, 2003
)
1.27
"Thalidomide has shown promise in the treatment of newly diagnosed multiple myeloma and relapsed/refractory disease, but side effects such as somnolence, constipation, and neuropathy limit its use. "( The role of immunomodulatory drugs in multiple myeloma.
Anderson, KC, 2003
)
1.76
"Thalidomide has significant clinical activity in patients with multiple myeloma. "( Thalidomide for patients with recurrent lymphoma.
Albitar, M; Cabanillas, F; Clemons, M; Dang, NH; Hagemeister, FB; McLaughlin, P; Pro, B; Rodriguez, MA; Romaguera, J; Samaniego, F; Younes, A, 2004
)
3.21
"Thalidomide has multiple actions, including anti-inflammatory and anti-angiogenic ones."( [Thalidomide--new prospective therapy in oncology].
Pałgan, I; Pałgan, K, 2003
)
1.95
"Thalidomide has been found to exhibit weak nitric oxide synthase (NOS)-inhibitory activity. "( Thalidomide as a nitric oxide synthase inhibitor and its structural development.
Hashimoto, Y; Miyachi, H; Sano, H; Shimazawa, R; Tanatani, A, 2004
)
3.21
"Thalidomide has been reported to have anti-AML activity and appears to cross the blood brain barrier (BBB)."( Thalidomide is highly effective in a patient with meningeal acute myeloid leukaemia.
Baird, R; Duddy, J; Iveson, A; Rassam, SM; van Zyl-Smit, RN, 2004
)
2.49
"Thalidomide has been shown to be an effective treatment in various immunologic diseases such as Crohn's disease and rheumatoid arthritis. "( Thalidomide induces apoptosis in human monocytes by using a cytochrome c-dependent pathway.
Domschke, W; Gockel, HR; Heidemann, J; Kucharzik, T; Lügering, A; Lügering, N; Schmidt, M, 2004
)
3.21
"Thalidomide which has antiangiogenic effects and direct cytotoxic effects was found to be effective in multiple myeloma and is considered as an established treatment modality for patients with refractory or relapsed multiple myeloma."( Antiangiogenic therapy in hematologic malignancies.
Goldschmidt, H; Hillengass, J; Ho, AD; Moehler, TM, 2004
)
1.04
"Thalidomide has demonstrated a remarkable efficacy in the treatment of multiple myeloma but its use may cause several toxicities. "( Common and rare side-effects of low-dose thalidomide in multiple myeloma: focus on the dose-minimizing peripheral neuropathy.
Brunori, M; Candela, M; Capelli, D; Catarini, M; Corvatta, L; Leoni, P; Malerba, L; Marconi, M; Mele, A; Montanari, M; Offidani, M; Olivieri, A; Rupoli, S, 2004
)
2.03
"Thalidomide has recently been recognized as an effective new agent for previously untreated, refractory or relapsed myeloma."( Low-dose thalidomide for multiple myeloma: interim analysis of a compassionate use program.
Gastl, G; Mitterer, M; Spizzo, G; Steurer, M, 2004
)
1.46
"Thalidomide has shown great promise in advanced or refractory multiple myeloma either alone or in combination with other agents."( The promise of thalidomide: evolving indications.
Joglekar, S; Levin, M, 2004
)
1.4
"Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). "( Response to thalidomide in multiple myeloma: impact of angiogenic factors.
Arenillas, L; Aymerich, M; Bladé, J; Cibeira, MT; Cid, MC; Esteve, J; Filella, X; Montserrat, E; Rosiñol, L; Rozman, M; Segarra, M, 2004
)
2.15
"Thalidomide has been shown to be effective in approximately 30% of patients with refractory or advanced multiple myeloma (MM). "( Possible multiple myeloma dedifferentiation following thalidomide therapy: a report of four cases.
Balleari, E; Falcone, A; Ghio, R; Musto, P, 2004
)
2.01
"s-Thalidomide has proven efficacy in multiple myeloma. "( s-thalidomide has a greater effect on apoptosis than angiogenesis in a multiple myeloma cell line.
Chaplin, T; Joel, SP; Liu, WM; Malpas, JS; Propper, DJ; Shahin, S; Strauss, SJ; Young, BD, 2004
)
1.77
"Thalidomide has already become part of standard therapy for the treatment of patients with relapsed and refractory multiple myeloma."( Thalidomid: current role in the treatment of non-plasma cell malignancies.
Kumar, S; Rajkumar, SV; Witzig, TE, 2004
)
1.04
"Thalidomide has demonstrated clinical activity in various malignancies including androgen-independent prostate cancer. "( Antitumor effects of thalidomide analogs in human prostate cancer xenografts implanted in immunodeficient mice.
Eger, K; Figg, WD; Gütschow, M; MacPherson, GR; Ng, SS, 2004
)
2.09
"Thalidomide has been shown to have antiangiogenic and immunomodulatory effects, including the inhibition of vascular endothelial growth factor, basic fibroblast growth factor and tumor necrosis factor alpha."( [A case of advanced pancreatic cancer with remarkable response to thalidomide, celecoxib and gemcitabine].
Hada, M; Mizutari, K, 2004
)
1.28
"Thalidomide-based therapy has the potential to produce durable responses in MMM-associated cytopenias, even after discontinuation of the drug."( Durable responses to thalidomide-based drug therapy for myelofibrosis with myeloid metaplasia.
Elliott, MA; Mesa, RA; Schroeder, G; Tefferi, A, 2004
)
1.36
"Thalidomide has long been recognized as an antiangiogenic molecule."( Thalidomide and analogues: current proposed mechanisms and therapeutic usage.
Brennen, WN; Brown, ML; Capitosti, S; Cooper, CR; Sikes, RA, 2004
)
2.49
"Thalidomide has re-emerged as a novel antineoplastic agent with immunomodulatory and antiangiogenic activities. "( Management of thalidomide toxicity.
Ghobrial, IM; Rajkumar, SV,
)
1.93
"Thalidomide has shown to inhibit, selectively and mainly the cytokine tumor necrosis factor-alpha (TNF-alpha), thus, thalidomide has inhibitory consequences on other cytokines; this is ascribed as an immunomodulatory effect. "( Immunomodulatory effects of thalidomide analogs on LPS-induced plasma and hepatic cytokines in the rat.
Fernández-Martínez, E; Morales-Ríos, MS; Muriel, P; Pérez-Alvarez, V, 2004
)
2.06
"Thalidomide has a variety of biological effects that vary considerably according to the species tested. "( Thalidomide pharmacokinetics and metabolite formation in mice, rabbits, and multiple myeloma patients.
Baguley, BC; Browett, P; Ching, LM; Chung, F; Kestell, P; Lu, J; Palmer, BD; Tingle, M, 2004
)
3.21
"Thalidomide has been proved to play an important role in rescue treatment of patients with refractory/relapsed multiple myeloma (MM). "( Aminoglycoside-associated severe renal failure in patients with multiple myeloma treated with thalidomide.
Bladé, J; Bosch, F; Montagut, C; Rosiñol, L; Villela, L, 2004
)
1.99
"Thalidomide has anti-angiogenic and immunomodulatory activity, exhibiting antitumour effects in patients with multiple myeloma and, more rarely, in several other solid tumours. "( Phase II study of thalidomide in patients with metastatic malignant melanoma.
Cancela, AI; Costa, TD; Di Leone, LP; Fernandes, S; Reiriz, AB; Richter, MF; Schwartsmann, G, 2004
)
2.1
"Thalidomide has been associated with venous thrombotic events, as reported in the post-marketing surveillance reports by Celgene Corporation; as well as case reports in the literature. "( Arterial thrombosis in four patients treated with thalidomide.
Brown, K; Chanan-Khan, A; Hahn, T; McCarthy, PL; Paplham, P; Roy, H; Scarpace, SL; van Besien, K, 2005
)
2.02
"Thalidomide has been shown in vitro to reduce antigen- or mitogen-activated macrophage production of TNF-alpha."( Effects of thalidomide on intracellular Mycobacterium leprae in normal and activated macrophages.
Shannon, EJ; Tadesse, A, 2005
)
1.44
"Thalidomide has been demonstrated to suppress tumor necrosis factor (TNF) release, which may be important at both the initial and chronic phases of the inflammation of sarcoidosis and appears to be crucial as part of the initial granulomatous response."( Newer therapies for cutaneous sarcoidosis: the role of thalidomide and other agents.
Baughman, RP; Lower, EE, 2004
)
1.29
"Thalidomide has gained an infamous history due to severe birth defects observed in patients who had taken the drug to control nausea during pregnancy. "( Complete resolution of generalized lichen planus after treatment with thalidomide.
Angel, TA; Hsu, S; Krishnan, RS; Maender, JL,
)
1.81
"Thalidomide has antiangiogenic and immunomodulatory properties and has recently been used in the management of human malignancies. "( Thalidomide and immunomodulatory drugs in the treatment of cancer.
Bamias, A; Dimopoulos, MA, 2005
)
3.21
"Thalidomide has been reported to yield anti-tumor activity in advanced renal cell carcinoma (RCC). "( Application of thalidomide/interleukin-2 in immunochemotherapy-refractory metastatic renal cell carcinoma.
Hegele, A; Heidenreich, A; Hofmann, R; Ohlmann, CH; Olbert, P; Schrader, AJ; Varga, Z; von Knobloch, R, 2005
)
2.12
"Thalidomide has several mechanisms of action: a hypnosedative effect, several immuno-modulatory properties and an anti-angiogenic action. "( [Thalidomide: new indications for an old drug].
Laffitte, E, 2005
)
2.68
"Thalidomide has undergone resurgence in the treatment of specific malignancies. "( Effect of thalidomide on colorectal cancer liver metastases in CBA mice.
Christophi, C; Daruwalla, J; Malcontenti-Wilson, C; Muralidharan, V; Nikfarjam, M, 2005
)
2.17
"Thalidomide has been reported as efficacious in refractory cutaneous lupus erythematosus (LE). "( Long-term thalidomide use in refractory cutaneous lesions of lupus erythematosus: a 65 series of Brazilian patients.
Cardoso, CR; Coelho, A; de Souza Papi, JA; Salgado, DR; Schmal, TR; Souto, MI; Waddington Cruz, M, 2005
)
2.17
"Thalidomide has been shown to be effective in previously untreated patients as monotherapy (36% remission), although greater remission is seen in combination therapy, for example, thalidomide with dexamethasone (72% remission)."( The future role of thalidomide in multiple myeloma.
Attal, M; Blade, J; Boccadoro, M; Palumbo, A, 2005
)
1.38
"Thalidomide has no activity in patients with advanced or recurrent gynecologic sarcomas and was not well-tolerated. "( Phase II trial of thalidomide for advanced and recurrent gynecologic sarcoma: a brief communication from the New York Phase II consortium.
Blank, SV; Christos, P; Fields, AL; Goldberg, GL; Murgo, A; Runowicz, CD; Timmins, P; Wadler, S; Yi-Shin Kuo, D, 2006
)
2.11
"Thalidomide has proven useful for patients with Langerhans cell histiocytosis of the skin and/or bone."( Drug therapy for the treatment of Langerhans cell histiocytosis.
McClain, KL, 2005
)
1.05
"Thalidomide has been used to treat a variety of diseases ranging from alleviation of autoimmune disorders to prevention of metastasis of cancers. "( Suppression of urokinase receptor expression by thalidomide is associated with inhibition of nuclear factor kappaB activation and subsequently suppressed ovarian cancer dissemination.
Haruta, S; Inagaki, K; Kanayama, N; Kawaguchi, R; Kitanaka, T; Kobayashi, H; Kondo, T; Kurita, N; Sakamoto, Y; Terao, T; Yagyu, T; Yamada, Y, 2005
)
2.03
"Thalidomide has demonstrated a broad spectrum of pharmacological and immunological effects, with potential therapeutic applications that span a wide spectrum of diseases: cancer and related conditions; infectious diseases; autoimmune diseases; dermatological diseases; and other disorders such as sarcoidosis, macular degeneration and diabetic retinopathy. "( Current therapeutic uses of lenalidomide in multiple myeloma.
Anderson, KC; Hideshima, T; Richardson, PG, 2006
)
1.78
"Thalidomide has been shown to have antiangiogenic and immunomodulatory effects, including the inhibition of vascular endothelial growth factor, basic fibroblast growth factor and tumor necrosis factor alpha."( [A case report of unresectable gallbladder cancer that responded remarkably to the combination of thalidomide, celecoxib, and gemcitabine].
Hada, M; Horiuchi, T; Shinji, H, 2006
)
1.27
"Thalidomide has changed the treatment paradigm for patients with myeloma."( Immunomodulatory analogues of thalidomide in the treatment of multiple myeloma.
Hussein, MA; Srkalovic, JG; Suppiah, R, 2006
)
1.34
"Thalidomide, which has anti-angiogenetic activity, has a 30-40% response rate, and the combination of thalidomide and dexamethasone has a 40-50% response rate."( [New treatment strategy of multiple myeloma for cure].
Handa, H; Murakami, H, 2006
)
1.06
"Thalidomide has gained renewed interest as a cancer therapeutic due to its potential antiangiogenic effects. "( Importance of the stress kinase p38alpha in mediating the direct cytotoxic effects of the thalidomide analogue, CPS49, in cancer cells and endothelial cells.
Dennis, PA; Figg, WD; Lepper, ER; Warfel, NA; Zhang, C, 2006
)
2
"Thalidomide has been shown to inhibit production of TNF-alpha."( Low-dose thalidomide in combination with oral fludarabine and cyclophosphamide is ineffective in heavily pre-treated patients with chronic lymphocytic leukemia.
Chiusolo, P; De Padua, L; Efremov, DG; Garzia, M; Laurenti, L; Leone, G; Piccioni, P; Piccirillo, N; Sica, S; Tarnani, M, 2007
)
1.48
"Thalidomide has shown promise for the treatment of patients with myelodysplastic syndrome. "( Thalidomide therapy in adult patients with myelodysplastic syndrome. A North Central Cancer Treatment Group phase II trial.
Alberts, SR; Colon-Otero, G; Geyer, SM; Hoering, A; Li, CY; Menke, DM; Moreno-Aspitia, A; Niedringhaus, RD; Tefferi, A; Vukov, A, 2006
)
3.22
"Thalidomide has been shown to decrease this inflammation by the suppression of TNF-alpha secretion."( Preparation and in vitro analysis of microcapsule thalidomide formulation for targeted suppression of TNF-alpha.
Amre, D; Chen, H; Das, SK; Haque, T; Metz, T; Prakash, S,
)
1.11
"Thalidomide has been demonstrated to be active as a first-line and salvage therapy in patients with multiple myeloma. "( The role of thalidomide in multiple myeloma.
Jagannath, S; Schwab, C, 2006
)
2.16
"Thalidomide has been reported as an effective treatment in at least 200 cases of severe DLE."( [Thalidomide therapy for discoid lupus erythematosus].
Baum, S; Lyakhovisky, A; Salomon, M; Shpiro, D; Trau, H, 2006
)
1.97
"Thalidomide has broad anticytokine properties, which might protect normal tissues in patients undergoing chemoradiotherapy. "( Assessing the ability of the antiangiogenic and anticytokine agent thalidomide to modulate radiation-induced lung injury.
Anscher, MS; Clough, R; Crawford, J; Dewhirst, MW; Dunphy, F; Garst, J; Herndon, JE; Larrier, N; Marino, C; Marks, LB; Shafman, TD; Vujaskovic, Z; Zhou, S, 2006
)
2.01
"As thalidomide has become an accepted component in therapeutic strategies for multiple myeloma, careful attention must be paid to the prevention of thrombosis."( [Deep vein thrombosis and pulmonary embolism in a patient with multiple myeloma treated with thalidomide and dexamethasone].
Handa, H; Irisawa, H; Karasawa, M; Matsushima, T; Miyazawa, Y; Murakami, H; Nojima, Y; Saitoh, T; Tsukamoto, N; Uchiumi, H, 2006
)
1.07
"Thalidomide may have been corticosteroid-sparing in a subgroup of these patients."( The effect of thalidomide on corticosteroid-dependent pulmonary sarcoidosis.
Byars, T; Cox, CE; Hartung, C; Judson, MA; Silvestri, J, 2006
)
1.42
"Thalidomide has been seen efficacious in the treatment of cutaneous disorders in patients with systemic lupus erythematosus and in mucocutaneous disease in Behcet's disease with a not dose-dependent response, even if it should be restricted to selected patients because of its important side effects."( [Thalidomide in treatment of connective diseases and vasculities].
Cantatore, FP; Maruotti, N; Ribatti, D,
)
1.76
"Thalidomide has been registered in the USA in combination with dexamethasone in newly diagnosed patients, but is not yet registered in the European Union."( Thalidomide in multiple myeloma: past, present and future.
Harousseau, JL, 2006
)
2.5
"Thalidomide has been used for the treatment of refractory multiple myeloma, the dosage in Japan is lower than in other countries; however, there is little information on the pharmacokinetics and their relationship with the drug response. "( The pharmacokinetics of low-dose thalidomide in Japanese patients with refractory multiple myeloma.
Asaoku, H; Ikawa, K; Iwato, K; Kamikawa, R; Morikawa, N; Sasaki, A, 2006
)
2.06
"Thalidomide has recently shown to improve LVEF in chronic heart failure patients, accompanied by a marked decrease in plasma levels of tumor necrosis factor alpha (TNF-alpha)."( Effects of thalidomide treatment in heart failure patients.
Arrieta-Rodríguez, O; Asensio-Lafuente, E; Castillo-Martínez, L; Dorantes-García, J; Granados-Arriola, J; Orea-Tejeda, A; Rodríguez-Reyna, T, 2007
)
1.45
"Thalidomide has been reported to have antiangiogenic and antimetastatic effects. "( A novel anticancer effect of thalidomide: inhibition of intercellular adhesion molecule-1-mediated cell invasion and metastasis through suppression of nuclear factor-kappaB.
Chen, CC; Lin, YC; Shun, CT; Wu, MS, 2006
)
2.07
"Thalidomide (Thal) has antiangiogenic and immunomodulatory activity. "( Thalidomide in multiple myeloma.
Glasmacher, A; Goldschmidt, H; Hillengass, J; Moehler, TM, 2006
)
3.22
"Thalidomide (Thal) has been used for a few years as salvage treatment for patients with multiple myeloma (MM). "( Prognostic factors for the efficacy of thalidomide in the treatment of multiple myeloma: a clinical study of 110 patients in China.
Chen, Y; Fu, W; Hou, J; Li, Y; Tao, Z; Wang, D; Yuan, Z, 2006
)
2.05
"Thalidomide has direct antimyeloma and immunomodulatory effects. "( Final report of toxicity and efficacy of a phase II study of oral cyclophosphamide, thalidomide, and prednisone for patients with relapsed or refractory multiple myeloma: A Hoosier Oncology Group Trial, HEM01-21.
Abonour, R; Ansari, RH; Cripe, LD; Fausel, C; Fisher, WB; Juliar, BE; Smith, GG; Suvannasankha, A; Wood, LL; Yiannoutsos, CT, 2007
)
2.01
"Thalidomide has been reported to have antitumor activity for treating metastatic hepatocellular carcinoma (HCC). "( Thalidomide for treating metastatic hepatocellular carcinoma: a pilot study.
Bang, SM; Cho, EK; Han, SH; Kim, JH; Kim, KK; Kim, SS; Kwon, OS; Kwon, SY; Lee, JH; Lee, JJ; Lee, JN; Nam, E; Park, SH; Park, YH; Shin, DB, 2006
)
3.22
"Thalidomide has been shown to be a highly effective drug for the treatment of ENL."( Double-blind trial of the efficacy of pentoxifylline vs thalidomide for the treatment of type II reaction in leprosy.
de Matos, HJ; Duppre, NC; Nery, JA; Sales, AM; Sampaio, EP; Sarno, EN, 2007
)
1.31
"Thalidomide has several mechanisms of action: several immuno-modulatory properties, an anti-angiogenic action and a hypnosedative effect. "( [The revival of thalidomide: an old drug with new indications].
Laffitte, E, 2006
)
2.12
"Thalidomide has been shown to be an effective treatment in Crohn's disease."( Thalidomide in luminal and fistulizing Crohn's disease resistant to standard therapies.
Kamm, MA; Ng, SC; Plamondon, S, 2007
)
3.23
"Thalidomide has been extensively studied alone and in combination in patients with relapsed myeloma, demonstrating substantial efficacy, and is therefore widely used in this setting."( The emerging role of novel therapies for the treatment of relapsed myeloma.
Anderson, KC; Hideshima, T; Mitsiades, C; Richardson, PG, 2007
)
1.06
"Thalidomide has been reported to downregulate the expression of tumor necrosis factor alpha (TNF-alpha), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohnos disease (CD)."( Therapeutic and prophylactic thalidomide in TNBS-induced colitis: synergistic effects on TNF-alpha, IL-12 and VEGF production.
Carneiro, AJ; Carvalho, AT; Carvalho, J; Castelo-Branco, M; Dines, I; Elia, C; Madi, K; Pereira Junior, FA; Pereira, MG; Rocha, E; Schanaider, A; Silv, F; Souza, H; Tortori, C, 2007
)
1.35
"Thalidomide (Thal) has been used in the treatment of multiple myeloma through the inhibitory effect on IL-6-dependent cell growth and angiogenesis."( Thalidomide prevents bleomycin-induced pulmonary fibrosis in mice.
Hisamori, S; Kadokawa, Y; Kubo, H; Mishima, M; Nakano, T; Tabata, C; Tabata, R; Takahashi, M, 2007
)
2.5
"Thalidomide has been used as a salvage regimen at the study institution since 1999. "( Time to first disease progression, but not beta2-microglobulin, predicts outcome in myeloma patients who receive thalidomide as salvage therapy.
Ambrosini, MT; Avonto, I; Boccadoro, M; Bringhen, S; Bruno, B; Caravita, T; Cavallo, F; Falco, P; Gay, F; Palumbo, A, 2007
)
1.99
"Thalidomide has been shown to decrease the secretion of TNF from phagocytic cells, therefore suppression of TNF and IL-1 production from activated phagocytic cells might be a successful treatment modality for prevention of systemic inflammatory response following severe burn."( Thalidomide decreases the plasma levels of IL-1 and TNF following burn injury: is it a new drug for modulation of systemic inflammatory response.
Eski, M; Ifran, A; Sahin, I; Sengezer, M; Serdar, M, 2008
)
2.51
"Thalidomide has a potent immunomodulatory property and has now a number of approved and off-label uses in dermatologic, oncologic, infectious and gastrointestinal conditions."( New cases of thalidomide embryopathy in Brazil.
Castilla, EE; de Sousa, AC; Luna, E; Maximino, C; Schuler-Faccini, L; Schwartz, IV; Soares, RC; Waldman, C, 2007
)
1.43
"Thalidomide has antiangiogenic and immunomodulatory properties and has recently been used in the management of human malignancies. "( A retrospective analysis of thalidomide therapy in non-HIV-related Kaposi's sarcoma.
Ben M'barek, L; Biet, I; Fardet, L; Kérob, D; Lebbe, C; Mebazaa, A; Morel, P; Thervet, E, 2007
)
2.08
"Thalidomide maintenance has unresolved issues regarding dosage and toxicity. "( Thalidomide maintenance following high-dose therapy in multiple myeloma: a UK myeloma forum phase 2 study.
Cocks, K; Feyler, S; Jackson, G; Johnson, RJ; Rawstron, A; Snowden, JA, 2007
)
3.23
"Thalidomide has been identified and its anti-inflammatory and immunomodulatory properties clarified. "( Thalidomide for treatment of intestinal involvement of juvenile-onset Behçet disease.
Akazawa, Y; Amano, Y; Minami, I; Nakamura, S; Uchida, N; Yamazaki, T; Yasui, K, 2008
)
3.23
"Thalidomide has been determined in formulations and, principally in biological fluids by a variety of methods such as high-performance liquid chromatography with ultraviolet detection and liquid chromatography coupled with tandem mass spectrometry."( Recent advances in analytical determination of thalidomide and its metabolites.
Bosch, ME; Ojeda, CB; Rojas, FS; Sánchez, AJ, 2008
)
1.32
"Thalidomide has become an important agent in the treatment of myeloma. "( Thalidomide induced impotence in male hematology patients: a common but ignored complication?
Murphy, PT; O'Donnell, JR, 2007
)
3.23
"Thalidomide has been associated with an increased risk of thromboembolic pulmonary hypertension (PH)."( Non-thromboembolic pulmonary hypertension in multiple myeloma, after thalidomide treatment: a pilot study.
Barbetakis, N; Bischiniotis, T; Lafaras, C; Mandala, E; Platogiannis, D; Verrou, E; Zervas, K, 2008
)
1.3
"Thalidomide has been used as a treatment for various human immunodeficiency virus (HIV)-associated and non-HIV-associated illnesses, generally in cases in which inflammatory disease is refractory to standard therapy. "( Thalidomide treatment for refractory HIV-associated colitis: a case series.
Hay, PE; Jarvis, JN; Johnson, L; Wilkins, EG, 2008
)
3.23
"Thalidomide has been estimated as a useful drug in therapy of refractory or relapsed multiple myeloma. "( Low-dose thalidomide regimens in therapy of relapsed or refractory multiple myeloma.
Adam, Z; Bacovsky, J; Gregora, E; Minarik, J; Pavlicek, P; Pika, T; Pour, L; Scudla, V; Zemanova, M, 2008
)
2.21
"Thalidomide has shown anti-inflammatory or immunosuppressive actions in several animal models."( Thalidomide for autoimmune disease.
Hendler, SS; McCarty, MF, 1983
)
2.43
"Thalidomide has been advocated as the treatment of choice for recalcitrant aphthae. "( Thalidomide-resistant HIV-associated aphthae successfully treated with granulocyte colony-stimulating factor.
Kostman, JR; Manders, SM; Mendez, L; Russin, VL, 1995
)
3.18
"Thalidomide has been reported to be an effective agent for treatment of chronic graft-versus-host disease (CGVHD). "( Thalidomide as salvage therapy for chronic graft-versus-host disease.
Blume, KG; Chao, N; Forman, SJ; Kashyap, A; Long, GD; Margolin, K; Molina, A; Nademanee, A; Negrin, RS; Niland, JC; O'Donnell, MR; Parker, PM; Planas, I; Schmidt, GM; Smith, EP; Snyder, DS; Somlo, G; Spielberger, R; Stein, AS; Stepan, DE; Wilsman, K; Zwingenberger, K, 1995
)
3.18
"Thalidomide has been reported to be effective in treating graft-versus-host disease, a condition with many clinical and pathological similarities to primary biliary cirrhosis. "( Thalidomide as therapy for primary biliary cirrhosis: a double-blind placebo controlled pilot study.
Burroughs, AK; Epstein, O; McCormick, PA; McIntyre, N; Scheuer, PJ; Scott, F, 1994
)
3.17
"Thalidomide has recently been shown to antagonize basic fibroblast growth factor-induced angiogenesis in the rat corneal micropocket assay. "( The effect of thalidomide on experimental tumors and metastases.
Clow, KA; Fryer, KH; Hayes, MM; Minchinton, AI; Wendt, KR, 1996
)
2.1
"Thalidomide, which has a long history of tragedy because of its ability to cause severe birth defects, is very effective in alleviating erythema nodosum leprosum in leprosy patients and aphthous ulcers in AIDS patients. "( Immunomodulatory assays to study structure-activity relationships of thalidomide.
Morales, MJ; Sandoval, F; Shannon, EJ, 1997
)
1.97
"Thalidomide has been shown to lead to a high rate of autism when exposure occurs during the 20th to 24th d of gestation. "( Linking etiologies in humans and animal models: studies of autism.
Croog, VJ; Ingram, JL; Rodier, PM; Tisdale, B,
)
1.57
"Thalidomide has been reported to be an effective agent for the treatment of chronic graft-vs.-host disease (GVHD). "( Paradoxical effect of thalidomide prophylaxis on chronic graft-vs.-host disease.
Blume, KG; Chao, NJ; Dagis, A; Forman, SJ; Gould, KA; Hu, WW; Long, GD; Nademanee, AP; Negrin, RS; Niland, JC; Parker, PM; Snyder, DS; Tierney, DK; Wong, RM; Zwingenberger, K, 1996
)
2.05
"Thalidomide therapy has been shown to cause increases in body weight in patients with HIV and tuberculosis infections. "( The metabolic and immunologic effects of short-term thalidomide treatment of patients infected with the human immunodeficiency virus.
Diakun, J; Freedman, VH; Haslett, P; Hempstead, M; Kaplan, G; Seidman, C; Vasquez, D, 1997
)
1.99
"That thalidomide has activity in this model suggests that an inflammatory process may be involved in the induction of lesions by MPTP in DAergic neurons."( Thalidomide reduces MPTP-induced decrease in striatal dopamine levels in mice.
Boireau, A; Bordier, F; Dubédat, P; Impérato, A; Pény, C, 1997
)
2.19
"Thalidomide (Thd) has been shown to have interesting immunosuppressive properties and strong action against TNF-alpha. "( In vitro and in vivo immunosuppressive potential of thalidomide and its derivative, N-hydroxythalidomide, alone and in combination with cyclosporin A.
Chuong, PH; Claude, JR; Galons, H; Huynh-Thien, D; Righenzi, S; Voisin, J; Warnet, JM; Zhu, J, 1997
)
1.99
"Thalidomide has been shown to selectively inhibit TNF-alpha production in vitro by lipopolysaccharide (LPS)-stimulated monocytes. "( Thalidomide protects mice against LPS-induced shock.
Kaplan, G; Moreira, AL; Sarno, EN; Wang, J, 1997
)
3.18
"Thalidomide has been described as an inhibitor of both angiogenesis (which may account for its teratogenic effects on limb bud formation) and tumor necrosis factor-alpha (TNF-alpha) production. "( The effect of thalidomide and 2 analogs on collagen induced arthritis.
Banquerigo, ML; Brahn, E; Cheng, TP; Oliver, SJ, 1998
)
2.1
"Thalidomide has a significant antiangiogenic effect against VEGF-induced neovasclar growth. "( Thalidomide inhibits corneal angiogenesis induced by vascular endothelial growth factor.
Becker, MD; Joussen, AM; Kruse, FE; Rohrschneider, K; Völcker, HE, 1998
)
3.19
"Thalidomide has been shown to be an inhibitor of angiogenesis in a rabbit cornea micropocket model; however, it has failed to demonstrate this activity in other models. "( Inhibition of angiogenesis by thalidomide requires metabolic activation, which is species-dependent.
Bauer, KS; Dixon, SC; Figg, WD, 1998
)
2.03
"Thalidomide has clearly been shown to be effective in mucocutaneous disease even at a dose of 100 mg/d."( Behçet's syndrome.
Hamuryudan, V; Yazici, H; Yurdakul, S, 1999
)
1.02
"Thalidomide, once banned, has returned to the center of controversy with the Food and Drug Administration's (FDA's) announcement that thalidomide will be placed on the market for the treatment of erythema nodosum leprosum, a severe dermatological complication of Hansen's disease."( Thalidomide and the Titanic: reconstructing the technology tragedies of the twentieth century.
Annas, GJ; Elias, S, 1999
)
2.47
"Thalidomide has anti-inflammatory properties and shows promise for treating a variety of infectious and autoimmune diseases, but it must be used with strict precautions."( Thalidomide's tightly controlled "comeback".
Calabrese, LH, 1999
)
3.19
"Thalidomide has one of the most notorious drug histories because of its teratogenicity. "( Thalidomide in children undergoing bone marrow transplantation: series at a single institution and review of the literature.
Graham-Pole, J; Kedar, A; Mehta, P; Skoda-Smith, S; Wingard, JR, 1999
)
3.19
"Thalidomide has also prompted commentators to celebrate American drug regulation and the American liability system; Professor Bernstein argues that these paeans are exaggerated."( Formed by thalidomide: mass torts as a false cure for toxic exposure.
Bernstein, A, 1997
)
1.42
"Thalidomide has been shown to have species- and metabolic-dependent antiangiogenic activity in vitro and in vivo, suggesting its potential in treating human angiogenesis-dependent pathologies such as solid tumors. "( Thalidomide up-regulates prostate-specific antigen secretion from LNCaP cells.
Bauer, KS; Dixon, SC; Figg, WD; Kruger, EA, 1999
)
3.19
"Thalidomide has subsequently been reported to be effective in treating a number of dermatoses, including cutaneous lupus erythematosus."( American experience with low-dose thalidomide therapy for severe cutaneous lupus erythematosus.
Duong, DJ; Gaspari, AA; Moxley, RT; Spigel, GT, 1999
)
1.3
"Thalidomide has been previously shown to inhibit angiogenesis induced by basic fibroblast growth factor in vivo, using the rabbit corneal micropocket assay."( Thalidomide and a thalidomide analogue inhibit endothelial cell proliferation in vitro.
Friedlander, DR; Kaplan, G; Moreira, AL; Shif, B; Zagzag, D, 1999
)
2.47
"Thalidomide has been shown to cause limb reduction defects in rabbits with much greater potency than in rats, possibly due to inherent biochemical differences between the two species. "( Differential alteration by thalidomide of the glutathione content of rat vs. rabbit conceptuses in vitro.
Carney, EW; Hansen, JM; Harris, C,
)
1.87
"Thalidomide has shown potential in treating some AIDS-related conditions [cachexia (weight loss and muscle wasting), and aphtous oral, oesophageal or genital ulcers]."( New uses for old drugs in HIV infection: the role of hydroxyurea, cyclosporin and thalidomide.
Lisziewicz, J; Lori, F; Ravot, E, 1999
)
1.25
"Thalidomide has inhibitory effects on angiogenesis in the corneal micropocket assay."( Effect of thalidomide and structurally related compounds on corneal angiogenesis is comparable to their teratological potency.
Germann, T; Joussen, AM; Kirchhof, B, 1999
)
1.43
"Thalidomide has been shown to selectively inhibit TNF-alpha production."( Analgesic effect of thalidomide on inflammatory pain.
Cunha, FQ; Ferreira, SH; Ribeiro, RA; Vale, ML, 2000
)
1.35
"Thalidomide has beneficial effects in a number of HIV-associated diseases."( Thalidomide suppresses Up-regulation of human immunodeficiency virus coreceptors CXCR4 and CCR5 on CD4+ T cells in humans.
Juffermans, NP; Olszyna, DP; Speelman, P; van Der Poll, T; van Deventer, SJ; Verbon, A, 2000
)
2.47
"Thalidomide has been shown to have antiinflammatory and, more recently, immunomodulating properties, which are beneficial for the treatment of an ever-increasing list of immune related diseases. "( Thalidomide stimulates splenic IgM antibody response and cytotoxic T lymphocyte activity and alters leukocyte subpopulation numbers in female B6C3F1 mice.
Brown, RD; Germolec, DR; Karrow, NA; McCay, JA; Munson, AE; Musgrove, DL; Pettit, DA; White, KL, 2000
)
3.19
"Thalidomide has been used to treat many inflammatory dermatologic conditions and has been reintroduced in the United States to treat immune-modulated diseases such as pyoderma gangrenosum."( Recalcitrant pyoderma gangrenosum treated with thalidomide.
Federman, DG; Federman, GL, 2000
)
1.29
"Thalidomide has antiangiogenic and immunomodulatory properties and is being investigated as an antineoplastic."( Effect of thalidomide on gastrointestinal toxic effects of irinotecan.
Broadwater, R; Govindarajan, R; Hauer-Jensen, M; Heaton, KM; Lang, NP; Zeitlin, A, 2000
)
1.43
"Thalidomide has significant immunomodulatory properties and has been used successfully in the treatment of oral ulcers and wasting in HIV patients. "( Thalidomide analogue CC-3052 reduces HIV+ neutrophil apoptosis in vitro.
Dalgleish, AG; Dransfield, I; Guckian, M; Hay, P, 2000
)
3.19
"Thalidomide has been successful in the treatment of several dermatologic conditions unresponsive to other agents. "( Thalidomide.
Levine, N; Radomsky, CL, 2001
)
3.2
"Thalidomide has been shown to block the activity of angiogenic substances like bFGF, VEGF and interleukin 6."( [Thalidomide. Clinical trials in cancer].
Politi, PM, 2000
)
1.94
"Thalidomide has recently enjoyed renewed interest as a treatment in many disorders, including plasma cell leukemia."( Thalidomide-associated hepatitis: a case report.
Fowler, R; Imrie, K, 2001
)
2.47
"Thalidomide has been shown to be an effective treatment for cutaneous forms of lupus erythematous refractory to other therapies. "( Update on therapy--thalidomide in the treatment of lupus.
Hughes, GR; Karim, MY; Khamashta, MA; Ruiz-Irastorza, G, 2001
)
2.08
"Thalidomide has been used at doses ranging from 200 to 800 mg with significant toxicity."( Low-dose thalidomide plus dexamethasone is an effective salvage therapy for advanced myeloma.
Bertola, A; Boccadoro, M; Bringhen, S; Gallo, E; Giaccone, L; Palumbo, A; Pileri, A; Pregno, P; Rus, C; Triolo, S, 2001
)
1.45
"Thalidomide has been reported to be an effective therapy for painful oral (mouth) ulcerations associated with AIDS that do not respond to the usual treatment options available. "( Thalidomide: an alternative therapy for treatment of apthous ulcers (canker sores).
Manesis, DA, 1995
)
3.18
"Thalidomide trials have been slow to recruit, therefore buyers clubs are working to make the drug available through their services."( Thalidomide and HIV: several possible uses.
Smith, D, 1995
)
2.46
"Thalidomide (Synovir) has been tested in eighteen patients who did not respond to other therapies."( Thalidomide shows benefit for microsporidial diarrhea.
Bartnof, HS, 1997
)
2.46
"Thalidomide has shown promise in treating wasting and contact information is provided for a compassionate use program."( Approaches to the AIDS Wasting Syndrome.
Corcoran, C, 1998
)
1.02
"Thalidomide has recently been shown to have significant activity in refractory multiple myeloma (MM). "( Thalidomide in the management of multiple myeloma.
Anaissie, E; Badros, A; Barlogie, B; Cromer, J; Fassas, A; Spencer, T; Tricot, G; Zangari, M, 2001
)
3.2
"Thalidomide has no clinical place as an immunosuppressant in solid organ transplantation."( Thalidomide: a re-look.
Gopalakrishna, R; Grover, JK; Ramam, M; Vats, V,
)
2.3
"Thalidomide has increasing clinical benefits, including the healing of aphthous ulcers in patients with HIV. "( Pharmacokinetics and pharmacodynamics of thalidomide in HIV patients treated for oral aphthous ulcers: ACTG protocol 251. AIDS Clinical Trials Group.
Aweeka, F; Bellibas, SE; Chernoff, M; Jacobson, J; Jayewardene, A; Lizak, P; Spritzler, J; Trapnell, C, 2001
)
2.02
"Thalidomide has a chiral centre, and the racemate of (R)- and (S)-thalidomide was introduced as a sedative drug in the late 1950s. "( Clinical pharmacology of thalidomide.
Björkman, S; Eriksson, T; Höglund, P, 2001
)
2.06
"Thalidomide has been shown to inhibit the ability of tumors to recruit new blood vessels."( A randomized phase II trial of docetaxel (taxotere) plus thalidomide in androgen-independent prostate cancer.
Arlen, P; Dahut, WL; Fedenko, K; Fernandez, P; Figg, WD; Gulley, J; Hamilton, M; Kruger, EA; Noone, M; Parker, C; Pluda, J, 2001
)
1.28
"Thalidomide has been used off-label with some success to treat a number of dermatologic diseases, including several inflammatory skin conditions."( Targeting tumor necrosis factor alpha. New drugs used to modulate inflammatory diseases.
Gaspari, AA; LaDuca, JR, 2001
)
1.03
"Thalidomide also has effect on aphthous stomatitis and Behçet's disease."( [Thalidomide--a dreaded drug with new indications].
Seidel, C; Waage, A, 2001
)
1.94
"Thalidomide has proven to be effective in the treatment of erythema nodosum leprosum and aphthous stomatitis. "( [Thalidomide--a dreaded drug with new indications].
Seidel, C; Waage, A, 2001
)
2.66
"Thalidomide also has steroid-sparing properties, and it is particularly useful in treating oral and fistulous complications of Crohn's disease."( Thalidomide treatment for refractory Crohn's disease: a review of the history, pharmacological mechanisms and clinical literature.
Dassopoulos, T; Ehrenpreis, ED; Ginsburg, PM, 2001
)
2.47
"Thalidomide has been used successfully in several other dermatologic disorders, including aphthous stomatitis, Behcet's syndrome, chronic cutaneous systemic lupus erythematosus, and graft-versus-host disease, the apparent shared characteristic of which is immune dysregulation."( Thalidomide: an antineoplastic agent.
Amato, RJ, 2002
)
2.48
"Thalidomide has recently shown antitumor activity in patients with refractory myeloma."( Thalidomide in refractory and relapsing multiple myeloma.
Bladé, J; Esteve, J; Montoto, S; Montserrat, E; Perales, M; Rosiñol, L; Tuset, M, 2001
)
2.47
"Thalidomide has been shown to have antiangiogenic effects in preclinical models as well as a significant antitumor effect in hematologic tumors such as multiple myeloma. "( Phase II study of the antiangiogenesis agent thalidomide in recurrent or metastatic squamous cell carcinoma of the head and neck.
Abbruzzese, JL; El-Naggar, AK; Ginsberg, LE; Glisson, BS; Herbst, RS; Hong, WK; Khuri, FR; Lawhorn, KN; Myers, JN; Pluda, JM; Roach, JS; Shin, DM; Steinhaus, GD; Teddy, S; Thall, PF; Tseng, JE; Wang, X; Zentgraf, RE, 2001
)
2.01
"Thalidomide has immunomodulatory and anti-angiogenic properties which may underlie its activity in cancer. "( Thalidomide in cancer.
Mehta, J; Singhal, S, 2002
)
3.2
"Thalidomide has been used in cases of Behçet's disease with some success."( Thalidomide in Behçet's disease.
Lim, DL; Shek, LP, 2002
)
2.48
"Thalidomide has recently been shown to be useful in the treatment of multiple myeloma and may also be useful in the treatment of other hematological malignancies. "( S-3-Amino-phthalimido-glutarimide inhibits angiogenesis and growth of B-cell neoplasias in mice.
Anderson, KC; Birsner, AE; D'Amato, RJ; LeBlanc, R; Lentzsch, S; Rogers, MS; Shah, JH; Treston, AM, 2002
)
1.76
"Thalidomide has recently proven to be a useful drug for treatment of refractory and relapsed multiple myeloma patients, up to 35% of whom achieve remission. "( The combination of thalidomide, cyclophosphamide and dexamethasone (ThaCyDex) is feasible and can be an option for relapsed/refractory multiple myeloma.
García-Sanz, R; González, M; González-Fraile, MI; López, C; San Miguel, JF; Sierra, M, 2002
)
2.09
"Thalidomide (Thalomid) has antiangiogenic properties, and angiogenesis has been shown to influence the outcome of colon cancer patients."( Irinotecan/thalidomide in metastatic colorectal cancer.
Govindarajan, R, 2002
)
1.43
"Thalidomide has been shown previously to require bio-activation to exert its anti-angiogenic effect in isolated blood vessels and endothelial cells."( Effects of putative hydroxylated thalidomide metabolites on blood vessel density in the chorioallantoic membrane (CAM) assay and on tumor and endothelial cell proliferation.
Fry, MO; Ihnat, MA; Li, PK; Marks, MG; Pokala, V; Shi, J; Trzyna, M; Xiao, Z, 2002
)
1.32
"Thalidomide has been shown to suppress TNF-alpha production from macrophages."( Thalidomide prevents alcoholic liver injury in rats through suppression of Kupffer cell sensitization and TNF-alpha production.
Enomoto, N; Hirose, M; Ikejima, K; Kitamura, T; Miwa, H; Sato, N; Takei, Y, 2002
)
2.48
"Thalidomide has been shown experimentally to be effective in treating GVHD."( Thalidomide for the treatment of chronic graft-versus-host disease.
Altamonte, V; Beschorner, WE; Colvin, OM; Corio, RL; Farmer, ER; Hess, AD; Jabs, DA; Levin, LS; Vogelsang, GB; Wingard, JR, 1992
)
2.45
"Thalidomide has been shown to cause a decrease in the ratio of CD4+ to CD8+ lymphocytes in the blood of healthy males."( Thalidomide's effectiveness in erythema nodosum leprosum is associated with a decrease in CD4+ cells in the peripheral blood.
Berhan, TY; Ejigu, M; Haile-Mariam, HS; Shannon, EJ; Tasesse, G, 1992
)
2.45
"Thalidomide has a role to play in the management of chronic GVHD and further studies are needed."( Thalidomide treatment for chronic graft-versus-host disease.
Bailey, CC; Barnard, DL; Heney, D; Lewis, IJ; Norfolk, DR; Wheeldon, J, 1991
)
2.45
"Thalidomide has been known to have immunosuppressive properties for over 20 years, but it has only recently been used in GVHD."( Thalidomide in the treatment of graft-versus-host disease.
Bailey, CC; Heney, D; Lewis, IJ, 1990
)
2.44
"Thalidomide has previously been reported to be of value in treatment of Behçet's syndrome, but to my knowledge never with such a dramatic effect on a severe colitis as reported in this case."( Treatment of severe colitis in Behçet's syndrome with thalidomide (CG-217).
Larsson, H, 1990
)
1.25
"Thalidomide has a beneficial effect on type II Lepra reaction especially chronic and recurrent reaction. "( Thalidomide in leprosy--study of 94 cases.
Ganapati, R; Parikh, DA; Revankar, CR,
)
3.02

Actions

Thalidomide (Thal) can suppress the growth of established, as well as explanted tumors in mice. Thalidomid displays remarkable species specificity, causing birth defects in humans and rabbits, but not rats or mice.

ExcerptReferenceRelevance
"Thalidomide may inhibit human fibroblast proliferation and it is worthy of further in vivo investigation."( The suppression effects of thalidomide on human lung fibroblasts: cell proliferation, vascular endothelial growth factor release, and collagen production.
Chang, KT; Hsiao, YH; Perng, DW; Su, KC; Su, VY; Tseng, CM; Wu, YC, 2013
)
2.13
"Thalidomide may inhibit TNF-α expression via down-regulation of the NFκB signaling pathway to alleviate acute pancreatitis-associated lung injury in rats."( Thalidomide alleviates acute pancreatitis-associated lung injury via down-regulation of NFκB induced TNF-α.
Fan, LJ; Ji, SS; Li, HY; Li, W; Lv, P, 2014
)
3.29
"Thalidomide, because of its anti-inflammatory properties, as re-emerged as an option for the treatment of Crohn's disease refractory to standard therapy. "( Effect of thalidomide on the healing of colonic anastomosis, in rats.
Campos, AD; Feres, O; Ramalho, FS; Ramalho, LN; Rocha, JJ; Veneziano, SG, 2008
)
2.19
"Thalidomide's ability to inhibit tumor necrosis factor alpha (TNF-alpha) in vitro has been proposed as a partial explanation of its effective treatment of ENL."( Thalidomide suppressed IL-1beta while enhancing TNF-alpha and IL-10, when cells in whole blood were stimulated with lipopolysaccharide.
Kamath, B; Noveck, R; Sandoval, F; Shannon, E, 2008
)
2.51
"Thalidomide can suppress the expression of HIF-1alpha and VEGF in HUVEC in vitro and then inhibit angiodysplasia, which may play a significant role in stopping the rebleeding in patients with recurrent gastrointestinal bleeding."( [The mechanisms of thalidomide in treatment of angiodysplasia due to hypoxia].
Chen, HM; Fang, JY; Ge, ZZ; Liu, WZ; Lu, H; Xiao, SD; Xu, CH, 2009
)
2.12
"Thalidomide can inhibit the formation of MNGC in a dose-dependent manner."( Thalidomide prevents formation of multinucleated giant cells (Langhans-type cells) from cultured monocytes: possible pharmaceutical applications for granulomatous disorders.
Kondo, Y; Manki, A; Morishima, T; Nagaoka, Y; Tsuge, M; Wada, T; Yashiro, M; Yasui, K,
)
2.3
"Thalidomide can inhibit the expression of AnxA2 mRNA and protein in RPMI8226 and HMEC-1 cells, which may be one of the mechanisms for the development of thrombosis induced by thalidomide in multiple myeloma patients."( [Effects of thalidomide on Annexin II gene regulation].
Bao, HY; Jiang, M; Ruan, CG; Shen, F; Zhu, MQ, 2009
)
2.17
"Thalidomide and IMiDs inhibit the cytokines tumour necrosis factor-alpha (TNF-alpha), interleukins (IL) 1-beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF)."( Pharmacological properties of thalidomide and its analogues.
Compagnone, R; De Sanctis, JB; Garmendia, J; Mijares, M; Moreno, D; Salazar-Bookaman, M; Suárez, A, 2010
)
1.37
"Thalidomide did not inhibit the activation of complement by zymosan, a known initiator of complement activation by the alternative pathway, or by M."( In vitro thalidomide does not interfere with the activation of complement by M. leprae.
Morales, MJ; Sandoval, FG; Shannon, EJ, 2011
)
1.51
"Thalidomide did not inhibit the JAK activation in response to IFN-γ."( Thalidomide inhibits interferon-γ-mediated nitric oxide production in mouse vascular endothelial cells.
Badamtseren, B; Haque, A; Hashimoto, S; Koide, N; Komatsu, T; Naiki, Y; Odkhuu, E; Yokochi, T; Yoshida, T, 2011
)
2.53
"Thalidomide (TD) displays remarkable species specificity, causing birth defects (teratogenesis) in humans and rabbits, but not rats or mice; yet, few determinants of species susceptibility have been identified. "( Resistance of CD-1 and ogg1 DNA repair-deficient mice to thalidomide and hydrolysis product embryopathies in embryo culture.
Gonçalves, LL; Lee, CJ; Wells, PG, 2011
)
2.06
"Thalidomide (Thal) can suppress the growth of established, as well as explanted tumors in mice. "( Thalidomide delayed the ability of 4T1 cells to amass into tumors in Balb/c mice.
Baghian, A; Israyelyan, A; Kearney, MT; Sandoval, F; Shannon, EJ, 2012
)
3.26
"Thalidomide can suppress VEGF, either induced by HIF-1α or bFGF."( Role of vascular endothelial growth factor in angiodysplasia: an interventional study with thalidomide.
Chen, H; Fang, J; Gao, Y; Ge, Z; Liu, W; Tan, H; Xiao, S; Xu, C, 2012
)
1.32
"Thalidomide is known to blunt the acute phase response."( Successful treatment of familial Mediterranean fever attacks with thalidomide in a colchicine resistant patient.
Masatlioglu, S; Ozdogan, H; Seyahi, E; Yazici, H,
)
1.09
"Thalidomide can inhibit these effects."( [Thalidomide inhibits the angiogenic activity of culture supernatants of multiple myeloma cell line].
Chen, W; Mirshahi, F; Mirshahi, M; Soria, C; Soria, J; Zhu, J, 2002
)
1.95
"Thalidomide could enhance the inhibition of Mabthera on colony formation of MM patients' myeloma cells, which is related to that thalidomide enhances CD20 antigen expression of myeloma cells."( [Combination of thalidomide and rituximab in suppressing myeloma cells in vitro].
Li, J; Luo, SK; Xiong, WJ; Zhou, ZH, 2002
)
2.1
"Thalidomide can not only inhibit angiogenesis, but also abrogate the adhesion of multiple myeloma cells to bone marrow stromal cells."( [Influence of thalidomide on bone marrow microenvironment in refractory and relapsed multiple myeloma].
Hong, WD; Li, J; Luo, SK; Zhou, ZH; Zou, WY, 2003
)
2.12
"Thalidomide did not inhibit dehydrogenase activity or growth of Ehrlich ascites tumor cells in agar. "( THALIDOMIDE: EFFECTS ON EHRLICH ASCITES TUMOR CELLS IN VITRO.
DIPAOLO, JA; WENNER, CE, 1964
)
3.13
"Thalidomide cannot inhibit VEGF mRNA expression of grafted H22 tumor in mouse."( [Effect of thalidomide on tumor growth in mouse hepatoma H22 model].
Lu, ZJ; Zhai, Y, 2003
)
1.43
"Thalidomide, because of its potent antiinflammatory and immunomodulatory properties, is being re-evaluated in several clinical fields."( Thalidomide as a potent inhibitor of neointimal hyperplasia after balloon injury in rat carotid artery.
Chae, IH; Choi, DJ; Jeon, SI; Kim, DH; Kim, HS; Koo, BK; Lee, MM; Oh, BH; Park, KW; Park, SJ; Park, YB; Yang, HM; Youn, SW, 2004
)
2.49
"Thalidomide can inhibit the growth and angiogenesis of human ovarian cancer transplanted subcutaneously in nude mice. "( [Study of thalidomide on the growth and angiogenesis of ovary cancer SKOV3 transplanted subcutaneously in nude mice].
Cao, ZY; Li, W; Peng, ZL, 2005
)
2.17
"Thalidomide was used because conventional medical treatment by steroids and immunosuppressives was ineffective."( [Thalidomide therapy for infantile-onset Crohn's disease].
Ikematsu, K; Joh, K; Kabuki, T; Kagimoto, S; Ogimi, C; Oh-Ishi, T; Tanaka, R, 2005
)
1.96
"Thalidomide could inhibit tumor growth in a concentration-dependent manner in MCF-7 and HL-60; its IC50s for them were 18.36+/-2.34 and 22.14+/-2.15 microM, respectively, while this effect was not observed in HeLa and K562."( Thalidomide inhibits growth of tumors through COX-2 degradation independent of antiangiogenesis.
Du, GJ; Lin, HH; Wang, MW; Xu, QT, 2005
)
2.49
"Thalidomide and IMiDs inhibit the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL) 1beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF)."( Properties of thalidomide and its analogues: implications for anticancer therapy.
Teo, SK, 2005
)
1.41
"Thalidomide seems to inhibit growth of intestinal angiodysplasias and may be useful for treatment of patients with bleeding related to angiodysplasias. "( Macroscopic appearance of intestinal angiodysplasias under antiangiogenic treatment with thalidomide.
Bauditz, J; Lochs, H; Voderholzer, W, 2006
)
2
"Thalidomide did not increase intra-tumoural TNF-alpha production induced with LPS, in sharp contrast to that obtained with DMXAA."( Thalidomide increases both intra-tumoural tumour necrosis factor-alpha production and anti-tumour activity in response to 5,6-dimethylxanthenone-4-acetic acid.
Baguley, BC; Browne, WL; Cao, Z; Ching, LM; Joseph, WR; Mountjoy, KG; Palmer, BD, 1999
)
2.47
"Thalidomide was found to inhibit PBMC-derived TNF-alpha, but not IL-2."( Selective down-regulation of T cell- and non-T cell-derived tumour necrosis factor alpha by thalidomide: comparisons with dexamethasone.
Dearman, RJ; Deighton, J; Ewan, PW; Kimber, I; McHugh, SM; Rowland, TL, 1999
)
1.24
"Thalidomide also did not inhibit metabolism of CYP-specific substrates and therefore any interactions with other drugs that are metabolized by the same enzyme system are unlikely."( Metabolism of thalidomide in human microsomes, cloned human cytochrome P-450 isozymes, and Hansen's disease patients.
Kook, KA; O'Brien, K; Sabourin, PJ; Teo, SK; Thomas, SD, 2000
)
1.39
"Thalidomide did not increase revertant frequencies in all bacterial strains."( Assessment of the in vitro and in vivo genotoxicity of Thalomid (thalidomide).
Morgan, M; Stirling, D; Teo, S; Thomas, S, 2000
)
1.27
"Thalidomide in lower intermittent doses is ineffective at preventing recurrence of aphthous ulcers in HIV-infected persons."( Thalidomide in low intermittent doses does not prevent recurrence of human immunodeficiency virus-associated aphthous ulcers.
Chernoff, M; Fahey, JL; Fox, L; Greenspan, JS; Hooton, TM; Jackson, JB; Jacobson, JM; Pulvirenti, JJ; Shikuma, C; Spritzler, J; Wohl, DA, 2001
)
2.47
"Thalidomide may cause birth defects, and larger doses can cause neuropathy or other adverse effects."( Wasting syndrome--affordable treatments.
James, JS, 1995
)
1.01
"Thalidomide is known to cause deformities in infants borne to pregnant women taking the drug."( Thalidomide effective treatment for AIDS-related mouth ulcers.
Randall, P, 1995
)
2.46
"Thalidomide failed to inhibit the growth of xenograft tumours. "( Renal cell carcinoma may adapt to and overcome anti-angiogenic intervention with thalidomide.
Douglas, ML; Hii, SI; Jonsson, JR; Nicol, DL; Reid, JL, 2002
)
1.98
"Thalidomide did not suppress the incidence of lymphocytic thyroiditis and serum anti-thyroglobulin antibodies or affect the serum concentrations of T4, T3 and TSH in this rat model."( Effect of thalidomide on the incidence of iodine-induced and spontaneous lymphocytic thyroiditis and spontaneous diabetes mellitus in the BB/Wor rat.
Abend, S; Alex, S; Appel, MC; Braverman, LE; Lueprasitsakul, W; Reinhardt, W, 1990
)
1.4

Treatment

Thalidomide as a treatment for refractory IBD in children and adolescents can improve clinical remission and achieve longer-term maintenance of remission.

ExcerptReferenceRelevance
"Thalidomide treatment significantly reduced serum levels of hepatic enzymes and TNF-α, IL-1-β, and IL-6."( Immunomodulatory effects of thalidomide in an experimental brain death liver donor model.
Andraus, W; Brasil, S; de Moraes, EL; de Oliveira-Braga, KA; de Sá Lima, L; Degaspari, S; Dellê, H; Figueiredo, EG; Nepomuceno, NA; Pêgo-Fernandes, PM; Pepineli, R; Ruiz, LM; Santana, AC; Scavone, C; Silva, FMO; Solla, DJF; Tullius, SG, 2021
)
1.64
"Thalidomide treatment also induced a significant decrease in the expression of ET-1 (1.4 ± 0.3 relative expression [BD + Thalid] vs."( Thalidomide modulates renal inflammation induced by brain death experimental model.
Andraus, W; Brasil, S; de Moraes, EL; de Oliveira-Braga, KA; Dellê, H; Dos Santos, MJ; Feliciano, R; Figueiredo, EG; Nepomuceno, NA; Neri, LHM; Pêgo-Fernandes, PM; Pepineli, R; Ruiz, LM; Sala, ACG; Santana, AC; Schust, AS; Silva, FMO, 2022
)
2.89
"In thalidomide-treated mice, there was a significant increase in the terminally differentiated mature CD27"( Antimetastatic effects of thalidomide by inducing the functional maturation of peripheral natural killer cells.
Hayakawa, Y; Miyazato, K; Tahara, H, 2020
)
1.37
"Thalidomide as a treatment for refractory IBD in children and adolescents can improve clinical remission and achieve longer-term maintenance of remission. "( Thalidomide as a treatment for inflammatory bowel disease in children and adolescents: A systematic review.
Cui, X; Li, H; Liu, C; Men, P; Qiu, T; Sun, T; Zhai, S, 2020
)
3.44
"Thalidomide-treated patients were more likely to have thrombocytopenia (P < .001) and high-risk disease (P = .02)."( Retrospective Analysis of the Clinical Use and Benefit of Lenalidomide and Thalidomide in Myelofibrosis.
Al Ali, N; Castillo-Tokumori, F; Komrokji, R; Kuykendall, AT; Lancet, J; Padron, E; Sallman, D; Sweet, K; Talati, C; Yun, S, 2020
)
1.51
"In thalidomide treated mice, blood urea nitrogen (BUN) (59.3 ± 19.6 vs."( Thalidomide reduces glycerol-induced acute kidney injury by inhibition of NF-κB, NLRP3 inflammasome, COX-2 and inflammatory cytokines.
Amirshahrokhi, K, 2021
)
2.58
"Thalidomide treatment also did not affect expression of GPIbα, GPVI or αIIbβ3, nor did it affect collagen- or ADP-induced platelet aggregation at threshold concentrations."( An absence of platelet activation following thalidomide treatment in vitro or in vivo.
Andrews, RK; Gardiner, EE; Ju, W; Li, D; Li, X; Liu, Y; Qi, K; Qiao, J; Wu, X; Wu, Y; Xu, K; Zeng, L, 2017
)
1.44
"Thalidomide treatment prevents CAV development in a rodent model and is therefore potentially useful in clinical applications to prevent post-transplant heart rejection."( Thalidomide treatment prevents chronic graft rejection after aortic transplantation in rats - an experimental study.
Bernstein, D; Deuse, T; Hu, X; Hua, X; Miller, KK; Neofytou, E; Reichenspurner, H; Renne, T; Schrepfer, S; Velden, J; Wang, D, 2017
)
2.62
"Thalidomide treatment reduced PTX3 in the serum 7 days after starting treatment."( Elevated Pentraxin-3 Concentrations in Patients With Leprosy: Potential Biomarker of Erythema Nodosum Leprosum.
Amadeu, TP; da Silva, CO; de Carvalho, DS; Ferreira, H; Hacker, MA; Mendes, MA; Nery, JAC; Pinheiro, RO; Prata, RBDS; Sampaio, EP; Sarno, EN; Schmitz, V; Silva, BJA, 2017
)
1.18
"Thalidomide treatment significantly decreased the infarct volume and neurological deficits of MCAO/R rats."( The Neuroprotective Effect of Thalidomide against Ischemia through the Cereblon-mediated Repression of AMPK Activity.
Asahi, T; Fujiwara, M; Hayashi, H; Sawamura, N; Takagi, N; Yamada, H; Yamada, M, 2018
)
1.49
"Thalidomide changed the treatment of patients with multiple myeloma, however, its effectiveness has been compromised due to its side effects. "( [Immunomodulator drugs for the treatment of multiple myeloma].
Caballero García, A; Córdova Martínez, A; Fernández-Lázaro, CI; Fernández-Lázaro, D, 2018
)
1.92
"Thalidomide treatment also significantly reduced tissue levels of the proinflammatory cytokines, MDA, MPO, and NO and increased anti-inflammatory cytokine IL-10."( Thalidomide ameliorates cisplatin-induced nephrotoxicity by inhibiting renal inflammation in an experimental model.
Amirshahrokhi, K; Khalili, AR, 2015
)
2.58
"Thalidomide pretreatment significantly reduced the levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity."( The effect of thalidomide on ethanol-induced gastric mucosal damage in mice: involvement of inflammatory cytokines and nitric oxide.
Amirshahrokhi, K; Khalili, AR, 2015
)
1.5
"Thalidomide (Thal) treatment of patients with multiple myeloma (MM) is associated with vascular thrombosis, but the underlying mechanism is unknown."( Thalidomide and multiple myeloma serum synergistically induce a hemostatic imbalance in endothelial cells in vitro.
Gao, Y; Liu, S; Ma, G; Su, Y; Teng, Y; Wang, Y, 2015
)
3.3
"Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide."( Thalidomide-induced limb abnormalities in a humanized CYP3A mouse model.
Abe, S; Akita, M; Kamataki, T; Kazuki, K; Kazuki, Y; Kobayashi, K; Ohta, R; Osaki, M; Oshimura, M; Satoh, D; Takehara, S; Yamazaki, H, 2016
)
2.6
"Thalidomide treatment demonstrated a significant mucositis-ameliorating effect during fractionated irradiation, which is likely to result from NF-κB inhibition. "( Modulation of radiation-induced oral mucositis by thalidomide : Preclinical studies.
Dörr, W; Frings, K; Gruber, S; Kleiter, M; Kuess, P, 2016
)
2.13
"Thalidomide-pretreatment increased engraftment and proliferation of transplanted hepatocytes due to decreased inflammation. "( Thalidomide promotes transplanted cell engraftment in the rat liver by modulating inflammation and endothelial integrity.
Gupta, P; Gupta, S; Kapoor, S; Viswanathan, P, 2016
)
3.32
"Thalidomide treatment poses a risk of bradycardia; however, the benefits are likely to exceed the risk."( Safety and efficacy of thalidomide in patients with POEMS syndrome: a multicentre, randomised, double-blind, placebo-controlled trial.
Aoyagi, R; Hanaoka, H; Ikeda, S; Kanda, T; Katayama, K; Kawachi, I; Kikuchi, S; Kira, J; Kohara, N; Koike, H; Kusunoki, S; Kuwabara, S; Misawa, S; Mitsui, Y; Nagashima, K; Nakashima, I; Nishizawa, M; Sasaki, H; Sato, Y; Sekiguchi, Y; Sobue, G; Takashima, H; Watanabe, O; Yabe, I, 2016
)
1.47
"Thalidomide treatment is extremely effective at ameliorating ENL symptoms."( Expression of CD64 on Circulating Neutrophils Favoring Systemic Inflammatory Status in Erythema Nodosum Leprosum.
Amadeu, TP; Barbosa, MG; Brandão, SS; Costa, Fda M; Dos Santos, JB; Ferreira, H; Hacker, Mde A; Machado, Ade M; Mendes, MA; Nery, JA; Pacheco, Fdos S; Pinheiro, RO; Prata, RB; Rodrigues, LS; Sales, AM; Sarno, EN; Schmitz, V, 2016
)
1.16
"Thalidomide treatment also dramatically suppressed the anchorage-independent growth of U-87 MG and other glioma cells by over a thousand fold without affecting its anchorage-dependent growth, which may be accomplished by knocking down endogenous bFGF expression in these cells."( The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma.
Mei, SC; Wu, RT, 2008
)
1.28
"Thalidomide effectively treats some dermatologic conditions that are refractory to standard medications. "( A case series of 48 patients treated with thalidomide.
Doherty, SD; Hsu, S, 2008
)
2.05
"Thalidomide treatment, however, was not an independent predictor of recurrence or cancer-specific mortality."( Randomized trial of adjuvant thalidomide versus observation in patients with completely resected high-risk renal cell carcinoma.
Jonasch, E; Lozano, M; Margulis, V; Matin, SF; Shen, Y; Swanson, DA; Tamboli, P; Tannir, N; Wood, CG, 2009
)
1.37
"Thalidomide treatment significantly decreased the invasive cells number through Matrigel and human umbilical vein endothelial cells when compared with the controls."( Thalidomide inhibits leukemia cell invasion and migration by upregulation of early growth response gene 1.
Li, J; Liu, P; Lu, H; Xu, B, 2009
)
2.52
"the thalidomide-alone treated mice showed 75% survival whereas 60% of the Augmentin-alone treated group survived."( A combination of thalidomide and augmentin protects BALB/c mice suffering from Klebsiella pneumoniae B5055-induced sepsis.
Chhibber, S; Harjai, K; Kumar, V, 2009
)
1.17
"His thalidomide treatment was withdrawn and his symptoms and HRCT findings improved."( [Case of thalidomide-induced interstitial pneumonia].
Hasejima, N; Matsushima, H; Oda, T; Sato, A; Takezawa, S; Yamamoto, M, 2009
)
1.25
"The thalidomide treatment was discontinued whereupon the hypoxaemia and the ground glass opacities resolved and the diffusion capacity impairment improved."( [Interstitial pneumonitis as an adverse effect of thalidomide].
Custers, FL; Lie, KS; Potjewijd, J; Scholte, JB; Voogt, PJ, 2009
)
1.09
"Thalidomide-treated cells also released less of other leaderless proteins, which require caspase-1 activity for their secretion."( Thalidomide inhibits activation of caspase-1.
Beer, HD; Keller, M; Sollberger, G, 2009
)
2.52
"Thalidomide treatment finally led to complete remission."( Disseminated cutaneous lymphoid hyperplasia of 12 years' duration triggered by vaccination.
Beylot-Barry, M; Doutre, MS; Pham-Ledard, A; Vergier, B, 2010
)
1.08
"The thalidomide treatment was discontinued whereupon the hypoxaemia and the ground glass opacities resolved and the diffusion capacity impairment improved."( [Interstitial pneumonitis as an adverse effect of thalidomide].
Custers, FL; Jie, KS; Potjewijd, J; Scholte, JB; Voogt, PJ, 2009
)
1.09
"Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway."( Integrated pathways for neutrophil recruitment and inflammation in leprosy.
Burdick, A; Carbone, RJ; Damoiseaux, R; Lee, DJ; Li, H; Modlin, RL; Ochoa, MT; Rea, TH; Sarno, EN; Tanaka, M, 2010
)
1.08
"Thalidomide-treated animals received thalidomide i.p."( The immunosuppressant drug, thalidomide, improves hepatic alterations induced by a high-fat diet in mice.
Bartchewsky, W; Carvalho, Pde O; Cintra, DE; Compri, CM; Fornari, JV; Gambero, A; Pedrazzoli, J; Pinto, Lde F; Ribeiro, ML; Saad, MJ; Trevisan, M; Velloso, LA, 2010
)
1.38
"Thalidomide treatment increased platelet-derived growth factor-B (PDGF-B) expression in endothelial cells and stimulated mural cell activation."( Thalidomide stimulates vessel maturation and reduces epistaxis in individuals with hereditary hemorrhagic telangiectasia.
Arthur, HM; Bréant, C; Disch, F; Eichmann, A; Freitas, C; Larrivée, B; Lebrin, F; Mager, JJ; Martin, S; Mathivet, T; Mummery, CL; Raymond, K; Snijder, RJ; Srun, S; Thomas, JL; van den Brink, S; Westermann, CJ, 2010
)
2.52
"Thalidomide treatment modulated pro-inflammatory function of alveolar macrophages by significantly (p<0.05) decreasing their phagocytic potential in terms of phagocytic uptake and intracellular killing, spreading and hydrogen peroxide (H2O2) release."( Thalidomide treatment modulates macrophage pro-inflammatory function and cytokine levels in Klebsiella pneumoniae B5055 induced pneumonia in BALB/c mice.
Chhibber, S; Harjai, K; Kumar, V, 2010
)
2.52
"Thalidomide was used as treatment in colitis and arthritis group, whereas etoricoxib was used in CWG group."( Correlation of seizures and biochemical parameters of oxidative stress in experimentally induced inflammatory rat models.
Khanduja, KL; Medhi, B; Pandhi, P; Rao, RS, 2010
)
1.08
"Thalidomide is a powerful treatment for inflammatory and cancer-based diseases. "( Apoptosis induction by thalidomide: critical for limb teratogenicity but therapeutic potential in idiopathic pulmonary fibrosis?
Jungck, D; Knobloch, J; Koch, A, 2011
)
2.12
"Thalidomide treatment was associated with significant down-regulation of nuclear NF-κB expression levels in residual neoplastic cells and microenvironments of responsive tumors, but not in t(11;18)(q21;q21)-positive, thalidomide-refractory tumors."( t(11;18)(q21;q21) translocation as predictive marker for non-responsiveness to salvage thalidomide therapy in patients with marginal zone B-cell lymphoma with gastric involvement.
Chen, LT; Cheng, AL; Hsu, CH; Kuo, SH; Lin, CW; Tzeng, YS; Wu, MS; Yeh, KH, 2011
)
1.31
"Thalidomide effectively treats PNH refractory to standard medications."( Thalidomide in 42 patients with prurigo nodularis Hyde.
Andersen, TP; Fogh, K, 2011
)
2.53
"Thalidomide was the only treatment that attenuated these increases."( The thalidomide analgesic effect is associated with differential TNF-α receptor expression in the dorsal horn of the spinal cord as studied in a rat model of neuropathic pain.
Andrade, P; Buurman, WA; Daemen, MA; Del Rosario, JS; Hoogland, G; Steinbusch, HW; Visser-Vandewalle, V, 2012
)
1.66
"Thalidomide treatment also leads to destruction of TNF-α mRNA thus, reducing the total expression of TNF-α protein."( TNF α signaling beholds thalidomide saga: a review of mechanistic role of TNF-α signaling under thalidomide.
Banerjee, S; Chatterjee, S; Majumder, S; Sreedhara, SR, 2012
)
1.41
"Thalidomide is the treatment of choice for severe or recurrent erythema nodosum leprosum. "( Deep vein thrombosis in a patient with lepromatous leprosy receiving thalidomide to treat leprosy reaction.
Burgués-Calderón, M; de la Hera, I; Fuertes, L; Hebe Petiti-Martin, G; Rivera-Díaz, R; Vanaclocha, F; Villar-Buill, M, 2013
)
2.07
"Thalidomide treatment prevented hyperglycemia and preserved pancreatic insulin secretion in the diabetic mice."( Thalidomide attenuates multiple low-dose streptozotocin-induced diabetes in mice by inhibition of proinflammatory cytokines.
Amirshahrokhi, K; Ghazi-Khansari, M, 2012
)
2.54
"Thalidomide treatment attenuated significantly STZ induced cognitive impairment and histopathological changes."( Thalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in rats.
Alan, S; Elçioğlu, H; Kabasakal, L; Karan, M; Salva, E; Tufan, F, 2013
)
2.55
"Thalidomide treatment significantly reduced gene expression of these cytokines and the activation of the NF-κB in the renal tissue and the circulating levels of cytokines."( Thalidomide suppresses inflammation in adenine-induced CKD with uraemia in mice.
Blanco, P; Catanozi, S; de Sá Lima, L; Degaspari, S; Dellê, H; Noronha, IL; Santana, AC; Scavone, C; Silva, C; Solez, K, 2013
)
2.55
"Thalidomide treatment was found to inhibit TNFalpha production in a dose-dependent manner in human macrophages exposed to Ti particles."( Thalidomide blocking of particle-induced TNFalpha release in vitro.
Bostrom, MP; Lin, JH; Yang, X, 2003
)
2.48
"Thalidomide treatment appeared to reverse the loss of weight and lean body mass over the 2-week trial period."( Oesophageal cancer and cachexia: the effect of short-term treatment with thalidomide on weight loss and lean body mass.
Austin, A; Cole, AT; Freeman, JG; Holt, M; Khan, ZH; MacDonald, I; Pye, D; Simpson, EJ, 2003
)
1.99
"Thalidomide + CCl(4) treated rats showed minor histological alterations and thinner bands of collagen."( Thalidomide ameliorates carbon tetrachloride induced cirrhosis in the rat.
Fernández-Martínez, E; García, J; Lara-Ochoa, F; Muriel, P; Pérez-Alvarez, V; Ponce, S; Shibayama, M; Tsutsumi, V, 2003
)
2.48
"Thalidomide treatment did not significantly alter tumor growth as compared with controls."( Thalidomide is anti-angiogenic in a xenograft model of neuroblastoma.
Beck, L; Frischer, JS; Huang, J; Kadenhe-Chiweshe, A; Kaicker, S; Kandel, JJ; McCrudden, KW; New, T; Serur, A; Yamashiro, DJ; Yokoi, A, 2003
)
2.48
"Thalidomide-treated and untreated animals showed the same amount of M."( Experimental murine mycobacteriosis: evaluation of the functional activity of alveolar macrophages in thalidomide- treated mice.
Arruda, MS; Oliveira, SM; Richini, VB; Vilani-Moreno, FR, 2004
)
1.26
"Thalidomide pretreatment did not affect NF-kappaB activity in HT-29 cells stimulated with LPS but production of TNF-alpha was depressed."( The effects of thalidomide on the stimulation of NF-kappaB activity and TNF-alpha production by lipopolysaccharide in a human colonic epithelial cell line.
Jung, HC; Kim, JS; Kim, YS; Song, IS, 2004
)
1.4
"Thalidomide treatment had no significant effect on markers of apoptosis including sunburn cell formation and terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labelling, which identifies single-strand breaks in DNA."( Photoprotection by thalidomide in patients with chronic cutaneous and systemic lupus erythematosus: discordant effects on minimal erythema dose and sunburn cell formation.
Cummins, DL; Gaspari, AA, 2004
)
1.37
"Thalidomide-treated group was given thalidomide (10mg/kg/day) intraperitoneally for 10 consecutive days."( Thalidomide salvages lethal hepatic necroinflammation and accelerates recovery from cirrhosis in rats.
Chen, MF; Ho, YP; Huang, SF; Jan, YY; Yeh, JN; Yeh, TS, 2004
)
2.49
"Thalidomide-treated patients had a prevalence of AVN similar to that of the control group (8% v 10%, respectively; P = .58)."( Avascular necrosis of femoral and/or humeral heads in multiple myeloma: results of a prospective study of patients treated with dexamethasone-based regimens and high-dose chemotherapy.
Anaissie, E; Angtuaco, E; Barlogie, B; Dong, L; Miceli, MH; Talamo, G; Tricot, G; Walker, RC; Zangari, M, 2005
)
1.05
"Thalidomide treatment compares favourably with other typical treatments for multiple myeloma."( The current status of thalidomide in the management of multiple myeloma.
Glasmacher, A; von Lilienfeld-Toal, M, 2005
)
1.36
"Thalidomide treatment did not protect normal mice from death but decreased remote lesion occurrence, with concurrent reduced bacterial counts recoverable from blood."( Lethal outcome caused by Porphyromonas gingivalis A7436 in a mouse chamber model is associated with elevated titers of host serum interferon-gamma.
Hu, SW; Huang, JH; Lai, YY; Lin, YY, 2006
)
1.06
"Thalidomide treatment before ischemic insult reduces early phase ischemia/reperfusion injury of the spinal cord in rabbits."( The effect of thalidomide on spinal cord ischemia/reperfusion injury in a rabbit model.
Kim, CS; Kim, KW; Lee, CJ; Lee, HM; Lim, YJ; Nahm, FS; Park, JH, 2007
)
2.14
"Thalidomide treatment is an adequate therapeutic measure in adult Langerhans cell histiocytosis, which is rare and difficult to treat. "( [Thalidomide in adult multisystem Langerhans cell histiocytosis: a case report].
Alioua, Z; Frikh, R; Ghfir, M; Hjira, N; Oumakhir, S; Rimani, M; Sedrati, O, 2006
)
2.69
"The thalidomide-treated group showed a significant increase of urinary protein on day 3. "( Postinflammatory glomerular recanalization is established under the accommodation of transformed mesangial cells.
Aoyagi, D; Chowdury, R; Otani, M; Shigematsu, H; Zhang, L,
)
0.69
"In thalidomide-treated mice, TNF-alpha RNA levels were reduced in the SCN."( Tumor necrosis factor alpha and macrophages in the brain of herpes simplex virus type 1-infected BALB/c mice.
Atherton, SS; Fields, M; Zhang, M; Zheng, M, 2006
)
0.85
"Thalidomide treatment decreased TNF and IL-1 significantly in both experimental groups at both the points (P<0.05)."( Thalidomide decreases the plasma levels of IL-1 and TNF following burn injury: is it a new drug for modulation of systemic inflammatory response.
Eski, M; Ifran, A; Sahin, I; Sengezer, M; Serdar, M, 2008
)
2.51
"Thalidomide treatment decreases PMNL infiltration, retinal edema, VEGF, and TNF-alpha synthesis following I/R injury to the guinea pig retina."( The effect of thalidomide on vascular endothelial growth factor and tumor necrosis factor-alpha levels in retinal ischemia/reperfusion injury.
Akpolat, N; Aydoğan, S; Celiker, U; Ilhan, N; Türkçüoğlu, P, 2008
)
2.15
"Thalidomide treatment increased retinal endostatin level in ischemia/reperfusion-injured guinea pig retinas."( Effect of thalidomide on endostatin levels in retinal ischemia/reperfusion injury.
Aydoğan, S; Celiker, U; Ilhan, N; Türkçüoğlu, P, 2007
)
2.18
"Thalidomide treatment in vivo was also associated with a significant reduction in hippocampal neuronal loss."( Thalidomide inhibition of perturbed vasculature and glial-derived tumor necrosis factor-alpha in an animal model of inflamed Alzheimer's disease brain.
McLarnon, JG; Ryu, JK, 2008
)
2.51
"Thalidomide treatment significantly reduced the degree of: 1) spinal cord inflammation and tissue injury (histological score); 2) neutrophil infiltration (myeloperoxidase evaluation); 3) iNOS, nitrotyrosine, lipid peroxidation, and cytokine expression (TNF-alpha and IL-1beta); 4) apoptosis (terminal deoxynucleotidyltransferase-mediated UTP end labeling staining, and Bax and Bcl-2 expression); and 5) nuclear factor-kappaB activation."( Effect of thalidomide on signal transduction pathways and secondary damage in experimental spinal cord trauma.
Bramanti, P; Caminiti, R; Cuzzocrea, S; Di Paola, R; Esposito, E; Genovese, T; Mazzon, E; Meli, R, 2008
)
1.47
"Thalidomide treatment should be further studied as a treatment for POEMS syndrome, particularly for patients who are not indicated for transplantation therapy."( Thalidomide reduces serum VEGF levels and improves peripheral neuropathy in POEMS syndrome.
Hattori, T; Kanai, K; Kuwabara, S; Misawa, S; Nakaseko, C; Nishimura, M; Sawai, S, 2008
)
3.23
"Thalidomide treatment was well tolerated, without serious adverse events. "( Thalidomide treatment reduces tumor necrosis factor alpha production and enhances weight gain in patients with pulmonary tuberculosis.
Akarasewi, P; Burroughs, M; Johnson, B; Kaplan, G; Klausner, JD; Makonkawkeyoon, S; Molloy, A; Rom, W; Tramontana, JM; Utaipat, U, 1995
)
3.18
"Thalidomide treatment reduces TNF alpha production both in vivo and in vitro and is associated with an accelerated weight gain during the study period."( Thalidomide treatment reduces tumor necrosis factor alpha production and enhances weight gain in patients with pulmonary tuberculosis.
Akarasewi, P; Burroughs, M; Johnson, B; Kaplan, G; Klausner, JD; Makonkawkeyoon, S; Molloy, A; Rom, W; Tramontana, JM; Utaipat, U, 1995
)
2.46
"Thalidomide treated rats had lower TNF levels at all time points (P = <0.01 at 90 and 120 min), with the inhibition being dose dependent."( Thalidomide inhibits TNF response and increases survival following endotoxin injection in rats.
Condon, M; Hsieh, J; Murphy, T; Rush, B; Schmidt, H; Simonian, G, 1996
)
2.46
"Thalidomide treatment reduces TNF-alpha production in both experimental systems, but has a greater effect on the more indolent gram positive inflammatory response in which peak TNF-alpha levels in the CSF are reduced by > 50%."( Effect of thalidomide on the inflammatory response in cerebrospinal fluid in experimental bacterial meningitis.
Burroughs, MH; Kaplan, G; Ossig, J; Sokol, K; Tsenova-Berkova, L; Tuomanen, E, 1995
)
1.41
"Thalidomide treatment (400 mg/day), however, dramatically improved the colitis within 7 days: fever and diarrhoea disappearing."( Treatment of colitis in Behçet's disease with thalidomide.
den Haan, P; Postema, PT; van Blankenstein, M; van Hagen, PM, 1996
)
1.27
"Thalidomide treatment increased HIV RNA levels (median increase, 0.42 log10 copies per milliliter; increase with placebo, 0.05; P=0.04)."( Thalidomide for the treatment of oral aphthous ulcers in patients with human immunodeficiency virus infection. National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group.
Chernoff, M; Fahey, JL; Fox, L; Greenspan, JS; Jackson, JB; Jacobson, JM; Ketter, N; MacPhail, LA; Spritzler, J; Vasquez, GJ; Wohl, DA; Wu, AW, 1997
)
2.46
"Thalidomide treatment did not interfere with the production of GM-CSF, IL-1 beta, or IFN-gamma."( Thalidomide protects mice against LPS-induced shock.
Kaplan, G; Moreira, AL; Sarno, EN; Wang, J, 1997
)
2.46
"When thalidomide treatment was combined with antibiotics, there was a marked reduction in TNF-alpha levels, leukocytosis, and brain pathology."( A combination of thalidomide plus antibiotics protects rabbits from mycobacterial meningitis-associated death.
Freedman, VH; Kaplan, G; Sokol, K; Tsenova, L, 1998
)
1.09
"Thalidomide treatment resulted in a significant reduction in tumor necrosis factor-alpha, interleukin 6 (IL-6) and IL-10 protein levels (blood) and mRNA expression (lungs)."( Effect of cytokine modulation by thalidomide on the granulomatous response in murine tuberculosis.
Freedman, VH; Freeman, S; Kaplan, G; Laochumroonvorapong, P; Moreira, AL; Tsenova-Berkova, L; Wang, J, 1997
)
1.3
"Thalidomide-treated LNCaP cells demonstrated increased PSA/cell levels at all concentrations tested compared to untreated control cells."( Thalidomide up-regulates prostate-specific antigen secretion from LNCaP cells.
Bauer, KS; Dixon, SC; Figg, WD; Kruger, EA, 1999
)
2.47
"Thalidomide treatment increased CD4+ and CD8+ T cell counts and lymphocyte proliferation to purified protein derivative."( Thalidomide-induced antigen-specific immune stimulation in patients with human immunodeficiency virus type 1 and tuberculosis.
Bekker, LG; Haslett, P; Kaplan, G; Maartens, G; Steyn, L, 2000
)
2.47
"Thalidomide treatment was found to cause potent and selective inhibition of IL-8 production in a dose-responsive manner."( Effect of thalidomide on chemokine production by human microglia.
Hu, S; Lokensgard, JR; Peterson, PK; Sheng, WS; van Fenema, EM, 2000
)
1.43
"In thalidomide-treated SSc patients, plasma levels of IL-12 and TNF-alpha increased, while plasma IL-5 and IL-10 levels remained unchanged."( Immune stimulation in scleroderma patients treated with thalidomide.
Kaplan, G; Moreira, A; Oliver, SJ, 2000
)
1.07
"Thalidomide treatment significantly reduced cell adhesion molecule expression in a dose-dependent fashion and inhibited HUVEC/CEM cell adhesion."( Down-regulation of cell adhesion molecules LFA-1 and ICAM-1 after in vitro treatment with the anti-TNF-alpha agent thalidomide.
Davis, MF; Ezell, T; Mack, C; Settles, B; Stevenson, A; Taylor, LD; Wilson, K, 2001
)
1.24
"Thalidomide treatment was successful in the majority of animals (16 of 18)."( Therapy of chronic graft-v-host disease in a rat model.
Friedman, KJ; Hess, AD; Santos, GW; Vogelsang, GB, 1989
)
1
"Treatment with thalidomide stopped the progression of the disease in two cases."( Progressive mucinous histiocytosis treated successfully with thalidomide: a rare case report.
Abdollahimajd, F; Diab, R; Kaddah, A; Rakhshan, A; Shahidi Dadras, M, 2023
)
1.49
"Treatment with thalidomide markedly stimulated the phosphorylation of AMPKα."( Renal-protective effect of thalidomide in streptozotocin-induced diabetic rats through anti-inflammatory pathway.
Li, R; Wang, B; Wang, Y; Yang, Y; Zhang, H, 2018
)
1.12
"Treatment with thalidomide is associated with an increased risk of developing peripheral neuropathy, which can be managed with dose reductions and discontinuation, and venous thromboembolism, which warrants thromboprophylaxis."( Role of thalidomide in the treatment of patients with multiple myeloma.
Davies, FE; Morgan, GJ, 2013
)
1.16
"Treatment with thalidomide is associated with vascular thrombosis. "( Increased PAC-1 expression among patients with multiple myeloma on concurrent thalidomide and warfarin.
Abdullah, D; Abdullah, WZ; Hussin, A; Roshan, TM; Zain, WS, 2013
)
0.97
"Treatment with thalidomide has proved to be effective in the management of these patients."( Scleromyxedema without paraproteinemia.
Abarzúa, AA; Giesen, LF; González, SB; Sandoval, MO, 2014
)
0.74
"Treatment with thalidomide and lenalidomide significantly inhibited osteoblast development in vitro, as reflected by a reduction of alkaline phosphatase activity and matrix mineralization."( Immunomodulatory drugs thalidomide and lenalidomide affect osteoblast differentiation of human bone marrow stromal cells in vitro.
Bolomsky, A; Hose, D; Ludwig, H; Meißner, T; Pfeifer, S; Schreder, M; Zojer, N, 2014
)
1.05
"Treatment with thalidomide restored malondialdehyde as well as reduction of myeloperoxidase and tumour necrosis factor-alpha towards normal levels."( Effect of different doses of thalidomide in experimentally induced inflammatory bowel disease in rats.
Medhi, B; Pandhi, P; Prakash, O; Saikia, UN, 2008
)
0.98
"Pretreatment with thalidomide also blocked the ocular hypotension induced by latanoprost; however, thalidomide pretreatment enhanced the duration of the initial hypertension."( Latanoprost-induced changes in rat intraocular pressure: direct or indirect?
Crosson, CE; Husain, S; Yates, PW, 2008
)
0.67
"The treatment with thalidomide is associated with an increased risk of thromboembolic events, in particular when it is combined with chemotherapy or dexamethasone. "( Disseminated intravascular coagulation during treatment with thalidomide. A case report.
Sartori, S; Tassinari, D; Tombesi, P,
)
0.7
"Treatment with thalidomide alone significantly (p<0.05) decreased interleukin-1 alpha (IL-1alpha), nitric oxide (NO) and malondialdehyde (MDA) levels in the serum without significantly (p<0.05) decreasing the bacterial count in blood."( A combination of thalidomide and augmentin protects BALB/c mice suffering from Klebsiella pneumoniae B5055-induced sepsis.
Chhibber, S; Harjai, K; Kumar, V, 2009
)
1.03
"Treatment with Thalidomide preserved VV spatial density [2.7 +/- 0.3 (N), 6.4 +/- 0.7 (HC), 3.5 +/- 0.8 (HC + Th); p = ns HC + Th vs."( Prevention of vasa vasorum neovascularization attenuates early neointima formation in experimental hypercholesterolemia.
Galili, O; Gössl, M; Herrmann, J; Lerman, A; Lerman, LO; Mannheim, D; Rajkumar, SV; Tang, H; Versari, D, 2009
)
0.69
"Treatment with thalidomide showed a significant remission of skin lesions compared to acetylsalicylic acid (aspirin) (RR 2.43; 95% CI 1.28 to 4.59) (1 trial, 92 participants)."( Interventions for erythema nodosum leprosum.
Lockwood, DN; Ramirez, J; Richardus, JH; van Brakel, WH; Van Veen, NH, 2009
)
0.69
"Rats treated with thalidomide showed significant increase in SC water compared with naive rats, but not vehicle-treated rats; their neutrophil infiltration and amount of spared/destroyed cord tissue was not different from vehicle-treated rats; and in no case was motor performance improved after thalidomide."( Thalidomide fails to be therapeutic following contusive spinal cord injury in rats.
Franco-Bourland, RE; Fuchs, B; Grijalva, I; Guízar-Sahagún, G; Madrazo, I; Martínez-Cruz, A; Reyes-Alva, HJ, 2009
)
2.12
"Treatment with thalidomide showed a significant benefit compared to aspirin (RR 2.43; 95% CI 1.28 to 4.59)."( Interventions for erythema nodosum leprosum. A Cochrane review.
Lockwood, DN; Ramirez, J; Richardus, JH; Van Brakel, WH; Van Veen, NH, 2009
)
0.69
"Pretreatment with thalidomide and analogues before activation was not different from simultaneous treatment."( Effect of thalidomide on nitric oxide production in lipopolysaccharide-activated RAW 264.7 cells.
Greig, N; Jung, E; Levis, WR; Park, E; Schuller-Levis, G, 2010
)
1.09
"Treatment with thalidomide resulted in a significant decrease in AUC, PI and IMAX compared with Group A (p<0.05)."( Quantitative evaluation of viable tissue perfusion changes with contrast-enhanced greyscale ultrasound in a mouse hepatoma model following treatment with different doses of thalidomide.
Cao, LH; Han, F; Li, AH; Liu, M; Luo, RZ; Wu, PH; Zheng, W; Zhou, JH, 2011
)
0.9
"Treatment with thalidomide resulted in a significant decrease in perfusion scores assigned to AUC, IMAX and PI parametric images as compared with control tumors (P < 0.001). "( Contrast-enhanced ultrasonic parametric perfusion imaging in the evaluation of antiangiogenic tumor treatment.
Cao, LH; Han, F; Li, AH; Liu, M; Luo, RZ; Wu, PH; Zheng, W; Zhou, JH, 2012
)
0.73
"Pretreatment with thalidomide did not induce statistically significant changes in overall tumor control induced by the"( Tumor blood vessel "normalization" improves the therapeutic efficacy of boron neutron capture therapy (BNCT) in experimental oral cancer.
Aromando, RF; Garabalino, MA; Heber, EM; Itoiz, ME; Miller, M; Molinari, AJ; Monti Hughes, A; Nigg, DW; Pozzi, EC; Schwint, AE; Thorp, SI; Trivillin, VA, 2012
)
0.7
"Treatment with thalidomide met the protocol specified goal of prolonging PFS at 6 months. "( A phase II trial of thalidomide in patients with refractory uterine carcinosarcoma and correlation with biomarkers of angiogenesis: a Gynecologic Oncology Group study.
Abulafia, O; Benbrook, DM; Darcy, KM; Hanjani, P; McMeekin, DS; Pearl, ML; Rose, PG; Rubin, SC; Sill, MW; Small, L, 2012
)
1.06
"Treatment with thalidomide significantly reduced serum urea, creatinine, phosphorus and iPTH levels and protected against tubulointerstitial injury."( Thalidomide suppresses inflammation in adenine-induced CKD with uraemia in mice.
Blanco, P; Catanozi, S; de Sá Lima, L; Degaspari, S; Dellê, H; Noronha, IL; Santana, AC; Scavone, C; Silva, C; Solez, K, 2013
)
2.17
"Treatment with thalidomide caused a preferential decrease in GFP expression in rabbit LBCs but not in rat LBCs."( Misregulation of gene expression in the redox-sensitive NF-kappab-dependent limb outgrowth pathway by thalidomide.
Gong, SG; Hansen, JM; Harris, C; Philbert, M, 2002
)
0.87
"Treatment with thalidomide was not shown to be effective and was associated with significantly higher mortality than placebo. "( Interventions for toxic epidermal necrolysis.
Majumdar, S; Mockenhaupt, M; Roujeau, J; Townshend, A, 2002
)
0.67
"Treatment with thalidomide, alone and in combination with other therapies, may improve survival for patients with advanced renal cell carcinoma."( Continuing education: The emergence of thalidomide in treating advanced renal cell carcinoma.
Monroe, D; Perez, C; Wood, LS,
)
0.75
"Mice treated with thalidomide had significantly smaller mean (7986 +/- 5189 vs 19607 +/- 10353 microns 2, p = 0.05) and maximum (15800 [12777-23675] vs 37169 [28000-41351] microns 2, p = 0.03) lesion sizes than those treated with placebo."( Thalidomide inhibits early atherogenesis in apoE-deficient mice.
Chew, M; Daugherty, A; Ellermann-Eriksen, S; Eriksson, T; Falk, E; Hansen, PR; Zhou, J, 2003
)
2.09
"We treated with thalidomide 17 patients (12 males, 5 females), average age 51 (range 42-73 years), mean time since diagnosis to the start of thalidomide treatment was 24 months (range 5-48)."( [Preliminary results of monotherapy with thalidomide in recurrent and treatment resistant cases of multiple myeloma].
Helbig, G; Hołowiecki, J; Kyrcz-Krzemień, S; Stella-Hołowiecka, B, 2003
)
0.92
"Treatment with thalidomide resulted in apoptosis of human peripheral blood monocytes in a time- and dose-dependent manner as demonstrated by annexin V staining."( Thalidomide induces apoptosis in human monocytes by using a cytochrome c-dependent pathway.
Domschke, W; Gockel, HR; Heidemann, J; Kucharzik, T; Lügering, A; Lügering, N; Schmidt, M, 2004
)
2.11
"Treatment with thalidomide, 100 mg/d. "( Thalidomide treatment for prurigo nodularis in human immunodeficiency virus-infected subjects: efficacy and risk of neuropathy.
Berger, T; Maurer, T; Poncelet, A, 2004
)
2.12
"Treatment with thalidomide is a potentially useful antitumor therapy for ovarian cancer."( [Study of thalidomide on the growth and angiogenesis of ovary cancer SKOV3 transplanted subcutaneously in nude mice].
Cao, ZY; Li, W; Peng, ZL, 2005
)
1.07
"We treated with thalidomide seven patients with primary MDS and observed reduction of the transfusion requirement in three cases and reduction of bone marrow blasts in one case. "( Thalidomide treatment reduces apoptosis levels in bone marrow cells from patients with myelodysplastic syndromes.
Ascari, E; Benatti, C; Brugnatelli, S; De Amici, M; Invernizzi, R; Ramajoli, I; Rovati, B; Travaglino, E, 2005
)
2.12
"Treatment with thalidomide resulted in complete resolution of the cutaneous lesions within one month of therapy."( Thalidomide in the treatment of recalcitrant Sweet's syndrome associated with myelodysplasia.
Browning, CE; Callen, JP; Dixon, JE; Malone, JC, 2005
)
2.11
"Treatment with thalidomide would prove more efficacious if the drug could be delivered directly to target areas in the gut, thereby reducing systemic circulation."( A new method for targeted drug delivery using polymeric microcapsules: implications for treatment of Crohn's disease.
Amre, D; Chen, H; Das, SK; Halim, T; Haque, T; Jones, ML; Metz, T; Mirzaei, M; Prakash, S, 2005
)
0.67
"Treatment with thalidomide resulted in significantly less potent inhibition of osteoclast formation and bone resorption."( Thalidomide derivative CC-4047 inhibits osteoclast formation by down-regulation of PU.1.
Anderson, G; Anderson, J; Donnenberg, A; Donnenberg, V; Ghobrial, I; Gries, M; Honjo, T; Kurihara, N; Lentzsch, S; Mapara, MY; Roodman, D; Stirling, D, 2006
)
2.12
"Treatment with thalidomide, 50-150 mg/d, and prednisolone, 25 mg/d, resulted in an increase in haemoglobin to 8.9 mmol/l during the following months."( [Refractory anaemia successfully treated with thalidomide].
Hansen, M; Hansen, PB, 2006
)
0.93
"We treated with thalidomide 200 mg/day after neurological examination."( [Thalidomide in adult multisystem Langerhans cell histiocytosis: a case report].
Alioua, Z; Frikh, R; Ghfir, M; Hjira, N; Oumakhir, S; Rimani, M; Sedrati, O, 2006
)
1.58
"Treatment with thalidomide seems an effective therapy for patients with frequently recurring gastrointestinal blood loss due to angiodysplasias who no longer tolerate conventional and invasive procedures due to their physical condition."( [Thalidomide for the treatment of recurrent gastrointestinal blood loss due to intestinal angiodysplasias].
de Koning, DB; Drenth, JP; Friederich, P; Nagengast, FM, 2006
)
1.58
"Treatment with thalidomide led to resolution of the disease."( Successful thalidomide therapy for actinic prurigo in a European woman.
Hofer, A; Holzer, A; Kerl, H; Legat, FJ; Wolf, P, 2006
)
1.06
"Treatment with thalidomide was started and great improvement of the lesion was noted as shown by a quality of life questionnaire similar to those used in rheumatoid arthritis."( Scleromyxedema: successful treatment with thalidomide in two patients.
Amini-Adle, M; Balme, B; Dalle, S; Thieulent, N; Thomas, L, 2007
)
0.94
"Treatment with thalidomide was associated with a significant decrease in plasma bFGF (p=0.008) and serum sEPCR (p=0.006), but not in plasma VEGF."( A phase II trial of thalidomide in patients with refractory leiomyosarcoma of the uterus and correlation with biomarkers of angiogenesis: a gynecologic oncology group study.
Benbrook, D; Darcy, KM; McMeekin, DS; Sill, MW; Stearns-Kurosawa, DJ; Waggoner, S; Webster, K, 2007
)
1
"Treatment with thalidomide was not associated with a significant improvement in survival of SCLC patients. "( Phase III double-blind, placebo-controlled study of thalidomide in extensive-disease small-cell lung cancer after response to chemotherapy: an intergroup study FNCLCC cleo04 IFCT 00-01.
Breton, JL; David, P; Gameroff, S; Genève, J; Gervais, R; Janicot, H; Maraninchi, D; Pujol, JL; Quoix, E; Tanguy, ML; Westeel, V, 2007
)
0.94
"The treatment with thalidomide was continued as maintenance for up to 2 years."( Phase II trial of thalidomide with chemotherapy and as maintenance therapy for patients with poor prognosis small-cell lung cancer.
Buchler, T; Ellis, P; Hackshaw, A; James, L; Lee, SM; Snee, M, 2008
)
1
"Treatment with thalidomide provides an effective alternative to steroid therapy, gives better long-term control and avoids the adverse effects of prolonged steroid therapy."( The role of thalidomide in the management of erythema nodosum leprosum.
Lockwood, DN; Walker, SL; Waters, MF, 2007
)
1.06
"Cotreatment with thalidomide (150 mg.kg(-1).day(-1) for 7 days) also reduced hyperreactivity to phenylephrine induced by isoproterenol."( Effects of isoproterenol treatment for 7 days on inflammatory mediators in the rat aorta.
Cachofeiro, V; Davel, AP; De Sá, LL; Fukuda, LE; Lahera, V; Munhoz, CD; Rossoni, LV; Sanz-Rosa, D; Scavone, C, 2008
)
0.67
"Treatment with thalidomide produced complete resolution of ulcers in 14 and significant improvement in the remaining patient."( Thalidomide in severe orogenital ulceration.
Allen, BR; Jenkins, JS; Littlewood, SM; Maurice, PD; Powell, RJ; Smith, NJ, 1984
)
2.05
"Treatment with thalidomide resulted in a dramatic clearing of skin lesions but failed to improve pathological laboratory tests."( [Treatment of subacute cutaneous lupus erythematosus with thalidomide].
Volc-Platzer, B; Wolff, K, 1983
)
0.85
"Treatment with thalidomide neither consistently altered mycobacterial burden in the spleens or livers of infected mice nor affected serum TNF-alpha levels."( Inhibition of tumor necrosis factor alpha alters resistance to Mycobacterium avium complex infection in mice.
Bala, S; Dempsey, WL; Hastings, KL; Inglis, S; Kazempour, K, 1998
)
0.64
"Treatment with thalidomide led to rapid regression."( [Bullous erythema nodosum leprosum. A case report in French Guiana].
About, V; Couppié, P; Heid, E; Pradinaud, R; Sainte-Marie, D, 1998
)
0.64
"Oral treatment of thalidomide or sulindac alone inhibited tumour growth by 55% and 35% respectively."( Combination oral antiangiogenic therapy with thalidomide and sulindac inhibits tumour growth in rabbits.
D'Amato, RJ; Panigrahy, D; Verheul, HM; Yuan, J, 1999
)
0.89
"Treatment with thalidomide resulted in prompt recovery of the mucocutaneous lesions and gastrointestinal manifestations."( Successful thalidomide treatment of severe infantile Behçet disease.
Bergman, R; Brik, R; Shamali, H,
)
0.86
"Treatment with thalidomide and dexamethasone was given to 26 patients with active, previously untreated multiple myeloma (MM). "( Therapeutic application of thalidomide in multiple myeloma.
Kyle, RA; Rajkumar, SV, 2001
)
0.96

Toxicity

Long term thalidomide is effective and safe for treating resistant ankylosing spondylitis and it has cumulative effect as duration prolongs. High-dose thalidmide has induced many adverse events, including in the nervous, gastrointestinal, and hematopoietic systems in approximately 20%-50% of patients. Severe skin reactions (exfoliative erythroderma, erythema multiforme, and toxic epidermal necrolysis) that required hospitalization and withdrawal of thalidamide developed in 3 patients receiving thalidumide and dexamethasone.

ExcerptReferenceRelevance
" Also the toxic dose to the mothers, 3000 mg/kg, given to rabbits in case of one FWA was without these effects."( Studies of embryo toxicity in rats and rabbits.
Lorke, D; Machemer, L, 1975
)
0.25
"The sedative thalidomide was withdrawn from the market 30 years ago because of its teratogenic and neurotoxic adverse effects."( Thalidomide in human immunodeficiency virus (HIV) patients. A review of safety considerations.
Günzler, V,
)
1.94
" Since reports on thalidomide neurotoxicity have shown that the neurological symptoms are long standing and possibly irreversible, it is obviously important to inform patients of this possible side effect and to evaluate them closely for the symptoms and electrophysiological signs of evolving neurological changes."( Thalidomide neurotoxicity.
Andersen, KE; Clemmensen, OJ; Olsen, PZ, 1984
)
2.04
" Thalidomide is a useful addition to the therapeutic armamentarium for treatment-resistant dermatoses as long as proper vigilance for adverse effects is maintained."( Rediscovering thalidomide: a review of its mechanism of action, side effects, and potential uses.
Pak, G; Pomeranz, MK; Shupack, JL; Tseng, S; Washenik, K, 1996
)
1.56
" In an interim analysis of nine patients, thalidomide had almost eliminated the dose-limiting gastrointestinal toxic effects of irinotecan, especially diarrhoea and nausea (each p<0."( Effect of thalidomide on gastrointestinal toxic effects of irinotecan.
Broadwater, R; Govindarajan, R; Hauer-Jensen, M; Heaton, KM; Lang, NP; Zeitlin, A, 2000
)
0.97
" During the first 18 months of spontaneous postmarketing adverse event surveillance for Thalomid, 1210 spontaneous postmarketing adverse event reports were received for patients treated with prescription thalidomide for all therapeutic indications, including off-label use."( Thalomid (Thalidomide) capsules: a review of the first 18 months of spontaneous postmarketing adverse event surveillance, including off-label prescribing.
Clark, TE; Edom, N; Larson, J; Lindsey, LJ, 2001
)
0.9
" Overall, adverse events were fatigue, constipation, rash, and neuropathy (grade 1 to 2 in most patients)."( Efficacy and safety of thalidomide in patients with acute myeloid leukemia.
Berdel, WE; Bieker, R; Buechner, T; Kessler, T; Kienast, J; Kropff, M; Mesters, RM; Padró, T; Ruiz, S; Steins, MB, 2002
)
0.63
" We conclude that severe lung toxicity should be included among the potential adverse effects of thalidomide."( [Lung toxicity due to thalidomide].
Bertomeu González, V; Carrión Valero, F, 2002
)
0.85
" We present the adverse effect profile of thalidomide in 23 relapsed or refractory MM patients treated with this drug over a period of 15 months."( The adverse effects of thalidomide in relapsed and refractory patients of multiple myeloma.
Grover, JK; Raina, V; Uppal, G, 2002
)
0.89
" In patients with advanced HF, thalidomide was safe and potentially effective when used at lower doses."( Preclinical and clinical assessment of the safety and potential efficacy of thalidomide in heart failure.
Agoston, I; Bozkurt, B; Dibbs, ZI; Mann, DL; Muller, G; Wang, F; Zeldis, JB, 2002
)
0.83
" Severe skin reactions (exfoliative erythroderma, erythema multiforme, and toxic epidermal necrolysis) that required hospitalization and withdrawal of thalidomide developed in 3 patients receiving thalidomide and dexamethasone."( Dermatologic side effects of thalidomide in patients with multiple myeloma.
Bouwhuis, S; El-Azhary, RA; Hall, VC; Rajkumar, SV, 2003
)
0.81
" As a result of adverse effects, salvage therapy had to be discontinued or reduced in 14 patients (26%)."( Outcome and toxicity of salvage treatment on patients relapsing after autologous hematopoietic stem cell transplantation--experience from a single center.
Berlanga, J; Büchler, T; Encuentra, M; Ferra, C; Gallardo, D; Grañena, A; Hermosilla, M; Sarra, J, 2003
)
0.32
"Thalidomide, an antiemetic administered in 60th of the 20th century to pregnant women, has become notorious for a range of adverse effects which led to its taking off market."( [Desirable and undesirable effects of thalidomide in patients with multiple myeloma].
Foldyna, D; Hájek, R; Kamelander, J; Krejcí, M, 2003
)
2.03
" In all, 87% of adverse effects were classified as grade 1 or grade 2 according to Common Toxicity Criteria and there were no serious adverse events attributable to CC-5013 treatment."( Phase I study to determine the safety, tolerability and immunostimulatory activity of thalidomide analogue CC-5013 in patients with metastatic malignant melanoma and other advanced cancers.
Bartlett, JB; Clarke, IA; Dalgleish, AG; Dredge, K; Kristeleit, H; Michael, A; Muller, GW; Nicholson, S; Pandha, H; Polychronis, A; Stirling, DI; Zeldis, J, 2004
)
0.55
"To determine the progression-free survival at 12 weeks, to evaluate the toxic effects, and to analyze the biological activity of thalidomide in patients with relapsed multiple myeloma (MM) after high-dose chemotherapy and stem cell transplantation."( Thalidomide for patients with relapsed multiple myeloma after high-dose chemotherapy and stem cell transplantation: results of an open-label multicenter phase 2 study of efficacy, toxicity, and biological activity.
Alsina, M; Anderson, K; Blood, E; Bosch, J; Dalton, W; Davies, F; Desikan, R; Doss, D; Freeman, A; Hideshima, T; Jagannath, S; Knight, R; Mitsiades, C; Patin, J; Richardson, P; Schlossman, R; Weller, E; Zeldis, J, 2004
)
1.97
"The optimal thalidomide dose varies, and adverse effects can be dose limiting."( Thalidomide for patients with relapsed multiple myeloma after high-dose chemotherapy and stem cell transplantation: results of an open-label multicenter phase 2 study of efficacy, toxicity, and biological activity.
Alsina, M; Anderson, K; Blood, E; Bosch, J; Dalton, W; Davies, F; Desikan, R; Doss, D; Freeman, A; Hideshima, T; Jagannath, S; Knight, R; Mitsiades, C; Patin, J; Richardson, P; Schlossman, R; Weller, E; Zeldis, J, 2004
)
2.15
" The incidence and severity of adverse events are related to dose and duration of therapy."( Management of thalidomide toxicity.
Ghobrial, IM; Rajkumar, SV,
)
0.49
"Neurotoxicity was the most troublesome and frequent toxic effect that was observed after long-term treatment, the incidence averaging 75%."( Neurological toxicity of long-term (>1 yr) thalidomide therapy in patients with multiple myeloma.
Baccarani, M; Cangini, D; Cavo, M; Cellini, C; Pastorelli, F; Perrone, G; Plasmati, R; Tacchetti, P; Tosi, P; Tura, S; Zamagni, E, 2005
)
0.59
" Their toxic profile is favorable, but during the drug development process some severe (sometimes lethal) toxicities have been observed, such as interstitial lung disease in patients treated with drugs targeting the epidermal growth factor receptor."( Side effects of anti-cancer molecular-targeted therapies (not monoclonal antibodies).
Awada, A; de Castro, G, 2006
)
0.33
" Adverse events, including thrombocytopenia and peripheral neuropathy, have affected 30% to 60% of patients overall, and interrupted therapy in 10% to 20%."( A multicenter retrospective analysis of adverse events in Korean patients using bortezomib for multiple myeloma.
Bang, SM; Cho, KS; Jo, DY; Kim, CC; Kim, CS; Kim, K; Lee, JH; Lee, JJ; Lee, KH; Lee, NR; Min, CK; Min, YH; Park, S; Seong, CM; Sohn, SK; Suh, C; Yoon, HJ; Yoon, SS, 2006
)
0.33
"Thalidomide is a relatively safe and efficacious form of therapy in the treatment of advanced, refractory multiple myeloma."( Thalidomide-induced severe hepatotoxicity.
Hanje, AJ; Meis, GM; Shamp, JL; Thomas, FB, 2006
)
3.22
"To examine dermatologic adverse effects of lenalidomide in patients with amyloidosis and multiple myeloma and to determine whether the adverse effects are different when lenalidomide is used alone compared with when it is used in combination with dexamethasone."( Dermatologic adverse effects of lenalidomide therapy for amyloidosis and multiple myeloma.
Davis, MD; Dispenzieri, A; Rajkumar, SV; Sviggum, HP, 2006
)
0.33
"The prevalence of dermatologic adverse effects in patients receiving lenalidomide was higher in those with amyloidosis than in those with multiple myeloma."( Dermatologic adverse effects of lenalidomide therapy for amyloidosis and multiple myeloma.
Davis, MD; Dispenzieri, A; Rajkumar, SV; Sviggum, HP, 2006
)
0.33
" Patients with comorbid disease had a significantly greater incidence of adverse reactions than those without (93."( Efficacy and safety of thalidomide in patients with hepatocellular carcinoma.
Chiou, HE; Liu, HW; Wang, TE; Wang, YY, 2006
)
0.64
" The majority of adverse events were grades 1-2, including fatigue (25/80 cycles), nausea/vomiting (23/80), constipation (13/80), abdominal pain (17/80), rash (12/80), neutropenia (12/80), and anemia (12/80)."( Safety and efficacy of lenalidomide (Revlimid) in recurrent ovarian and primary peritoneal carcinoma.
Chan, JK; Guo, HY; Husain, A; Teng, NN; Zhang, MM, 2007
)
0.34
" Neuropathy is the main adverse effect, but appears to be cumulative dose-dependent, thus allowing long-term remission before drug suspension."( Efficacy and safety of thalidomide in children and young adults with intractable inflammatory bowel disease: long-term results.
Bradaschia, F; Lazzerini, M; Marchetti, F; Martelossi, S; Ronfani, L; Scabar, A; Ventura, A, 2007
)
0.65
"In all studies, thalidomide was selectively toxic to development."( Evaluation of the developmental toxicity of lenalidomide in rabbits.
Christian, MS; Hoberman, A; Laskin, OL; Latriano, L; Sharper, V; Stirling, DI, 2007
)
0.69
" Unlike thalidomide, lenalidomide affected embryo-fetal development only at maternally toxic dosages, confirming that structure-activity relationships may not predict maternal or developmental effects."( Evaluation of the developmental toxicity of lenalidomide in rabbits.
Christian, MS; Hoberman, A; Laskin, OL; Latriano, L; Sharper, V; Stirling, DI, 2007
)
0.77
" The most common Grade 3/4 adverse events experienced on thalidomide monotherapy were venous thrombosis (3."( Systematic review to establish the safety profiles for direct and indirect inhibitors of p38 Mitogen-activated protein kinases for treatment of cancer. A systematic review of the literature.
Claflin, JE; Crean, S; Lahn, M; Linz, H; Noel, JK; Ranganathan, G, 2008
)
0.59
" Other toxic effects included infections, skin reactions."( Long term use of thalidomide: safe and effective.
Grover, J; Kumar, R; Raina, V; Sharma, A; Uppal, G,
)
0.47
" Serious adverse events including tumor flare and tumor lysis are summarized."( Higher doses of lenalidomide are associated with unacceptable toxicity including life-threatening tumor flare in patients with chronic lymphocytic leukemia.
Andritsos, LA; Awan, F; Blum, W; Byrd, JC; Chen, CS; Jarjoura, D; Johnson, AJ; Kefauver, C; Knight, RD; Lapalombella, R; Lehman, A; Lozanski, G; May, SE; Raymond, CA; Ruppert, AS; Smith, LL; Wang, DS, 2008
)
0.35
"Four consecutive patients were treated with lenalidomide; all had serious adverse events."( Higher doses of lenalidomide are associated with unacceptable toxicity including life-threatening tumor flare in patients with chronic lymphocytic leukemia.
Andritsos, LA; Awan, F; Blum, W; Byrd, JC; Chen, CS; Jarjoura, D; Johnson, AJ; Kefauver, C; Knight, RD; Lapalombella, R; Lehman, A; Lozanski, G; May, SE; Raymond, CA; Ruppert, AS; Smith, LL; Wang, DS, 2008
)
0.35
"Lenalidomide administered at 25 mg/d in relapsed CLL is associated with unacceptable toxicity; the rapid onset and adverse clinical effects of tumor flare represent a significant limitation of lenalidomide use in CLL at this dose."( Higher doses of lenalidomide are associated with unacceptable toxicity including life-threatening tumor flare in patients with chronic lymphocytic leukemia.
Andritsos, LA; Awan, F; Blum, W; Byrd, JC; Chen, CS; Jarjoura, D; Johnson, AJ; Kefauver, C; Knight, RD; Lapalombella, R; Lehman, A; Lozanski, G; May, SE; Raymond, CA; Ruppert, AS; Smith, LL; Wang, DS, 2008
)
0.35
" Thalidomide has been reported to be effective for these patients; however, high-dose thalidomide has induced many adverse events, including in the nervous, gastrointestinal, and hematopoietic systems in approximately 20%-50% of patients."( A pharmacokinetic study evaluating the relationship between treatment efficacy and incidence of adverse events with thalidomide plasma concentrations in patients with refractory multiple myeloma.
Abe, M; Iida, S; Kodama, T; Miyata, A; Murakami, H; Ozaki, S; Sakai, A; Sawamura, M; Shimazaki, C; Wakayama, T, 2009
)
1.47
" When severe adverse events did not develop, the dose was increased to 200 mg/day in the second week and was continued until progression."( A pharmacokinetic study evaluating the relationship between treatment efficacy and incidence of adverse events with thalidomide plasma concentrations in patients with refractory multiple myeloma.
Abe, M; Iida, S; Kodama, T; Miyata, A; Murakami, H; Ozaki, S; Sakai, A; Sawamura, M; Shimazaki, C; Wakayama, T, 2009
)
0.56
" Severe adverse events, including grade > 2 nonhematologic and grade > 3 hematologic adverse events, were observed in 21 patients (46."( A pharmacokinetic study evaluating the relationship between treatment efficacy and incidence of adverse events with thalidomide plasma concentrations in patients with refractory multiple myeloma.
Abe, M; Iida, S; Kodama, T; Miyata, A; Murakami, H; Ozaki, S; Sakai, A; Sawamura, M; Shimazaki, C; Wakayama, T, 2009
)
0.56
"The thalidomide concentration in the plasma does not predict treatment efficacy and the development of adverse events."( A pharmacokinetic study evaluating the relationship between treatment efficacy and incidence of adverse events with thalidomide plasma concentrations in patients with refractory multiple myeloma.
Abe, M; Iida, S; Kodama, T; Miyata, A; Murakami, H; Ozaki, S; Sakai, A; Sawamura, M; Shimazaki, C; Wakayama, T, 2009
)
1.12
" The most common grade 3 or 4 adverse events were neutropenia (60%), thrombocytopenia (39%), and anemia (20%), which proved manageable with dose reduction."( Safety and efficacy of single-agent lenalidomide in patients with relapsed and refractory multiple myeloma.
Anderson, KC; Badros, AZ; Bensinger, W; Berenson, J; Hussein, M; Irwin, D; Jagannath, S; Kenvin, L; Knight, R; Olesnyckyj, M; Richardson, P; Singhal, S; Vescio, R; Williams, SF; Yu, Z; Zeldis, J, 2009
)
0.35
" The most common adverse events (AEs) were haematological (49%), gastrointestinal (59%), and fatigue (55%)."( Expanded safety experience with lenalidomide plus dexamethasone in relapsed or refractory multiple myeloma.
Abonour, R; Alsina, M; Bahlis, NJ; Boccia, RV; Chen, C; Coutre, SE; Knight, RD; Kumar, S; Matous, J; Niesvizky, R; Pietronigro, D; Rajkumar, V; Reece, DE; Richardson, P; Siegel, D; Stadtmauer, EA; Vescio, R; Zeldis, JB, 2009
)
0.35
"These data indicate that intravitreal application of thalidomide can be an effective and safe way to treat retinal neovascularisation."( Intravitreal thalidomide reduces experimental preretinal neovascularisation without induction of retinal toxicity.
Erber, R; Hammes, HP; Jonas, JB; Kamppeter, BA; Vom Hagen, F, 2010
)
0.98
" In conclusion, bortezomib-based regimens are safe and effective and should be considered as appropriate treatment options for MM patients with any degree of RI."( Safety and efficacy of bortezomib-based regimens for multiple myeloma patients with renal impairment: a retrospective study of Italian Myeloma Network GIMEMA.
Baldini, L; Boccadoro, M; Bringhen, S; Callea, V; Casulli, AF; Catalano, L; Cavo, M; Ciolli, S; Di Raimondo, F; Galimberti, S; Gentile, M; Mannina, D; Mele, G; Morabito, F; Musto, P; Offidani, M; Palmieri, S; Palumbo, A; Petrucci, MT; Pinotti, G; Piro, E; Tosi, P, 2010
)
0.36
" Thalidomide, in combination with MP, is associated with adverse events (AEs) including peripheral neuropathy and venous thromboembolism."( Consensus guidelines for the optimal management of adverse events in newly diagnosed, transplant-ineligible patients receiving melphalan and prednisone in combination with thalidomide (MPT) for the treatment of multiple myeloma.
Bladé, J; Davies, F; Delforge, M; Facon, T; Garcia Sanz, R; Kropff, M; Leal da Costa, F; Moreau, P; Morgan, G; Palumbo, A; Schey, S, 2010
)
1.46
" Most adverse events were of mild degree and manageable."( Bortezomib, doxorubicin, and dexamethasone combination therapy followed by thalidomide and dexamethasone consolidation as a salvage treatment for relapsed or refractory multiple myeloma: analysis of efficacy and safety.
Bang, SM; Chung, J; Do, YR; Jin, JY; Joo, YD; Kang, HJ; Kim, BS; Kim, HY; Kim, K; Lee, DS; Lee, GW; Lee, JH; Lee, JJ; Lee, MH; Lee, SS; Park, J; Ryoo, HM; Shim, H; Suh, C; Yoon, SS, 2010
)
0.59
" The major adverse events associated with these treatments are somnolence (thalidomide), venous thromboembolism (thalidomide and lenalidomide), myelosuppression (lenalidomide and bortezomib), gastrointestinal disturbance, and peripheral neuropathy (thalidomide and bortezomib)."( Management of treatment-related adverse events in patients with multiple myeloma.
Mateos, MV, 2010
)
0.59
"The results from this study indicated that, with careful monitoring of the CLCr level and adverse events as well as appropriate dose adjustments, lenalidomide plus dexamethasone is an effective and well tolerated treatment option for patients with multiple myeloma who have RI."( The efficacy and safety of lenalidomide plus dexamethasone in relapsed and/or refractory multiple myeloma patients with impaired renal function.
Alegre, A; de Castro, CM; Dimopoulos, M; Goldschmidt, H; Masliak, Z; Olesnyckyj, M; Reece, D; Stadtmauer, EA; Weber, DM; Yu, Z; Zonder, JA, 2010
)
0.36
" Nonhematologic grade 3/4 adverse events were reported in 35% of once-weekly patients and 51% of twice-weekly patients (P = ."( Efficacy and safety of once-weekly bortezomib in multiple myeloma patients.
Benevolo, G; Boccadoro, M; Bringhen, S; Callea, V; Cangialosi, C; Cavalli, M; Cavo, M; De Rosa, L; Evangelista, A; Falcone, AP; Gaidano, G; Gentili, S; Genuardi, M; Grasso, M; Guglielmelli, T; Larocca, A; Levi, A; Liberati, AM; Musto, P; Nozzoli, C; Palumbo, A; Patriarca, F; Ria, R; Rizzo, V; Rossi, D, 2010
)
0.36
" Three patients experienced a grade 4 adverse reaction; two pulmonary emboli and one cerebral ischemia."( Phase I safety study of lenalidomide and dacarbazine in patients with metastatic melanoma previously untreated with systemic chemotherapy.
Bassett, R; Bedikian, A; Hwu, P; Hwu, WJ; Kim, KB; Knight, RD; Papadopoulos, NE; Patnana, M, 2010
)
0.36
" Fludarabine was highly toxic to the cells, producing very high levels of cell death; however, thalidomide did not increase this effect."( Thalidomide enhances cyclophosphamide and dexamethasone-mediated cytotoxicity towards cultured chronic lymphocytic leukaemia cells.
Allsup, D; Bailey, J; Eagle, G; Evans, P; Greenman, J; Pointon, JC, 2010
)
2.02
"8%) withdrew from the study because of adverse events."( [The efficacy and safety of long-term thalidomide in the treatment of ankylosing spondylitis].
Huang, F; Zhang, JL; Zhu, J, 2010
)
0.63
"Long term thalidomide is effective and safe for treating resistant ankylosing spondylitis and it has cumulative effect as duration prolongs."( [The efficacy and safety of long-term thalidomide in the treatment of ankylosing spondylitis].
Huang, F; Zhang, JL; Zhu, J, 2010
)
1.03
" On the other hand, when new drugs are used it is very important to know their associated toxicity, since adequate management of the adverse effects can help to avoid unnecessary treatment interruptions - thereby undoubtedly contributing to improvement in the efficacy of therapy."( Management of the adverse effects of lenalidomide in multiple myeloma.
González Rodríguez, AP, 2011
)
0.37
" The major adverse events (AEs) associated with lenalidomide include: hematological toxicities (myelosuppression), mainly neutropenia, venous thromboembolism, gastrointestinal disturbance, skin toxicity, atrial fibrillation, asthenia, and decreased peripheral blood stem cell yield during stem cell collection when lenalidomide is used after a long period of time."( Lenalidomide treatment for patients with multiple myeloma: diagnosis and management of most frequent adverse events.
García Sánchez, PJ; González Rodríguez, AP; Mesa, MG; Pérez Persona, E, 2011
)
0.37
" However, these benefits are accompanied by increases in treatment-related adverse events (AEs), which may be particularly pronounced in older individuals."( Practical management of adverse events in multiple myeloma: can therapy be attenuated in older patients?
Bringhen, S; Mateos, MV; Palumbo, A; San Miguel, JF, 2011
)
0.37
" The most common adverse events were mild to moderate (grades 1, 2)."( [The efficacy and safety of bortezomib plus thalidomide in treatment of newly diagnosed multiple myeloma].
Chen, SL; Gao, W; Jiang, B; Qiu, LG; Yu, L; Zhong, YP, 2011
)
0.63
" Febrile neutropenia was rare (4%) and there were no toxic deaths."( Lenalidomide can be safely combined with R-CHOP (R2CHOP) in the initial chemotherapy for aggressive B-cell lymphomas: phase I study.
Ansell, SM; Habermann, TM; Inwards, DJ; Johnston, PB; Klebig, RR; LaPlant, B; Macon, WR; Micallef, IN; Nowakowski, GS; Porrata, LF; Reeder, CB; Rivera, CE; Witzig, TE, 2011
)
0.37
" We conclude that pulmonary toxicity is a potential adverse effect of pomalidomide therapy and encourage physicians to remain cognizant of its clinical presentation."( Acute lung toxicity related to pomalidomide.
Geyer, HL; Lacy, MQ; Leslie, KO; Mikhael, JR; Stewart, K; Viggiano, RW; Witzig, TE, 2011
)
0.37
" In both arms, greater rates of severe hematologic adverse events were associated with RI (eGFR < 50 mL/min), however, therapy discontinuation rates were unaffected."( Safety and efficacy of bortezomib-melphalan-prednisone-thalidomide followed by bortezomib-thalidomide maintenance (VMPT-VT) versus bortezomib-melphalan-prednisone (VMP) in untreated multiple myeloma patients with renal impairment.
Baldini, L; Benevolo, G; Boccadoro, M; Bringhen, S; Cascavilla, N; Cavo, M; Di Raimondo, F; Gentile, M; Grasso, M; Guglielmelli, T; Majolino, I; Marasca, R; Mazzone, C; Montefusco, V; Morabito, F; Musolino, C; Musto, P; Nozzoli, C; Offidani, M; Palumbo, A; Patriarca, F; Petrucci, MT; Ria, R; Rossi, D; Vincelli, I, 2011
)
0.62
" Common adverse events included fatigue, injection site reactions, constipation, nausea, pruritus and febrile neutropenia."( Safety, efficacy and biological predictors of response to sequential azacitidine and lenalidomide for elderly patients with acute myeloid leukemia.
Abdel-Wahab, O; Berube, C; Bhattacharya, S; Coutre, S; Figueroa, ME; Gallegos, L; Gotlib, JR; Kohrt, HE; Levine, R; Liedtke, M; Medeiros, BC; Melnick, A; Mitchell, BS; Pollyea, DA; Zehnder, J; Zhang, B, 2012
)
0.38
" Most adverse events occur early during the course of treatment and are manageable."( The clinical safety of lenalidomide in multiple myeloma and myelodysplastic syndromes.
Fenaux, P; Freeman, J; Palumbo, A; Weiss, L, 2012
)
0.38
"The combination of thalidomide and tegafur/uracil was safe and demonstrated modest activity in patients with advanced HCC."( Efficacy, safety, and potential biomarkers of thalidomide plus metronomic chemotherapy for advanced hepatocellular carcinoma.
Cheng, AL; Hsiao, CH; Hsu, C; Hsu, CH; Huang, CC; Lee, KD; Lin, ZZ; Lu, YS; Shao, YY; Shen, YC, 2012
)
0.97
" All subjects tolerated apremilast well with no serious adverse events or withdrawal due to side effects."( A phase 2, open-label, investigator-initiated study to evaluate the safety and efficacy of apremilast in subjects with recalcitrant allergic contact or atopic dermatitis.
Au, SC; Dumont, N; Gottlieb, AB; Scheinman, P; Volf, EM, 2012
)
0.38
" Serum ferritin (SF) was measured monthly, and safety assessment included monitoring of adverse events during treatment and of liver and renal parameters."( Deferasirox treatment for myelodysplastic syndromes: "real-life" efficacy and safety in a single-institution patient population.
Alimena, G; Breccia, M; Colafigli, G; Federico, V; Finsinger, P; Latagliata, R; Loglisci, G; Petrucci, L; Salaroli, A; Santopietro, M; Serrao, A, 2012
)
0.38
" The main objective was to estimate the risk of serious adverse events and their impact on outcome."( Safety of thalidomide in newly diagnosed elderly myeloma patients: a meta-analysis of data from individual patients in six randomized trials.
Baldi, I; Beksac, M; Boccadoro, M; Ciccone, G; Galli, M; Gay, F; Gimsing, P; Hulin, C; Juliusson, G; Kolb, B; Leleu, X; Lokhorst, H; Palumbo, A; Pégourié, B; Pezzatti, S; Rodon, P; Rolke, J; Schaafsma, M; Sonneveld, P; Sucak, G; Turesson, I; van der Holt, B; Waage, A; Wetterwald, M; Wijermans, P; Zweegman, S, 2013
)
0.79
" The most common adverse events were headache, nasopharyngitis, diarrhoea and nausea."( Efficacy and safety of apremilast in subjects with moderate to severe plaque psoriasis: results from a phase II, multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison study.
Hu, C; Kaufmann, R; Papp, KA; Rohane, P; Sutherland, D; Thaçi, D, 2013
)
0.39
" These agents have specific adverse event (AE) profiles, and it is especially important to consider severe AEs that may lead to premature discontinuation, negatively affecting outcomes."( How to maintain patients on long-term therapy: understanding the profile and kinetics of adverse events.
Mateos, MV, 2012
)
0.38
" There were two serious treatment-related adverse events during the treatment period (cerebrovascular accident, placebo; worsening thrombocytopenia, romiplostim 500 μg)."( A randomized, double-blind, placebo-controlled phase 2 study evaluating the efficacy and safety of romiplostim treatment of patients with low or intermediate-1 risk myelodysplastic syndrome receiving lenalidomide.
Gandhi, S; Hu, K; Larson, RA; Liu, D; Lyons, RM; Matei, C; Scott, B; Wang, ES; Yang, AS, 2012
)
0.38
"Lenalidomide appears to be efficacious and safe in patients with refractory CLE, but clinical relapse is frequent after its withdrawal."( Efficacy and safety of lenalidomide for refractory cutaneous lupus erythematosus.
Ávila, G; Cortés-Hernández, J; Ordi-Ros, J; Vilardell-Tarrés, M, 2012
)
0.38
"Cutaneous toxicity is a frequent side effect of new anticancer targeted therapies."( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects.
Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014
)
0.4
"This study evaluates the impact of cutaneous adverse drug reactions (cADR) of the new therapies bortezomib and lenalidomide and presents a review of their skin side effects."( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects.
Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014
)
0.4
" Three adverse events linked to bortezomib and 4 to lenalidomide forced to a complete withdrawal of the drug, while 3 reactions due to bortezomib mandated a dose reduction."( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects.
Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014
)
0.4
" Our study suggests that cutaneous toxicities, when researched by Dermatologists, are a side effect even more frequent than the reported data."( Cutaneous adverse reactions linked to targeted anticancer therapies bortezomib and lenalidomide for multiple myeloma: new drugs, old side effects.
Brandi, G; Dika, E; Maibach, H; Patrizi, A; Tacchetti, P; Venturi, M, 2014
)
0.4
" Low-dose lenalidomide therapy was effective and safe against MM with a bortezomib-associated lung disorder."( Safety and effectiveness of low-dose lenalidomide therapy for multiple myeloma complicated with bortezomib-associated interstitial pneumonia.
Ihara, K; Inomata, H; Kato, J; Kikuchi, S; Koyama, R; Muramatsu, H; Nagamachi, Y; Nishisato, T; Nozawa, E; Okamoto, T; Ono, K; Tanaka, S; Yamada, H; Yamauchi, N; Yano, T, 2013
)
0.39
"Patients received oral lenalidomide 25mg once daily on days 1-21 of each 28-day cycle for a maximum of 24 months, until disease progression or development of unacceptable adverse events (AEs)."( A phase 2, multicentre, single-arm, open-label study to evaluate the safety and efficacy of single-agent lenalidomide (Revlimid) in subjects with relapsed or refractory peripheral T-cell non-Hodgkin lymphoma: the EXPECT trial.
Bosly, A; Coiffier, B; Delarue, R; Fitoussi, O; Gabarre, J; Glaisner, S; Haioun, C; Li, J; Lister, J; Morschhauser, F; Quach, H; Thieblemont, C, 2013
)
0.39
" Central hypothyroidism is a well-recognized side effect of bexarotene."( Thyroid dysfunction as an unintended side effect of anticancer drugs.
Appetecchia, M; Baldelli, R; Barnabei, A; Corsello, SM; Paragliola, R; Torino, F, 2013
)
0.39
" The most common adverse events observed were neutropenia (56%), thrombocytopenia (50%), and anemia (40%)."( [Effectiveness and safety of lenalidomide in myelofibrosis patients: a case series from the Spanish compassionate use program].
Asensio, A; Blanes, M; Boqué, C; Castillo, I; Hermosilla, MM; Ojea, MA,
)
0.13
" Grade 3-4 hematologic adverse events were: neutropenia in 28% of the courses, thrombocytopenia in 9%, and anemia in 3%."( Lenalidomide plus cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab is safe and effective in untreated, elderly patients with diffuse large B-cell lymphoma: a phase I study by the Fondazione Italiana Linfomi.
Baldi, I; Bottelli, C; Carella, AM; Castellino, A; Chiappella, A; Ciccone, G; De Masi, P; Gaidano, G; Ladetto, M; Liberati, AM; Orsucci, L; Palumbo, A; Pavone, V; Perticone, S; Rossi, G; Rossini, B; Salvi, F; Tucci, A; Vitolo, U; Zanni, M, 2013
)
0.39
" Adverse events were reported in 68."( "Real-world" data on the efficacy and safety of lenalidomide and dexamethasone in patients with relapsed/refractory multiple myeloma who were treated according to the standard clinical practice: a study of the Greek Myeloma Study Group.
Anagnostopoulos, N; Anargyrou, K; Briasoulis, E; Giannakoulas, N; Hatzimichael, E; Karras, G; Katodritou, E; Kotsopoulou, M; Kyriakou, D; Kyrtsonis, MC; Lalagianni, C; Maniatis, A; Matsouka, P; Michali, E; Papageorgiou, G; Spanoudakis, E; Symeonidis, A; Terpos, E; Tsakiridou, A; Tsionos, K; Vadikolia, C; Zikos, P, 2014
)
0.4
"The median age of the patients was 58 years, with 30% of the patients aged >65 years, 49% having an International Staging System stage of 2 and 3, 12% having severe renal insufficiency, and 8% demonstrating an adverse result on fluorescence in situ hybridization."( Efficacy and safety profile of long-term exposure to lenalidomide in patients with recurrent multiple myeloma.
Avet Loiseau, H; Bonnet, S; Debarri, H; Demarquette, H; Facon, T; Fouquet, G; Gay, J; Guidez, S; Herbaux, C; Hulin, C; Leleu, X; Michel, J; Miljkovic, D; Perrot, A; Serrier, C; Tardy, S, 2013
)
0.39
"The intravitreal implants delivered safe doses of thalidomide that were also effective to induce vessels regression in CAMs."( In vivo release and retinal safety of intravitreal implants of thalidomide in rabbit eyes and antiangiogenic effect on the chorioallantoic membrane.
Fialho, SL; Fulgêncio, GO; Haddad, A; Jorge, R; Messias, A; Miranda, MM; Pereira, BG; Silva-Cunha, A; Souza, PA, 2013
)
0.88
" These results provide a path for toxicological assessment of complex chemical mixtures and in detail show the toxic potential of TD and its PTPs as well as its HTPs."( Identification of phototransformation products of thalidomide and mixture toxicity assessment: an experimental and quantitative structural activity relationships (QSAR) approach.
Kümmerer, K; Leder, C; Mahmoud, WM; Menz, J; Schneider, M; Toolaram, AP, 2014
)
0.66
" Adverse events were manageable and mostly included thrombocytopenia and neutropenia."( Efficacy and safety of lenalinomide combined with rituximab in patients with relapsed/refractory diffuse large B-cell lymphoma.
Aurran-Schleinitz, T; Blaise, D; Bouabdallah, R; Broussais-Guillaumot, F; Chetaille, B; Coso, D; Esterni, B; Ivanov, V; Olive, D; Schiano, JM; Stoppa, AM, 2014
)
0.4
" Salvage therapy must be tailored according to an individual patient's clinical profile, with the risks and potential effects of treatment-related adverse events being major determinants of the choice of therapy."( Treatment-related adverse events in patients with relapsed/refractory multiple myeloma.
Vij, R, 2011
)
0.37
" In conclusion, low-dose lenalidomide plus dexamethasone therapy is an effective and safe regimen for patients with relapsed or refractory POEMS syndrome."( Efficacy and safety of low-dose lenalidomide plus dexamethasone in patients with relapsed or refractory POEMS syndrome.
Cai, H; Cai, QQ; Cao, XX; Li, J; Wang, C; Zhou, DB, 2015
)
0.42
" The most common grade 3 or 4 adverse events were neutropenia (38 [35%] of 110 patients), muscle pain (ten [9%]), rash (eight [7%]), cough, dyspnoea, or other pulmonary symptoms (five [5%]), fatigue (five [5%]), thrombosis (five [5%]), and thrombocytopenia (four [4%])."( Safety and activity of lenalidomide and rituximab in untreated indolent lymphoma: an open-label, phase 2 trial.
Baladandayuthapani, V; Claret, LC; Davis, RE; Fanale, MA; Fayad, LE; Feng, L; Fowler, NH; Hagemeister, FB; Kwak, LW; McLaughlin, P; Muzzafar, T; Nastoupil, L; Neelapu, SS; Oki, Y; Orlowski, RZ; Rawal, S; Romaguera, JE; Samaniego, F; Shah, J; Tsai, KY; Turturro, F; Wang, M; Westin, JR, 2014
)
0.4
" Four dose-limiting toxic events were noted in phase 1: one at a dose of ixazomib of 2·97 mg/m(2) and three at 3·95 mg/m(2)."( Safety and tolerability of ixazomib, an oral proteasome inhibitor, in combination with lenalidomide and dexamethasone in patients with previously untreated multiple myeloma: an open-label phase 1/2 study.
Berdeja, JG; Berg, D; Di Bacco, A; Estevam, J; Gupta, N; Hamadani, M; Hari, P; Hui, AM; Kaufman, JL; Kumar, SK; Laubach, JP; Liao, E; Lonial, S; Niesvizky, R; Rajkumar, V; Richardson, PG; Roy, V; Stewart, AK; Vescio, R, 2014
)
0.4
" The outcomes included overall response (OR) rate, complete response (CR) rate, 3-year progression-free survival (PFS) rate, 3-year overall survival (OS) rate, and different types of treatment-related adverse events."( Efficacy and Safety of Lenalidomide in the Treatment of Multiple Myeloma: A Systematic Review and Meta-analysis of Randomized Controlled Trials.
Guo, XN; Qiao, SK; Ren, HY; Ren, JH, 2015
)
0.42
"3% of patients randomized to placebo and apremilast, respectively, had 1 or more adverse events."( Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1).
Chimenti, S; Day, RM; Gordon, KB; Griffiths, CE; Hu, C; Kircik, L; Korman, NJ; Langley, RG; Leonardi, CL; Papp, K; Reich, K; Stevens, RM, 2015
)
0.42
" The most frequent adverse events ≥ grade 3 at 15 mg were 14% anemia and 43% neutropenia."( Lenalidomide is safe and active in Waldenström macroglobulinemia.
Arnulf, B; Bakala, J; Banos, A; Bories, C; Brice, P; Choquet, S; Demarquette, H; Dib, M; Fouquet, G; Guidez, S; Herbaux, C; Karlin, L; Leblond, V; LeGouill, S; Leleu, X; Louni, C; Martin, A; Morel, P; Nudel, M; Ohyba, B; Petillon, MO; Poulain, S; Salles, G; Thielemans, B; Tournilhac, O, 2015
)
0.42
" Twenty-one (49%) patients had at least one drug-related grade ≥3 adverse event (AE); the most common were neutropenia (19%), diarrhea (14%), and thrombocytopenia (12%)."( Pharmacokinetics and safety of ixazomib plus lenalidomide-dexamethasone in Asian patients with relapsed/refractory myeloma: a phase 1 study.
Chim, CS; Chng, WJ; Esseltine, DL; Goh, YT; Gupta, N; Hanley, MJ; Hui, AM; Kim, K; Lee, JH; Min, CK; Venkatakrishnan, K; Wong, RS; Yang, H, 2015
)
0.42
" The exposure-adjusted incidence of adverse events did not increase with continued apremilast treatment for up to 52 weeks."( Efficacy and safety of apremilast, an oral phosphodiesterase 4 inhibitor, in patients with moderate-to-severe plaque psoriasis over 52 weeks: a phase III, randomized controlled trial (ESTEEM 2).
Cather, J; Crowley, J; Day, RM; Ferrandiz, C; Girolomoni, G; Gooderham, M; Gottlieb, AB; Hu, C; Mrowietz, U; Paul, C; Poulin, Y; Shah, K; Stevens, RM, 2015
)
0.42
"Nephrotoxicity is a major side effect for the antineoplastic drug cisplatin."( Additive Renoprotection by Pioglitazone and Fenofibrate against Inflammatory, Oxidative and Apoptotic Manifestations of Cisplatin Nephrotoxicity: Modulation by PPARs.
El-Mas, MM; Helmy, MM; Helmy, MW, 2015
)
0.42
"0%) and lack of 3/4 grade adverse events (R(2)=1."( Efficacy and safety of lenalidomide treatment in multiple myeloma (MM) patients--Report of the Polish Myeloma Group.
Becht, R; Bołkun, Ł; Butrym, A; Błońska, D; Charliński, G; Dębski, J; Dmoszyńska, A; Druzd-Sitek, A; Dytfeld, D; Hałka, J; Hołojda, J; Hus, M; Januszczyk, J; Jurczyszyn, A; Knopińska-Posłuszny, W; Kuliczkowski, K; Kłoczko, J; Lech-Marańda, E; Legieć, W; Malenda, A; Nowicki, A; Pogrzeba, J; Rymko, M; Rzepecki, P; Stella-Hołowiecka, B; Subocz, E; Torosian, T; Urbanowicz, A; Urbańska-Ryś, H; Usnarska-Zubkiewicz, L; Zaucha, JM; Zdziarska, B; Zubkiewicz-Kucharska, A, 2016
)
0.43
"LEN is an effective and safe therapeutic option, even in intensively treated resistant and relapsed MM patients, as well as in patients with stable disease and previous treatment-induced neurological complications."( Efficacy and safety of lenalidomide treatment in multiple myeloma (MM) patients--Report of the Polish Myeloma Group.
Becht, R; Bołkun, Ł; Butrym, A; Błońska, D; Charliński, G; Dębski, J; Dmoszyńska, A; Druzd-Sitek, A; Dytfeld, D; Hałka, J; Hołojda, J; Hus, M; Januszczyk, J; Jurczyszyn, A; Knopińska-Posłuszny, W; Kuliczkowski, K; Kłoczko, J; Lech-Marańda, E; Legieć, W; Malenda, A; Nowicki, A; Pogrzeba, J; Rymko, M; Rzepecki, P; Stella-Hołowiecka, B; Subocz, E; Torosian, T; Urbanowicz, A; Urbańska-Ryś, H; Usnarska-Zubkiewicz, L; Zaucha, JM; Zdziarska, B; Zubkiewicz-Kucharska, A, 2016
)
0.43
" We followed up patients each month to assess epistaxis severity score and transfusion need, and any adverse events were reported."( Efficacy and safety of thalidomide for the treatment of severe recurrent epistaxis in hereditary haemorrhagic telangiectasia: results of a non-randomised, single-centre, phase 2 study.
Balduini, CL; Bastia, R; Bellistri, F; Benazzo, M; Chu, F; Danesino, C; Grignani, P; Invernizzi, R; Klersy, C; Matti, E; Olivieri, C; Ornati, F; Pagella, F; Plumitallo, S; Quaglia, F; Spinozzi, G, 2015
)
0.73
" Patients had only non-serious, grade 1 adverse effects, the most common of which were constipation (21 patients), drowsiness (six patients), and peripheral oedema (eight patients)."( Efficacy and safety of thalidomide for the treatment of severe recurrent epistaxis in hereditary haemorrhagic telangiectasia: results of a non-randomised, single-centre, phase 2 study.
Balduini, CL; Bastia, R; Bellistri, F; Benazzo, M; Chu, F; Danesino, C; Grignani, P; Invernizzi, R; Klersy, C; Matti, E; Olivieri, C; Ornati, F; Pagella, F; Plumitallo, S; Quaglia, F; Spinozzi, G, 2015
)
0.73
"Low-dose thalidomide seems to be safe and effective for the reduction of epistaxis in patients with hereditary haemorrhagic telangiectasia."( Efficacy and safety of thalidomide for the treatment of severe recurrent epistaxis in hereditary haemorrhagic telangiectasia: results of a non-randomised, single-centre, phase 2 study.
Balduini, CL; Bastia, R; Bellistri, F; Benazzo, M; Chu, F; Danesino, C; Grignani, P; Invernizzi, R; Klersy, C; Matti, E; Olivieri, C; Ornati, F; Pagella, F; Plumitallo, S; Quaglia, F; Spinozzi, G, 2015
)
1.14
" The most common grade ≥3 adverse events (AEs) were neutropenia and thrombocytopenia."( Safety and efficacy of different lenalidomide starting doses in patients with relapsed or refractory chronic lymphocytic leukemia: results of an international multicenter double-blinded randomized phase II trial.
Buhler, A; Chanan-Khan, A; De Bedout, S; Dürig, J; Fraser, GA; Gribben, JG; Hallek, M; Hillmen, P; Kalaycio, M; Kipps, TJ; Mei, J; Michallet, AS; Purse, B; Stilgenbauer, S; Wendtner, CM; Zhang, J, 2016
)
0.43
"Pomalidomide and dexamethasone favored prolonged and safe exposure to treatment in 40% of heavily treated and end-stage RRMM, a paradigm shift in the natural history of RRMM characterized with a succession of shorter disease-free intervals and ultimately shorter survival."( Safe and prolonged survival with long-term exposure to pomalidomide in relapsed/refractory myeloma.
Arnulf, B; Attal, M; Avet-Loiseau, H; Banos, A; Benbouker, L; Brechiniac, S; Caillot, D; Decaux, O; Escoffre-Barbe, M; Facon, T; Fermand, JP; Fouquet, G; Garderet, L; Hulin, C; Karlin, L; Kolb, B; Leleu, X; Macro, M; Marit, G; Mathiot, C; Moreau, P; Pegourie, B; Petillon, MO; Richez, V; Rodon, P; Roussel, M; Royer, B; Stoppa, AM; Wetterwald, M, 2016
)
0.43
" All patients had ≥ 1 adverse event (AE)."( Pharmacokinetics and Safety of Elotuzumab Combined With Lenalidomide and Dexamethasone in Patients With Multiple Myeloma and Various Levels of Renal Impairment: Results of a Phase Ib Study.
Badros, A; Berdeja, J; Bleickardt, E; Gupta, M; Jagannath, S; Kaufman, JL; Lynch, M; Manges, R; Paliwal, P; Tendolkar, A; Vij, R; Zonder, J, 2016
)
0.43
" Complete response (CR), progression-free survival (PFS), overall survival (OS), and adverse events (AE) were combined."( Efficacy and Safety of Novel Agent-Based Therapies for Multiple Myeloma: A Meta-Analysis.
Li, Y; Wang, X; Yan, X, 2016
)
0.43
" LenDex was interrupted in three cases because of adverse events (infections and cutaneous events); 78 % of the patients were on thromboprophylaxis with aspirin."( Lenalidomide is effective and safe for the treatment of patients with relapsed multiple myeloma and very severe renal impairment.
Coelho, I; Esteves, GV; Esteves, S; Freitas, J; Geraldes, C; Gomes, F; João, C; Lúcio, P; Neves, M, 2016
)
0.43
" Most frequent grade 3/4 treatment-emergent adverse events were hematologic (neutropenia [49."( Safety and efficacy of pomalidomide plus low-dose dexamethasone in STRATUS (MM-010): a phase 3b study in refractory multiple myeloma.
Anttila, P; Blanchard, MJ; Cafro, AM; Cavo, M; Corradini, P; de Arriba, F; Delforge, M; Di Raimondo, F; Dimopoulos, MA; Doyen, C; Goldschmidt, H; Hansson, M; Herring, J; Kaiser, M; Knop, S; Miller, N; Moreau, P; Morgan, G; Ocio, EM; Oriol, A; Palumbo, A; Peluso, T; Petrini, M; Raymakers, R; Röllig, C; San-Miguel, J; Simcock, M; Sternas, L; Vacca, A; Weisel, KC; Zaki, MH, 2016
)
0.43
" The primary endpoint was the proportion of grade ≥3 non-haematological adverse events (AEs); other endpoints included the number of dose reductions/discontinuations and efficacy."( Elotuzumab in combination with thalidomide and low-dose dexamethasone: a phase 2 single-arm safety study in patients with relapsed/refractory multiple myeloma.
Blade, J; Bleickardt, E; Gironella, M; Granell, M; Hernandez, MT; Lynch, M; Martín, J; Martinez-Lopez, J; Mateos, MV; Oriol, A; Paliwal, P; San-Miguel, J; Singhal, A, 2016
)
0.72
" Five patients had serious adverse events: three in the thalidomide group (transient cardiac arrest, heart failure, and dehydration) and two in the placebo group (ileus and fever)."( Safety and efficacy of thalidomide in patients with POEMS syndrome: a multicentre, randomised, double-blind, placebo-controlled trial.
Aoyagi, R; Hanaoka, H; Ikeda, S; Kanda, T; Katayama, K; Kawachi, I; Kikuchi, S; Kira, J; Kohara, N; Koike, H; Kusunoki, S; Kuwabara, S; Misawa, S; Mitsui, Y; Nagashima, K; Nakashima, I; Nishizawa, M; Sasaki, H; Sato, Y; Sekiguchi, Y; Sobue, G; Takashima, H; Watanabe, O; Yabe, I, 2016
)
0.99
"The aim of the study was to evaluate the incidence of adverse events (AEs) in female dogs diagnosed with advanced clinical stage mammary gland neoplasms following treatment with thalidomide."( Absence of significant adverse events following thalidomide administration in bitches diagnosed with mammary gland carcinomas.
Amorim, RL; Camargo Nunes, F; Carneiro, RA; Cassali, GD; de Campos, CB; Fialho Ligório, S; Lavalle, GE, 2016
)
0.88
" All four children completed the protocol without any significant adverse effects and remain in complete and durable remission 15-18 months posttreatment."( Excellent remission rates with limited toxicity in relapsed/refractory Langerhans cell histiocytosis with pulse dexamethasone and lenalidomide in children.
Bakane, A; Raj, R; Ramachandrakurup, S; Subburaj, D; Uppuluri, R, 2017
)
0.46
" Venous thromboembolism (VTE), other adverse effects (AEs), and the changes of D-dimer and fibrinogen levels were monitored."( Efficacy and Safety of Danshen Compound Tablets in Preventing Thalidomide-Associated Thromboembolism in Patients with Multiple Myeloma: A Multicenter Retrospective Study.
Ai, H; Chen, L; Liu, XJ; Mi, RH; Wei, XD; Yin, JJ; Yin, QS, 2016
)
0.67
" Most common adverse events (≥5%) with apremilast, including nausea, diarrhoea, upper respiratory tract infection, nasopharyngitis, tension headache and headache, were mild or moderate in severity; diarrhoea and nausea generally resolved in the first month."( The efficacy and safety of apremilast, etanercept and placebo in patients with moderate-to-severe plaque psoriasis: 52-week results from a phase IIIb, randomized, placebo-controlled trial (LIBERATE).
Bewley, A; Day, RM; Goncalves, J; Gooderham, M; Green, L; Khanskaya, I; Piguet, V; Reich, K; Shah, K; Soung, J; Zhang, Z, 2017
)
0.46
" Group 2, served as the toxic group, received CFZ (4 mg/kg, intraperitoneally [i."( Apremilast reversed carfilzomib-induced cardiotoxicity through inhibition of oxidative stress, NF-κB and MAPK signaling in rats.
Ahmad, SF; Al-Harbi, MM; Al-Harbi, NO; Aljerian, K; Almukhlafi, TS; Almutairi, MM; Alshammari, M; Ansari, MA; Ansari, MN; Imam, F, 2016
)
0.43
" Safety was evaluated based on the occurrence rates of grades 3-4 adverse events (AEs)."( Efficacy and Safety of Lenalidomide for Treatment of Low-/Intermediate-1-Risk Myelodysplastic Syndromes with or without 5q Deletion: A Systematic Review and Meta-Analysis.
Deng, ZQ; He, PF; Lian, XY; Lin, J; Qian, J; Wen, XM; Xu, ZJ; Yang, L; Yao, DM; Zhang, ZH, 2016
)
0.43
" We focused on adverse events associated with such agents and described how they should be managed."( Management of adverse events induced by next-generation immunomodulatory drug and proteasome inhibitors in multiple myeloma.
Boccadoro, M; Bonello, F; Larocca, A; Salvini, M, 2017
)
0.46
" The adverse events during TAS were generally tolerable, but 39 (10."( Efficacy and toxicity of the combination chemotherapy of thalidomide, alkylating agent, and steroid for relapsed/refractory myeloma patients: a report from the Korean Multiple Myeloma Working Party (KMMWP) retrospective study.
Choi, YS; Eom, HS; Han, JJ; Kang, HJ; Kim, HJ; Kim, K; Kim, MK; Kim, SH; Kwon, J; Lee, JH; Lee, JJ; Lee, JO; Lee, WS; Min, CK; Moon, JH; Yoon, DH; Yoon, SS, 2017
)
0.7
" We demonstrated that CK1α inactivation, while toxic for myeloma cells, is dispensable for the survival of healthy B lymphocytes and stromal cells."( Inactivation of CK1α in multiple myeloma empowers drug cytotoxicity by affecting AKT and β-catenin survival signaling pathways.
Barilà, G; Bonaldi, L; Cabrelle, A; Carrino, M; Costacurta, M; Gianesin, K; Macaccaro, P; Manni, S; Manzoni, M; Martines, A; Neri, A; Nunes, SC; Piazza, F; Semenzato, G; Taiana, E; Trentin, L; Tubi, LQ; Zambello, R, 2017
)
0.46
" CIPN is a common dose limiting side effect in patients with MM."( The magnitude of neurotoxicity in patients with multiple myeloma and the impact of dose modifications: results from the population-based PROFILES registry.
Beijers, AJ; Eurelings, M; Minnema, MC; Mols, F; Oerlemans, S; van de Poll-Franse, LV; Vreugdenhil, A, 2017
)
0.46
"Among the 25 participants, 14 (56%) terminated early due to adverse events, dramatically decreasing the power of the study."( Poor Safety and Tolerability Hamper Reaching a Potentially Therapeutic Dose in the Use of Thalidomide for Alzheimer's Disease: Results from a Double-Blind, Placebo-Controlled Trial.
Ahmadi, M; Belden, C; Decourt, B; Drumm-Gurnee, D; Gonzales, A; Jacobson, S; Macias, M; Powell, J; Sabbagh, MN; Shill, H; Sirrel, S; Walker, A; Wilson, J, 2017
)
0.68
" Most common adverse events (AEs) with placebo, apremilast 20 and apremilast 30 (0-16 weeks) were nasopharyngitis (8."( Apremilast, an oral phosphodiesterase 4 inhibitor, in the treatment of Japanese patients with moderate to severe plaque psoriasis: Efficacy, safety and tolerability results from a phase 2b randomized controlled trial.
Chen, P; Day, RM; Imafuku, S; Komine, M; Maroli, A; Nemoto, O; Ohtsuki, M; Okubo, Y; Petric, R, 2017
)
0.46
" During 0 to ≤52 weeks, the adverse events (AEs) that occurred in ≥5% of patients included diarrhea, nausea, upper respiratory tract infection, nasopharyngitis, tension headache, and headache."( Long-term safety and tolerability of apremilast in patients with psoriasis: Pooled safety analysis for ≥156 weeks from 2 phase 3, randomized, controlled trials (ESTEEM 1 and 2).
Cather, JC; Chen, R; Crowley, J; Day, RM; Ferrándiz, C; Goncalves, J; Joly, P; Papp, KA; Peris, K; Shah, K; Thaçi, D, 2017
)
0.46
" The main concerns on adverse events were thrombosis/embolism events, peripheral neuropathy, and second primary malignancies."( Efficacy and safety of bortezomib, thalidomide, and lenalidomide in multiple myeloma: An overview of systematic reviews with meta-analyses.
Aguiar, PM; Colleoni, GWB; de Mendonça Lima, T; Storpirtis, S, 2017
)
0.73
" Safety data from TOURMALINE-MM1 are reviewed and guidance for managing clinically relevant adverse events associated with IRd is provided."( Management of adverse events associated with ixazomib plus lenalidomide/dexamethasone in relapsed/refractory multiple myeloma.
Avivi, I; Berg, D; Einsele, H; Esseltine, DL; Gupta, N; Hájek, R; Hari, P; Kumar, S; Liberati, AM; Lin, J; Lonial, S; Ludwig, H; Masszi, T; Mateos, MV; Minnema, MC; Moreau, P; Richardson, PG; Romeril, K; Shustik, C; Spencer, A, 2017
)
0.46
"Heavily pretreated patients with relapsed and refractory multiple myeloma are susceptible to treatment-related adverse events (AEs)."( Adverse event management in patients with relapsed and refractory multiple myeloma taking pomalidomide plus low-dose dexamethasone: A pooled analysis.
Anttila, P; Bahlis, N; Biyukov, T; Cavo, M; Chen, C; Cook, G; Corradini, P; Delforge, M; Dimopoulos, MA; Hansson, M; Herring, J; Hong, K; Joao, C; Kaiser, M; Moreau, P; O'Gorman, P; Oriol, A; Raymakers, R; Richardson, PG; San-Miguel, J; Siegel, DS; Slaughter, A; Song, K; Sternas, L; Weisel, K; Yu, X; Zaki, M, 2017
)
0.46
" Haemocytopenia was the predominant adverse effect, and acute toxicity was moderate, tolerable and well managed in both arms."( The efficacy and safety of gemcitabine, cisplatin, prednisone, thalidomide versus CHOP in patients with newly diagnosed peripheral T-cell lymphoma with analysis of biomarkers.
Chang, Y; Duan, W; Fu, X; Li, L; Li, X; Li, Z; Nan, F; Sun, Z; Wang, X; Wu, J; Yan, J; Young, KH; Zhang, L; Zhang, M; Zhang, X, 2017
)
0.69
" The number of serious adverse events was not significantly different among the apremilast, secukinumab, ustekinumab, and placebo groups."( Relative efficacy and safety of apremilast, secukinumab, and ustekinumab for the treatment of psoriatic arthritis.
Lee, YH; Song, GG, 2018
)
0.48
" Most adverse events were mild or moderate; most common were diarrhea, headache, nausea, upper respiratory tract infection, decreased appetite, and vomiting."( Efficacy and Safety of Apremilast in Patients With Moderate Plaque Psoriasis With Lower BSA: Week 16 Results from the UNVEIL Study.
Bagel, J; Callis Duffin, K; Chen, R; Goncalves, J; Jackson, JM; Lebwohl, M; Levi, E; Stein Gold, L; Strober, B, 2017
)
0.46
" While this medication is considered safe with a very low risk of serious side effects, a few common (≥5% of patients) mild to moderate side effects have been reported, including diarrhea, nausea, headache, and nasopharyngitis."( Management of Common Side Effects of Apremilast.
Beecker, J; Langley, A,
)
0.13
" Its efficacy and safety data are limited; hence, real-world outcomes are important for elucidating the full spectrum of its adverse events (AEs) and expanding generalizability of clinical trial findings."( Efficacy and Safety of Apremilast Monotherapy for Moderate to Severe Psoriasis: Retrospective Study.
Georgakopoulos, JR; Ighani, A; Shear, N; Walsh, S; Yeung, J; Zhou, LL,
)
0.13
"Psoriasis is a chronic inflammatory skin disease, which requires long-term, safe and effective treatment."( Real-world data on the efficacy and safety of apremilast in patients with moderate-to-severe plaque psoriasis.
Kokkalis, G; Papadavid, E; Rigopoulos, D; Rompoti, N; Theodoropoulos, K, 2018
)
0.48
" Secondary endpoints were the evaluation at week 16 of (i) PASI; (ii) Dermatology Life Quality Index (DLQI); (iii) Physician Global Assessment (PGA); (iv) Psoriasis Scalp Severity Index (PSSI); and (v) the percentage of patients who achieved ΔPASI50, ΔPASI75, ΔPASI90 and ΔPASI100; (vi) adverse events (AE); (vii) reasons for drug discontinuation; and (viii) drug survival."( Real-world data on the efficacy and safety of apremilast in patients with moderate-to-severe plaque psoriasis.
Kokkalis, G; Papadavid, E; Rigopoulos, D; Rompoti, N; Theodoropoulos, K, 2018
)
0.48
" Patients discontinued apremilast (28%), mostly during the first 4 weeks due to adverse events (12%) with gastrointestinal symptoms being the most common, and later due to lack of efficacy (16%)."( Real-world data on the efficacy and safety of apremilast in patients with moderate-to-severe plaque psoriasis.
Kokkalis, G; Papadavid, E; Rigopoulos, D; Rompoti, N; Theodoropoulos, K, 2018
)
0.48
"Apremilast is a safe and efficacious treatment for psoriasis patients as it produces ΔPASI75 and ΔPASI50 responses combined with DLQI ≤ 5 in 16 weeks in 70."( Real-world data on the efficacy and safety of apremilast in patients with moderate-to-severe plaque psoriasis.
Kokkalis, G; Papadavid, E; Rigopoulos, D; Rompoti, N; Theodoropoulos, K, 2018
)
0.48
" The most common adverse events (≥5% of patients) through week 52 were diarrhea (28."( Efficacy and Safety of Apremilast in Systemic- and Biologic-Naive Patients With Moderate Plaque Psoriasis: 52-Week Results of UNVEIL.
Bagel, J; Chen, R; Duffin, KC; Goncalves, J; Jackson, JM; Lebwohl, M; Levi, E; Stein Gold, L, 2018
)
0.48
" Carfilzomib (CFZ) has high selectivity and minimal off-target adverse effects including lower rates of PNP."( Efficacy and toxicity profile of carfilzomib based regimens for treatment of multiple myeloma: A systematic review.
Abraham, I; Anwer, F; Iftikhar, A; Kapoor, V; Latif, A; McBride, A; Mushtaq, A; Riaz, IB; Zahid, U, 2018
)
0.48
" Most frequent grade 3/4 treatment-emergent adverse events were hematologic (neutropenia 24."( The efficacy and safety of pomalidomide in relapsed/refractory multiple myeloma in a "real-world" study: Polish Myeloma Group experience.
Bernatowicz, P; Charlinski, G; Dmoszynska, A; Grzasko, N; Guzicka-Kazimierczak, R; Janczarski, M; Jurczyszyn, A; Lech-Maranda, E; Swiderska, A; Szczepaniak, A; Szeremet, A; Waszczuk-Gajda, A; Wichary, R, 2018
)
0.48
"The therapeutic efficacy of different doses of dexamethasone combined with bortezomib and thalidomide for patients with multiple myeloma is similar, can obviously enhance remission rate, prolong the survival time, promote life quality, but the incidence of adverse reactions in low dose dexamethason rigemen is significantly reduced, and the safety is better."( [Clinical Efficacy and Safety of Different Doses of Dexamethasone Combined with Bortezomib and Thalidomide for Treating Patients with Multiple Myeloma].
Fu, LP; Ji, Y; Li, CS; Zhang, WP, 2018
)
0.92
" Adverse events (AEs) occurred in 69 (57."( Efficacy and safety of lenalidomide and dexamethasone in patients with relapsed/\ refractory multiple myeloma: a real-life experience
Duran, M; Durusoy, R; Patır, P; Şahin, F; Saydam, G; Soyer, N; Töbü, M; Tombuloğlu, M; Ünal, HD; Uysal, A; Vural, F, 2018
)
0.48
" The overall incidence of adverse events (AEs) was similar in IRd and placebo-Rd groups."( [Safety and management of adverse events of ixazomib/lenalidomide/dexamethasone therapy in Japanese patients with relapsed/refractory multiple myeloma].
Aotsuka, N; Berg, D; Handa, H; Iida, S; Ishida, T; Izumi, T; Kase, Y; Komeno, T; Soeda, J; Sunami, K,
)
0.13
" Recently, apremilast, a selective inhibitor of phosphodiesterase E4 has been suggested to be a safe and effective therapeutic option in HIV-infected population with psoriatic arthritis."( Apremilast efficacy and safety in a psoriatic arthritis patient affected by HIV and HBV virus infections.
Bianchi, L; Campione, E; Esposito, M; Giunta, A; Manfreda, V, 2019
)
0.51
" The HHT working group within the ERN for Rare Multisystemic Vascular Diseases (VASCERN), developed a questionnaire-based retrospective capture of adverse events (AEs) classified using the Common Terminology Criteria for Adverse Events."( Safety of thalidomide and bevacizumab in patients with hereditary hemorrhagic telangiectasia.
Botella, LM; Buscarini, E; Dupuis-Girod, S; Geisthoff, U; Kjeldsen, AD; Mager, HJ; Pagella, F; Shovlin, CL; Suppressa, P; Zarrabeitia, R, 2019
)
0.92
" Fatal adverse events were more common in males (p = 0."( Safety of thalidomide and bevacizumab in patients with hereditary hemorrhagic telangiectasia.
Botella, LM; Buscarini, E; Dupuis-Girod, S; Geisthoff, U; Kjeldsen, AD; Mager, HJ; Pagella, F; Shovlin, CL; Suppressa, P; Zarrabeitia, R, 2019
)
0.92
" Data were extracted for ACR20/50, HAQ-DI, SF-36 and adverse/serious adverse events after 16-24 weeks."( Efficacy and safety of systemic treatments in psoriatic arthritis: a systematic review, meta-analysis and GRADE evaluation.
Dressler, C; Eisert, L; Nast, A; Pham, PA, 2019
)
0.51
" We observed no significant differences in the incidence of serious adverse events after treatment with tofacitinib 10 mg, apremilast 30 mg, tofacitinib 5 mg, apremilast 20 mg, or placebo."( Comparison of the Efficacy and Safety of Tofacitinib and Apremilast in Patients with Active Psoriatic Arthritis: A Bayesian Network Meta-Analysis of Randomized Controlled Trials.
Lee, YH; Song, GG, 2019
)
0.51
"In patients with active psoriatic arthritis, tofacitinib 10 mg and apremilast 30 mg were the most efficacious interventions and were not associated with a significant risk of serious adverse events."( Comparison of the Efficacy and Safety of Tofacitinib and Apremilast in Patients with Active Psoriatic Arthritis: A Bayesian Network Meta-Analysis of Randomized Controlled Trials.
Lee, YH; Song, GG, 2019
)
0.51
" Data from several phase III clinical trials and real-world studies showed a good benefit-risk profile, with diarrhea and nausea as the most common adverse events."( [Gastrointestinal side effects of apremilast : Characterization and management].
Beigel, F; Beissert, S; Gerdes, S; Homey, B; Körber, A; Mössner, R; Pinter, A; Radtke, MA; Staubach-Renz, P, 2019
)
0.51
"Thalidomide, used to treat erythema nodosum leprosum (ENL), is associated with severe adverse events (AEs) and is highly teratogenic."( Adverse events in patients with leprosy on treatment with thalidomide.
Carvalho, GO; Drummond, PLM; Pádua, CAM; Santos, RMMD, 2019
)
2.2
"Even as treatment of psoriasis becomes safer, it is important to recognize both common and uncommon adverse effects of treatment."( A safety review of recent advancements in the treatment of psoriasis: analysis of clinical trial safety data.
Cline, A; Feldman, SR; Kepley, AL; Kolli, SS, 2019
)
0.51
" All adverse events (AEs) were recorded during follow-up."( Efficacy and safety of apremilast for Behçet's syndrome: a real-life single-centre Italian experience.
Boffini, N; Campochiaro, C; Cariddi, A; Cavalli, G; Dagna, L; De Luca, G; Tomelleri, A; Vanni, D, 2020
)
0.56
" Adverse reactions were recorded."( The efficacy and safety of thalidomide on the recurrence interval of continuous recurrent aphthous ulceration: A randomized controlled clinical trial.
Shi, J; Shi, X; Yang, J; Yang, M; Zeng, Q; Zhao, W; Zhao, X; Zhou, H, 2020
)
0.86
" The incidence of adverse reactions was similar between two groups (P = ."( The efficacy and safety of thalidomide on the recurrence interval of continuous recurrent aphthous ulceration: A randomized controlled clinical trial.
Shi, J; Shi, X; Yang, J; Yang, M; Zeng, Q; Zhao, W; Zhao, X; Zhou, H, 2020
)
0.86
" However, soon after their introduction into clinical practice, chemotherapy-induced peripheral neurotoxicity (CIPN) emerged as their main non-hematological and among dose-limiting adverse events."( Vinca alkaloids, thalidomide and eribulin-induced peripheral neurotoxicity: From pathogenesis to treatment.
Alberti, P; Argyriou, AA; Islam, B; Kolb, N; Lustberg, M; Staff, NP, 2019
)
0.85
" The clinical response and adverse events of the thalidomide treatment were recorded."( CYP2C19 polymorphism has no correlation with the efficacy and safety of thalidomide in the treatment of immune-related bowel disease.
Chen, BL; Chen, MH; Feng, R; He, Y; Mao, R; Qiu, Y; Xu, PP; Zeng, ZR; Zhang, SH, 2020
)
1.04
"CYP2C19 polymorphisms do not seem to be associated with efficacy of thalidomide and the incidence of adverse events in treating IRBD."( CYP2C19 polymorphism has no correlation with the efficacy and safety of thalidomide in the treatment of immune-related bowel disease.
Chen, BL; Chen, MH; Feng, R; He, Y; Mao, R; Qiu, Y; Xu, PP; Zeng, ZR; Zhang, SH, 2020
)
1.03
" Common adverse events with apremilast were diarrhea (30."( Efficacy and safety of apremilast in patients with moderate to severe plaque psoriasis of the scalp: Results of a phase 3b, multicenter, randomized, placebo-controlled, double-blind study.
Cauthen, A; Lebwohl, M; Lynde, C; Paris, M; Sofen, H; Stein Gold, L; Strober, B; Tyring, S; Van Voorhees, AS; Wang, Y; Zhang, Z, 2020
)
0.56
" In this systematic review, associations of the efficacy of each approved regimen with adverse events (AEs) and the total cost per cycle were compared with a Bayesian network meta-analysis (NMA) of phase 3 randomized controlled trials (RCTs)."( Association of adverse events and associated cost with efficacy for approved relapsed and/or refractory multiple myeloma regimens: A Bayesian network meta-analysis of phase 3 randomized controlled trials.
Aryal, M; Chhabra, S; D'Souza, A; Dhakal, B; Ghose, S; Giri, S; Hamadani, M; Hari, PN; Janz, S; Narra, RK; Pathak, LK; Smunt, TL; Szabo, A, 2020
)
0.56
"9%) and adverse events (15."( Real-world effectiveness and safety of apremilast in psoriasis at 52 weeks: a retrospective, observational, multicentre study by the Spanish Psoriasis Group.
Armesto, S; Belinchón, I; Carrascosa, JM; Carretero, G; Del Alcázar, E; Ferran, M; Herranz, P; Herrera-Acosta, E; Hospital, M; Llamas, M; López-Ferrer, A; Martín, I; Mitxelena, MJ; Mollet, J; Montesinos, E; Muñoz, C; Pérez-Barrio, S; Rivera, R; Ruiz-Genao, DP; Ruiz-Villaverde, R; Sahuquillo-Torralba, A; Suárez-Pérez, JA; Valentí, F; Vidal, D; Vilarrasa, E, 2020
)
0.56
" Although the drug has a good safety profile, adverse gastrointestinal effects are common."( Real-world effectiveness and safety of apremilast in psoriasis at 52 weeks: a retrospective, observational, multicentre study by the Spanish Psoriasis Group.
Armesto, S; Belinchón, I; Carrascosa, JM; Carretero, G; Del Alcázar, E; Ferran, M; Herranz, P; Herrera-Acosta, E; Hospital, M; Llamas, M; López-Ferrer, A; Martín, I; Mitxelena, MJ; Mollet, J; Montesinos, E; Muñoz, C; Pérez-Barrio, S; Rivera, R; Ruiz-Genao, DP; Ruiz-Villaverde, R; Sahuquillo-Torralba, A; Suárez-Pérez, JA; Valentí, F; Vidal, D; Vilarrasa, E, 2020
)
0.56
" At least one adverse event was experienced by 56/96 patients, and 11/56 events required drug withdrawal."( Long-term efficacy and safety of apremilast in psoriatic arthritis: Focus on skin manifestations and special populations.
Balato, A; Bianchi, L; Campione, E; Cirillo, T; Fabbrocini, G; Malara, G; Trifirò, C, 2020
)
0.56
" Our experience suggests that apremilast is effective and safe for treating palmar-plantar psoriasis and plaques at other locations but not for treating scalp psoriasis."( Treatment Persistence and Safety of Apremilast in Psoriasis: Experience With 30 Patients in Routine Clinical Practice.
Botella Estrada, R; de Unamuno Bustos, B; Monte Boquet, E; Rodríguez Serna, M; Sahuquillo-Torralba, A, 2020
)
0.56
" However, its clinical use is limited because of its known adverse effect profile, including teratogenicity, peripheral neuropathy, and thromboembolic risk."( Thalidomide use in the management of oromucosal disease: A 10-year review of safety and efficacy in 12 patients.
Harte, MC; Hodgson, TA; Saunsbury, TA, 2020
)
2
" Data on patient response to treatment and major/minor adverse events were obtained from their clinical and electrophysiologic records."( Thalidomide use in the management of oromucosal disease: A 10-year review of safety and efficacy in 12 patients.
Harte, MC; Hodgson, TA; Saunsbury, TA, 2020
)
2
" No other major adverse effects were reported."( Thalidomide use in the management of oromucosal disease: A 10-year review of safety and efficacy in 12 patients.
Harte, MC; Hodgson, TA; Saunsbury, TA, 2020
)
2
" Demographic data and details regarding psoriasis and adverse events (AEs) were collected from patient medical records."( Real-World Effectiveness and Safety of Apremilast in Older Patients with Psoriasis.
Bastien, M; Beauchet, A; Begon, E; Beneton, N; Boulard, C; Chaby, G; Cinotti, E; Delaunay, J; Fougerousse, AC; Maccari, F; Mahé, E; Mery-Bossard, L; Parier, J; Phan, C; Prignano, F; Reguiai, Z; Romanelli, M; Samimi, M; Thomas-Beaulieu, D, 2020
)
0.56
"Apremilast seems to be an effective and safe therapeutic option for psoriasis in the elderly."( Real-World Effectiveness and Safety of Apremilast in Older Patients with Psoriasis.
Bastien, M; Beauchet, A; Begon, E; Beneton, N; Boulard, C; Chaby, G; Cinotti, E; Delaunay, J; Fougerousse, AC; Maccari, F; Mahé, E; Mery-Bossard, L; Parier, J; Phan, C; Prignano, F; Reguiai, Z; Romanelli, M; Samimi, M; Thomas-Beaulieu, D, 2020
)
0.56
" We conclude that the PluriBeat assay is a novel method for predicting chemicals' adverse effects on embryonic development."( A novel human pluripotent stem cell-based assay to predict developmental toxicity.
Emnéus, JK; Holst, B; Lauschke, K; Meiser, I; Neubauer, JC; Rasmussen, MA; Rosenmai, AK; Schmidt, K; Taxvig, C; Vinggaard, AM, 2020
)
0.56
"The incidence of grade 3 or more haematological and grade 2 or more non-haematological adverse events was lower in the dose-escalation group than in the standard-dose group, and only that of diarrhoea was significantly lower."( Safety and Effectiveness of Ixazomib Dose-escalating Strategy in Ixazomib-Lenalidomide-Dexamethasone Treatment for Relapsed/Refractory Multiple Myeloma.
Boku, S; Higai, K; Kagoo, T; Niijima, D; Ogawa, C; Ohashi, Y; Tani, K; Ueno, H; Yachi, Y; Yano, T; Yatabe, M; Yokoyama, A,
)
0.13
"A dose-escalation strategy to optimise ixazomib dosing may reduce treatment interruption due to adverse events without compromising its antitumor activity."( Safety and Effectiveness of Ixazomib Dose-escalating Strategy in Ixazomib-Lenalidomide-Dexamethasone Treatment for Relapsed/Refractory Multiple Myeloma.
Boku, S; Higai, K; Kagoo, T; Niijima, D; Ogawa, C; Ohashi, Y; Tani, K; Ueno, H; Yachi, Y; Yano, T; Yatabe, M; Yokoyama, A,
)
0.13
" In routine practice, few patients received ixazomib-based induction therapy due to reasons including (1) patients' preference on oral regimens, (2) concerns on adverse events (AEs) of other intravenous/subcutaneous regimens, (3) requirements for less center visits, and (4) fears of COVID-19 and other infectious disease exposures."( Ixazomib-based frontline therapy in patients with newly diagnosed multiple myeloma in real-life practice showed comparable efficacy and safety profile with those reported in clinical trial: a multi-center study.
Bao, L; Chen, B; Ding, K; Fu, C; Hua, L; Huang, Y; Li, B; Li, J; Liu, P; Luo, J; Wang, L; Wang, S; Wang, W; Wu, G; Xia, Z; Xu, T; Yang, W; Yang, Y; Zhang, W; Zhou, X, 2020
)
0.56
"We present a series of general and specific recommendations based on pathophysiologic considerations for managing the most common adverse effects of apremilast that lead to treatment discontinuation: diarrhea, nausea, and headache."( Multidisciplinary Management of the Adverse Effects of Apremilast.
Alonso Suárez, J; Beltrán Catalán, E; Blasco Maldonado, C; Daudén Tello, E; García-Merino, A; Herrero Manso, MC; Jiménez Morales, A; Marín-Jiménez, I; Martín-Arranz, MD; Porta Etessam, J; Rodríguez-Sagrado, MA; Rosas Gómez de Salazar, J; Salgado-Boquete, L; Trujillo Martín, E, 2021
)
0.62
" The disease phenotypes, laboratory data, concomitant medication use, and adverse events were also investigated."( Efficacy and safety of apremilast for 3 months in Behçet's disease: A prospective observational study.
Hirahara, L; Kirino, Y; Mizuki, N; Nakajima, H; Soejima, Y; Takase-Minegishi, K; Takeno, M; Takeuchi, M; Yoshimi, R, 2021
)
0.62
" Cal/BD foam plus apremilast appeared to be safe and well tolerated."( Efficacy and Safety of Calcipotriene 0.005%/Betamethasone Dipropionate 0.064% Foam With Apremilast for Moderate Plaque Psoriasis.
Kircik, LH; Schlesinger, TE; Tanghetti, E, 2020
)
0.56
"Acitretin, apremilast, and methotrexate are safe and effective modalities for ICI-mediated psoriasis."( Immune checkpoint-mediated psoriasis: A multicenter European study of 115 patients from the European Network for Cutaneous Adverse Event to Oncologic Drugs (ENCADO) group.
Annunziata, MC; Apalla, Z; Carrera, C; Fabbrocini, G; Fattore, D; Giacchero, D; Lallas, A; Lallas, K; Lazaridou, E; Nikolaou, V; Ortiz-Brugués, A; Patri, A; Peris, K; Riganti, J; Rigopoulos, D; Romano, MC; Rossi, E; Sibaud, V; Sollena, P; Stratigos, AJ; Voudouri, D, 2021
)
0.62
" The most tolerable common adverse reactions were drowsiness (10/35), dry mouth (8/35), constipation (8/35), dandruff (7/35), dizziness (4/35)."( Efficacy and safety of thalidomide on psychological symptoms and sleep disturbances in the patient with refractory ankylosing spondylitis.
Chen, Z; Gao, F; He, J; Lin, D; Lin, H; Liu, J; Wu, Y; Zhang, S, 2021
)
0.93
" No severe adverse effects was reported by patients of any group."( Comparison of efficacy and safety of thalidomide vs hydroxyurea in patients with Hb E-β thalassemia - a pilot study from a tertiary care Centre of India.
Baul, SN; Chakrabarti, P; De, R; Dolai, TK; Ghosh, P; Jain, M; Mandal, PK, 2021
)
0.89
" Hypothyroidism is an uncommon side effect of pomalidomide."( Hyponatraemia due to hypothyroidism: a rare side effect from pomalidomide.
Qureshi, A; Rhee, JH, 2021
)
0.62
" Changes in m-PPPASI and Dermatology Life Quality Index scores from baseline, the proportion of patients achieving m-PPPASI 75, and adverse events were assessed."( Comparison of the Efficacy and Safety of Apremilast and Methotrexate in Patients with Palmoplantar Psoriasis: A Randomized Controlled Trial.
Dogra, S; Handa, S; Kt, S; Narang, T; Thakur, V, 2021
)
0.62
" Five patients discontinued thalidomide due to adverse events."( Clinical-therapeutic study on the efficacy and safety of thalidomide in the management of discoid lupus erythematosus. A single-centre, retrospective study.
Aguilar-Mena, C; Bonifaz, A; Hernández-Salgado, Y; Rodriguez-Mendoza, A; Tirado-Sánchez, A, 2021
)
1.16
"Apremilast has been approved as an effective and safe treatment for psoriasis, but clinical trial results may differ from real-life data."( Is apremilast for psoriasis as effective and safe as reported in clinical trials? Five-year experience from a Greek tertiary hospital: long-term real-life efficacy and safety of apremilast in Greece.
Bakirtzi, K; Ioannides, D; Lallas, A; Papadimitriou, I; Sideris, N; Sotiriou, E; Tsentemeidou, A; Vakirlis, E, 2021
)
0.62
" The adverse drug reaction rate was 21."( Effectiveness and safety of apremilast in biologic-naïve patients with moderate psoriasis treated in routine clinical practice in Greece: the APRAISAL study.
Anagnostopoulos, Z; Anastasiadis, G; Antonakopoulos, N; Antoniou, C; Aronis, P; Bassukas, I; Chasapi, V; Drosos, A; Georgiou, S; Ioannides, D; Ioannidou, D; Katsantonis, I; Krasagakis, K; Lazaridou, E; Lefaki, I; Neofotistou, O; Papageorgiou, M; Papakonstantis, M; Patsatsi, A; Protopapa, A; Rigopoulos, D; Roussaki-Schulze, AV; Satra, F, 2021
)
0.62
"This analysis allows us to think beyond the safe use of thalidomide, but the safety provided by any type of monitoring system."( Comparative analysis of the use and control of thalidomide in Brazil and different countries: is it possible to say there is safety?
de Jesus, SM; Leite, SN; Santana, RS, 2022
)
1.22
" Majority of the studies used a dose of 2-6 mg/kg/day and around 24% suffered from at least one adverse effect, with a mortality of 5%."( Efficacy and Safety of Thalidomide in Patients with Complicated Central Nervous System Tuberculosis: A Systematic Review and Meta-Analysis.
Dawman, L; Panda, P; Panda, PK; Sharawat, IK; Sihag, RK, 2021
)
0.93
" Safety was assessed by adverse effects related to thalidomide."( Efficacy and Safety of Thalidomide in Patients With Transfusion-Dependent Thalassemia.
Chandra, J; Goel, M; Parakh, N; Pemde, H; Sharma, S; Singh, N, 2021
)
1.18
" In 32 children, 47 adverse events were observed."( Efficacy and Safety of Thalidomide in Patients With Transfusion-Dependent Thalassemia.
Chandra, J; Goel, M; Parakh, N; Pemde, H; Sharma, S; Singh, N, 2021
)
0.93
"Thalidomide resulted in major/moderate response in majority of children with transfusion-dependent thalassemia with satisfactory adverse effect profile."( Efficacy and Safety of Thalidomide in Patients With Transfusion-Dependent Thalassemia.
Chandra, J; Goel, M; Parakh, N; Pemde, H; Sharma, S; Singh, N, 2021
)
2.37
" The most commonly reported adverse events (≥ 5%) with apremilast were diarrhea, headache, nausea, nasopharyngitis, and upper respiratory tract infection, consistent with prior studies."( Efficacy and safety of apremilast in patients with mild-to-moderate plaque psoriasis: Results of a phase 3, multicenter, randomized, double-blind, placebo-controlled trial.
Albrecht, L; Bhatia, N; Callis Duffin, K; Chen, M; Gooderham, M; Green, L; Papp, K; Paris, M; Pariser, D; Sofen, H; Stein Gold, L; Wang, Y, 2022
)
0.72
" The patient treatment course, including adverse events (AEs), was reported."( Safety Profile of Ixazomib in Patients with Relapsed/Refractory Multiple Myeloma in Japan: An All-case Post-marketing Surveillance.
Chou, T; Hashimoto, M; Hiraizumi, M; Hoshino, M; Kakimoto, Y; Shimizu, K, 2022
)
0.72
" The secondary endpoints included the red blood cell (RBC) units transfused and adverse effects."( Safety and efficacy of thalidomide in patients with transfusion-dependent β-thalassemia: a randomized clinical trial.
Cai, N; Chen, JM; Chen, SJ; Chen, SY; Chen, XQ; He, S; Hu, ML; Huang, K; Huang, L; Huang, Y; Li, GH; Li, JM; Li, JY; Li, RL; Liu, J; Liu, SH; Lu, QY; Luo, TY; Qu, LW; Tan, Y; Wang, GZ; Wang, WD; Wei, JH; Wu, WQ; Xu, JQ; Xu, WW; Yang, HJ; Zhou, GB; Zhou, MG; Zhu, WJ, 2021
)
0.93
" The novel quadruplet combination was overall well-tolerated, with clinically manageable adverse events."( A phase 2 trial of the efficacy and safety of elotuzumab in combination with pomalidomide, carfilzomib and dexamethasone for high-risk relapsed/refractory multiple myeloma.
Berenson, JR; Eades, B; Eshaghian, S; Ghermezi, M; Lim, S; Martinez, D; Schwartz, G; Spektor, TM; Swift, RA; Vescio, R; Yashar, D, 2022
)
0.72
" We evaluated tumor responses (including participants who had a second course), adverse events, progression-free survival (PFS), and long-term outcomes."( Safety, Activity, and Long-term Outcomes of Pomalidomide in the Treatment of Kaposi Sarcoma among Individuals with or without HIV Infection.
George, J; Goncalves, P; Lurain, K; Polizzotto, MN; Ramaswami, R; Steinberg, SM; Uldrick, TS; Whitby, D; Widell, A; Wyvill, KM; Yarchoan, R, 2022
)
0.72
"Pomalidomide is a safe and active chemotherapy-sparing agent for the treatment of KS among individuals with or without HIV."( Safety, Activity, and Long-term Outcomes of Pomalidomide in the Treatment of Kaposi Sarcoma among Individuals with or without HIV Infection.
George, J; Goncalves, P; Lurain, K; Polizzotto, MN; Ramaswami, R; Steinberg, SM; Uldrick, TS; Whitby, D; Widell, A; Wyvill, KM; Yarchoan, R, 2022
)
0.72
" The secondary end points were mouth and throat soreness (MTS), weight loss, short-term efficacy, and adverse events."( Efficacy and safety of thalidomide in preventing oral mucositis in patients with nasopharyngeal carcinoma undergoing concurrent chemoradiotherapy: A multicenter, open-label, randomized controlled trial.
Hu, K; Jiang, L; Liang, L; Lin, Z; Liu, Z; Ning, X; Shi, Z; Wang, H; Wang, R; Wei, Y; Yan, H; Zhu, H, 2022
)
1.03
" Apremilast was well tolerated and the reported adverse events were in line with the known safety profile."( Real-World Efficacy and Safety of Apremilast in Belgian Patients with Psoriatic Arthritis: Results from the Prospective Observational APOLO Study.
de Vlam, K; Di Romana, S; Kaiser, MJ; Lories, R; Remans, P; Toukap, AN; Van den Berghe, M; Van den Bosch, F; Vanhoof, J, 2022
)
0.72
" The adverse drug reaction rate was 19."( A real-world, non-interventional, prospective study of the effectiveness and safety of apremilast in bio-naïve adults with moderate plaque psoriasis treated in the routine care in Greece - the 'APRAISAL' study.
Anagnostopoulos, Z; Anastasiadis, G; Antonakopoulos, N; Aronis, P; Bassukas, I; Chasapi, V; Drosos, A; Ioannides, D; Kalinou, C; Kekki, A; Krasagakis, K; Lazaridou, E; Lefaki, I; Neofotistou, O; Oikonomou, C; Papadavid, E; Papageorgiou, M; Papakonstantis, M; Pokas, E; Protopapa, A; Rigopoulos, D; Rovithi, E; Tampouratzi, E; Zafiriou, E, 2022
)
0.72
"Apremilast is a safe and effective treatment for bio-naïve patients with moderate psoriasis and specific psoriasis manifestations."( A real-world, non-interventional, prospective study of the effectiveness and safety of apremilast in bio-naïve adults with moderate plaque psoriasis treated in the routine care in Greece - the 'APRAISAL' study.
Anagnostopoulos, Z; Anastasiadis, G; Antonakopoulos, N; Aronis, P; Bassukas, I; Chasapi, V; Drosos, A; Ioannides, D; Kalinou, C; Kekki, A; Krasagakis, K; Lazaridou, E; Lefaki, I; Neofotistou, O; Oikonomou, C; Papadavid, E; Papageorgiou, M; Papakonstantis, M; Pokas, E; Protopapa, A; Rigopoulos, D; Rovithi, E; Tampouratzi, E; Zafiriou, E, 2022
)
0.72
" We sought to evaluate the following outcomes: psoriasis area and severity index score (PASI)-50, PASI-75, PASI-90, static Physician Global Assessment (sPGA), and adverse events."( Efficacy and safety of apremilast monotherapy in moderate-to-severe plaque psoriasis: A systematic review and meta-analysis.
Alahmadi, RA; Alamri, AM; Aljefri, YE; Alkhamisi, TA; Alkhunani, TA; Alraddadi, AA; Ghaddaf, AA, 2022
)
0.72
" Treatment continued until disease progression or intolerable adverse events (AEs)."( Efficacy and safety of pomalidomide and low-dose dexamethasone in Chinese patients with relapsed or refractory multiple myeloma: a multicenter, prospective, single-arm, phase 2 trial.
Bai, H; Fang, BJ; Fu, WJ; Liao, AJ; Lu, J; Niu, T; Wang, YF; Zhao, HG, 2022
)
0.72
" The most common grade 3 and 4 treatment-emergent adverse events (TEAEs) were neutropenia (63."( Efficacy and safety of pomalidomide and low-dose dexamethasone in Chinese patients with relapsed or refractory multiple myeloma: a multicenter, prospective, single-arm, phase 2 trial.
Bai, H; Fang, BJ; Fu, WJ; Liao, AJ; Lu, J; Niu, T; Wang, YF; Zhao, HG, 2022
)
0.72
"Pomalidomide in combination with low-dose dexamethasone is effective and safe in Chinese RRMM patients."( Efficacy and safety of pomalidomide and low-dose dexamethasone in Chinese patients with relapsed or refractory multiple myeloma: a multicenter, prospective, single-arm, phase 2 trial.
Bai, H; Fang, BJ; Fu, WJ; Liao, AJ; Lu, J; Niu, T; Wang, YF; Zhao, HG, 2022
)
0.72
"We aimed to compare incidence rates of adverse events of special interest identified a priori, in patients receiving apremilast with those receiving other systemic treatments for psoriasis or psoriatic arthritis."( Safety of Apremilast in Patients with Psoriasis and Psoriatic Arthritis: Findings from the UK Clinical Practice Research Datalink.
Cordey, M; Jick, S; Paris, M; Persson, R, 2022
)
0.72
" Incidence rates of adverse events of special interest were estimated for four matched cohorts: apremilast-exposed and three matched non-apremilast cohorts (oral only, injectable only, and oral and injectable psoriasis or psoriatic arthritis treatments)."( Safety of Apremilast in Patients with Psoriasis and Psoriatic Arthritis: Findings from the UK Clinical Practice Research Datalink.
Cordey, M; Jick, S; Paris, M; Persson, R, 2022
)
0.72
" Similar incidence rates of all-cause mortality, major adverse cardiac events, tachyarrhythmias, and solid malignancies were recorded in the apremilast and non-apremilast cohorts."( Safety of Apremilast in Patients with Psoriasis and Psoriatic Arthritis: Findings from the UK Clinical Practice Research Datalink.
Cordey, M; Jick, S; Paris, M; Persson, R, 2022
)
0.72
" A total of 21 adverse events appeared in the included studies, with neutropenia being the highest incidence of hematologic adverse events (32."( The efficacy and safety of triplet regimens based on pomalidomide and dexamethasone for treatment of relapsed/refractory multiple myeloma: a systematic review and meta-analysis.
Chen, XM; Huang, CL; Liao, KY; Liu, Y; Xiong, H; Zhang, XW, 2022
)
0.72
"Three-drug regimens based on pomalidomide and dexamethasone could yield excellent overall response rate to relapsed/refractory multiple myeloma, but there are still various adverse events; therefore, consequent studies should address these adverse events."( The efficacy and safety of triplet regimens based on pomalidomide and dexamethasone for treatment of relapsed/refractory multiple myeloma: a systematic review and meta-analysis.
Chen, XM; Huang, CL; Liao, KY; Liu, Y; Xiong, H; Zhang, XW, 2022
)
0.72
"In conclusion, replacing Revlimid® with its generic version Rivelime® in singlet, doublet or triplet lenalidomide containing RRMM regimens seems not to compromise the efficacy of treatment, and to yield a similarly improved response rates and survival outcome and no additional toxic effects, enabling a long-term therapy."( Generic Lenalidomide Rivelime Versus Brand-name Revlimid® in the Treatment of Relapsed/Refractory Multiple Myeloma: A Retrospective Single-center Experience on Efficacy, Safety and Survival Outcome.
Beksac, M; Gurman, G; Ilhan, O; Koyun, D; Seval, GC; Topcuoglu, P; Yuksel, MK, 2023
)
0.91
" Pomalidomide combinations were well tolerated, no patient discontinued treatment due to adverse events."( Pomalidomide combinations are a safe and effective option after daratumumab failure.
Binder, M; Brioli, A; Engelhardt, M; Ernst, T; Gengenbach, L; Heidel, FH; Hilgendorf, I; Hochhaus, A; Mancuso, K; Stauch, T; von Lilienfeld-Toal, M; Zamagni, E, 2023
)
0.91
"These data show that pomalidomide-based combinations can be an effective and safe salvage regimen for daratumumab-refractory patients, including those with EMM."( Pomalidomide combinations are a safe and effective option after daratumumab failure.
Binder, M; Brioli, A; Engelhardt, M; Ernst, T; Gengenbach, L; Heidel, FH; Hilgendorf, I; Hochhaus, A; Mancuso, K; Stauch, T; von Lilienfeld-Toal, M; Zamagni, E, 2023
)
0.91
" We examined the time-to-onset and outcome of lung adverse events (LAEs) related to pomalidomide in Japanese patients based on information obtained from the spontaneous reporting system of the Japanese Adverse Drug Event Report database (JADER) of the Pharmaceuticals and Medical Devices Agency."( Assessment of Time-to-onset and Outcome of Lung Adverse Events With Pomalidomide from a Pharmacovigilance Study.
Kawahara, Y; Murata, S; Shimizu, T; Uchida, M; Uesawa, Y,
)
0.13
"We analyzed adverse events (AEs) reports recorded between April 2004 and March 2021 from JADER."( Assessment of Time-to-onset and Outcome of Lung Adverse Events With Pomalidomide from a Pharmacovigilance Study.
Kawahara, Y; Murata, S; Shimizu, T; Uchida, M; Uesawa, Y,
)
0.13
" The primary outcomes were Overall Survival (OS) and Progression Free Survival (PFS, measured as time to next treatment), and the secondary outcomes were Adverse Events (AE)."( Real-world effectiveness and safety of multiple myeloma treatments based on thalidomide and bortezomib: A retrospective cohort study from 2009 to 2020 in a Brazilian metropolis.
Costa, IHFD; Drummond, PLM; Malta, JS; Menezes de Pádua, CA; Reis, AMM; Santos, RMMD; Silveira, LP, 2023
)
1.14
" Mild adverse events were reported in 48 (9%) patients and serious adverse events, including cerebral vascular accident and portal vein thrombosis were reported in two patients each."( Long-term clinical efficacy and safety of thalidomide in patients with transfusion-dependent β-thalassemia: results from Thal-Thalido study.
Ali, M; Ali, Z; Ismail, M; Khan, MTM; Rani, GF; Rehman, IU, 2023
)
1.17
" The efficacy and adverse events were evaluated and recorded every 3 months."( Efficacy and safety of thalidomide in children with monogenic autoinflammatory diseases: a single-center, real-world-evidence study.
Gao, S; Gou, L; Li, J; Ma, M; Song, H; Wang, C; Wang, L; Wang, W; Yu, Z; Zhang, C; Zhong, L; Zhou, Y, 2023
)
1.22
" Anorexia and nausea occurred in 2 cases, with no other reported drug-related adverse reactions."( Efficacy and safety of thalidomide in children with monogenic autoinflammatory diseases: a single-center, real-world-evidence study.
Gao, S; Gou, L; Li, J; Ma, M; Song, H; Wang, C; Wang, L; Wang, W; Yu, Z; Zhang, C; Zhong, L; Zhou, Y, 2023
)
1.22
" Thalidomide is relatively safe in monogenic AIDs."( Efficacy and safety of thalidomide in children with monogenic autoinflammatory diseases: a single-center, real-world-evidence study.
Gao, S; Gou, L; Li, J; Ma, M; Song, H; Wang, C; Wang, L; Wang, W; Yu, Z; Zhang, C; Zhong, L; Zhou, Y, 2023
)
2.13

Pharmacokinetics

This phase II study evaluated the combination of semaxanib, a small molecule tyrosine kinase inhibitor of vascular endothelial growth factor (VEGF) receptor-2, and thalidomide in patients with metastatic melanoma. The pharmacokinetic profiles of plasma concentrations were evaluated with both noncompartmental and compartmental methods.

ExcerptReferenceRelevance
"Absorption, blood level course, renal, fecal, and biliary elimination and the metabolisation of 2-(bicyclo[2,2,1]-heptane-2-endo-3-endo-dicarboximido)-glutarimide (taglutimide, K-2004), a new hypnotic-sedative substance, were studied in the rat, and the pharmacokinetic constants were calculated."( Pharmacokinetics and metabolism of taglutimide (K-2004) in the rat.
Fiebrich, F; Koch, H; Pischek, G, 1979
)
0.26
" The mean plasma elimination half-life was in the range of 5 h for the enantiomers, as well as for the racemic mixture, although there was a tendency toward slower elimination and higher plasma AUC values of the S-enantiomer: thus, after administration of the (greater than 99%) pure enantiomers, the plasma AUC value of the administered S-enantiomer was found to be more than one-third higher than that of the administered R-enantiomer."( The enantiomers of the teratogenic thalidomide analogue EM 12: 1. Chiral inversion and plasma pharmacokinetics in the marmoset monkey.
Nau, H; Neubert, D; Schmahl, HJ, 1988
)
0.55
" No changes were observed for other pharmacokinetic parameters assessed for either ethinyl estradiol or norethindrone."( Thalidomide does not alter the pharmacokinetics of ethinyl estradiol and norethindrone.
Abernethy, DR; Collins, JM; Donahue, SR; Flockhart, DA; Thacker, D; Trapnell, CB, 1998
)
1.74
" Furthermore, no changes were seen for other pharmacokinetic parameters assessed for thalidomide between days 1 and 21."( Thalidomide does not alter the pharmacokinetics of ethinyl estradiol and norethindrone.
Abernethy, DR; Collins, JM; Donahue, SR; Flockhart, DA; Thacker, D; Trapnell, CB, 1998
)
1.97
" Serial serum or blood samples were obtained for pharmacokinetic assessment after administration of a single oral dose or multiple daily dosing of thalidomide and were assayed by reversed-phase HPLC."( Pharmacokinetics of thalidomide in an elderly prostate cancer population.
Bauer, KS; Bergan, R; Chen, A; Figg, WD; Hamilton, M; Pluda, J; Raje, S; Reed, E; Tompkins, A; Venzon, D, 1999
)
0.83
" The pharmacokinetic profiles of plasma concentrations of thalidomide were evaluated with both noncompartmental and compartmental methods, whereas those of ethinyl estradiol and norethindrone were calculated with noncompartmental methods."( Thalidomide does not alter estrogen-progesterone hormone single dose pharmacokinetics.
Colburn, W; Kook, KA; Scheffler, MR; Thomas, SD, 1999
)
1.99
" There were no significant differences between pharmacokinetic parameters for thalidomide after 1 dose and those after 18 consecutive doses."( Thalidomide does not alter estrogen-progesterone hormone single dose pharmacokinetics.
Colburn, W; Kook, KA; Scheffler, MR; Thomas, SD, 1999
)
1.97
" Pharmacokinetic parameters were determined using compartmental methods for the two Celgene formulations and using noncompartmental methods for all three formulations."( Single-dose oral pharmacokinetics of three formulations of thalidomide in healthy male volunteers.
Colburn, WA; Teo, SK; Thomas, SD, 1999
)
0.55
" Pharmacokinetic modelling predicted that varying the infusion time of a fixed dose of S-thalidomide between 10 min and 6h would have little influence on the maximal blood concentration of formed R-thalidomide."( Intravenous formulations of the enantiomers of thalidomide: pharmacokinetic and initial pharmacodynamic characterization in man.
Björkman, S; Eriksson, T; Höglund, P; Roth, B, 2000
)
0.79
" The aim of this study was to further investigate these pharmacokinetic DMXAA-drug interactions in the rat model."( A difference between the rat and mouse in the pharmacokinetic interaction of 5,6-dimethylxanthenone-4-acetic acid with thalidomide.
Ching, LM; Kestell, P; Paxton, JW; Tingle, MD; Zhou, S, 2001
)
0.52
" The cause of the species difference in the pharmacokinetic response to thalidomide by DMXAA is unknown, and indicates difficulties in predicting the outcome of such a combination in patients."( A difference between the rat and mouse in the pharmacokinetic interaction of 5,6-dimethylxanthenone-4-acetic acid with thalidomide.
Ching, LM; Kestell, P; Paxton, JW; Tingle, MD; Zhou, S, 2001
)
0.75
" In both of these cases, thalidomide extends the half-life (t(1/2)) of the other drug."( Modulation of thalidomide pharmacokinetics by cyclophosphamide or 5,6-dimethylxanthenone-4-acetic acid (DMXAA) in mice: the role of tumour necrosis factor.
Baguley, BC; Ching, LM; Chung, F; Kestell, P; Wang, LC, 2004
)
0.99
"Both cyclophosphamide and DMXAA have a pharmacokinetic interaction with thalidomide, increasing t(1/2) and AUC."( Modulation of thalidomide pharmacokinetics by cyclophosphamide or 5,6-dimethylxanthenone-4-acetic acid (DMXAA) in mice: the role of tumour necrosis factor.
Baguley, BC; Ching, LM; Chung, F; Kestell, P; Wang, LC, 2004
)
0.92
" After a single oral dose of thalidomide 200 mg (as the US-approved capsule formulation) in healthy volunteers, absorption is slow and extensive, resulting in a peak concentration (C(max)) of 1-2 mg/L at 3-4 hours after administration, absorption lag time of 30 minutes, total exposure (AUC( infinity )) of 18 mg."( Clinical pharmacokinetics of thalidomide.
Colburn, WA; Jaworsky, MS; Kook, KA; Laskin, OL; Scheffler, MA; Stirling, DI; Teo, SK; Thomas, SD; Tracewell, WG, 2004
)
0.91
"Plasma concentration-time profiles for the individual patients were very similar to each other, but widely different pharmacokinetic properties were found between patients compared with those in mice or rabbits."( Thalidomide pharmacokinetics and metabolite formation in mice, rabbits, and multiple myeloma patients.
Baguley, BC; Browett, P; Ching, LM; Chung, F; Kestell, P; Lu, J; Palmer, BD; Tingle, M, 2004
)
1.77
" We performed a phase I and pharmacokinetic study of thalidomide with carboplatin in children with refractory solid tumors."( Phase I and pharmacokinetic study of thalidomide with carboplatin in children with cancer.
Aleksic, A; Berg, SL; Blaney, SM; Bomgaars, LR; Chintagumpala, M; Klenke, RA; Kuttesch, JF, 2004
)
0.85
" In addition, we have characterized the pharmacokinetic behavior of thalidomide in children."( Phase I and pharmacokinetic study of thalidomide with carboplatin in children with cancer.
Aleksic, A; Berg, SL; Blaney, SM; Bomgaars, LR; Chintagumpala, M; Klenke, RA; Kuttesch, JF, 2004
)
0.83
" Further studies are warranted to explore the pharmacokinetic and pharmacodynamic interactions between CPT-11 and thalidomide."( Determination of thalidomide by high performance liquid chromatography: plasma pharmacokinetic studies in the rat.
Chan, E; Chan, SY; Duan, W; Goh, BC; Ho, PC; Hu, Z; Yang, X; Zhou, S, 2005
)
0.88
" Pharmacokinetic studies were performed at the first dose level and repeated at the second dose level of each patient."( Phase I and pharmacokinetic study of oral thalidomide in patients with advanced hepatocellular carcinoma.
Chang, JY; Chao, Y; Chen, LT; Chen, PJ; Chin, YH; Chuang, TR; Huang, JD; Liu, TW; Shiah, HS; Whang-Peng, J; Yao, TJ, 2006
)
0.6
" The pharmacokinetic analysis were performed on 16 patients."( Irinotecan in combination with thalidomide in patients with advanced solid tumors: a clinical study with pharmacodynamic and pharmacokinetic evaluation.
Allegrini, G; Amatori, F; Bocci, G; Cerri, E; Cupini, S; Danesi, R; Del Tacca, M; Di Paolo, A; Falcone, A; Marcucci, L; Masi, G, 2006
)
0.62
" This study aimed to investigate whether combination of thalidomide modulated the toxicities of CPT-11 using a rat model and the possible role of the altered pharmacokinetic component in the toxicity modulation using in vitro models."( Pharmacokinetic mechanisms for reduced toxicity of irinotecan by coadministered thalidomide.
Bian, JS; Boelsterli, UA; Chan, E; Chan, SY; Chen, YZ; Duan, W; Ho, PC; Hu, ZP; Huang, M; Ng, KY; Yang, XX; Zhou, SF, 2006
)
0.81
"This phase II study evaluated the combination of semaxanib, a small molecule tyrosine kinase inhibitor of vascular endothelial growth factor (VEGF) receptor-2, and thalidomide in patients with metastatic melanoma to assess the efficacy, tolerability, pharmacokinetic (PK) and pharmacodynamic (PD) characteristics of the combination."( A phase II, pharmacokinetic, and biologic study of semaxanib and thalidomide in patients with metastatic melanoma.
Beeram, M; Berg, K; de Bono, JS; Eckhart, SG; Forero, L; Hammond, LA; Izbicka, E; Mita, AC; Mita, MM; Patnaik, A; Rowinsky, EK; Simmons, P; Takimoto, C; Tolcher, AW; Weiss, GR, 2007
)
0.77
" This pharmacokinetic difference may explain the dose difference between Japan and other countries."( The pharmacokinetics of low-dose thalidomide in Japanese patients with refractory multiple myeloma.
Asaoku, H; Ikawa, K; Iwato, K; Kamikawa, R; Morikawa, N; Sasaki, A, 2006
)
0.62
" The differences in pharmacokinetic parameters between normal renal function and mild renal impairment were minor to modest (11%-32%)."( Pharmacokinetics of lenalidomide in subjects with various degrees of renal impairment and in subjects on hemodialysis.
Chen, N; Knight, R; Kong, L; Kumar, G; Laskin, OL; Lau, H; Zeldis, JB, 2007
)
0.34
"Twenty-four patients who were enrolled in a large randomized trial of thalidomide vs no thalidomide maintenance therapy for myeloma, in which all patients also received zoledronic acid, were recruited to a pharmacokinetic and renal safety sub-study, and followed for up to 16 months."( Renal safety of zoledronic acid with thalidomide in patients with myeloma: a pharmacokinetic and safety sub-study.
Bilic, S; Copeman, M; Cremers, S; Kennedy, N; Lynch, K; Neeman, T; Ravera, C; Roberts, A; Schran, H; Spencer, A, 2008
)
0.85
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
Lombardo, F; Obach, RS; Waters, NJ, 2008
)
0.35
" Pharmacokinetic data when irinotecan was administered as a single agent in each arm were compared to data when the two study agents were co-administered using paired t tests."( The effect of thalidomide on the pharmacokinetics of irinotecan and metabolites in advanced solid tumor patients.
Cohen, EE; House, LK; Innocenti, F; Janisch, L; Karrison, T; Ramírez, J; Ratain, MJ; Wu, K, 2011
)
0.73
"The differences in pharmacokinetic parameters and metabolic markers after thalidomide administration were small and unlikely to be clinically significant."( The effect of thalidomide on the pharmacokinetics of irinotecan and metabolites in advanced solid tumor patients.
Cohen, EE; House, LK; Innocenti, F; Janisch, L; Karrison, T; Ramírez, J; Ratain, MJ; Wu, K, 2011
)
0.96
" Pharmacokinetic parameters were estimated using noncompartmental methods."( Plasma and cerebrospinal fluid pharmacokinetics of thalidomide and lenalidomide in nonhuman primates.
Berg, SL; Dauser, RC; Gibson, BW; McGuffey, LH; Muscal, JA; Nuchtern, JG; Sun, Y, 2012
)
0.63
"9 mL/min/kg, the median plasma AUC was 80 μM h, and the median terminal half-life (t(½)) was 13."( Plasma and cerebrospinal fluid pharmacokinetics of thalidomide and lenalidomide in nonhuman primates.
Berg, SL; Dauser, RC; Gibson, BW; McGuffey, LH; Muscal, JA; Nuchtern, JG; Sun, Y, 2012
)
0.63
" The dosage of thalidomide, concentrations of (R)- and (S)-thalidomide in whole blood, and clinical laboratory test results were used as pharmacokinetic and pharmacodynamic indices."( Influence of cytochrome P450 2C19 gene variations on pharmacokinetic parameters of thalidomide in Japanese patients.
Ishida, F; Matsuda, M; Matsuzawa, N; Nakamura, K; Ohmori, S, 2012
)
0.96
" The terminal elimination half-life (t (½)) was 3-4 h at doses up to 50 mg and was not affected by food."( Single-dose pharmacokinetics of lenalidomide in healthy volunteers: dose proportionality, food effect, and racial sensitivity.
Chen, N; Kasserra, C; Lau, H; Liu, L; Reyes, J, 2012
)
0.38
" Murine pharmacokinetic characterization necessary for translational and further preclinical investigations has not been published."( Pharmacokinetics and tissue disposition of lenalidomide in mice.
Byrd, JC; Gao, Y; Herman, SE; Jarjoura, D; Johnson, AJ; Li, X; Mahoney, E; Phelps, MA; Rozewski, DM; Shin, JD; Stefanovski, MR; Towns, WH; Yang, X, 2012
)
0.38
" However, there have been few studies of the pharmacokinetic changes occurring during thalidomide therapy."( Clinical evidence of pharmacokinetic changes in thalidomide therapy.
Ando, Y; Matsunaga, T; Matsuzawa, N; Nakamura, K; Ohmori, S; Yamazaki, H, 2013
)
0.87
"Herein, the authors review the chemistry, the mechanism of action and the pharmacokinetic properties of pomalidomide."( Pharmacokinetic evaluation of pomalidomide for the treatment of myeloma.
Bringhen, S; Gay, F; Mina, R; Troia, R, 2013
)
0.39
"This article describes, for the first time, a highly sensitive and specific enzyme-linked immunosorbent assay (ELISA) for therapeutic monitoring and pharmacokinetic studies of lenalidomide (LND), the potent drug for treatment of multiple myeloma (MM)."( A highly sensitive polyclonal antibody-based ELISA for therapeutic monitoring and pharmacokinetic studies of lenalidomide.
Abuhejail, RM; Alzoman, NZ; Darwish, IA, 2014
)
0.4
" A simple and robust HPLC assay with fluorescence detection for pomalidomide over the range of 1-500ng/mL has been developed for application to pharmacokinetic studies in ongoing clinical trials in various other malignancies."( A sensitive and robust HPLC assay with fluorescence detection for the quantification of pomalidomide in human plasma for pharmacokinetic analyses.
Aleman, K; Figg, WD; Peer, CJ; Polizzotto, MN; Roth, J; Shahbazi, S; Uldrick, TS; Wyvill, KM; Yarchoan, R; Zeldis, JB, 2014
)
0.4
" Pharmacokinetic (PK) analyses were conducted to determine the PK disposition of the isomers from their PK profiles in humans and monkeys."( Modeling and simulation to probe the pharmacokinetic disposition of pomalidomide R- and S-enantiomers.
Hoffmann, M; Kumar, G; Li, Y; Palmisano, M; Zhou, S, 2014
)
0.4
"4) and Cmax (from 290 vs."( The impact of co-administration of ketoconazole and rifampicin on the pharmacokinetics of apremilast in healthy volunteers.
Liu, Y; Palmisano, M; Wan, Y; Wu, A; Zhou, S, 2014
)
0.4
" The analytical method was applied to support a pharmacokinetic study of simultaneous estimation of lenalidomide, ibrutinib, and its active metabolite PCI-45227 in Wistar rat."( Simultaneous quantification of lenalidomide, ibrutinib and its active metabolite PCI-45227 in rat plasma by LC-MS/MS: application to a pharmacokinetic study.
Govindarajulu, B; Rangasamy, M; Thappali, S; Vakkalanka, S; Veeraraghavan, S; Viswanadha, S, 2015
)
0.42
" Here we evaluated the clinical and pharmacodynamic effects of continuous or intermittent dosing strategies of pomalidomide/dexamethasone in lenalidomide-refractory myeloma in a randomized trial."( Clinical and pharmacodynamic analysis of pomalidomide dosing strategies in myeloma: impact of immune activation and cereblon targets.
Breider, M; Cooper, D; Couto, S; Das, R; Deng, Y; Dhodapkar, KM; Dhodapkar, MV; Hansel, D; Kocoglu, M; Koduru, S; Ren, Y; Sehgal, K; Seropian, S; Thakurta, A; Vasquez, J; Verma, R; Wang, M; Yao, X; Zhang, L, 2015
)
0.42
" Pharmacodynamic effects of apremilast on plasma biomarkers associated with inflammation were evaluated in a PALACE 1 substudy."( The pharmacodynamic impact of apremilast, an oral phosphodiesterase 4 inhibitor, on circulating levels of inflammatory biomarkers in patients with psoriatic arthritis: substudy results from a phase III, randomized, placebo-controlled trial (PALACE 1).
Chen, P; Chopra, R; Fang, L; Schafer, PH; Wang, A, 2015
)
0.42
" The objective of this study was to evaluate the pharmacokinetic and pharmacodynamic drug interactions between lenalidomide and warfarin in healthy volunteers."( Evaluation of pharmacokinetic and pharmacodynamic interactions when lenalidomide is co-administered with warfarin in a randomized clinical trial setting.
Chen, N; Knight, R; Palmisano, M; Weiss, D; Zhou, S, 2015
)
0.42
"The 90 % confidence intervals (CI) for the ratio of AUC or Cmax geometric means between co-administration with lenalidomide and placebo were within the 80-125 % bioequivalence bounds for R-warfarin and S-warfarin."( Evaluation of pharmacokinetic and pharmacodynamic interactions when lenalidomide is co-administered with warfarin in a randomized clinical trial setting.
Chen, N; Knight, R; Palmisano, M; Weiss, D; Zhou, S, 2015
)
0.42
" This study was conducted to investigate the pharmacokinetic and safety profiles of ixazomib, administered with lenalidomide-dexamethasone, in East Asian patients with relapsed/refractory MM."( Pharmacokinetics and safety of ixazomib plus lenalidomide-dexamethasone in Asian patients with relapsed/refractory myeloma: a phase 1 study.
Chim, CS; Chng, WJ; Esseltine, DL; Goh, YT; Gupta, N; Hanley, MJ; Hui, AM; Kim, K; Lee, JH; Min, CK; Venkatakrishnan, K; Wong, RS; Yang, H, 2015
)
0.42
" Simulation of human plasma concentrations of thalidomide were achieved with a simplified physiologically based pharmacokinetic model in accordance with reported thalidomide concentrations."( Simulation of Human Plasma Concentrations of Thalidomide and Primary 5-Hydroxylated Metabolites Explored with Pharmacokinetic Data in Humanized TK-NOG Mice.
Guengerich, FP; Nishiyama, S; Shibata, N; Suemizu, H; Yamazaki, H, 2015
)
0.94
"A wide linearity range analytical method for the determination of lenalidomide in patients with multiple myeloma for pharmacokinetic studies is required."( A Wide Linearity Range Method for the Determination of Lenalidomide in Plasma by High-Performance Liquid Chromatography: Application to Pharmacokinetic Studies.
Climente-Martí, M; Guglieri-López, B; Martinez-Gómez, MA; Merino-Sanjuán, M; Pérez-Pitarch, A; Porta-Oltra, B, 2016
)
0.43
"A rapid, sensitive and selective ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS-MS) was developed and validated for the determination and pharmacokinetic investigation of apremilast in rat plasma."( Determination of Apremilast in Rat Plasma by UPLC-MS-MS and Its Application to a Pharmacokinetic Study.
Chen, LG; Lai, X; Li, T; Pan, Y; Wang, S; Wang, Z, 2016
)
0.43
" Simulation of human plasma concentrations of the teratogen thalidomide and its human metabolites is possible with a simplified physiologically based pharmacokinetic model based on data obtained in chimeric mice, in accordance with reported clinical thalidomide concentrations."( Combining Chimeric Mice with Humanized Liver, Mass Spectrometry, and Physiologically-Based Pharmacokinetic Modeling in Toxicology.
Guengerich, FP; Mitsui, M; Shimizu, M; Suemizu, H; Yamazaki, H, 2016
)
0.68
" Simulations of human plasma concentrations of pomalidomide were achieved with simplified physiologically-based pharmacokinetic models in both groups of mice in accordance with reported pomalidomide concentrations after low dose administration in humans."( Metabolic profiles of pomalidomide in human plasma simulated with pharmacokinetic data in control and humanized-liver mice.
Guengerich, FP; Mitsui, M; Shibata, N; Shimizu, M; Suemizu, H; Yamazaki, H, 2017
)
0.46
" Plasma apremilast and metabolite M12 concentrations were determined, and pharmacokinetic parameters were calculated from samples obtained predose and up to 72 hours postdose."( Impact of Renal Impairment on the Pharmacokinetics of Apremilast and Metabolite M12.
Assaf, M; Liu, Y; Nissel, J; Palmisano, M; Zhou, S, 2016
)
0.43
" A set of blood samples was taken in order to develop a pharmacokinetic model accounting for lenalidomide concentrations in this setting."( Pharmacokinetics of lenalidomide during high cut-off dialysis in a patient with multiple myeloma and renal failure.
Buclin, T; Burnier, M; Dao, K; Figg, WD; Kissling, S; Lu, Y; Peer, CJ; Stadelmann, R, 2017
)
0.46
" The aim of this study was to conduct a population pharmacokinetic analysis of lenalidomide in multiple myeloma patients to identify and evaluate non-studied covariates that could be used for dose individualization."( Population pharmacokinetics of lenalidomide in multiple myeloma patients.
Climente-Martí, M; Guchelaar, HJ; Guglieri-López, B; Merino-Sanjuán, M; Moes, DJ; Pérez-Pitarch, A; Porta-Oltra, B, 2017
)
0.46
" Nonlinear mixed-effects modeling was used to develop a population pharmacokinetic model and perform covariate analysis."( Population pharmacokinetics of lenalidomide in multiple myeloma patients.
Climente-Martí, M; Guchelaar, HJ; Guglieri-López, B; Merino-Sanjuán, M; Moes, DJ; Pérez-Pitarch, A; Porta-Oltra, B, 2017
)
0.46
" In addition, the developed population pharmacokinetic model can be used to individualize lenalidomide dose in multiple myeloma patients, taking into account not only creatinine clearance but also body surface area."( Population pharmacokinetics of lenalidomide in multiple myeloma patients.
Climente-Martí, M; Guchelaar, HJ; Guglieri-López, B; Merino-Sanjuán, M; Moes, DJ; Pérez-Pitarch, A; Porta-Oltra, B, 2017
)
0.46
" Simulations of human plasma concentrations of lenalidomide were achieved with simplified physiologically-based pharmacokinetic models in control and humanized-liver mice or by the direct fitting analysis of reported human data, in accordance with reported lenalidomide concentrations after low dose administration in humans."( Association of pharmacokinetic profiles of lenalidomide in human plasma simulated using pharmacokinetic data in humanized-liver mice with liver toxicity detected by human serum albumin RNA.
Guengerich, FP; Kamiya, Y; Kusama, T; Mitsui, M; Murayama, N; Shimizu, M; Suemizu, H; Uehara, S; Yamazaki, H, 2018
)
0.48
" In the same way, the two methods were successfully used to study the pharmacokinetic parameters of both THD and DEX after their intra-peritoneal administration."( Simultaneous Determination of Thalidomide and Dexamethasone in Rat Plasma by Validated HPLC and HPTLC With Pharmacokinetic Study.
Abdelkawy, MM; Abdelwahab, NS; Ali, NW; Sharkawi, SMZ; Zaki, MM, 2019
)
0.8
" Population pharmacokinetic analyses were conducted to determine the pharmacokinetics of intravenous daratumumab in combination therapy versus monotherapy, evaluate the effect of patient- and disease-related covariates on drug disposition, and examine the relationships between daratumumab exposure and efficacy/safety outcomes."( Pharmacokinetics and Exposure-Response Analyses of Daratumumab in Combination Therapy Regimens for Patients with Multiple Myeloma.
Belch, A; Capra, M; Clemens, PL; Dimopoulos, MA; Gomez, D; Ho, PJ; Iida, S; Jansson, R; Leiba, M; Medvedova, E; Min, CK; Schecter, J; Sonneveld, P; Sun, YN; Xu, XS; Zhang, L, 2018
)
0.48
" The F3 nanoparticles were further evaluated for in vitro release and in vivo pharmacokinetic studies in rats."( Preparation of sustained release apremilast-loaded PLGA nanoparticles: in vitro characterization and in vivo pharmacokinetic study in rats.
Alalaiwe, A; Anwer, MK; Ezzeldin, E; Fatima, F; Iqbal, M; Mohammad, M, 2019
)
0.51
"A population pharmacokinetic (PPK) model to describe the pharmacokinetics of thalidomide in different patient populations was developed using data pooled from healthy subjects and patients with Hansen's disease, human immunodeficiency virus (HIV), and multiple myeloma (MM)."( Population Pharmacokinetic Model to Assess the Impact of Disease State on Thalidomide Pharmacokinetics.
Chen, N; Gaudy, A; Hwang, R; Palmisano, M, 2020
)
1.02
"Maternofoetal physiologically-based pharmacokinetic models integrating multi-compartmental maternal and foetal units were developed using Simbiology® to estimate prenatal drug exposure."( Using mechanistic physiologically-based pharmacokinetic models to assess prenatal drug exposure: Thalidomide versus efavirenz as case studies.
Adejuyigbe, E; Atoyebi, SA; Bolaji, O; Olagunju, A; Owen, A; Rajoli, RKR; Siccardi, M, 2019
)
0.73
"Finding biomarkers that provide shared link between disease severity, drug-induced pharmacodynamic effects and response status in human trials can provide number of values for patient benefits: elucidating current therapeutic mechanism-of-action, and, back-translating to fast-track development of next-generation therapeutics."( Large-scale Analyses of Disease Biomarkers and Apremilast Pharmacodynamic Effects.
Ai, J; Eisinger, D; LaBrie, ST; Medvedeva, IV; Schafer, P; Stokes, ME; Trotter, MWB; Yang, R, 2020
)
0.56
"We evaluated the pharmacodynamic effects of apremilast in 69 patients who were included in biomarker subanalyses of a phase 2b study that demonstrated the long-term safety and efficacy of apremilast in Japanese adults with moderate to severe psoriasis."( Pharmacodynamic analysis of apremilast in Japanese patients with moderate to severe psoriasis: Results from a phase 2b randomized trial.
Imafuku, S; Komine, M; Nemoto, O; Ohtsuki, M; Okubo, Y; Petric, R; Schafer, P, 2021
)
0.62
" Apremilast was rapidly absorbed (maximum concentration: ~2-3 h postdose), and eliminated according to a monoexponential pattern with a terminal-phase elimination half-life of 8-9 h."( Pharmacokinetics and tolerability of apremilast in healthy Korean adult men.
Choi, Y; Huh, KY; Lee, H; Liu, L; Nissel, J; Palmisano, M; Ramirez-Valle, F; Wang, X, 2021
)
0.62
" The aims of this analysis were to develop a population pharmacokinetic (PPK) model of apremilast based on observed data from phase 1 studies combined with clinical trial data from subjects with moderate to severe psoriasis, and to develop exposure-response (E-R) models to determine whether Japanese subjects with moderate to severe psoriasis achieve response to apremilast treatment similar to that observed in non-Japanese, predominantly Caucasian subjects with moderate to severe psoriasis."( Population pharmacokinetic and exposure-response analysis of apremilast in Japanese subjects with moderate to severe psoriasis.
Imafuku, S; Kassir, N; Komine, M; Nemoto, O; Ohtsuki, M; Okubo, Y; Petric, R, 2021
)
0.62

Compound-Compound Interactions

The therapeutic efficacy of different doses of dexamethasone combined with bortezomib and thalidomide for patients with multiple myeloma is similar, can obviously enhance remission rate, prolong the survival time. The incidence of adverse reactions in low dose Dexamethason rigemen is significantly reduced, and the safety is better.

ExcerptReferenceRelevance
" The purpose of this work was to evaluate the in vitro and in vivo immunosuppressive effects of Thd and its derivative, N-Hydroxythalidomide (H-Thd), alone and in combination with cyclosporin A (CsA), upon different in vitro lymphocyte activation pathways and in vivo local graft-versus-host-reaction (GvHR)."( In vitro and in vivo immunosuppressive potential of thalidomide and its derivative, N-hydroxythalidomide, alone and in combination with cyclosporin A.
Chuong, PH; Claude, JR; Galons, H; Huynh-Thien, D; Righenzi, S; Voisin, J; Warnet, JM; Zhu, J, 1997
)
0.75
" Additionally, we investigated a potential enhancement of the antitumoral action of thalidomide when combined with a low dose of the antineoplastic carmustine."( Antiproliferative effect of thalidomide alone and combined with carmustine against C6 rat glioma.
Arrieta, O; Guevara, P; Rembao, D; Rivera, E; Sotelo, J; Tamariz, J, 2002
)
0.83
" Thalidomide, both alone and in combination with dexamethasone, has been demonstrated to be useful in patients with advanced MM, as responses could be achieved in 30-60% of the cases."( Thalidomide alone or in combination with dexamethasone in patients with advanced, relapsed or refractory multiple myeloma and renal failure.
Baccarani, M; Cangini, D; Cavo, M; Cellini, C; Tacchetti, P; Tosi, P; Tura, S; Zamagni, E, 2004
)
2.68
"To quantify changes of bone marrow microcirculation in multiple myeloma (MM) using contrast enhanced dynamic MRI (dMRI) during thalidomide as antiangiogenic monotherapy or in combination with chemotherapy (cyclophosphamide, etoposide, dexamethasone)."( [Dynamic MRI of the bone marrow for monitoring multiple myeloma during treatment with thalidomide as monotherapy or in combination with CED chemotherapy].
Delorme, S; Düber, C; Goldschmidt, H; Heiss, J; Hillengass, J; Kauczor, HU; Moehler, T; Neben, K; Nosas, S; Wasser, K, 2004
)
0.75
"dMRI can quantify significant changes of bone marrow microcirculation solely during treatment with thalidomide combined with chemotherapy, not with thalidomide alone."( [Dynamic MRI of the bone marrow for monitoring multiple myeloma during treatment with thalidomide as monotherapy or in combination with CED chemotherapy].
Delorme, S; Düber, C; Goldschmidt, H; Heiss, J; Hillengass, J; Kauczor, HU; Moehler, T; Neben, K; Nosas, S; Wasser, K, 2004
)
0.76
"The present study aimed to evaluate the side-effects and efficacy of thalidomide in combination with an anthracycline-containing chemotherapy regimen in previously untreated myeloma patients."( Thalidomide in combination with vincristine, epirubicin and dexamethasone (VED) for previously untreated patients with multiple myeloma.
Bojko, P; Brandhorst, D; Buttkereit, U; Ebeling, P; Flasshove, M; Hense, J; Hoiczyk, M; Metz, K; Moritz, T; Nowrousian, MR; Opalka, B; Schütt, P; Seeber, S, 2005
)
2.01
"The aim of this study was to assess the side effects and the efficacy of thalidomide alone or in combination with dexamethasone in relapsed multiple myeloma (MM) and to evaluate possible predictive factors for response rate and survival."( Thalidomide in combination with dexamethasone for pretreated patients with multiple myeloma: serum level of soluble interleukin-2 receptor as a predictive factor for response rate and for survival.
Brandhorst, D; Buttkereit, U; Ebeling, P; Flasshove, M; Moritz, T; Müller, S; Nowrousian, MR; Opalka, B; Poser, M; Schütt, P; Seeber, S, 2005
)
2
"Thalidomide in combination with IL-2 is tolerable and can produce durable, active responses in patients with MRCC."( Phase I/II study of thalidomide in combination with interleukin-2 in patients with metastatic renal cell carcinoma.
Amato, RJ; Morgan, M; Rawat, A, 2006
)
2.1
"Recent clinical studies have demonstrated a reduction of irinotecan (CPT-11) gastrointestinal toxicities when the CPT-11 is administered in combination with thalidomide in patients with diagnosis of colorectal cancer."( Irinotecan in combination with thalidomide in patients with advanced solid tumors: a clinical study with pharmacodynamic and pharmacokinetic evaluation.
Allegrini, G; Amatori, F; Bocci, G; Cerri, E; Cupini, S; Danesi, R; Del Tacca, M; Di Paolo, A; Falcone, A; Marcucci, L; Masi, G, 2006
)
0.82
" Pharmacokinetic data suggested a decreased metabolism of irinotecan into SN-38 and SN-38-glucuronide when it was administered with thalidomide."( Irinotecan in combination with thalidomide in patients with advanced solid tumors: a clinical study with pharmacodynamic and pharmacokinetic evaluation.
Allegrini, G; Amatori, F; Bocci, G; Cerri, E; Cupini, S; Danesi, R; Del Tacca, M; Di Paolo, A; Falcone, A; Marcucci, L; Masi, G, 2006
)
0.82
" This article provides the clinical rationale for the use of PLD in combination with immunomodulatory drugs to treat patients with MM and summarizes the clinical experience with these combinations to date."( Pegylated liposomal doxorubicin and immunomodulatory drug combinations in multiple myeloma: rationale and clinical experience.
Chanan-Khan, AA; Lee, K, 2007
)
0.34
" The animals, which received thalidomide alone orally or in combination with augmentin, 30 min prior to bacterial instillation into the lungs via intranasal route, showed significant (P<0."( Anti-inflammatory effect of thalidomide alone or in combination with augmentin in Klebsiella pneumoniae B5055 induced acute lung infection in BALB/c mice.
Chhibber, S; Kumar, V, 2008
)
0.93
" Lenalidomide in combination with dexamethasone has been approved by the United States Food and Drug Administration and the European Medicines Agency for the treatment of patients with MM who have received at least one prior therapy."( Lenalidomide in combination with dexamethasone for the treatment of relapsed or refractory multiple myeloma.
Attal, M; Dimopoulos, M; Harousseau, JL; Hussein, M; Knop, S; Ludwig, H; Palumbo, A; San Miguel, J; Sonneveld, P; von Lilienfeld-Toal, M, 2009
)
0.35
" Food and Drug Administration (FDA) on June 29, 2006, for use in combination with dexamethasone in patients with multiple myeloma (MM) who have received at least one prior therapy."( Lenalidomide in combination with dexamethasone for the treatment of multiple myeloma after one prior therapy.
Booth, B; Dagher, R; Farrell, A; Hazarika, M; Justice, R; Pazdur, R; Rock, E; Sridhara, R; Williams, G, 2008
)
0.35
"The aim of the present study was to evaluate the effectiveness of bortezomib combined with epirubicin, dexamethasone, and thalidomide (BADT) for the treatment of multiple myeloma (MM)."( Bortezomib in combination with epirubicin, dexamethasone and thalidomide is a highly effective regimen in the treatment of multiple myeloma: a single-center experience.
Hu, X; Huang, C; Lü, S; Ni, X; Qiu, H; Wang, J; Xu, X; Yang, J, 2009
)
0.8
" 60 MM patients including 19 de novo patients, out of them 14 patients received the treatment using regimen of bortezomib in combination with thalidomide (BT), 5 patients received bortezomib-methylprednisolone regimen (BMP)."( [Bortezomib combined with other drugs for treating 60 cases of multiple myeloma].
Chen, SL; Hu, Y; Li, X; Zhang, JJ; Zhong, YP, 2009
)
0.55
"Novel agents have demonstrated enhanced efficacy when combined with other antimyeloma agents especially dexamethasone."( Bortezomib in combination with pegylated liposomal doxorubicin and thalidomide is an effective steroid independent salvage regimen for patients with relapsed or refractory multiple myeloma: results of a phase II clinical trial.
Ailawadhi, S; Barcos, M; Bernstein, ZP; Chanan-Khan, A; Czuczman, MS; Iancu, D; Lee, K; Miller, KC; Mohr, A; Musial, L; Padmanabhan, S; Patel, M; Sher, T; Yu, J, 2009
)
0.59
" We evaluated thalidomide, an anti-angiogenic agent, when combined with chemotherapy and as maintenance treatment."( Anti-angiogenic therapy using thalidomide combined with chemotherapy in small cell lung cancer: a randomized, double-blind, placebo-controlled trial.
Ali, K; Ferry, D; Hackshaw, A; James, L; Jitlal, M; Lee, SM; Middleton, G; O'Brien, M; Rudd, R; Spiro, S; Woll, PJ, 2009
)
1
"In this large randomized trial, thalidomide in combination with chemotherapy did not improve survival of patients with SCLC but was associated with an increased risk of thrombotic events."( Anti-angiogenic therapy using thalidomide combined with chemotherapy in small cell lung cancer: a randomized, double-blind, placebo-controlled trial.
Ali, K; Ferry, D; Hackshaw, A; James, L; Jitlal, M; Lee, SM; Middleton, G; O'Brien, M; Rudd, R; Spiro, S; Woll, PJ, 2009
)
0.93
"NP regimen combined with thalidomide can significantly prolong the median time to tumor progression in patients with advanced NSCLC."( [Randomized study of thalidomide combined with vinorelbine and cisplatin chemotherapy for the treatment of advanced non-small cell lung cancer].
Gu, AQ; Han, BH; Qi, DJ; Shen, J; Song, YY; Xin, Y; Xiong, LW; Zhang, XY, 2009
)
0.98
"The purpose of this study was to investigate the effect of thalidomide (THD) combined with dexamethasone (Dx) on multiple myeloma KM3 cells and its mechanism."( [Effect of thalidomide combined with dexamethasone on multiple myeloma KM3 cells].
Gao, B; Gao, N; Gu, J; He, B; Li, JY; Zhang, Y; Zhou, W, 2009
)
0.99
" We hypothesized that thalidomide, an oral antiangiogenic agent, when combined with chemotherapy, and as maintenance treatment, would improve survival in patients with advanced non-small-cell lung cancer (NSCLC)."( Randomized double-blind placebo-controlled trial of thalidomide in combination with gemcitabine and Carboplatin in advanced non-small-cell lung cancer.
Gilligan, D; Gower, N; Hackshaw, A; Jitlal, M; Lee, SM; Ottensmeier, C; Price, A; Rudd, R; Spiro, S; Woll, PJ, 2009
)
0.92
"In this large trial of patients with NSCLC, thalidomide in combination with chemotherapy did not improve survival overall, but increased the risk of thrombotic events."( Randomized double-blind placebo-controlled trial of thalidomide in combination with gemcitabine and Carboplatin in advanced non-small-cell lung cancer.
Gilligan, D; Gower, N; Hackshaw, A; Jitlal, M; Lee, SM; Ottensmeier, C; Price, A; Rudd, R; Spiro, S; Woll, PJ, 2009
)
0.86
" The results of five phase III trials assessing thalidomide in combination with melphalan and prednisone (MPT) have demonstrated significantly improved response rates compared with melphalan and prednisone (MP) alone."( Consensus guidelines for the optimal management of adverse events in newly diagnosed, transplant-ineligible patients receiving melphalan and prednisone in combination with thalidomide (MPT) for the treatment of multiple myeloma.
Bladé, J; Davies, F; Delforge, M; Facon, T; Garcia Sanz, R; Kropff, M; Leal da Costa, F; Moreau, P; Morgan, G; Palumbo, A; Schey, S, 2010
)
0.81
" We have investigated the role of artemisone (ATM), a novel derivative of artemisinin (ART) in a cancer setting both alone and in combination with established chemotherapeutic agents."( In vitro study of the anti-cancer effects of artemisone alone or in combination with other chemotherapeutic agents.
Chan, WC; Dalgleish, AG; Gravett, AM; Haynes, RK; Krishna, S; Liu, WM; Wilson, NL, 2011
)
0.37
" Finally, ART and ATM were combined with the common anti-cancer agents oxaliplatin, gemcitabine and thalidomide."( In vitro study of the anti-cancer effects of artemisone alone or in combination with other chemotherapeutic agents.
Chan, WC; Dalgleish, AG; Gravett, AM; Haynes, RK; Krishna, S; Liu, WM; Wilson, NL, 2011
)
0.59
" This phase 1/2 dose-escalation study aimed to determine the maximum tolerated dose (MTD) of lenalidomide in combination with melphalan and dexamethasone (M-dex), and assess the efficacy and tolerability of this therapy for patients with de novo AL amyloidosis."( Lenalidomide in combination with melphalan and dexamethasone in patients with newly diagnosed AL amyloidosis: a multicenter phase 1/2 dose-escalation study.
Alakl, M; Benboubker, L; Bridoux, F; Fermand, JP; Harousseau, JL; Hermine, O; Jaccard, A; Leblond, V; Leleu, X; Moreau, P; Planche, L; Roussel, M; Royer, B; Salles, G, 2010
)
0.36
" This factorial design phase I/II protocol tested dose-dense temozolomide alone and combined with cytostatic agents."( A phase I factorial design study of dose-dense temozolomide alone and in combination with thalidomide, isotretinoin, and/or celecoxib as postchemoradiation adjuvant therapy for newly diagnosed glioblastoma.
Chang, E; Colman, H; Conrad, C; de Groot, J; Giglio, P; Gilbert, MR; Gonzalez, J; Groves, MD; Hess, K; Hunter, K; Levin, V; Mahajan, A; Puduvalli, V; Woo, S; Yung, WK, 2010
)
0.58
"Thalidomide used in combination with TAE enhanced anti-tumour effects in rabbits bearing VX2 liver tumours."( Anti-tumour effects of transcatheter arterial embolisation administered in combination with thalidomide in a rabbit VX2 liver tumour model.
Murata, K; Nitta, N; Nitta-Seko, A; Ohta, S; Otani, H; Sonoda, A; Takahashi, M; Tsuchiya, K, 2011
)
2.03
" This phase I study was performed to identify the optimal dose of pomalidomide to be used in combination with gemcitabine in the treatment of patients with metastatic pancreatic cancer."( A phase I, dose-escalation study of pomalidomide (CC-4047) in combination with gemcitabine in metastatic pancreas cancer.
Bendell, JC; Burris, HA; Hainsworth, JD; Infante, JR; Jones, SF; Messersmith, WA; Spigel, DR; Weekes, CD; Yardley, DA, 2011
)
0.37
"A total of thirty-seven patients with MDS-RCMD or-RAEB-I were treated with CsA in combination with thalidomide."( [Cyclosporine A in combination with thalidomide for the treatment of patients with myelodysplastic syndromes].
Hao, YS; Liu, KQ; Qin, TJ; Xiao, ZJ; Xu, ZF; Zhang, Y, 2010
)
0.85
"CsA in combination with thalidomide appears to be effective mainly in inducing HI-E and relatively well-tolerated for the treatment of patients with MDS."( [Cyclosporine A in combination with thalidomide for the treatment of patients with myelodysplastic syndromes].
Hao, YS; Liu, KQ; Qin, TJ; Xiao, ZJ; Xu, ZF; Zhang, Y, 2010
)
0.94
"We evaluated the in vitro antimyeloma activity of AT9283 alone and in combination with lenalidomide and the in vivo efficacy by using a xenograft mouse model of human MM."( Antimyeloma activity of a multitargeted kinase inhibitor, AT9283, via potent Aurora kinase and STAT3 inhibition either alone or in combination with lenalidomide.
Anderson, KC; Bandi, M; Chauhan, D; Cirstea, D; Gorgun, G; Hideshima, T; Hu, Y; Mahindra, A; Munshi, NC; Nelson, EA; Patel, K; Pozzi, S; Raje, N; Rodig, S; Santo, L; Squires, M; Unitt, C; Vallet, S, 2011
)
0.37
" We conducted a phase I trial to establish the maximum tolerated dose of lenalidomide that could be combined with R-CHOP (rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone)."( Lenalidomide can be safely combined with R-CHOP (R2CHOP) in the initial chemotherapy for aggressive B-cell lymphomas: phase I study.
Ansell, SM; Habermann, TM; Inwards, DJ; Johnston, PB; Klebig, RR; LaPlant, B; Macon, WR; Micallef, IN; Nowakowski, GS; Porrata, LF; Reeder, CB; Rivera, CE; Witzig, TE, 2011
)
0.37
" In conclusion, thalidomide alone, or in combination with cisplatin/gemcitabine, controlled disease for >6 months in ∼30% of patients."( The predictive role of serum VEGF in an advanced malignant mesothelioma patient cohort treated with thalidomide alone or combined with cisplatin/gemcitabine.
Abraham, R; Clarke, S; Cullen, M; Davey, R; Harvie, R; Kao, SC; Kerestes, Z; Marx, G; Paturi, F; Pavlakis, N; Taylor, R, 2012
)
0.94
"Patients were randomly assigned to the control arm (PC) involving two cycles of induction paclitaxel 225 mg/m(2) and carboplatin area under the curve (AUC) 6 followed by 60 Gy thoracic radiation administered concurrently with weekly paclitaxel 45 mg/m(2) and carboplatin AUC 2, or to the experimental arm (TPC), receiving the same treatment in combination with thalidomide at a starting dose of 200 mg daily."( Randomized phase III study of thoracic radiation in combination with paclitaxel and carboplatin with or without thalidomide in patients with stage III non-small-cell lung cancer: the ECOG 3598 study.
Belinsky, SA; Dahlberg, SE; Fitzgerald, TJ; Hoang, T; Johnson, DH; Mehta, MP; Schiller, JH, 2012
)
0.76
" In preclinical and clinical studies, panobinostat showed good anti-myeloma activity in combination with several agents."( Phase II study of melphalan, thalidomide and prednisone combined with oral panobinostat in patients with relapsed/refractory multiple myeloma.
Alesiani, F; Ballanti, S; Boccadoro, M; Caraffa, P; Catarini, M; Cavallo, F; Corvatta, L; Gentili, S; Leoni, P; Liberati, AM; Offidani, M; Palumbo, A; Polloni, C; Pulini, S, 2012
)
0.67
"This study was purposed to analyze the clinical features and evaluate the efficacy of thalidomide combined with VAD regimen for treatment of osteosclerotic myeloma (POEMS syndrome)."( [Clinical observation of thalidomide combined with VAD regimen for treatment of osteosclerotic myeloma (POEMS syndrome)].
Gan, SL; Liu, YF; Meng, XL; Sun, H; Sun, L; Wan, DM; Zhou, JW, 2012
)
0.91
"Ezatiostat was administered to 19 patients with non-deletion(5q) myelodysplastic syndrome (MDS) at one of two doses (2000 mg or 2500 mg/day) in combination with 10 mg of lenalidomide on days 1-21 of a 28-day cycle."( Phase 1 dose-ranging study of ezatiostat hydrochloride in combination with lenalidomide in patients with non-deletion (5q) low to intermediate-1 risk myelodysplastic syndrome (MDS).
Boccia, R; Brown, GL; Galili, N; Garcia-Manero, G; Lyons, RM; Mesa, RA; Mulford, D; Raza, A; Sekeres, MA; Smith, SE; Steensma, DP, 2012
)
0.38
"The tolerability and activity profile of ezatiostat co-administered with lenalidomide supports the further development of ezatiostat in combination with lenalidomide in MDS and also encourages studies of this combination in other hematologic malignancies where lenalidomide is active."( Phase 1 dose-ranging study of ezatiostat hydrochloride in combination with lenalidomide in patients with non-deletion (5q) low to intermediate-1 risk myelodysplastic syndrome (MDS).
Boccia, R; Brown, GL; Galili, N; Garcia-Manero, G; Lyons, RM; Mesa, RA; Mulford, D; Raza, A; Sekeres, MA; Smith, SE; Steensma, DP, 2012
)
0.38
" We aimed to identify the maximum tolerated dose (MTD) of lenalidomide when combined with rituximab in a phase 1 trial and to assess the efficacy and safety of this combination in a phase 2 trial in patients with relapsed or refractory MCL."( Lenalidomide in combination with rituximab for patients with relapsed or refractory mantle-cell lymphoma: a phase 1/2 clinical trial.
Badillo, M; Bejarano, M; Bell, N; Byrne, C; Cabanillas, F; Champlin, R; Chen, W; Chen, Y; Fanale, M; Fayad, L; Feng, L; Fowler, N; Hagemeister, F; Hartig, K; Kwak, L; McLaughlin, P; Neelapu, SS; Newberry, KJ; Romaguera, J; Samaniego, F; Sun, L; Wagner-Bartak, N; Wang, M; Younes, A; Young, KH; Zeldis, J; Zhang, L, 2012
)
0.38
" A total of 704 patients (390 aged <65 years, 232 aged 65-74 years, and 82 aged ≥75 years) received lenalidomide or placebo, both in combination with dexamethasone."( Lenalidomide in combination with dexamethasone improves survival and time-to-progression in patients ≥65 years old with relapsed or refractory multiple myeloma.
Borrello, I; Chanan-Khan, AA; Dimopoulos, M; Foà, R; Hellmann, A; Knight, R; Lonial, S; Swern, AS; Weber, D, 2012
)
0.38
" Rats with implanted liver tumors were randomized into four treatment groups: 1) Zd6126 (Zd); 2) Thalidomide (Tha); 3) Zd in combination with Tha (ZdTha); and 4) controls."( Enhanced antitumor efficacy of a vascular disrupting agent combined with an antiangiogenic in a rat liver tumor model evaluated by multiparametric MRI.
Chen, F; Cona, MM; De Geest, B; De Keyzer, F; Feng, Y; Jiang, Y; Li, J; Marchal, G; Ni, Y; Oyen, R; Verfaillie, C; Wang, H; Yu, J; Zheng, K, 2012
)
0.6
"Preclinical and clinical studies have shown that proteasome inhibitors (PIs) have anti-MM activity in combination with dexamethasone or lenalidomide."( CEP-18770 (delanzomib) in combination with dexamethasone and lenalidomide inhibits the growth of multiple myeloma.
Berenson, JR; Chen, H; Hunter, K; Jones-Bolin, S; Li, J; Li, M; Ruggeri, B; Sanchez, E; Wang, C, 2012
)
0.38
"To evaluate the efficacy and tolerability of capecitabine combined with thalidomide in patients with advanced pancreatic cancer (APC) who have previously received gemcitabine-based therapy."( Phase II trial of capecitabine combined with thalidomide in second-line treatment of advanced pancreatic cancer.
Liu, QY; Niu, ZX; Shi, SB; Tang, XY; Wang, M,
)
0.62
"Capecitabine combined with thalidomide is a well-tolerated second-line regimen, in patients with APC refractory to gemcitabine."( Phase II trial of capecitabine combined with thalidomide in second-line treatment of advanced pancreatic cancer.
Liu, QY; Niu, ZX; Shi, SB; Tang, XY; Wang, M,
)
0.69
"To evaluate the 6-mo overall survival, safety and tolerability of lenalidomide in combination with standard gemcitabine as first-line treatment for patients with metastatic pancreatic cancer."( Lenalidomide in combination with gemcitabine as first-line treatment for patients with metastatic carcinoma of the pancreas: a Sarah Cannon Research Institute phase II trial.
Arkenau, HT; Bendell, JC; Burris, HA; Hainsworth, JD; Infante, JR; Jones, GT; Lane, CM; Rubin, MS; Spigel, DR; Waterhouse, D, 2013
)
0.39
"This phase I/IIA study evaluated the maximum-tolerated dose (MTD), safety, and clinical benefit of pomalidomide, an immunomodulatory drug (IMiD), combined with cisplatin+etoposide chemotherapy, in treatment-naive patients with extensive-stage (ES) small-cell lung cancer (SCLC)."( A phase I study of pomalidomide (CC-4047) in combination with cisplatin and etoposide in patients with extensive-stage small-cell lung cancer.
Beck, R; Ellis, PM; Fandi, A; Jungnelius, U; Shepherd, FA; Zhang, J, 2013
)
0.39
"Thalidomide, the first clinically available immunomodulatory drug, reaches monotherapy treatment response in about 1/ 3 of significantly pretreated patients with multiple myeloma, and in combination with glucocorticoids approximately 50% response rate."( [Thalidomide in the treatment of multiple myeloma: focus on combination with bortezomib].
Gumulec, J; Hájek, R; Plonková, H, 2013
)
2.74
"We conducted a phase I dose escalation study to determine the maximal tolerated dose of bortezomib that could be combined with standard dose lenalidomide in patients with MDS or AML."( Phase I dose escalation study of bortezomib in combination with lenalidomide in patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
Amrein, PC; Attar, EC; Ballen, KK; Deangelo, DJ; Fathi, AT; Foster, J; Fraser, JW; McAfee, S; Neuberg, D; Steensma, DP; Stone, RM; Wadleigh, M, 2013
)
0.39
" Furthermore, reported for the first time is the effect of lenalidomide in combination with cetuximab on T cell function, including increases in circulating naïve and central memory T cells."( Immunomodulatory effects in a phase II study of lenalidomide combined with cetuximab in refractory KRAS-mutant metastatic colorectal cancer patients.
Chopra, R; Gandhi, AK; Jungnelius, U; Li, M; Romano, A; Schafer, PH; Shi, T; Siena, S; Tabernero, J, 2013
)
0.39
" In conclusion, the poor results obtained with lenalidomide in combination with vorinostat and dexamethasone provide no arguments that could justify further investigation of this drug combination for the treatment of relapsed PTCL."( Lenalidomide in combination with vorinostat and dexamethasone for the treatment of relapsed/refractory peripheral T cell lymphoma (PTCL): report of a phase I/II trial.
Egle, A; Greil, R; Hopfinger, G; Lang, A; Linkesch, W; Melchardt, T; Nösslinger, T; Weiss, L, 2014
)
0.4
" The C max of digoxin was slightly higher (+14 %) when administered with lenalidomide versus placebo."( No clinically significant drug interactions between lenalidomide and P‑glycoprotein substrates and inhibitors: results from controlled phase I studies in healthy volunteers.
Chen, N; Kasserra, C; Kumar, G; Liu, L; Palmisano, M; Reyes, J; Wang, X; Weiss, D; Weiss, L; Zhou, S, 2014
)
0.4
"Thalidomide can down-regulate serum VEGF level in EC patients, and combined with radiotherapy may improve treatment outcome."( Clinical trial of thalidomide combined with radiotherapy in patients with esophageal cancer.
Hu, LJ; Li, DQ; Li, Y; Ni, XC; Sun, SP; Sun, ZQ; Wang, J; Yu, JP, 2014
)
2.18
" Xenografts acquired resistance to two generations of immunomodulatory drugs (IMiDs; lenalidomide and pomalidomide) in combination with dexamethasone, that was reversible after a wash-out period."( In vivo murine model of acquired resistance in myeloma reveals differential mechanisms for lenalidomide and pomalidomide in combination with dexamethasone.
Bjorklund, CC; Corchete, LA; Couto, S; Delgado, M; Díaz-Rodríguez, E; Fernández-Lázaro, D; Garayoa, M; García-Gómez, A; Gutiérrez, NC; López-Corral, L; Mateos, MV; Montero, JC; Ocio, EM; Paíno, T; Pandiella, A; San-Miguel, JF; San-Segundo, L; Wang, M, 2015
)
0.42
" We demonstrated that lenalidomide can be safely combined with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone); this new combination is known as R2CHOP."( Lenalidomide combined with R-CHOP overcomes negative prognostic impact of non-germinal center B-cell phenotype in newly diagnosed diffuse large B-Cell lymphoma: a phase II study.
Ansell, SM; Foran, JM; Gascoyne, RD; Habermann, TM; Inwards, DJ; Johnston, PB; LaPlant, B; Macon, WR; Micallef, IN; Nelson, GD; Nowakowski, GS; Porrata, LF; Reeder, CB; Rivera, CE; Thompson, CA; Witzig, TE, 2015
)
0.42
"Low-dose THAL together with PRED appeared to be effective in the treatment of PMF-associated anemia, and the response duration would prolong significantly if combined with DANA."( [Comparison of low-dose thalidomide and prednisone combined with or without danazol for the treatment of primary myelofibrosis-associated anemia].
Fang, L; Hu, N; Li, B; Pan, L; Qin, T; Qu, S; Xiao, Z; Xu, J; Xu, Z; Zhang, H; Zhang, Y, 2014
)
0.71
" Little is known about pomalidomide's potential for drug-drug interactions (DDIs); as pomalidomide clearance includes hydrolysis and cytochrome P450 (CYP450)-mediated hydroxylation, possible DDIs via CYP450 and drug-transporter proteins were investigated in vitro and in a clinical study."( Pomalidomide: evaluation of cytochrome P450 and transporter-mediated drug-drug interaction potential in vitro and in healthy subjects.
Assaf, M; Hoffmann, M; Kasserra, C; Kumar, G; Li, Y; Liu, L; Palmisano, M; Wang, X, 2015
)
0.42
" Bendamustine was administered with a cumulative dose of up to 200 mg/m(2)."( Bendamustine in combination with thalidomide and dexamethasone is a viable salvage option in myeloma relapsed and/or refractory to bortezomib and lenalidomide.
Aitchison, R; Blesing, N; Lau, IJ; Peniket, A; Rabin, N; Ramasamy, K; Roberts, P; Smith, D; Yong, K, 2015
)
0.7
" The effect of the drug alone and in combination with radiotherapy using Cobalt 60 (60Co) at 45 Gy on the enzymatic activity of substance‑P degrading A disintegrin and metalloproteinase (ADAM)10 and neprilysin (NEP) was investigated in the mouse breast cancer cell lines 4T1 and 4T1 heart metastases post‑capsaicin (4THMpc)."( Thalidomide combined with irradiation alters the activity of two proteases.
Aydemir, E; Fişkın, K; Korcum, AF; Şimşek, E, 2015
)
1.86
" In a phase 1/2 trial we aimed to assess the safety, tolerability, and activity of ixazomib in combination with lenalidomide and dexamethasone in newly diagnosed multiple myeloma."( Safety and tolerability of ixazomib, an oral proteasome inhibitor, in combination with lenalidomide and dexamethasone in patients with previously untreated multiple myeloma: an open-label phase 1/2 study.
Berdeja, JG; Berg, D; Di Bacco, A; Estevam, J; Gupta, N; Hamadani, M; Hari, P; Hui, AM; Kaufman, JL; Kumar, SK; Laubach, JP; Liao, E; Lonial, S; Niesvizky, R; Rajkumar, V; Richardson, PG; Roy, V; Stewart, AK; Vescio, R, 2014
)
0.4
"In this Phase 1b study, the safety and tolerability of maintenance therapy, comprising lenalidomide (0-25 mg, days 5-25) in combination with azacitidine (50-75 mg/m(2) , days 1-5) every 28 d, was explored in 40 patients with acute myeloid leukaemia (AML) in complete remission after chemotherapy."( Maintenance lenalidomide in combination with 5-azacitidine as post-remission therapy for acute myeloid leukaemia.
Avery, S; Fleming, S; Govindaraj, C; McManus, J; Patil, S; Perruzza, S; Plebanski, M; Spencer, A; Stevenson, W; Tan, P; Wei, A, 2015
)
0.42
"On August 5, 2013, a marketing authorization valid throughout the European Union (EU) was issued for pomalidomide in combination with dexamethasone for the treatment of adult patients with relapsed and refractory multiple myeloma (MM) who have received at least two prior treatment regimens, including both lenalidomide and bortezomib, and have demonstrated disease progression on the last therapy."( The European medicines agency review of pomalidomide in combination with low-dose dexamethasone for the treatment of adult patients with multiple myeloma: summary of the scientific assessment of the committee for medicinal products for human use.
Camarero, J; Flores, B; Gisselbrecht, C; Hanaizi, Z; Hemmings, R; Laane, E; Pignatti, F; Salmonson, T; Sancho-Lopez, A, 2015
)
0.42
" The maximum tolerated dose (MTD) of lenalidomide given in combination with gemcitabine was defined as the highest dose level at which no more than one out of four (25%) subjects experiences a dose-limiting toxicity (DLT)."( A phase I dose-escalation study of lenalidomide in combination with gemcitabine in patients with advanced pancreatic cancer.
Liljefors, M; Rossmann, E; Ullenhag, GJ, 2015
)
0.42
"Treatment with dose-adjusted Len combined with low-dose Dex is an effective and safe therapy for older RRMM patients exhibiting renal impairment after receiving Bor-based therapies."( Dose-adjusted Lenalidomide Combined with Low-dose Dexamethasone Rescues Older Patients with Bortezomib-resistant Multiple Myeloma.
Kadowaki, M; Kohno, K; Okamura, S; Takase, K; Yamasaki, S, 2015
)
0.42
" This chart review evaluated the use of methotrexate alone and in combination with 7 other systemic therapies in 48 patients with palmoplantar psoriasis."( The Use of Methotrexate, Alone or in Combination With Other Therapies, for the Treatment of Palmoplantar Psoriasis.
Klufas, DM; Strober, BE; Wald, JM, 2015
)
0.42
"To explore the inhibitory effect of thalidomide combined with interferon (IFN) on the human acute myeloid leukemia cell line Kasumi- 1 and its mechanism."( [Inhibitory effect of thalidomide combined with interferon on the proliferation of Kasumi-1 cells].
Fan, R; Mi, R; Wang, X; Wei, X; Xu, H; Yin, Q, 2015
)
1.01
"LTD) combined with chemotherapy in treating patients with advanced colorectal cancer."( Thalidomide Combined with Chemotherapy in Treating Patients with Advanced Colorectal Cancer.
Deng, LC; Gu, HG; Gu, M; Huang, XE; Ji, ZQ; Li, L; Liu, MY; Liu, Y; Qian, T; Shen, HL; Wang, L; Yan, XC, 2015
)
1.86
"A consecutive cohort of pretreated patients with advanced colorectal cancer were treated with thalidomide combined with chemotherapy."( Thalidomide Combined with Chemotherapy in Treating Patients with Advanced Colorectal Cancer.
Deng, LC; Gu, HG; Gu, M; Huang, XE; Ji, ZQ; Li, L; Liu, MY; Liu, Y; Qian, T; Shen, HL; Wang, L; Yan, XC, 2015
)
2.08
"Thalidomide combined with chemotherapy was safe and mildly effective in treating patients with advanced colorectal cancer."( Thalidomide Combined with Chemotherapy in Treating Patients with Advanced Colorectal Cancer.
Deng, LC; Gu, HG; Gu, M; Huang, XE; Ji, ZQ; Li, L; Liu, MY; Liu, Y; Qian, T; Shen, HL; Wang, L; Yan, XC, 2015
)
3.3
"Elotuzumab combined with lenalidomide and dexamethasone in patients with relapsed multiple myeloma showed acceptable safety and efficacy that seems better than that previously noted with lenalidomide and dexamethasone only."( Elotuzumab in combination with lenalidomide and dexamethasone in patients with relapsed multiple myeloma: final phase 2 results from the randomised, open-label, phase 1b-2 dose-escalation study.
Anderson, KC; Benboubker, L; Bleickardt, E; Facon, T; Jagannath, S; Jakubowiak, AJ; Lonial, S; Moreau, P; Raab, MS; Reece, DE; Richardson, PG; Singhal, AK; Tsao, LC; Vij, R; White, D; Zonder, J, 2015
)
0.42
"Proteasome inhibitors (PIs) in combination with immunomodulatory drugs (IMiDs) have been shown to be effective against relapsed/refractory multiple myeloma (RRMM)."( Phase I study of once weekly treatment with bortezomib in combination with lenalidomide and dexamethasone for relapsed or refractory multiple myeloma.
Hagiwara, S; Iida, S; Ishida, T; Ito, A; Kanamori, T; Kato, C; Kinoshita, S; Komatsu, H; Kusumoto, S; Masuda, A; Murakami, S; Nakashima, T; Narita, T; Ri, M; Suzuki, N; Totani, H; Yoshida, T, 2016
)
0.43
"The present study evaluated the pharmacokinetics and safety of elotuzumab, a humanized IgG1 monoclonal antibody against signaling lymphocyte activation molecule-F7, combined with lenalidomide and dexamethasone, in patients with multiple myeloma (MM) and renal impairment."( Pharmacokinetics and Safety of Elotuzumab Combined With Lenalidomide and Dexamethasone in Patients With Multiple Myeloma and Various Levels of Renal Impairment: Results of a Phase Ib Study.
Badros, A; Berdeja, J; Bleickardt, E; Gupta, M; Jagannath, S; Kaufman, JL; Lynch, M; Manges, R; Paliwal, P; Tendolkar, A; Vij, R; Zonder, J, 2016
)
0.43
" We conducted a phase I study of lenalidomide in combination with FOLFOX (5-fluorouracil, leucovorin, and oxaliplatin) in patients with advanced cancer."( Phase I clinical trial of lenalidomide in combination with 5-fluorouracil, leucovorin, and oxaliplatin in patients with advanced cancer.
Falchook, G; Fu, S; Hong, DS; Naing, A; Piha-Paul, S; Said, R; Tsimberidou, AM; Wheler, JJ; Ye, Y, 2016
)
0.43
"Lenalidomide in combination with FOLFOX was well tolerated."( Phase I clinical trial of lenalidomide in combination with 5-fluorouracil, leucovorin, and oxaliplatin in patients with advanced cancer.
Falchook, G; Fu, S; Hong, DS; Naing, A; Piha-Paul, S; Said, R; Tsimberidou, AM; Wheler, JJ; Ye, Y, 2016
)
0.43
" We conducted a phase 1b trial to determine the maximum tolerated dose (MTD) of lenalidomide in combination with R-ESHAP (rituximab, etoposide, cisplatin, cytarabine, methylprednisolone) (LR-ESHAP) in patients with relapsed or refractory DLBCL."( Lenalidomide in combination with R-ESHAP in patients with relapsed or refractory diffuse large B-cell lymphoma: a phase 1b study from GELTAMO group.
Caballero, D; Canales, M; Dlouhy, I; González-Barca, E; López-Guillermo, A; Martín, A; Montes-Moreno, S; Ocio, EM; Redondo, AM; Salar, A, 2016
)
0.43
"To evaluate the short term-efficacy and safety of apremilast in combination with at least one form of photo-, systemic, or biologic therapy in the treatment of chronic plaque psoriasis."( Use of Apremilast in Combination With Other Therapies for Treatment of Chronic Plaque Psoriasis: A Retrospective Study.
AbuHilal, M; Shear, N; Walsh, S, 2016
)
0.43
"A total of 81 patients with plaque psoriasis were treated with apremilast in combination with at least 1 other therapy (NB-UVB, methotrexate, acitretin, cyclosporin, etanercept, adalimumab, infliximab, or ustekinumab)."( Use of Apremilast in Combination With Other Therapies for Treatment of Chronic Plaque Psoriasis: A Retrospective Study.
AbuHilal, M; Shear, N; Walsh, S, 2016
)
0.43
"Apremilast can be safely and effectively combined with phototherapy, systemic, and/or biological agents in patients with plaque psoriasis not responding adequately to these agents alone."( Use of Apremilast in Combination With Other Therapies for Treatment of Chronic Plaque Psoriasis: A Retrospective Study.
AbuHilal, M; Shear, N; Walsh, S, 2016
)
0.43
"To explore the efficacy and prognostic factors of induction therapy combined with autogenetic peripheral blood stem cells transplantation (APBSCT)in patients with multiple myeloma (MM)."( [Efficacy and prognostic factors of induction therapy combined with autologous stem cell transplantation in 201 patients with multiple myeloma].
Chang, H; Du, J; Fan, J; Fu, W; He, H; Hou, J; Jiang, H; Jin, L; Xi, H; Zeng, T; Zhang, C; Zhou, L, 2016
)
0.43
"To investigate the clinical efficacy and safety between CHOPE regimen alone and it combined with thalidomide for relapsed and refractory non-Hodgkin's lymphoma."( [Clinical Efficacy Comparison between CHOPE Regimen alone and It Combined with Thalidomide for Relapsed and Refractory Non-Hodgkin's Lymphoma].
Yang, YZ, 2016
)
0.88
"Compared with CHOPE regimen alone, CHOPE regimen combined with thalidomide for relapsed and refractory non-Hodgkin's lymphoma can efficiently delay the disease progression, reduce tumor burden level, enhance the long-term survival rate, morever did not increase the risk of toxic side effects."( [Clinical Efficacy Comparison between CHOPE Regimen alone and It Combined with Thalidomide for Relapsed and Refractory Non-Hodgkin's Lymphoma].
Yang, YZ, 2016
)
0.9
"Pomalidomide is an IMiD(®) immunomodulatory agent, which has shown clinically significant benefits in relapsed and/or refractory multiple myeloma (rrMM) patients when combined with dexamethasone, regardless of refractory status to lenalidomide or bortezomib."( Pomalidomide in combination with dexamethasone results in synergistic anti-tumour responses in pre-clinical models of lenalidomide-resistant multiple myeloma.
Bjorklund, CC; Cathers, BE; Chopra, R; Daniel, TO; Gandhi, AK; Leisten, J; Lopez-Girona, A; Lu, L; Mendy, D; Miller, K; Narla, RK; Ning, Y; Orlowski, RZ; Raymon, HK; Rychak, E; Shi, T; Thakurta, A, 2016
)
0.43
" We developed a phase I study to evaluate the safety and tolerability of Len in combination with intermediate dose AraC (1."( A phase I study of intermediate dose cytarabine in combination with lenalidomide in relapsed/refractory acute myeloid leukemia.
Brady, WE; Dickey, NM; Ford, LA; Griffiths, EA; L Bashaw, H; Sperrazza, J; Tan, W; Thompson, JE; Vigil, CE; Wang, ES; Wetzler, M, 2016
)
0.43
" Lenalidomide has a manageable safety profile whether administered as a single agent or in combination with rituximab."( Clinical experience with lenalidomide alone or in combination with rituximab in indolent B-cell and mantle cell lymphomas.
Martin, P; Ruan, J; Schuster, SJ; Shah, B, 2016
)
0.43
"Fourteen patients with advanced lung cancer were scheduled to receive chemotherapy combined with thalidomide."( Thalidomide Combined with Chemotherapy in Treating Patients with Advanced lung Cancer.
Huang, XE; Li, L, 2016
)
2.09
"Our results demonstrate that thalidomide combined with chemotherapy is mildly effective and safe for treating patients with advanced lung cancer."( Thalidomide Combined with Chemotherapy in Treating Patients with Advanced lung Cancer.
Huang, XE; Li, L, 2016
)
2.17
"To investigate the clinical efficacy of regimen consisting of lenalidomide combined with chemotherapy for acute leukemia and its impact on vascular endothilial growth factor (vEGF) and basic fibroblast growth factor (bFGF), and to analyze the relationship lenalidomide with therapeutic efficacy of leukemia."( [Clinical Curative Efficacy of Lenalidomide Combined with Chemotherapy for Acute Leukemia and Its Impact on VEGF].
Ma, LM; Ruan, LH; Yang, XW; Zhao, XQ, 2016
)
0.43
"The lenalidomide combined with chemotherapy can significantly decrease the expression level of VEGF and bFGF, and enhance the remission rate of patients with AML."( [Clinical Curative Efficacy of Lenalidomide Combined with Chemotherapy for Acute Leukemia and Its Impact on VEGF].
Ma, LM; Ruan, LH; Yang, XW; Zhao, XQ, 2016
)
0.43
"To evaluate the efficacy and adverse effects of low dose thalidomide (TD) combined with modified VCMP (vincristine+cyclophosphamide+melphalan+prednisone) (TD+mVCMP) and VAD (vincristine+doxorubicin+dexamethsone) (TD+VAD) regimens for treating aged patients with MM."( [Efficacy Comparison of Low dose Thalidomide Combined with Modified VCMP and VAD regimens for Treatment of Aged MM Patients].
Liu, HB; Wang, W, 2016
)
0.96
"Low dose TD combined with modified VCMP regimen for treatment of newly diagnosed aged patients with MM is safe and effective, which may be used as the first line treatment regimen for population in aged MM patients."( [Efficacy Comparison of Low dose Thalidomide Combined with Modified VCMP and VAD regimens for Treatment of Aged MM Patients].
Liu, HB; Wang, W, 2016
)
0.72
" We evaluated the safety and tolerability of elotuzumab 10 mg/kg combined with thalidomide 50-200 mg and dexamethasone 40 mg (with/without cyclophosphamide 50 mg) in patients with relapsed/refractory multiple myeloma (RRMM)."( Elotuzumab in combination with thalidomide and low-dose dexamethasone: a phase 2 single-arm safety study in patients with relapsed/refractory multiple myeloma.
Blade, J; Bleickardt, E; Gironella, M; Granell, M; Hernandez, MT; Lynch, M; Martín, J; Martinez-Lopez, J; Mateos, MV; Oriol, A; Paliwal, P; San-Miguel, J; Singhal, A, 2016
)
0.95
"The use of carfilzomib/pomalidomide single-agent or in combination with other agents in patients with refractory/relapsed multiple myeloma (RRMM) was not clearly clarified in clinical practice."( Carfilzomib/pomalidomide single-agent or in combination with other agents for the management of relapsed/refractory multiple myeloma: a meta-analysis of 37 trials.
Fan, L; Hu, C; Ma, X; Ran, X; Yu, H; Zou, Y, 2017
)
0.46
"To investigate the effects of interferon-α2b combined with thalidomid(THD) on the proliferation and apoptosis of HEL cells, and expression of JAK2V617F-mutated gene."( [Effect of Interferon Combined with Thalidomid on HEL Cell Apoptosis and JAK2V617F Mutation Gene Expression].
Cai, ZM; Wang, Y; Wu, XX; Xue, LG; Zhao, LD, 2016
)
0.43
"The cell survival rates were assayed by CCK-8 after HEL cells were treated by interferon-α2b, thalidomid and thalidomid combined with interferon-α2b for 24, 48 and 72 hours, while the apoptosis and expression of JAK2V617F mutation gene were detected by flow cytometry and fluorescence quantitative PCR respectively after treatmemt for 48 hours."( [Effect of Interferon Combined with Thalidomid on HEL Cell Apoptosis and JAK2V617F Mutation Gene Expression].
Cai, ZM; Wang, Y; Wu, XX; Xue, LG; Zhao, LD, 2016
)
0.43
"IFN-α2b combined with THD could more obviously inhibit the proliferation of HEL cells than IFN-α2b or THD alone for 24 and 48 and 72 hours, and the differences between groups were statistically significant(P<0."( [Effect of Interferon Combined with Thalidomid on HEL Cell Apoptosis and JAK2V617F Mutation Gene Expression].
Cai, ZM; Wang, Y; Wu, XX; Xue, LG; Zhao, LD, 2016
)
0.43
"IFN-α2b combined with THD can obviously inhibit the proliferation and induce apoptosis of HEL cells more than that of IFN-α2b alone, but the effect of reducing JAK2V617F mutation gene expression is not different."( [Effect of Interferon Combined with Thalidomid on HEL Cell Apoptosis and JAK2V617F Mutation Gene Expression].
Cai, ZM; Wang, Y; Wu, XX; Xue, LG; Zhao, LD, 2016
)
0.43
" We have previously shown in a retrospective analysis that lenalidomide combined with continuous low-dose cyclophosphamide and prednisone (REP) had remarkable activity in heavily pretreated, lenalidomide-refractory MM patients."( Phase 1/2 study of lenalidomide combined with low-dose cyclophosphamide and prednisone in lenalidomide-refractory multiple myeloma.
Beeker, A; Bloem, AC; Bos, GMJ; Broijl, A; Faber, LM; Franssen, LE; Klein, SK; Koene, HR; Levin, MD; Lokhorst, HM; Mutis, T; Nijhof, IS; Oostvogels, R; Raymakers, R; Sonneveld, P; van de Donk, NWCJ; van der Spek, E; van Kessel, B; van Spronsen, DJ; van Velzen, J; Westerweel, PE; Ypma, PF; Zweegman, S, 2016
)
0.43
"In 12 patients with relapsed or refractory acute myelogenous leukemia (AML), the efficacy and safety of a novel regimen, namely thalidomide combined with interferon and interleukin 2 (IL-2), were initially explored."( [Thalidomide combined with interferon and interleukin-2 in treatment of relapsed or refractory acute myelogenous leukemia].
Ai, H; Chen, L; Hao, QM; Mi, RH; Song, YP; Wang, P; Wei, XD; Yin, QS; Yuan, FF, 2016
)
1.55
"Clinical trials of vorinostat, a Class I/II histone deacetylase inhibitor, in combination with proteasome inhibitors and immunomodulatory agents have shown activity in relapsed/refractory multiple myeloma."( A phase IIb trial of vorinostat in combination with lenalidomide and dexamethasone in patients with multiple myeloma refractory to previous lenalidomide-containing regimens.
Anand, P; Bilotti, E; Biran, N; Ivanovski, K; McBride, L; Richter, JR; Sanchez, L; Siegel, DS; Vesole, DH, 2017
)
0.46
"We report the first clinical investigation conducted in Japan to confirm the safety, tolerability, and pharmacokinetics of ixazomib alone and combined with lenalidomide-dexamethasone (Rd) in Japanese patients with relapsed/refractory multiple myeloma."( Phase 1 study of ixazomib alone or combined with lenalidomide-dexamethasone in Japanese patients with relapsed/refractory multiple myeloma.
Chou, T; Handa, H; Ishizawa, K; Kase, Y; Suzuki, K; Takubo, T, 2017
)
0.46
" In a previous phase 3 study in patients with relapsed/refractory multiple myeloma (RRMM), elotuzumab (10 mg/kg, ∼3-h infusion), combined with lenalidomide and dexamethasone, demonstrated durable efficacy and acceptable safety; 10% (33/321) of patients had infusion reactions (IRs; Grade 1/2: 29; Grade 3: 4)."( A phase 2 safety study of accelerated elotuzumab infusion, over less than 1 h, in combination with lenalidomide and dexamethasone, in patients with multiple myeloma.
Badarinath, S; Berenson, J; Cartmell, A; Harb, W; Lyons, R; Manges, R; McIntyre, K; Mohamed, H; Nourbakhsh, A; Rifkin, R, 2017
)
0.46
"On November 30, 2015, the FDA approved elotuzumab (Empliciti; Bristol-Myers Squibb) in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who received one to three prior therapies."( FDA Drug Approval: Elotuzumab in Combination with Lenalidomide and Dexamethasone for the Treatment of Relapsed or Refractory Multiple Myeloma.
Deisseroth, A; Farrell, AT; Goldberg, KB; Gormley, NJ; Kaminskas, E; Ko, CW; Kormanik, N; Nie, L; Pazdur, R, 2017
)
0.46
" These studies provide further support for clinical trials evaluating OPZ in combination with Pom and Dex."( Anti-angiogenic and anti-multiple myeloma effects of oprozomib (OPZ) alone and in combination with pomalidomide (Pom) and/or dexamethasone (Dex).
Berenson, JR; Chen, H; Gillespie, A; Li, M; Sanchez, E; Tang, G; Wang, CS, 2017
)
0.46
"Randomized controlled trials(RCTs) about efficacy and safety of thalidomide combined with TACE for primary HCC were identified from the Cochrane Library, Pubmed, Embase, CNKI, and Wan Fang until August, 2016."( Thalidomide combined with transcatheter artierial chemoembolzation for primary hepatocellular carcinoma: a systematic review and meta-analysis.
Cao, DD; Gao, SF; Ge, W; Liu, L; Xu, HL; Xu, XM; Zheng, YF, 2017
)
2.14
"Our findings suggest that thalidomide combined with TACE shows better clinical efficacy and tolerable adverse events in patients with primary HCC when compared with TACE alone."( Thalidomide combined with transcatheter artierial chemoembolzation for primary hepatocellular carcinoma: a systematic review and meta-analysis.
Cao, DD; Gao, SF; Ge, W; Liu, L; Xu, HL; Xu, XM; Zheng, YF, 2017
)
2.2
" This phase I/II study was conducted to determine the maximum tolerated dose (MTD), safety, and efficacy of lenalidomide combined with panobinostat in relapsed/refractory HL."( A Phase I/II Trial of Panobinostat in Combination With Lenalidomide in Patients With Relapsed or Refractory Hodgkin Lymphoma.
Bartlett, NL; Blum, KA; Christian, BA; Devine, SM; Fehniger, TA; Jaglowski, SM; Maly, JJ; Phelps, MA; Sexton, JL; Wagner-Johnston, ND; Wei, L; Zhu, X, 2017
)
0.46
"Our results demonstrated that thalidomide combined with capecitabine was mildly effective and safe for treating elderly patients with advanced GC."( Thalidomide combined with chemotherapy in treating elderly patients with advanced gastric cancer.
Chu, Y; Li, Y; Song, R; Xu, F, 2018
)
2.21
"To discuss and assess the clinical value of treating lung cancer cachexia with thalidomide combined with cinobufagin."( Clinical study on thalidomide combined with cinobufagin to treat lung cancer cachexia.
Bao, Y; Bu, K; Chen, X; Lu, Y; Qin, S; Xie, M, 2018
)
1.04
"Using thalidomide combined with cinobufagin to treat patients with lung cancer cachexia will significantly improve their nutritional status and quality of life."( Clinical study on thalidomide combined with cinobufagin to treat lung cancer cachexia.
Bao, Y; Bu, K; Chen, X; Lu, Y; Qin, S; Xie, M, 2018
)
1.3
"This phase 1 study investigated the safety of the anthracycline amrubicin combined with lenalidomide and dexamethasone in adults with relapsed or refractory multiple myeloma."( A phase I, open-label, dose-escalation study of amrubicin in combination with lenalidomide and weekly dexamethasone in previously treated adults with relapsed or refractory multiple myeloma.
Berube, C; Coutré, SE; Dinner, S; Dunn, TJ; Gotlib, J; Kaufman, GP; Liedtke, M; Medeiros, BC; Price, E, 2018
)
0.48
"To study the clinical efficacy and safety of dexamethasone of different doses combined with bortezomib and thalidomide for treatment of primary multiple myeloma."( [Clinical Efficacy and Safety of Different Doses of Dexamethasone Combined with Bortezomib and Thalidomide for Treating Patients with Multiple Myeloma].
Fu, LP; Ji, Y; Li, CS; Zhang, WP, 2018
)
0.91
"The therapeutic efficacy of different doses of dexamethasone combined with bortezomib and thalidomide for patients with multiple myeloma is similar, can obviously enhance remission rate, prolong the survival time, promote life quality, but the incidence of adverse reactions in low dose dexamethason rigemen is significantly reduced, and the safety is better."( [Clinical Efficacy and Safety of Different Doses of Dexamethasone Combined with Bortezomib and Thalidomide for Treating Patients with Multiple Myeloma].
Fu, LP; Ji, Y; Li, CS; Zhang, WP, 2018
)
0.92
"Thalidomide in combination with chemotherapy is an alternative treatment option for elderly patients with AML."( Thalidomide in Combination with Chemotherapy in Treating Elderly Patients with Acute Myeloid Leukemia.
Chen, C; Xu, W; Yang, J, 2018
)
3.37
" The treatment outcomes of MAbs versus HDACi in combination with bortezomib or lenalidomide plus dexamethasone remain unknown."( Monoclonal Antibodies versus Histone Deacetylase Inhibitors in Combination with Bortezomib or Lenalidomide plus Dexamethasone for the Treatment of Relapsed or Refractory Multiple Myeloma: An Indirect-Comparison Meta-Analysis of Randomized Controlled Trial
Chen, X; Feng, J; Gao, G; Shen, H; Tang, H; Xu, L; Zhang, N; Zheng, Y, 2018
)
0.48
"\ In practice, clinicians have attempted to use thalidomide(TLD) combined with transcatheter arterial chemoembolization\ (TACE) for treating liver cancer."( Thalidomide Combined with Transcatheter Arterial Chemoembolization (TACE) for Intermediate or Advanced Hepatocellular Carcinoma: A Systematic Review and GRADE Approach
Chen, Y; Hong, Q; Huang, L; Kang, D; Wang, D; Wen, S; Yang, W, 2018
)
2.18
"Lenalidomide in combination with R-CHOP had an acceptable safety profile and showed anti-cancer activity in patients with previously untreated high burden follicular lymphoma."( Lenalidomide in combination with R-CHOP (R2-CHOP) as first-line treatment of patients with high tumour burden follicular lymphoma: a single-arm, open-label, phase 2 study.
Becker, S; Bouabdallah, R; Cabeçadas, J; Casasnovas, O; Feugier, P; Gabarre, J; Gouill, SL; Haioun, C; Jardin, F; Lamy, T; Molina, TJ; Morschhauser, F; Mounier, N; Salles, G; Tilly, H; Tournilhac, O, 2018
)
0.48
"Pomalidomide is a third generation immunomodulatory drug which in combination with dexamethasone, has been shown to be active in relapsed/refractory multiple myeloma."( Pomalidomide and dexamethasone combination with additional cyclophosphamide in relapsed/refractory multiple myeloma (AMN001)-a trial by the Asian Myeloma Network.
Asaoku, H; Chim, CS; Chng, WJ; Durie, B; Gopalakrishnan, SK; Huang, SY; Kim, JS; Kim, K; Kimura, H; Kosugi, H; Lee, JH; Lee, JJ; Lee, SL; Min, CK; Moorakonda, R; Nagarajan, C; Sakamoto, J; Soekojo, CY; Takezako, N; Wei, Y; Yoon, SS, 2019
)
0.51
" We conducted a Bayesian network meta-analysis to compare the prophylactic efficacy of these agents in combination with PALO-DEX."( Efficacy of olanzapine, neurokinin-1 receptor antagonists, and thalidomide in combination with palonosetron plus dexamethasone in preventing highly emetogenic chemotherapy-induced nausea and vomiting: a Bayesian network meta-analysis.
Aapro, M; Abraham, I; Alatawi, Y; Alharbi, AS; Alhifany, AA; Almutairi, AR; Babiker, H; Cheema, E; MacDonald, K; McBride, A; Shahbar, A, 2020
)
0.8
" After 24 weeks, patients who responded (decreased Vitiligo Area Scoring Index >30%) were rerandomized to receive apremilast or placebo, combined with twice-weekly NB-UVB for 24 additional weeks."( Apremilast in Combination with Narrowband UVB in the Treatment of Vitiligo: A 52-Week Monocentric Prospective Randomized Placebo-Controlled Study.
Fontas, E; Khemis, A; Lacour, JP; Montaudié, H; Moulin, S; Passeron, T, 2020
)
0.56
"CUR inhibited proliferation and induced apoptosis in both KG-1 and U937 cells and this effect increased by combination with THAL."( Curcumin Combined with Thalidomide Reduces Expression of
Babakhani, D; Bahadoran, M; Chahardouli, B; Dashti, N; Haghi, A; Mohammadi Kian, M; Mohammadi, S; Nikbakht, M; Rostami, S; Salemi, M, 2020
)
0.87
" Here we demonstrated that DC vaccination in combination with pomalidomide and programmed death-ligand 1 (PD-L1) blockade inhibited tumor growth of a multiple myeloma (MM) mouse model."( Potent anti-myeloma efficacy of dendritic cell therapy in combination with pomalidomide and programmed death-ligand 1 blockade in a preclinical model of multiple myeloma.
Chu, TH; Jung, SH; Kim, HJ; Lakshmi, TJ; Lee, JJ; Park, HS; Vo, MC, 2021
)
0.62
" The combination of cyclophosphamide and dexamethasone (CD) is a recognised treatment option for patients with relapsed refractory multiple myeloma (RRMM) who have relapsed after treatment with bortezomib and lenalidomide, whilst also often being combined with newer proteasome inhibitors."( The MUK eight protocol: a randomised phase II trial of cyclophosphamide and dexamethasone in combination with ixazomib, in relapsed or refractory multiple myeloma (RRMM) patients who have relapsed after treatment with thalidomide, lenalidomide and a prote
Auner, HW; Bailey, L; Brown, S; Brudenell Straw, F; Cook, G; Cook, M; Dawkins, B; Flanagan, L; Hinsley, S; Kaiser, MF; McKee, S; Meads, D; Reed, S; Sherratt, D; Walker, K, 2020
)
0.74
" The primary objective of the trial is to evaluate whether ixazomib in combination with cyclophosphamide and dexamethasone (ICD) has improved clinical activity compared to CD in terms of progression-free survival (PFS)."( The MUK eight protocol: a randomised phase II trial of cyclophosphamide and dexamethasone in combination with ixazomib, in relapsed or refractory multiple myeloma (RRMM) patients who have relapsed after treatment with thalidomide, lenalidomide and a prote
Auner, HW; Bailey, L; Brown, S; Brudenell Straw, F; Cook, G; Cook, M; Dawkins, B; Flanagan, L; Hinsley, S; Kaiser, MF; McKee, S; Meads, D; Reed, S; Sherratt, D; Walker, K, 2020
)
0.74
" Previous studies investigating the safety and efficacy of ICD in patients with RRMM demonstrate a toxicity profile consistent with ixazomib in combination with lenalidomide and dexamethasone, whilst the combination showed possible activity in RRMM patients."( The MUK eight protocol: a randomised phase II trial of cyclophosphamide and dexamethasone in combination with ixazomib, in relapsed or refractory multiple myeloma (RRMM) patients who have relapsed after treatment with thalidomide, lenalidomide and a prote
Auner, HW; Bailey, L; Brown, S; Brudenell Straw, F; Cook, G; Cook, M; Dawkins, B; Flanagan, L; Hinsley, S; Kaiser, MF; McKee, S; Meads, D; Reed, S; Sherratt, D; Walker, K, 2020
)
0.74
"This phase 2 study evaluated isatuximab as monotherapy or combined with dexamethasone in relapsed/refractory multiple myeloma (RRMM)."( Isatuximab as monotherapy and combined with dexamethasone in patients with relapsed/refractory multiple myeloma.
Anttila, P; Bringhen, S; Capra, M; Cavo, M; Cole, C; Dimopoulos, M; Gasparetto, C; Hellet, M; Hungria, V; Jenner, M; Macé, S; Paiva, B; Ruiz, EY; Saleem, R; Vij, R; Vorobyev, V; Yin, JY, 2021
)
0.62
"The aim was to evaluate the safety and effectiveness of thalidomide, an immunomodulatory agent, in combination with glucocorticoid, for the treatment of COVID-19 patients with life-threatening symptoms."( Thalidomide combined with short-term low-dose glucocorticoid therapy for the treatment of severe COVID-19: A case-series study.
Chen, C; Chen, Y; Li, J; Li, X; Li, Y; Pan, J; Qi, F; Shi, K; Wu, G; Xia, J; Yu, Z; Zhou, T, 2021
)
2.31
"Purpose: To investigate the clinical therapeutic effect and safety of thalidomide combined with temozolomide (TMZ) and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z,
)
0.68
"Methods: The clinical data of 108 patients with high-grade gliomas undergoing operation in our hospital from September 2014 to December 2016 were retrospectively analyzed, of which 54 received thalidomide combined with TMZ and three-dimensional conformal radiotherapy (thalidomide group) and 54 received TMZ combined with three-dimensional conformal radiotherapy (control group)."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z,
)
0.64
"Conclusions: The application of thalidomide combined with TMZ and three-dimensional conformal radiotherapy for high-grade glioma patients after operation can prominently enhance the clinical therapeutic effect, improve patient quality of life, prolong survival, and produce tolerable adverse reactions."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z,
)
0.73
"To explore the efficacy and safety of 125 I radioactive seed implantation combined with intermittent hormonal therapy (IHT) in the clinical treatment of moderate- and high-risk non-metastatic prostate cancer."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z,
)
0.45
"125 I seed implantation combined with IHT is safe and effective in the clinical treatment of patients with moderate- and high-risk non-metastatic prostate cancer."( Therapeutic effect of thalidomide combined with temozolomide and three-dimensional conformal radiotherapy for patients with high-grade gliomas after operation.
Li, Y; Shen, X; Sui, L; Xu, Z,
)
0.45
" On May 30, 2020, a marketing authorization valid through the European Union (EU) was issued for isatuximab in combination with pomalidomide and dexamethasone (IsaPd) for the treatment of adult patients with relapsed and refractory (RR) multiple myeloma (MM)."( EMA Review of Isatuximab in Combination with Pomalidomide and Dexamethasone for the Treatment of Adult Patients with Relapsed and Refractory Multiple Myeloma.
Delgado, J; Enzmann, H; Gisselbrecht, C; Moreau, A; Pignatti, F; van Hennik, PB; Zienowicz, M, 2021
)
0.62
" This phase 2 study evaluated the efficacy and safety of elotuzumab in combination with pomalidomide, carfilzomib, and low-dose dexamethasone for patients with high-risk relapsed/refractory (RR)MM (NCT03104270)."( A phase 2 trial of the efficacy and safety of elotuzumab in combination with pomalidomide, carfilzomib and dexamethasone for high-risk relapsed/refractory multiple myeloma.
Berenson, JR; Eades, B; Eshaghian, S; Ghermezi, M; Lim, S; Martinez, D; Schwartz, G; Spektor, TM; Swift, RA; Vescio, R; Yashar, D, 2022
)
0.72
" An exposure-response (E-R) analysis using data from patients with relapsed/refractory multiple myeloma (RRMM) enrolled in a phase Ib clinical study who received isatuximab at doses from 5 to 20 mg/kg weekly for 1 cycle (4 weeks) followed by every 2 weeks thereafter (qw/q2w) in combination with pomalidomide/dexamethasone (n = 44) was first used to determine the optimal dose/schedule for the phase III ICARIA-MM study."( Exposure-response analyses for selection/confirmation of optimal isatuximab dosing regimen in combination with pomalidomide/dexamethasone treatment in patients with multiple myeloma.
Brillac, C; Fau, JB; Gaudel-Dedieu, N; Koiwai, K; Nguyen, L; Rachedi, F; Sebastien, B; Semiond, D; Thai, HT; van de Velde, H; Veyrat-Follet, C, 2022
)
0.72
" This pilot study assesses the effect of twice-weekly maintenance doses of Cal/BD foam after 4 weeks of standard once-daily treatment in combination with apremilast."( The Maintenance Effect of Calcipotriene 0.05% and Betamethasone Dipropionate 0.064% (Cal/BD) Aerosol Foam in Combination With Apremilast.
Kircik, L; Ozyurekoglu, E, 2022
)
0.72

Bioavailability

The aim of the present study has been to develop aqueous Thalidomide (THA) eye drops in order to minimize systemic side effects and to improve bioavailability following topical application. The safety, tolerability, and pharmacokinetics of a formulation of thalidomides with improved bioavailability in HIV-infected persons was examined in a placebo-controlled phase 1 study.

ExcerptReferenceRelevance
" Due to the variable absorption rate there is a need for an intravenous formulation of thalidomide, and in addition the search for more active and possibly less teratogenic derivatives must be intensified."( Thalidomide--the need for a new clinical evaluation of an old drug.
Eger, K; Ehninger, G; Schuler, U; Stuhler, A, 1993
)
1.95
"The aim of the present study has been to develop aqueous Thalidomide (THA) eye drops in order to minimize systemic side effects and to improve bioavailability following topical application."( Influence of cyclodextrins on the in vitro corneal permeability and in vivo ocular distribution of thalidomide.
Hartmann, C; Keipert, S; Müller, M; Pleyer, U; Siefert, B, 1999
)
0.77
" Terminal half-life for Tortuga was two to three times longer compared to the Celgene formulations and is clear evidence for absorption rate limitations."( Single-dose oral pharmacokinetics of three formulations of thalidomide in healthy male volunteers.
Colburn, WA; Teo, SK; Thomas, SD, 1999
)
0.55
" However, its use is limited by its poor bioavailability due to low solubility and short half life in solution, and teratogenic and neurotoxic side-effects."( Thalidomide analogue CC-3052 reduces HIV+ neutrophil apoptosis in vitro.
Dalgleish, AG; Dransfield, I; Guckian, M; Hay, P, 2000
)
1.75
"The effect of food on the oral pharmacokinetics of thalidomide and the relative bioavailability of two oral thalidomide formulations were determined in an open label, single dose, randomized, three-way crossover study."( Effect of a high-fat meal on thalidomide pharmacokinetics and the relative bioavailability of oral formulations in healthy men and women.
Colburn, WA; Kook, KA; Scheffler, MR; Stirling, DI; Teo, SK; Thomas, SD; Tracewell, WG, 2000
)
0.85
" It is orally bioavailable and can be administered in once daily dosing."( Thalidomide: a remarkable comeback.
Jacobson, JM, 2000
)
1.75
" The oral bioavailability of thalidomide has not been unequivocally determined, but available data suggest that it is high."( Clinical pharmacology of thalidomide.
Björkman, S; Eriksson, T; Höglund, P, 2001
)
0.91
" The safety, tolerability, and pharmacokinetics of a formulation of thalidomide with improved bioavailability in HIV-infected persons was examined in a placebo-controlled, dose-escalating phase 1 study."( Safety, tolerability, and pharmacokinetic effects of thalidomide in patients infected with human immunodeficiency virus: AIDS Clinical Trials Group 267.
Aweeka, FT; Bell, D; Cherng, DW; Fox, L; Holohan, MK; Kaplan, G; Pomerantz, R; Robinson, W; Schmitz, J; Simpson, D; Spritzler, J; Teppler, H; Thomas, S; Wohl, DA, 2002
)
0.8
" Lenalidomide is an orally bioavailable analogue of thalidomide with more potent immunomodulatory, antiangiogenic, and antitumor activities than the parent compound and with a better safety profile."( Emerging data on IMiDs in the treatment of myelodysplastic syndromes (MDS).
List, AF, 2005
)
0.58
" Most of the new compounds demonstrate medium to high predicted biological activity and good bioavailability as estimated by the octanol-water partition coefficient ClogP."( A preliminary in silico lead series of 2-phthalimidinoglutaric acid analogues designed as MMP-3 inhibitors.
Amin, EA; Welsh, WJ,
)
0.13
" Since thalidomide exhibits low oral bioavailability due to limitations in solubility, inclusion complexation using sulfobutyl ether-7 beta-cyclodextrin was used to improve the delivery of thalidomide."( Molecular encapsulation of thalidomide with sulfobutyl ether-7 beta-cyclodextrin for immediate release property: enhanced in vivo antitumor and antiangiogenesis efficacy in mice.
Juvekar, A; Kale, R; Saraf, M; Tayade, P, 2008
)
1.1
"Defibrotide is a novel orally bioavailable polydisperse oligonucleotide with anti-thrombotic and anti-adhesive effects."( Melphalan, prednisone, thalidomide and defibrotide in relapsed/refractory multiple myeloma: results of a multicenter phase I/II trial.
Anderson, K; Benevolo, G; Boccadoro, M; Bringhen, S; Cavallo, F; Gaidano, G; Gay, F; Genuardi, M; Iacobelli, M; Kotwica, K; Larocca, A; Magarotto, V; Masini, L; Mitsiades, C; Palumbo, A; Richardson, P; Rossi, D; Rus, C, 2010
)
0.67
" Studies herein define mouse plasma pharmacokinetics and tissue distribution after intravenous (IV) bolus administration and bioavailability after oral and intraperitoneal delivery."( Pharmacokinetics and tissue disposition of lenalidomide in mice.
Byrd, JC; Gao, Y; Herman, SE; Jarjoura, D; Johnson, AJ; Li, X; Mahoney, E; Phelps, MA; Rozewski, DM; Shin, JD; Stefanovski, MR; Towns, WH; Yang, X, 2012
)
0.38
" Both of these analogs displayed oral bioavailability in rat."( Isosteric analogs of lenalidomide and pomalidomide: synthesis and biological activity.
Babusis, D; Capone, L; Chen, R; Corral, L; Kang, J; Man, HW; Moghaddam, MF; Muller, GW; Parton, A; Ruchelman, AL; Schafer, PH; Shirley, MA; Tang, Y; Zhang, W, 2013
)
0.39
" Neither the rate nor the capacity of lenalidomide renal excretion was affected by quinidine or temsirolimus, in addition lenalidomide absorption rate and bioavailability remained unchanged."( No clinically significant drug interactions between lenalidomide and P‑glycoprotein substrates and inhibitors: results from controlled phase I studies in healthy volunteers.
Chen, N; Kasserra, C; Kumar, G; Liu, L; Palmisano, M; Reyes, J; Wang, X; Weiss, D; Weiss, L; Zhou, S, 2014
)
0.4
"Nonobvious controlled polymeric pharmaceutical excipient, chitosan nanoparticles (CS-NPs) for lenalidomide encapsulation were geared up by the simple ionic cross linking method to get better bioavailability and to reduce under as well as overloading of hydrophobic and sparingly soluble drug lenalidomide towards cancer cells."( Studies on drug-polymer interaction, in vitro release and cytotoxicity from chitosan particles excipient.
Gomathi, T; Govindarajan, C; Imran, PK; Kim, SK; Rose H R, MH; Sudha, PN; Venkatesan, J, 2014
)
0.4
" As an orally bioavailable immunomodulator with antineoplastic, immunologic, and antiproliferative activity in B-cell lymphoma, lenalidomide has emerged as one such option."( The evolving role of lenalidomide in non-Hodgkin lymphoma.
Galanina, N; Nabhan, C; Petrich, A, 2016
)
0.43
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
"Many lead compounds fail to reach clinical trials despite being potent because of low bioavailability attributed to their insufficient solubility making solubility a primary and crucial factor in early phase drug discovery."( Structural modification aimed for improving solubility of lead compounds in early phase drug discovery.
Baidya, ATK; Das, B; Kumar, R; Mathew, AT; Yadav, AK, 2022
)
0.72
" This new development may allow for once-daily drug administration and improve both bioavailability and patient compliance."( Development of an amorphous based sustained release system for apremilast a selective phosphodiesterase 4 (PDE4) inhibitor.
Blass, B; Durig, T; Fassihi, R; Zhang, Q, 2022
)
0.72

Dosage Studied

Thirty male patients with treatment-refractory ankylosing spondylitis were recruited into a 12-month open study. The dosage of thalidomide ranged from 33 to 200 mg/d. A dosage of 400 mg/kg per day was efficient in reducing inflammation whether given in three doses (at -24 h, -4 h and +4 h)

ExcerptRelevanceReference
" The minimum dosage used by the authors seems to be adequate on the basis of the results obtained."( [Fixed lupus erythematosus (its treatment with thalidomide)].
Barba Rubio, J; Franco González, F, 1977
)
0.51
" The initial dosage of either of the drugs was 300 mg daily administered in divided doses of 100 mg three times a day."( Treatment of steroid dependant cases of recurrent lepra reaction with a combination of thalidomide and clofazimine.
Girdhar, A; Ramu, G, 1979
)
0.48
" Within 1 h 82% of the dose given were absorbed, and 12 h after the dosing 88% had been excreted again."( Pharmacokinetics and metabolism of taglutimide (K-2004) in the rat.
Fiebrich, F; Koch, H; Pischek, G, 1979
)
0.26
" We concluded that thalidomide in a dosage of 100 mg/d is an effective treatment of severe aphthous stomatitis but is not without some risk."( Crossover study of thalidomide vs placebo in severe recurrent aphthous stomatitis.
Bonnetblanc, JM; Claudy, A; Dallac, S; Guillaume, JC; Hans, P; Janier, M; Klene, C; Marchand, C; Revuz, J; Souteyrand, P, 1990
)
0.94
" Stereoselective differences between the enantiomers of 2a and 2b were observed only when a dose of 200 mg/kg was applied, whereas the higher activity of the (S)-enantiomers of 2c, 1b + c was obtained already with a lower dosage range."( [Stereoselective differences of central nervous system-depressive action of a homologous series of 3-alkyl-thalidomide analysis].
Büch, HP; Knabe, J; Omlor, G, 1990
)
0.49
" At the most, there is only a marginal loss of sensitivity in respect of detecting the lowest dosage at which effects may occur."( An indirect assessment of the Chernoff/Kavlock assay.
Palmer, AK, 1987
)
0.27
" after dosing and the radioactivity persists for more than 58hr."( The fate of[14C]thalidomide in the pregnant rabbit.
Fabro, S; Smith, RL; Williams, RT, 1967
)
0.59
" A correlation between total dosage and severeness of polyneuropathy could not be found."( [Electrophysiologic changes in thalidomide neuropathy in the treatment of discoid lupus erythematosus].
Ludolph, A; Matz, DR, 1982
)
0.55
" Only after subchronic treatment with an elevated dosage of supidimide (greater than or equal to 150 mg/kg) is a reversible induction of cytochrome P-450 observed."( The metabolic fate of supidimide in the rat.
Becker, R; Flohé, L; Frankus, E; Graudums, I; Günzler, WA; Helm, FC, 1982
)
0.26
" Ten of the studies are dose-response evaluations."( Sleep spindles: pharmacological effects in humans.
Hirshkowitz, M; Karacan, I; Thornby, JI, 1982
)
0.26
" Whereas a pronounced loss of the receptor density of CD49d was observed and only few cells with high epitope density were left in the blood at the end of the complete dosing schedule, no such effect was observable on cells bearing the CD49b epitope."( Thalidomide and the immune system. 3. Simultaneous up- and down-regulation of different integrin receptors on human white blood cells.
Helge, H; Neubert, D; Neubert, R; Nogueira, AC, 1994
)
1.73
"A therapeutic regimen of thalidomide administered at a dosage of 100 mg/d for 2 months is able to suppress the clinical symptoms of Jessner-Kanof lymphocytic infiltration of the skin."( Crossover study of thalidomide vs placebo in Jessner's lymphocytic infiltration of the skin.
Bonnetblanc, JM; Claudy, A; Daniel, F; Dieng, MT; Guillaume, JC; Morel, P; Moulin, G; Poli, F; Souteyrand, P; Vaillant, L, 1995
)
0.92
"The dose-response of the teratogenic potency of the thalidomide (Thd) derivative EM12 was evaluated in the common marmoset (Callithrix jacchus)."( Embryotoxic effects of thalidomide derivatives in the non-human primate callithrix jacchus. IV. Teratogenicity of micrograms/kg doses of the EM12 enantiomers.
Felies, A; Heger, W; Klug, S; Merker, HJ; Nau, H; Neubert, D; Schmahl, HJ, 1994
)
0.85
" Thalidomide, at the dosage used in this study, had no effect on peripheral CD4+ T cells nor on HIV viral burden in PBMC."( Effects of thalidomide on HIV-associated wasting syndrome: a randomized, double-blind, placebo-controlled clinical trial.
Arroyo-Figueroa, H; Calva, JJ; Martínez del Cerro, V; Pasquetti, A; Reyes-Terán, G; Ruiz-Palacios, GM; Sierra-Madero, JG, 1996
)
1.59
" A dosage of 100 mg/d is as effective as a dosage of 300 mg/day."( Thalidomide in the treatment of the mucocutaneous lesions of the Behçet syndrome. A randomized, double-blind, placebo-controlled trial.
Hamuryudan, V; Mat, C; Ozyazgan, Y; Saip, S; Siva, A; Yazici, H; Yurdakul, S; Zwingenberger, K, 1998
)
1.74
"Important determinants or principles in developmental toxicology are: (1) genotype; (2) developmental stage when an insult is hitting; (3) mechanisms of action; (4) pharmacokinetics of the drug in the mother, conceptus and the neonate; (5) the manifestations of embryo/foeto- and neonatal toxicity such as death, malformations, growth inhibition and functional disturbances; and (6) dose-effect and dose-response relationships."( Susceptibility in utero and upon neonatal exposure.
Dencker, L; Eriksson, P, 1998
)
0.3
" The initial dosage was 200 mg a day, which was increased to 400 mg a day after 4 months."( Disfiguring cutaneous manifestation of sarcoidosis treated with thalidomide: a case report.
Koblenzer, PS; Lee, JB, 1998
)
0.54
" Serial serum or blood samples were obtained for pharmacokinetic assessment after administration of a single oral dose or multiple daily dosing of thalidomide and were assayed by reversed-phase HPLC."( Pharmacokinetics of thalidomide in an elderly prostate cancer population.
Bauer, KS; Bergan, R; Chen, A; Figg, WD; Hamilton, M; Pluda, J; Raje, S; Reed, E; Tompkins, A; Venzon, D, 1999
)
0.83
"Though thalidomide in a dosage of 100 mg/day is the standard treatment for recurrent oral and genital ulcers (OGU), its toxicity would be less important with lower dosage, while its efficacy would be identical."( [Treatment of recurrent ulceration with low doses of thalidomide. Pilot study in 17 patients].
Berthier, S; de Wazières, B; Dupond, JL; Gil, H; Magy, N; Vuitton, DA, 1999
)
1.01
" The initial dosage of thalidomide was 50 mg/day (1 tablet) for 1 month."( [Treatment of recurrent ulceration with low doses of thalidomide. Pilot study in 17 patients].
Berthier, S; de Wazières, B; Dupond, JL; Gil, H; Magy, N; Vuitton, DA, 1999
)
0.86
" A 200-mg/8 days dosage induced prolonged remission in 12 patients."( [Treatment of recurrent ulceration with low doses of thalidomide. Pilot study in 17 patients].
Berthier, S; de Wazières, B; Dupond, JL; Gil, H; Magy, N; Vuitton, DA, 1999
)
0.55
"A dosage of 50 mg/day is initially efficacious in most cases, provided that the patient is carefully followed up to allow early detection of potential peripheral neuropathy."( [Treatment of recurrent ulceration with low doses of thalidomide. Pilot study in 17 patients].
Berthier, S; de Wazières, B; Dupond, JL; Gil, H; Magy, N; Vuitton, DA, 1999
)
0.55
" TNFalpha was the most sensitive to thalidomide, showing dose-response inhibition at concentrations of 20 microg/ml, 50 microg/ml and 250 microg/ml."( Mycoplasma fermentans-induced inflammatory response of astrocytes: selective modulation by aminoguanidine, thalidomide, pentoxifylline and IL-10.
Brenner, T; Gallily, R; Kipper-Galperin, M, 1999
)
0.79
" An equal dosage of EM12, however, resulted in significant weight loss of the animals, but did not increase angiogenic activity compared with lower doses."( Effect of thalidomide and structurally related compounds on corneal angiogenesis is comparable to their teratological potency.
Germann, T; Joussen, AM; Kirchhof, B, 1999
)
0.71
" Sixteen HIV-infected patients with clinical and histological diagnosis of oral recurrent aphthous ulcerations received randomly an 8-week course of either thalidomide or placebo, with an initial oral dosage of 400 mg/d for 1 week, followed by 200 mg/d for 7 weeks."( Thalidomide as therapy for human immunodeficiency virus-related oral ulcers: a double-blind placebo-controlled clinical trial.
Esquivel-Pedraza, L; Gonzalez-Guevara, M; Ponce-de-Leon, S; Ramirez-Amador, VA; Reyes-Teran, G; Sierra-Madero, JG, 1999
)
1.94
" Thalidomide was administered via nasogastric tube in a dosage of 6 mg/kg/day, 12 mg/kg/day, or 24 mg/kg/day."( Adjunctive thalidomide therapy of childhood tuberculous meningitis: possible anti-inflammatory role.
Bekker, LG; Donald, PR; Hanekom, WA; Haslett, PA; Kaplan, G; Ravenscroft, A; Schoeman, JF; Springer, P; van Rensburg, AJ, 2000
)
1.61
" The remaining 8 animals (2/sex/group; high-dose and control groups) were dosed for 53 weeks, euthanized, and necropsied at 58 weeks after a 5-week recovery period."( Safety profile of thalidomide after 53 weeks of oral administration in beagle dogs.
Brockman, MJ; Ehrhart, J; Evans, MG; Morgan, JM; Stirling, DI; Teo, SK; Thomas, SD, 2001
)
0.64
" They were dosed at 43, 200 or 1000 mg/kg for 53 weeks followed by a 4-week treatment-free recovery period."( Lack of peripheral neuropathy in Beagle dogs after 53 weeks oral administration of thalidomide capsules.
Allen, D; Brockman, M; Ehrhart, J; Evans, M; Morgan, M; Stirling, D; Teo, S; Thomas, S, 2000
)
0.53
" The Food and Drug Administration (FDA), Celgene, and AIDS activists eliminated the randomized dose portion of the program to allow physicians to determine the dosage to use."( Thalidomide's elusive access.
Gilden, D, 1995
)
1.73
" Response rates were higher and survival was longer especially in high-risk patients given more than 42 g THAL in 3 months (median cumulative dose) (landmark analysis); this supports a THAL dose-response effect in advanced MM."( Extended survival in advanced and refractory multiple myeloma after single-agent thalidomide: identification of prognostic factors in a phase 2 study of 169 patients.
Anaissie, E; Ayers, D; Badros, A; Barlogie, B; Desikan, R; Eddlemon, P; Epstein, J; Munshi, N; Shaughnessy, J; Spencer, T; Spoon, D; Tricot, G; Zangari, M; Zeldis, J, 2001
)
0.54
" In the present study, we investigated the oedematogenic activity of both toxins, characterizing the time-course and dose-response of this pro-inflammatory event."( The effect of tumour necrosis factor (TNF) inhibitors in Clostridium difficile toxin-induced paw oedema and neutrophil migration.
Carneiro-Filho, BA; Lima, AA; Ribeiro, RA; Souza, ML, 2001
)
0.31
" Patients were orally dosed with 100 mg of thalidomide/day for 8 weeks."( Thalidomide is distributed into human semen after oral dosing.
Burke, AB; Harden, JL; Johnson, MA; Noormohamed, FH; Peters, BS; Stirling, DI; Teo, SK; Thomas, SD; Youle, M, 2001
)
2.02
" Comparing response and survival by thalidomide dose for low- and high-risk groups revealed a thalidomide dose-response effect in the high-risk group of patients."( Thalidomide in the management of multiple myeloma.
Anaissie, E; Barlogie, B; Tricot, G, 2001
)
2.03
" Thalidomide was administered in an initial dosage of 200 mg/d for 2 weeks and then increased as tolerated (in 200-mg increments at 2-week intervals) to a maximum daily dose of 800 mg."( Therapeutic application of thalidomide in multiple myeloma.
Kyle, RA; Rajkumar, SV, 2001
)
1.52
" Optimum dosing with antiangiogenic agents is currently under investigation."( Phase II study of thalidomide in the treatment of recurrent glioblastoma multiforme.
Bell, DR; Biggs, M; Boyle, FM; Cook, R; Levi, JA; Little, N; Marx, GM; McCowatt, S; Pavlakis, N; Wheeler, HR, 2001
)
0.64
" Moreover, the dose-response relationship has not been defined."( Thalidomide in low doses is effective for the treatment of resistant or relapsed multiple myeloma and for plasma cell leukaemia.
Abdalla, SH; Johnston, RE, 2002
)
1.76
"Thirty male patients with treatment-refractory ankylosing spondylitis were recruited into a 12-month open study using thalidomide at a dosage of 200 mg/day."( One-year open-label trial of thalidomide in ankylosing spondylitis.
Gu, J; Huang, F; Yu, DT; Zhang, J; Zhao, W; Zhu, J, 2002
)
0.81
"Although thalidomide (Thal) was introduced successfully in the treatment of multiple myeloma (MM), the optimal Thal dosage and schedule are still controversial."( Dose-dependent effect of thalidomide on overall survival in relapsed multiple myeloma.
Benner, A; Egerer, G; Goldschmidt, H; Ho, AD; Kraemer, A; Moehler, T; Neben, K, 2002
)
1.04
"From December 1998 to March 2001, 83 patients with relapsed MM were enrolled in a clinical Phase II trial and treated with a maximum Thal dosage of 400 mg daily."( Dose-dependent effect of thalidomide on overall survival in relapsed multiple myeloma.
Benner, A; Egerer, G; Goldschmidt, H; Ho, AD; Kraemer, A; Moehler, T; Neben, K, 2002
)
0.62
"Our retrospective analysis demonstrates that the cumulative 3-month Thal dosage is one of the major prognostic factors for OS, supporting the hypothesis of a dose-dependent effect of Thal in relapsed MM."( Dose-dependent effect of thalidomide on overall survival in relapsed multiple myeloma.
Benner, A; Egerer, G; Goldschmidt, H; Ho, AD; Kraemer, A; Moehler, T; Neben, K, 2002
)
0.62
" The dose-response relationship, if any, of thalidomide for renal cell carcinoma is unclear."( A phase II study of thalidomide in advanced metastatic renal cell carcinoma.
Damico, LA; Elias, L; Meng, G; Minor, DR; Monroe, D; Suryadevara, U, 2002
)
0.9
" The initial dosage of thalidomide was 100 approximately 200 mg/d with a weekly escalation of 50 mg/d to 450 approximately 650 mg/d."( [Therapeutic effectiveness of thalidomide to multiple myeloma and its mechanism].
Li, Y; Liu, Y; Wang, M; Wu, H, 2002
)
0.91
" The dosage of 450 approximately 650 mg/d might be effective in refractory or initial MM."( [Therapeutic effectiveness of thalidomide to multiple myeloma and its mechanism].
Li, Y; Liu, Y; Wang, M; Wu, H, 2002
)
0.6
" They were given oral thalidomide at a dosage of 200 mg/d for 2 weeks, which was then increased as tolerated to a maximum of 800 mg/d."( Response rate, durability of response, and survival after thalidomide therapy for relapsed multiple myeloma.
Dispenzieri, A; Fonseca, R; Gertz, MA; Geyer, SM; Greipp, PR; Hayman, SR; Iturria, NL; Kumar, S; Kyle, RA; Lacy, MQ; Lust, JA; Rajkumar, SV; Witzig, TE, 2003
)
0.88
"To evaluate the literature regarding the dosing of thalidomide in multiple myeloma."( Thalidomide dosing in patients with relapsed or refractory multiple myeloma.
Hansen, LA; Thompson, JL, 2003
)
2.01
"The antiangiogenic effect of interferon (IFN) may improve with frequent dosing and by combination with other agents with antiangiogenic activity."( Interferon alfa-2b three times daily and thalidomide in the treatment of metastatic renal cell carcinoma.
Ahtinen, H; Bono, P; Hernberg, M; joensuu, H; Mäenpää, H; Virkkunen, P, 2003
)
0.58
"The combination of frequently dosed IFN-alpha-2b and low-dose thalidomide is feasible and active in advanced RCC, but the clinical benefit may remain small compared with that of IFN alone."( Interferon alfa-2b three times daily and thalidomide in the treatment of metastatic renal cell carcinoma.
Ahtinen, H; Bono, P; Hernberg, M; joensuu, H; Mäenpää, H; Virkkunen, P, 2003
)
0.83
" Since a significant gain of therapeutic effects could not be observed as thalidomide dosage was escalated, the optimal dose of thalidomide remains to be determined."( Low dose thalidomide in patients with relapsed or refractory multiple myeloma.
Ackermann, J; Dimou, G; Drach, J; Gisslinger, H; Kees, M; Lechner, K; Sillaber, C, 2003
)
0.97
"Thalidomide had no adverse effects on mating and fertility in male and female rabbits dosed up to 500 and 100 mg/kg/day, respectively, for 14 days prior to mating."( Effects of thalidomide on reproductive function and early embryonic development in male and female New Zealand white rabbits.
Denny, KH; Hoberman, AM; Morseth, SL; Stirling, DI; Teo, SK; Thomas, SD, 2004
)
2.16
" Data collection included viral hepatitis, grade of cirrhosis, total dosage of thalidomide, side effect, stage of hepatoma by Okuda and CLIP classification, and prognosis."( Salvage therapy for hepatocellular carcinoma with thalidomide.
Chang, WH; Chu, CH; Hsieh, RK; Kao, CR; Lin, J; Lin, SC; Wang, TE, 2004
)
0.8
" These trials also indicated a possible dose-response relationship of thalidomide and identified several poor prognostic factors, including advanced age, high lactose dehydrogenase level, low platelet count, and low hemoglobin level."( Thalidomide in relapsed/refractory multiple myeloma: pivotal trials conducted outside the United States.
Anagnostopoulos, A; Dimopoulos, MA, 2003
)
2
" The patients received PTX at the initiating dosage until complete clinical cure."( [Pentoxifylline in the treatment of erythema nodosum leprosum: results of an open study].
Achirafi, A; de Carsalade, GY; Flageul, B, 2003
)
0.32
" Median thalidomide dosage was 200 mg/day."( Combined thalidomide and temozolomide treatment in patients with glioblastoma multiforme.
Baumann, F; Baumert, BG; Bernays, RL; Bjeljac, M; Brandner, S; Kollias, SS; Rousson, V; Yonekawa, Y,
)
0.98
"The present study determined effects of thalidomide on three successive generations of New Zealand White rabbits after oral dosing to F0 maternal rabbits during the later third of gestation (post major organogenesis) and lactation."( Effects of thalidomide on developmental, peri- and postnatal function in female New Zealand white rabbits and offspring.
Denny, KH; Hoberman, AM; Morseth, S; Stirling, DI; Teo, SK; Thomas, SD, 2004
)
0.98
" Depending on dosage and agent used symptoms resolve completely or not."( [Neurotoxic effects of medications: an update].
Arné-Bès, MC, 2004
)
0.32
"The dosage of thalidomide ranged from 33 to 200 mg/d."( Thalidomide treatment for prurigo nodularis in human immunodeficiency virus-infected subjects: efficacy and risk of neuropathy.
Berger, T; Maurer, T; Poncelet, A, 2004
)
2.13
" Only the 200 mg of thalidomide arm of this trial met our definition of a tolerable maintenance therapy, defined as no dose reductions or discontinuation due to toxicity in at least 65% of patients for a minimum of 6 months, thus establishing a dosing schedule for phase III trials."( Results of a multicenter randomized phase II trial of thalidomide and prednisone maintenance therapy for multiple myeloma after autologous stem cell transplant.
Belch, AR; Chen, CI; Ding, K; Howson-Jan, K; Kovacs, MJ; Meyer, RM; Roy, J; Sadura, A; Shepherd, L; Shustik, C; Stewart, AK; White, D, 2004
)
0.9
" The usual dosage has recently been investigated in a dose-escalation trial, with the majority of patients responding to 100 mg/day."( Newer therapies for cutaneous sarcoidosis: the role of thalidomide and other agents.
Baughman, RP; Lower, EE, 2004
)
0.57
" The dosage of thalidomide was 400 mg/day and the dosage of dexamethasone 20 mg/m2 daily for 4 consecutive days every 3 weeks."( Thalidomide in combination with dexamethasone for pretreated patients with multiple myeloma: serum level of soluble interleukin-2 receptor as a predictive factor for response rate and for survival.
Brandhorst, D; Buttkereit, U; Ebeling, P; Flasshove, M; Moritz, T; Müller, S; Nowrousian, MR; Opalka, B; Poser, M; Schütt, P; Seeber, S, 2005
)
2.12
" Further studies will be necessary to determine the dosage of thalidomide that does not elicit side effects, but thalidomide seems to be effective in patients with refractory CD."( [Thalidomide therapy for infantile-onset Crohn's disease].
Ikematsu, K; Joh, K; Kabuki, T; Kagimoto, S; Ogimi, C; Oh-Ishi, T; Tanaka, R, 2005
)
1.48
" Prednisolone in standard dosage schedule as recommended by WHO is now being widely used in control programmes."( Reactions and their management.
Ganapati, R; Pai, VV, 2004
)
0.32
" The total dosage of medication given to each patient ranged from 3200 mg to 40,500 mg."( Phase II trial of thalidomide for advanced and recurrent gynecologic sarcoma: a brief communication from the New York Phase II consortium.
Blank, SV; Christos, P; Fields, AL; Goldberg, GL; Murgo, A; Runowicz, CD; Timmins, P; Wadler, S; Yi-Shin Kuo, D, 2006
)
0.67
" The initial thalidomide dosage was 200 mg daily and was adjusted for toxicity."( Thalidomide in advanced hepatocellular carcinoma with optional low-dose interferon-alpha2a upon progression.
Goldenberg, A; Lehrer, D; Liebes, L; Mandeli, J; Schwartz, JD; Schwartz, M; Sung, M; Volm, M, 2005
)
2.14
" The favorable effects of CR and rapidly sequenced second transplantation attest to the validity of a melphalan dose-response effect in myeloma."( Total therapy 2 without thalidomide in comparison with total therapy 1: role of intensified induction and posttransplantation consolidation therapies.
Anaissie, E; Barlogie, B; Crowley, J; Epstein, J; Fassas, A; Hollmig, K; Pineda-Roman, M; Rasmussen, E; Shaughnessy, J; Tricot, G; van Rhee, F; Zangari, M, 2006
)
0.64
" Thirty-two trials used an escalating dosing regimen and four a fixed dose regimen (one dose with 50 mg/d, three doses with 200 mg/d)."( A systematic review of phase-II trials of thalidomide monotherapy in patients with relapsed or refractory multiple myeloma.
Glasmacher, A; Goldschmidt, H; Gorschlüter, M; Hahn, C; Hoffmann, F; Naumann, R; Orlopp, K; Schmidt-Wolf, I; von Lilienfeld-Toal, M, 2006
)
0.6
" We investigated the efficacy and safety of a 24-wk course of thalidomide at a dosage of 200 mg/day in eight patients with HCV chronic hepatitis nonresponders to interferon alpha plus ribavirin."( Thalidomide in the treatment of chronic hepatitis C unresponsive to alfa-interferon and ribavirin.
Biasin, M; Clerici, M; Galli, M; Gatti, N; Milazzo, L; Moroni, M; Niero, F; Piacentini, L; Riva, A; Zanone Poma, B, 2006
)
2.02
"The combined dosing of paclitaxel (100 mg/m(2) weekly), doxorubicin (20 mg/m(2) weekly), and thalidomide (300 mg daily) is tolerated by men with AIPC and merits continued phase II study."( A phase I study of paclitaxel/doxorubicin/ thalidomide in patients with androgen- independent prostate cancer.
Amato, RJ; Sarao, H, 2006
)
0.82
" Two patients had early death (one from massive cerebral ischemic stroke, the other from dementia and progressive renal failure), one patient progressed during Thali-Dexa (thalidomide 200mg) and was rescued with chemotherapy, two patients required increasing thalidomide dosage (to 200 and 400mg, respectively) because of progressive disease, three patients had stable disease remission lasting from 4m+ to 16m+."( Low-dose thalidomide plus monthly high-dose oral dexamethasone (Thali-Dexa): results, prognostic factors and side effects in eight patients previously treated with multiple myeloma.
Bemardeschi, P; Dentico, P; Fiorentini, G; Giustarini, G; Rossi, S; Turano, E, 2003
)
0.93
" Data about BNP dosage for cardiovascular monitoring of patients with ALA on renal replacement therapy are lacking."( Role of B-type natriuretic peptide in cardiovascular state monitoring in a hemodialysis patient with primary amyloidosis.
Cantelli, S; Catizone, L; Fabbian, F; Molino, C; Russo, G; Russo, M; Sartori, S; Stabellini, N, 2006
)
0.33
" However, a high incidence of side effects at the dosage initially recommended (400 mg/day) justified further studies with lower doses of thalidomide given alone or in combination with dexamethasone or chemotherapy."( Thalidomide in multiple myeloma: past, present and future.
Harousseau, JL, 2006
)
1.98
"Thalidomide has been used for the treatment of refractory multiple myeloma, the dosage in Japan is lower than in other countries; however, there is little information on the pharmacokinetics and their relationship with the drug response."( The pharmacokinetics of low-dose thalidomide in Japanese patients with refractory multiple myeloma.
Asaoku, H; Ikawa, K; Iwato, K; Kamikawa, R; Morikawa, N; Sasaki, A, 2006
)
2.06
" The initial dose of thalidomide was 100 mg once a day, and it was increased to 100 mg twice a day after a period of 10 days, if the prior dosage was well-tolerated."( Effects of thalidomide treatment in heart failure patients.
Arrieta-Rodríguez, O; Asensio-Lafuente, E; Castillo-Martínez, L; Dorantes-García, J; Granados-Arriola, J; Orea-Tejeda, A; Rodríguez-Reyna, T, 2007
)
1.05
" According to our data, increasing thalidomide dosage and/or adding further drugs does not generally produce significant improvement."( Thalidomide plus monthly high-dose dexamethasone in chemorefractory myeloma. Results of a phase II clinical study.
Bernardeschi, P; Dentico, P; Fiorentini, G; Giustarini, G; Montenora, I; Rossi, S; Turano, E; Turrisi, G,
)
1.85
" However, the best dosing scheme has not yet been discovered and is the subject of research in a number of clinical studies today."( [Low-dose thalidomide in refractory and relapsing multiple myeloma].
Maisnar, V; Radocha, J, 2007
)
0.74
" Caution should be exercised when lenalidomide therapy is commenced and CrCl should be incorporated as a determinant of the initial dosing of lenalidomide in MM patients."( Lenalidomide-induced myelosuppression is associated with renal dysfunction: adverse events evaluation of treatment-naïve patients undergoing front-line lenalidomide and dexamethasone therapy.
Chen-Kiang, S; Christos, PJ; Coleman, M; Ely, S; Furst, JR; Jalbrzikowski, J; Jayabalan, D; Lent, R; Leonard, JP; Mark, T; Mazumdar, M; Naib, T; Niesvizky, R; Pearse, RN; Zafar, F, 2007
)
0.34
" Clinical trials of relapsed and refractory MM have shown that lenalidomide is clinically efficacious at a dosage of 25 mg/day when administered in combination with dexamethasone."( Lenalidomide in myelodysplastic syndrome and multiple myeloma.
Shah, SR; Tran, TM, 2007
)
0.34
"The pharmacology, clinical use, adverse effects, dosage and administration, and cost of lenalidomide in the treatment of multiple myeloma (MM) are reviewed."( Lenalidomide in the treatment of multiple myeloma.
Rao, KV, 2007
)
0.34
" The optimal dosing regimen of thalidomide is not known."( Monotherapy with low-dose thalidomide for relapsed or refractory multiple myeloma: better response rate with earlier treatment.
Bláha, V; Büchler, T; Hájek, R; Maisnar, V; Malý, J; Radocha, J, 2007
)
0.93
" The median daily thalidomide dosage was 100 mg and the median duration of drug treatment was 16 weeks."( A retrospective analysis of thalidomide therapy in non-HIV-related Kaposi's sarcoma.
Ben M'barek, L; Biet, I; Fardet, L; Kérob, D; Lebbe, C; Mebazaa, A; Morel, P; Thervet, E, 2007
)
0.97
"Thalidomide maintenance has unresolved issues regarding dosage and toxicity."( Thalidomide maintenance following high-dose therapy in multiple myeloma: a UK myeloma forum phase 2 study.
Cocks, K; Feyler, S; Jackson, G; Johnson, RJ; Rawstron, A; Snowden, JA, 2007
)
3.23
" In our experience a cumulative dosage at >20 gm and long-term administration for >10 months seem to increase the risk of peripheral neuropathy."( Childhood thalidomide neuropathy: a clinical and neurophysiologic study.
Alpigiani, MG; Buoncompagni, A; Calevo, MG; De Grandis, E; De Negri, E; Gandullia, P; Giribaldi, G; Grosso, P; Lamba, LD; Priolo, T; Veneselli, E; Viola, S, 2008
)
0.75
"HNPC patients (n = 21) with evidence of progression demonstrated by 3 consecutive rises in PSA and no evidence of radiographic involvement were treated on a chronic dosing schedule with GM-CSF."( Phase 2 study of granulocyte-macrophage colony-stimulating factor plus thalidomide in patients with hormone-naïve adenocarcinoma of the prostate.
Amato, RJ; Henary, H; Hernandez-McClain, J,
)
0.36
" Most patients suffered toxicities at a dose of 400 mg per day, but there was no clear dose-response relationship."( Single-institute phase 2 study of thalidomide treatment for refractory or relapsed multiple myeloma: prognostic factors and unique toxicity profile.
Hattori, Y; Ikeda, Y; Kakimoto, T; Morita, K; Okamoto, S; Shimada, N; Tanigawara, Y, 2008
)
0.63
" Future studies with lenalidomide in CLL should focus on understanding this toxicity, investigating patients at risk, and investigating alternative safer dosing schedules."( Higher doses of lenalidomide are associated with unacceptable toxicity including life-threatening tumor flare in patients with chronic lymphocytic leukemia.
Andritsos, LA; Awan, F; Blum, W; Byrd, JC; Chen, CS; Jarjoura, D; Johnson, AJ; Kefauver, C; Knight, RD; Lapalombella, R; Lehman, A; Lozanski, G; May, SE; Raymond, CA; Ruppert, AS; Smith, LL; Wang, DS, 2008
)
0.35
" The threshold neurotoxic dosage is lower than previously reported."( Thalidomide and sensory neurotoxicity: a neurophysiological study.
Arienti, S; Doria, A; Ermani, M; Rondinone, R; Zara, G, 2008
)
1.79
" The recommended phase II dosing schedule is thalidomide 100 mg twice daily with docetaxel 25 mg/m(2)/week."( Phase I trial of docetaxel and thalidomide: a regimen based on metronomic therapeutic principles.
Bokar, JA; Brell, JM; Cooney, MM; Dowlati, A; Gibbons, J; Krishnamurthi, S; Ness, A; Nock, C; Remick, SC; Sanborn, SL, 2008
)
0.89
" The goal of dosing 200 mg per day was achieved in just 17 of 31 patients, and the median tolerated thalidomide dose was 100 mg per day."( Thalidomide maintenance following high-dose melphalan with autologous stem cell support in myeloma.
Callander, NS; Chang, JE; Gangnon, RE; Juckett, MB; Kahl, BS; Longo, WL; Mitchell, TL, 2008
)
2
" The 45 patients received a total number of 192 cycles, respectively a median of three cycles; the median dosage of dexamethasone was 240 mg per cycle."( Effective prophylaxis of thromboembolic complications with low molecular weight heparin in relapsed multiple myeloma patients treated with lenalidomide and dexamethasone.
Goldschmidt, H; Hegenbart, U; Hillengass, J; Ho, AD; Hundemer, M; Klein, U; Kosely, F; Moehler, T; Neben, K; Schmitt, S, 2009
)
0.35
"To investigate the efficacy and toxicity of bortezomib based combination therapy for Chinese patients with relapsed or refractory multiple myeloma (MM), and to determine the combination regimen, dosage and cycles in application of bortezomib for MM therapy."( [Bortezomib-based combination therapy for relapsed or refractory multiple myeloma].
Chen, YB; Fu, WJ; Hou, J; Wang, DX; Xi, H; Yuan, ZG, 2008
)
0.35
" With these drug therapies has come a more targeted approach to treatment enabling not only improved antimyeloma efficacy but also the use of decreased dosing enhancing the safety and tolerability of these regimens."( New drugs in multiple myeloma.
Berenson, JR; Yellin, O, 2008
)
0.35
" Intended therapy consisted of daily thalidomide (200 mg for 2 weeks, then 400 mg for 50 weeks) and rituximab (375 mg/m(2) per week) dosed on weeks 2 to 5 and 13 to 16."( Thalidomide and rituximab in Waldenstrom macroglobulinemia.
Anderson, KC; Boedeker, H; Branagan, AR; Briccetti, FM; Chu, L; Chua, C; Ciccarelli, BT; Cooper, RB; Garbo, L; Hatjiharissi, E; Hill, J; Howard, J; Hunter, ZR; Ioakimidis, L; Lovett, DR; Moore, M; Musto, P; Nantel, SH; Pasmantier, M; Patterson, CJ; Rauch, A; Sonneborn, H; Soumerai, JD; Treon, SP; Zimbler, H, 2008
)
2.06
" Eight patients had permitted escalation of thalidomide dosage up to 200 mg daily."( Clarithromycin with low dose dexamethasone and thalidomide is effective therapy in relapsed/refractory myeloma.
Boyd, K; Clarke, P; Drake, M; Hull, DR; Jones, FC; Kettle, PJ; Morris, TC; Morrison, A; O'Reilly, P; Quinn, J, 2008
)
0.86
" The initial thalidomide dosage of 100 mg/day was escalated in 100 mg steps weekly up to 300 mg/day based on tolerability."( Thalidomide in advanced hepatocellular carcinoma as antiangiogenic treatment approach: a phase I/II trial.
Müller, C; Peck-Radosavljevic, M; Pinter, M; Plank, C; Schmid, K; Wichlas, M; Wrba, F, 2008
)
2.16
"Effectiveness and adverse events of 102 MM patients treated with thalidomide at a median dosage of 200 mg/d."( [The efficacy of thalidomide for multiple myeloma: a clinical analysis of 102 Chinese patients].
Li, YN; Qi, PJ; Qiu, LG; Wang, YF; Xiao, ZJ; Xu, Y; Zhao, YZ; Zou, DH, 2008
)
0.92
" The recommended phase II dosing is docetaxel 75 mg/m(2) on day 1, lenalidomide 25 mg on days 1-14, and pegfilgrastim 6 mg on day 2, given every 3 weeks."( Phase I trial of docetaxel given every 3 weeks and daily lenalidomide in patients with advanced solid tumors.
Bako, J; Bokar, JA; Brell, JM; Cooney, MM; Dowlati, A; Gibbons, J; Horvath, N; Krishnamurthi, S; Nock, C; Remick, SC; Sanborn, SL, 2009
)
0.35
" 4) The most common adverse events were 1-2 grade and tolerable 3 patients had to reduce the bortezomib dosage because of peripheral neuropathy or sinus bradycardia."( [Outcome of bortezomib plus chemotherapy with or without stem cell transplantation for treatment of multiple myeloma].
Deng, SH; Qiu, LG; Wang, Y; Wang, YF; Wu, T; Xu, Y; Zhao, YZ; Zou, DH, 2008
)
0.35
"Intended therapy consisted of 48 weeks of lenalidomide (25 mg/d for 3 weeks and then 1 week off) along with rituximab (375 mg/m(2)/wk) dosed on weeks 2 to 5 and 13 to 16."( Lenalidomide and rituximab in Waldenstrom's macroglobulinemia.
Anderson, KC; Baron, AD; Branagan, AR; Chu, L; Hunter, ZR; Hyman, PM; Ioakimidis, L; Kash, JJ; Munshi, NC; Musto, P; Nawfel, EL; Nunnink, JC; Patterson, CJ; Sharon, DJ; Soumerai, JD; Terjanian, TO; Treon, SP, 2009
)
0.35
"Thalidomide presents polymorphism and is a problematic drug due to its poor solubility and difficult tablet processability, which is the dosage form available in Brazil."( Solid state evaluation of some thalidomide raw materials.
Carini, JP; Fialho, SL; Machado, G; Mayorga, P; Mexias, AS; Pavei, C; Pereira, VP; Silva, AP, 2009
)
2.08
" Improvement was noted within 1 month at a dosage of 5 mg/d in one case and was maintained for 10 months before the dosage was doubled to 10 mg/d for 12 months because of a slight worsening of symptoms."( Lenalidomide for the treatment of resistant discoid lupus erythematosus.
Albrecht, J; Bonilla-Martinez, Z; Okawa, J; Rose, M; Rosenbach, M; Shah, A; Werth, VP, 2009
)
0.35
" From these results, even in Japanese patients, the thalidomide dosage need not be modified for renal insufficiency and HD."( [Analysis of plasma concentration of thalidomide in Japanese patients of multiple myeloma with renal dysfunction].
Arai, A; Fukuda, T; Hirota, A; Miura, O; Mori, Y; Sasaki, S; Terada, Y; Tohda, S, 2009
)
0.88
" Lenalidomide was well tolerated up to a 35-mg/d intermittent dosing schedule at doses higher than previously indicated for hematologic malignancies."( Phase I study of oral lenalidomide in patients with refractory metastatic cancer.
Aragon-Ching, JB; Arlen, PM; Dahut, WL; Figg, WD; Gulley, JL; Tohnya, TM; Ventiz, J; Woo, S; Wright, JJ, 2009
)
0.35
" Treatment with corticosteroids and antibiotics resulted in significant improvement, but at reduction of steroid dosage the skin lesions reappeared."( Prurigo nodularis of Hyde treated with low-dose thalidomide.
Cottone, M; Orlando, A; Renna, S,
)
0.39
" Moreover no agreement exists concerning the effects of thalidomide dosage on the clinical and electrophysiological findings."( Clinical and electrophysiological evaluation of patients with thalidomide-induced neuropathy.
Aki, Z; Erdogmus, NI; Haznedar, R; Kocer, B; Kuruoglu, R; Sucak, G, 2009
)
0.84
" The initial daily dosing of lenalidomide is 10 mg for MDS with a 5q deletion and 25 mg for relapsed or refractory multiple myeloma."( The clinical utility of lenalidomide in multiple myeloma and myelodysplastic syndromes.
Bonkowski, J; Kolesar, JM; Vermeulen, LC, 2010
)
0.36
"Thalidomide was given to 2 patients with EOS (a 16-year-old girl and an 8-year-old boy) at an initial dosage of 2 mg/kg/day, and the dosage was increased if necessary."( Thalidomide dramatically improves the symptoms of early-onset sarcoidosis/Blau syndrome: its possible action and mechanism.
Manki, A; Morishima, T; Takemoto, K; Tsuge, M; Yamamoto, M; Yashiro, M; Yasui, K, 2010
)
3.25
" With dosing of lenalidomide according to renal function, LenDex can be administered to patients with RI (who may not have other treatment options) without excessive toxicity."( Lenalidomide and dexamethasone for the treatment of refractory/relapsed multiple myeloma: dosing of lenalidomide according to renal function and effect on renal impairment.
Christoulas, D; Dimopoulos, MA; Efstathiou, E; Gavriatopoulou, M; Grapsa, I; Kastritis, E; Matsouka, C; Migkou, M; Mparmparoussi, D; Psimenou, E; Roussou, M; Terpos, E, 2010
)
0.36
"The impact of cumulative dosing and premature drug discontinuation (PMDD) of bortezomib (V), thalidomide (T), and dexamethasone (D) on overall survival (OS), event-free survival (EFS), time to next therapy, and post-relapse survival in Total Therapy 3 were examined, using time-dependent methodology, relevant to induction, peritransplantation, consolidation, and maintenance phases."( Total Therapy 3 for multiple myeloma: prognostic implications of cumulative dosing and premature discontinuation of VTD maintenance components, bortezomib, thalidomide, and dexamethasone, relevant to all phases of therapy.
Alsayed, Y; Anaissie, E; Barlogie, B; Crowley, J; Hoering, A; Nair, B; Petty, N; Shaughnessy, JD; Szymonifka, J; van Rhee, F; Waheed, S, 2010
)
0.78
"Lenalidomide (25 mg daily) treatment was then initiated in a continuous dosing schedule."( Lenalidomide induced good clinical response in a patient with multiple relapsed and refractory Hodgkin's lymphoma.
Kolonic, SO; Mandac, I, 2010
)
0.36
" Intermittent dosing of pomalidomide allowed substantially higher doses than were previously reported with a continuous schedule."( A phase I, dose-escalation study of pomalidomide (CC-4047) in combination with gemcitabine in metastatic pancreas cancer.
Bendell, JC; Burris, HA; Hainsworth, JD; Infante, JR; Jones, SF; Messersmith, WA; Spigel, DR; Weekes, CD; Yardley, DA, 2011
)
0.37
" Pharmacokinetic analysis demonstrated that the lenalidomide area under the concentration-time curve from 0 to 24 hours and maximum plasma concentration increased with dosage over the range studied."( Phase I trial of lenalidomide in pediatric patients with recurrent, refractory, or progressive primary CNS tumors: Pediatric Brain Tumor Consortium study PBTC-018.
Blaney, SM; Boyett, JM; Fangusaro, J; Goldman, S; Jakacki, R; Kun, LE; Macdonald, T; Packer, R; Pollack, IF; Schaiquevich, P; Stewart, CF; Wallace, D; Warren, KE, 2011
)
0.37
" Nevertheless, such a memantine dosing regimen did not affect dopamine metabolism in mPFC and Acb."( Memantine abolishes the formation of cocaine-induced conditioned place preference possibly via its IL-6-modulating effect in medial prefrontal cortex.
Cherng, CG; Lin, KY; Lin, LC; Lu, RB; Yang, FR; Yu, L, 2011
)
0.37
"Quantification of tumor blood flow by using contrast-enhanced destruction-replenishment US shows the potential to guide drug dosage during antiangiogenic therapy."( Quantitative assessment of tumor blood flow in mice after treatment with different doses of an antiangiogenic agent with contrast-enhanced destruction-replenishment US.
Cao, LH; Han, F; Li, AH; Liu, JB; Liu, M; Luo, RZ; Zheng, W; Zhou, JH, 2011
)
0.37
" Of note, once-weekly bortezomib dosing (in combination with MP±T) was shown to reduce the incidence of peripheral neuropathy and gastrointestinal events compared with twice-weekly dosing, while maintaining efficacy."( Practical management of adverse events in multiple myeloma: can therapy be attenuated in older patients?
Bringhen, S; Mateos, MV; Palumbo, A; San Miguel, JF, 2011
)
0.37
" Lenalidomide was dosed 10 mg on days 1 to 21 of a 28-day schedule for a total of 24 cycles."( Lenalidomide maintenance after nonmyeloablative allogeneic stem cell transplantation in multiple myeloma is not feasible: results of the HOVON 76 Trial.
Bruijnen, CP; Cornelisse, PB; Cornelissen, JJ; Emmelot, M; Huisman, C; Huls, G; Janssen, JJ; Kersten, MJ; Kneppers, E; Lokhorst, HM; Meijer, E; Minnema, MC; Mutis, T; Sonneveld, P; van der Holt, B; Zweegman, S, 2011
)
0.37
" Although well tolerated, this phase II trial did not show superior efficacy compared with conventional dosing and scheduling of these agents."( Phase II trial of syncopated thalidomide, lenalidomide, and weekly dexamethasone in patients with newly diagnosed multiple myeloma.
Anand, P; Bello, E; Bendarz, U; Bilotti, E; McBride, L; McNeill, A; Olivo, K; Siegel, DS; Tufail, M; Vesole, DH, 2012
)
0.67
" However the response rate, even using lenalidomide at 50 mg, was not superior to standard dosing of thalidomide or lenalidomide plus dexamethasone."( Phase II trial of syncopated thalidomide, lenalidomide, and weekly dexamethasone in patients with newly diagnosed multiple myeloma.
Anand, P; Bello, E; Bendarz, U; Bilotti, E; McBride, L; McNeill, A; Olivo, K; Siegel, DS; Tufail, M; Vesole, DH, 2012
)
0.89
" The dosage of thalidomide, concentrations of (R)- and (S)-thalidomide in whole blood, and clinical laboratory test results were used as pharmacokinetic and pharmacodynamic indices."( Influence of cytochrome P450 2C19 gene variations on pharmacokinetic parameters of thalidomide in Japanese patients.
Ishida, F; Matsuda, M; Matsuzawa, N; Nakamura, K; Ohmori, S, 2012
)
0.96
" A prospective cohort study in 50 patients with RRMM has reported that when Len/Dex dosing was adjusted according to renal function, response rates and survival outcomes were similar in patients with and without RI, and there was no increase in adverse events in patients with RI."( Treatment with lenalidomide and dexamethasone in patients with multiple myeloma and renal impairment.
Alegre, A; Dimopoulos, MA; Goldschmidt, H; Mark, T; Niesvizky, R; Terpos, E, 2012
)
0.38
" Phase III clinical trials are currently underway and will better elucidate appropriate dosing of apremilast and further illuminate its side effect profile."( Apremilast as a treatment for psoriasis.
Feldman, S; Pellerin, M; Shutty, B; West, C, 2012
)
0.38
" The patient was administered an increasing dosage of thalidomide, up to 300 mg/day, with thromboembolism prophylaxis for 3 months, with no clinical response."( [High-dose thalidomide for severe idiopathic obscure gastrointestinal bleeding in a patient at high-thrombotic risk].
Gonzalez-Santiago, JM; Martín-Noguerol, E; Martinez-Alcalá, C; Molina-Infante, J; Vara-Brenes, D, 2013
)
1.03
"Treatment with apremilast at a dosage of 20 mg twice per day or 40 mg once per day demonstrated efficacy in comparison with placebo and was generally well tolerated in patients with active PsA."( Oral apremilast in the treatment of active psoriatic arthritis: results of a multicenter, randomized, double-blind, placebo-controlled study.
de Vlam, KL; Hu, C; Joos, R; Papp, K; Rodrigues, JF; Schett, G; Stevens, R; Vessey, AR; Wollenhaupt, J, 2012
)
0.38
" Two different dosing schedules were explored."( Phase I trial of pomalidomide given for patients with advanced solid tumors.
Bokar, J; Cooney, MM; Dowlati, A; Dreicer, R; Gibbons, J; Krishnamurthi, S; Ness, A; Nock, C; Remick, SC; Rodal, MB, 2012
)
0.38
"Pomalidomide was well tolerated and the recommended phase II dosing schedules are 7 mg daily given for 21 days followed by a 7-day rest or pomalidomide 4 mg given on an uninterrupted daily schedule."( Phase I trial of pomalidomide given for patients with advanced solid tumors.
Bokar, J; Cooney, MM; Dowlati, A; Dreicer, R; Gibbons, J; Krishnamurthi, S; Ness, A; Nock, C; Remick, SC; Rodal, MB, 2012
)
0.38
" However, phase III trials were dosed without regard to food; therefore, clinical relevance of the food effect was minimal."( Single-dose pharmacokinetics of lenalidomide in healthy volunteers: dose proportionality, food effect, and racial sensitivity.
Chen, N; Kasserra, C; Lau, H; Liu, L; Reyes, J, 2012
)
0.38
" We observed dose-dependent kinetics over the evaluated dosing range."( Pharmacokinetics and tissue disposition of lenalidomide in mice.
Byrd, JC; Gao, Y; Herman, SE; Jarjoura, D; Johnson, AJ; Li, X; Mahoney, E; Phelps, MA; Rozewski, DM; Shin, JD; Stefanovski, MR; Towns, WH; Yang, X, 2012
)
0.38
" This dosage form permits the prolonged drug release."( Evaluation of the effects of thalidomide-loaded biodegradable devices in solid Ehrlich tumor.
Dantas Cassali, G; Ligorio Fialho, S; Maria de Souza, C; Pereira, BG; Silva-Cunha, A, 2013
)
0.68
" Lenalidomide even in lower dosed combined with steroids can induce complete responses in patients with refractory AITL."( Therapy refractory angioimmunoblastic T-cell lymphoma in complete remission with lenalidomide.
Beckers, MM; Huls, G, 2013
)
0.39
" CRd was administered on 28-day dosing cycles: carfilzomib 15 to 27 mg/m(2) on days 1, 2, 8, 9, 15, and 16; lenalidomide 10 to 25 mg on days 1 to 21; and dexamethasone 40 mg weekly."( Phase Ib dose-escalation study (PX-171-006) of carfilzomib, lenalidomide, and low-dose dexamethasone in relapsed or progressive multiple myeloma.
Alsina, M; Bensinger, WI; Kunkel, LA; Lee, S; Martin, TG; Niesvizky, R; Orlowski, RZ; Siegel, DS; Wang, M; Wong, AF, 2013
)
0.39
" Dosage adjustment was made according to improvement of symptoms or patient's own choice."( Thalidomide improves clinical symptoms of primary cutaneous amyloidosis: report of familiar and sporadic cases.
An, Q; Chen, HD; Gao, XH; Hong, Y; Lin, J; Zhang, L; Zheng, S,
)
1.57
" The most common adverse events (incidence ≥20 %) occurring in lenalidomide recipients were thrombocytopenia and neutropenia, which were generally managed by dosage reductions and/or interruptions, and/or pharmacotherapy."( Lenalidomide: a review of its use in patients with transfusion-dependent anaemia due to low- or intermediate-1-risk myelodysplastic syndrome associated with 5q chromosome deletion.
Scott, LJ; Syed, YY, 2013
)
0.39
"Preclinical models show that an antiangiogenic regimen at low-dose daily (metronomic) dosing may be effective against chemotherapy-resistant tumors."( A phase II trial of a multi-agent oral antiangiogenic (metronomic) regimen in children with recurrent or progressive cancer.
Allen, JC; Bendel, AE; Campigotto, F; Chi, SN; Chordas, CA; Comito, MA; Goldman, S; Hubbs, SM; Isakoff, MS; Khatib, ZA; Kieran, MW; Kondrat, L; Manley, PE; Neuberg, DS; Pan, WJ; Pietrantonio, JB; Robison, NJ; Rubin, JB; Turner, CD; Werger, AM; Zimmerman, MA, 2014
)
0.4
" The post-implantation loss rate and number of placental remnants were increased and the number of live fetuses was decreased in both of the strains in the EFD study and in Kbl:NZW at 300 mg/kg dosed on GD 7-8 in the SP study."( Common nature in the effects of thalidomide on embryo-fetal development in Kbl:JW and Kbl:NZW rabbits.
Awatsuji, H; Kawamura, Y; Matsumoto, K; Sato, K; Shirotsuka, Y, 2014
)
0.69
" The dosage of hemoglobin in sponge and in circulation was performed and the ratio between the values was tested using nonparametric Mann-Whitney test."( Standardization of a method to study angiogenesis in a mouse model.
Azzalis, LA; Feder, CK; Feder, D; Fonseca, FL; Forsait, S; Junqueira, PE; Junqueira, VB; Pereira, EC; Perrazo, FF, 2013
)
0.39
" Drugs for multiple myeloma therapy are significantly removed with both HCO and PFX, with important implications for the dosing and timing of administration, particularly in patients with cast nephropathy receiving extended dialysis."( Clearance of drugs for multiple myeloma therapy during in vitro high-cutoff hemodialysis.
Devine, E; Krause, B; Krieter, DH; Lemke, HD; Storr, M; Wanner, C, 2014
)
0.4
" The optimal dosing schedule of granulocyte colony-stimulating factor (G-CSF) is unclear."( Intermittent granulocyte colony-stimulating factor for neutropenia management in patients with relapsed or refractory multiple myeloma treated with lenalidomide plus dexamethasone.
Atenafu, EG; Chen, C; Kukreti, V; Masih-Khan, E; Reece, DE; Sun, HL; Trudel, S; Winter, A; Yeboah, E, 2015
)
0.42
" High-dose cytarabine is clearly effective and there definitely is a dose-response relationship for cytarabine and remission duration."( Optimal therapy for adult patients with acute myeloid leukemia in first complete remission.
Wiernik, PH, 2014
)
0.4
" The MTD was found to be continuous dosing of lenalidomide 10 mg/day plus sunitinib 37."( A phase I/II study of lenalidomide in combination with sunitinib in patients with advanced or metastatic renal cell carcinoma.
Beck, R; Burris, HA; Fandi, A; Garcia, JA; Infante, JR; Jungnelius, U; Li, S; Redman, B; Rini, B, 2014
)
0.4
"Adequate dosing of lenalidomide in Chronic Lymphocytic Leukemia (CLL) remains unclear."( A dose escalation feasibility study of lenalidomide for treatment of symptomatic, relapsed chronic lymphocytic leukemia.
Andritsos, LA; Browning, R; Byrd, JC; Flynn, J; Gao, Y; Harper, E; Jiang, Y; Johnson, AJ; Jones, J; Kefauver, C; Maddocks, K; Phelps, MA; Poi, M; Rozewski, DM; Ruppert, AS, 2014
)
0.4
" A total of 43 patients were recruited into three CPT plus thalidomide cohorts based on CPT dosage in sequence: 5 mg/kg (n = 11), 8 mg/kg (n = 17), and 10 mg/kg (n = 15)."( A multicenter, open-label phase II study of recombinant CPT (Circularly Permuted TRAIL) plus thalidomide in patients with relapsed and refractory multiple myeloma.
Chen, WM; Geng, C; Hou, J; Huang, Z; Ke, X; Liu, Y; Qiu, L; Wang, F; Wang, Z; Wei, N; Wei, P; Xi, H; Yang, S; Zhao, Y; Zheng, X; Zhu, B, 2014
)
0.87
"The pharmacology, pharmacokinetics, clinical efficacy, safety, dosage and administration, and place in therapy of pomalidomide for the management of refractory multiple myeloma are reviewed."( Pomalidomide for the management of refractory multiple myeloma.
Cole, SW; Olin, JL; Summers, BB, 2014
)
0.4
" For patients with small lymphocytic lymphoma, dosing began at 10 mg/day to avoid tumour flare, with an escalation of 5 mg/month to 20 mg/day."( Safety and activity of lenalidomide and rituximab in untreated indolent lymphoma: an open-label, phase 2 trial.
Baladandayuthapani, V; Claret, LC; Davis, RE; Fanale, MA; Fayad, LE; Feng, L; Fowler, NH; Hagemeister, FB; Kwak, LW; McLaughlin, P; Muzzafar, T; Nastoupil, L; Neelapu, SS; Oki, Y; Orlowski, RZ; Rawal, S; Romaguera, JE; Samaniego, F; Shah, J; Tsai, KY; Turturro, F; Wang, M; Westin, JR, 2014
)
0.4
" Treatment-specific tools and clinical assessments can be useful for optimizing dosing and schedule adjustments to increase therapy duration, and implementing supportive care strategies (e."( Treatment-related symptom management in patients with multiple myeloma: a review.
Colson, K, 2015
)
0.42
" In addition to appropriate drug dosing and administration, effective supportive care and health maintenance are crucial for maximizing quality of life and disease control."( Treatment-related symptom management in patients with multiple myeloma: a review.
Colson, K, 2015
)
0.42
" The tolerability profile demonstrated in the dose escalation schedule of lenalidomide suggests the dosing of lenalidomide to be 25 mg daily on days 1-21 with standard dosing of gemcitabine and merits further evaluation in a phase II trial."( A phase I dose-escalation study of lenalidomide in combination with gemcitabine in patients with advanced pancreatic cancer.
Liljefors, M; Rossmann, E; Ullenhag, GJ, 2015
)
0.42
" Here we evaluated the clinical and pharmacodynamic effects of continuous or intermittent dosing strategies of pomalidomide/dexamethasone in lenalidomide-refractory myeloma in a randomized trial."( Clinical and pharmacodynamic analysis of pomalidomide dosing strategies in myeloma: impact of immune activation and cereblon targets.
Breider, M; Cooper, D; Couto, S; Das, R; Deng, Y; Dhodapkar, KM; Dhodapkar, MV; Hansel, D; Kocoglu, M; Koduru, S; Ren, Y; Sehgal, K; Seropian, S; Thakurta, A; Vasquez, J; Verma, R; Wang, M; Yao, X; Zhang, L, 2015
)
0.42
"The biologic endpoint of full KIR occupancy was achieved across the IPH2101 dosing interval."( A Phase I Trial of the Anti-KIR Antibody IPH2101 and Lenalidomide in Patients with Relapsed/Refractory Multiple Myeloma.
Andre, P; Benson, DM; Caligiuri, MA; Cohen, AD; Efebera, YA; Hofmeister, CC; Jagannath, S; Munshi, NC; Spitzer, G; Zerbib, R, 2015
)
0.42
" The 90 % CI for the ratio of area under the INR curve from time zero until 144 hours after dosing (AUCINR, 0-144) or the peak INR geometric means between co-administration with lenalidomide versus placebo was also within the 85-125 % bounds."( Evaluation of pharmacokinetic and pharmacodynamic interactions when lenalidomide is co-administered with warfarin in a randomized clinical trial setting.
Chen, N; Knight, R; Palmisano, M; Weiss, D; Zhou, S, 2015
)
0.42
" Alternate approaches such as sequential dosing need to be evaluated when considering novel combination strategies for myelofibrosis."( Ruxolitinib in combination with lenalidomide as therapy for patients with myelofibrosis.
Borthakur, G; Cortes, J; Daver, N; Jabbour, E; Kadia, T; Kantarjian, H; Newberry, K; Pemmaraju, N; Pierce, S; Ravandi, F; Sasaki, K; Verstovsek, S; Wang, X; Zhou, L, 2015
)
0.42
"In this issue of Blood, Sehgal et al report on the clinical and pharmacodynamics analysis of pomalidomide dosing strategies in multiple myeloma (MM) and their impact on immune activation and cereblon targets."( Toward optimizing pomalidomide therapy in MM patients.
Podar, K, 2015
)
0.42
" We point the attention on open issues, including drug dosage and administration schedule, prediction of clinical response to lenalidomide, and combination therapeutic strategies."( Lenalidomide in chronic lymphocytic leukemia: the present and future in the era of tyrosine kinase inhibitors.
Colaci, E; Fiorcari, S; Luppi, M; Maffei, R; Marasca, R; Martinelli, S; Potenza, L, 2016
)
0.43
" Thalidomide was orally administered at a dosage of 50mg/day to 150 mg/day before sleeping for at least 14 days."( Thalidomide Combined with Chemotherapy in Treating Patients with Advanced Colorectal Cancer.
Deng, LC; Gu, HG; Gu, M; Huang, XE; Ji, ZQ; Li, L; Liu, MY; Liu, Y; Qian, T; Shen, HL; Wang, L; Yan, XC, 2015
)
2.77
" Pomalidomide at a dosage of 4 mg orally on days 1-21 of repeated 28-day cycles associated with fixed low-dose dexamethasone (40 mg on days 1, 8, 15 and 22 of each 28-day cycle), outside of the clinical trials, was started as a final attempt."( Response to pomalidomide plus fixed low-dose dexamethasone in a case of secondary plasma cell leukaemia.
Coppi, MR; Guaragna, G; Mele, G; Melpignano, A; Spina, A, 2016
)
0.43
" This analysis of the pivotal phase 3 FIRST trial examined the impact of renally adapted dosing of lenalidomide and dexamethasone on outcomes of patients with different degrees of renal impairment."( Impact of renal impairment on outcomes with lenalidomide and dexamethasone treatment in the FIRST trial, a randomized, open-label phase 3 trial in transplant-ineligible patients with multiple myeloma.
Belhadj, K; Bensinger, W; Chen, G; Cheung, MC; Derigs, HG; Dib, M; Dimopoulos, MA; Eom, H; Ervin-Haynes, A; Facon, T; Gamberi, B; Hall, R; Jaccard, A; Jardel, H; Karlin, L; Kolb, B; Lenain, P; Leupin, N; Liu, T; Marek, J; Rigaudeau, S; Roussel, M; Schots, R; Tosikyan, A; Van der Jagt, R, 2016
)
0.43
" To determine the optimal dosing schedule of once weekly bortezomib (BTZ) combined with lenalidomide (LEN) and dexamethasone (DEX), especially in the outpatient setting, we conducted a phase I dose escalation study."( Phase I study of once weekly treatment with bortezomib in combination with lenalidomide and dexamethasone for relapsed or refractory multiple myeloma.
Hagiwara, S; Iida, S; Ishida, T; Ito, A; Kanamori, T; Kato, C; Kinoshita, S; Komatsu, H; Kusumoto, S; Masuda, A; Murakami, S; Nakashima, T; Narita, T; Ri, M; Suzuki, N; Totani, H; Yoshida, T, 2016
)
0.43
" In ECG evaluations performed after dosing with pomalidomide 4 mg (therapeutic dose) or 20 mg (supratherapeutic dose), the upper limit of the two-sided 90 % CI for mean change from baseline and placebo-corrected QTcF was <10 ms at all postdose time points, which is below the defined threshold of regulatory concern."( A Phase 1, double-blind, 4-period crossover study to investigate the effects of pomalidomide on QT interval in healthy male subjects.
Assaf, M; Liu, L; Mondal, SA; O'Mara, E, 2016
)
0.43
" To establish safety, lenalidomide dosing in this combination was escalated in a conventional 3 + 3 design (15, 20 and 25 mg daily for 2 weeks followed by 1 week off)."( Phase II trial of docetaxel, bevacizumab, lenalidomide and prednisone in patients with metastatic castration-resistant prostate cancer.
Adesunloye, BA; Arlen, PM; Beedie, SL; Chen, C; Chun, G; Cordes, L; Couvillon, A; Dahut, WL; Dawson, NA; Figg, WD; Gulley, JL; Harold, N; Huang, X; Karzai, FH; Lee, MJ; Lee, S; Madan, RA; McLeod, DG; Ning, YM; Rosner, I; Sissung, T; Steinberg, SM; Theoret, MR; Tomita, Y; Trepel, JB, 2016
)
0.43
" A significant correlation was observed between platelet (Plt) count prior to the start of Len therapy (pre-treatment Plt) and the difference between pre-treatment Plt and the minimum Plt up to the point in time of treatment discontinuation, prolongation, or dosage reduction (min-Plt) (r=0."( The Establishment of Indicators of Thrombocytopenia in Patients Receiving Lenalidomide Therapy.
Goto, C; Goto, H; Ichihashi, A; Kasahara, S; Nagaya, K; Osawa, T; Tachi, T; Takahashi, T; Teramachi, H; Umeda, M; Yasuda, M, 2015
)
0.42
" The present review examines the drug's pharmacokinetics, discusses the main adverse renal effects that are associated with lenalidomide treatment, and makes recommendations for dosage adjustment in patients with underlying renal impairment."( [Lenalidomide nephrotoxicity].
Izzedine, H; Kheder El-Fekih, R, 2016
)
0.43
" Conventionally dosed lenalidomide has activity in 5q-MDS."( A study of high-dose lenalidomide induction and low-dose lenalidomide maintenance therapy for patients with hypomethylating agent refractory myelodysplastic syndrome.
Cashen, AF; Cherian, MA; DiPersio, JF; Fiala, M; Fletcher, T; Gao, F; Jacoby, MA; Stockerl-Goldstein, K; Tibes, R; Uy, GL; Vij, R; Westervelt, P, 2016
)
0.43
" The dosing and safety profile of POM + LoDEX was similar across RI subgroups."( Pomalidomide plus low-dose dexamethasone in patients with relapsed/refractory multiple myeloma and moderate renal impairment: a pooled analysis of three clinical trials.
Baz, R; Cavo, M; Delforge, M; Dimopoulos, MA; Goldschmidt, H; Hong, K; Jagannath, S; Moreau, P; Palumbo, A; Richardson, P; San Miguel, JF; Siegel, DS; Song, KW; Sternas, L; Weisel, KC; Yu, X; Zaki, M, 2016
)
0.43
" Dosing was based on the lenalidomide label."( Pharmacokinetics, safety, and efficacy of lenalidomide plus dexamethasone in patients with multiple myeloma and renal impairment.
Abraham, J; Arnulf, B; Bridoux, F; Chen, N; Desport, E; Fermand, JP; Jaccard, A; Moreau, S; Moumas, E, 2016
)
0.43
" When co-administrated with anti-CD20 mAbs, dosage of lenalidomide was not the key factor of ORR in combination therapy."( Efficacy of lenalidomide in relapsed/refractory chronic lymphocytic leukemia patient: a systematic review and meta-analysis.
Hu, X; Liang, L; Liu, H; Yang, LP; Zhao, M; Zhu, YC, 2016
)
0.43
" Overall, lenalidomide is a suitable therapeutic option for R/R DLBCL, especially in non-GCB DLBCL, and 25 mg/day dosing should be preferred."( Lenalidomide in Relapsed or Refractory Diffuse Large B-Cell Lymphoma: Is It a Valid Treatment Option?
Cuzzocrea, S; Ferrero, S; Ghione, P; Marabese, A; Mian, M; Mondello, P; Pitini, V; Steiner, N; Willenbacher, W, 2016
)
0.43
" Moreover, thalidomide prevented the morphine-induced shift to the right of the ED50 in the dose-response curve."( A new pharmacological role for thalidomide: Attenuation of morphine-induced tolerance in rats.
Amini, H; Hassanzadeh, K; Izadpanah, E; Khodadadi, B; Moloudi, MR; Rahmani, MR, 2016
)
1.11
" This prompted us to explore the concept of less intense drug dosing with shorter intervals between courses with the aim of preventing inter-course relapse."( Dose-dense and less dose-intense Total Therapy 5 for gene expression profiling-defined high-risk multiple myeloma.
Alapat, D; Avery, D; Bailey, C; Barlogie, B; Crowley, J; Epstein, J; Heuck, CJ; Hoering, A; Jethava, Y; Khan, R; Mitchell, A; Morgan, G; Petty, N; Sawyer, J; Schinke, C; Smith, R; Stein, C; Steward, D; Thanendrarajan, S; Tian, E; van Rhee, F; Waheed, S; Yaccoby, S; Zangari, M, 2016
)
0.43
" Reduction in steroid dosage was reported in 109/152 (71."( Thalidomide for inflammatory bowel disease: Systematic review.
Bramuzzo, M; Lazzerini, M; Martelossi, S; Ventura, A, 2016
)
1.88
" Continous high dosing schedules are poorly tolerated and minimally active."( A phase 2 trial of high dose lenalidomide in patients with relapsed/refractory higher-risk myelodysplastic syndromes and acute myeloid leukaemia with trilineage dysplasia.
Carraway, HE; DeZern, A; Gojo, I; Gore, SD; Smith, BD; Zeidan, AM, 2017
)
0.46
" Initial dosage level was 5 mg once per day for 21 days per 28-day cycle, with a de-escalated level of 3 mg if not tolerable, and aspirin 81 mg once per day thromboprophylaxis."( Pomalidomide for Symptomatic Kaposi's Sarcoma in People With and Without HIV Infection: A Phase I/II Study.
Aleman, K; Bevans, M; Figg, WD; Goncalves, PH; Khetani, V; Maldarelli, F; Marshall, V; Peer, CJ; Polizzotto, MN; Sereti, I; Steinberg, SM; Uldrick, TS; Whitby, D; Wyvill, KM; Yarchoan, R; Zeldis, JB, 2016
)
0.43
" However, a dosage adjustment was needed because of pancytopenia."( Efficacy of pomalidomide in a multiple myeloma patient requiring hemodialysis.
Hangaishi, A; Hirao, M; Iizuka, H; Kida, M; Usuki, K, 2016
)
0.43
" The developed model was used to simulate dose schedules in order to explore the need of different dosing regimens in patients with different covariate values."( Population pharmacokinetics of lenalidomide in multiple myeloma patients.
Climente-Martí, M; Guchelaar, HJ; Guglieri-López, B; Merino-Sanjuán, M; Moes, DJ; Pérez-Pitarch, A; Porta-Oltra, B, 2017
)
0.46
" Dosing comprised elotuzumab 10 mg/kg intravenously (weekly, Cycles 1-2; biweekly, Cycles 3+), lenalidomide 25 mg (daily, Days 1-21), and dexamethasone (28 mg orally and 8 mg intravenously, weekly, Cycles 1-2; 40 mg orally, weekly, Cycles 3+), in 28-day cycles."( A phase 2 safety study of accelerated elotuzumab infusion, over less than 1 h, in combination with lenalidomide and dexamethasone, in patients with multiple myeloma.
Badarinath, S; Berenson, J; Cartmell, A; Harb, W; Lyons, R; Manges, R; McIntyre, K; Mohamed, H; Nourbakhsh, A; Rifkin, R, 2017
)
0.46
" Further study should focus on guidelines for dosing and course and investigate how to reduce the adverse effects."( Thalidomide for Epistaxis in Patients with Hereditary Hemorrhagic Telangiectasia: A Preliminary Study.
Chen, X; Fang, J; Guan, J; Su, K; Ye, H; Zhang, W; Zhu, B, 2017
)
1.9
" Median duration of dosing was 36."( A phase 1b study of isatuximab plus lenalidomide and dexamethasone for relapsed/refractory multiple myeloma.
Baz, R; Benson, DM; Campana, F; Charpentier, E; Lendvai, N; Lesokhin, AM; Martin, T; Munster, P; Vij, R; Wack, C; Wolf, J, 2017
)
0.46
" Patients received daratumumab 16 mg/kg at the recommended dosing schedule, pomalidomide 4 mg daily for 21 days of each 28-day cycle, and dexamethasone 40 mg weekly."( Daratumumab plus pomalidomide and dexamethasone in relapsed and/or refractory multiple myeloma.
Ahmadi, T; Arnulf, B; Chari, A; Chiu, C; Comenzo, R; Fay, JW; Ifthikharuddin, JJ; Kaufman, JL; Khokhar, NZ; Krishnan, A; Lentzsch, S; Lonial, S; Nottage, K; Suvannasankha, A; Wang, J; Weiss, BM, 2017
)
0.46
" The basis of the RI treatment in MM is bortizomib-based regimen, which does not require dosage adjustment in patients with dialysis or renal insufficiency."( [Expert consensus for the diagnosis and treatment of patients with renal impairment of multiple myeloma].
, 2017
)
0.46
" Although the POM dosage was reduced to 1-2 mg/day due to somnolence, which was reported as an adverse event, stringent complete response (sCR) was achieved and sustained for 10 months following 11 cycles of low-dose POM monotherapy."( [Achievement of a stringent complete response with low-dose pomalidomide monotherapy in a multiple myeloma patient].
Endo, T; Hamada, T; Hatta, Y; Iriyama, N; Koike, T; Kurihara, K; Miura, K; Nakagawa, M; Otake, S; Sato, H; Takahashi, H; Takei, M; Uchino, Y,
)
0.13
"Pomalidomide is an immunomodulatory drug and the dosage of 4 mg per day taken orally on days 1-21 of repeated 28-day cycles has been approved in the European Union and United States to treat patients with relapsed/refractory multiple myeloma."( An Open-Label, Phase 1 Study to Assess the Effects of Hepatic Impairment on Pomalidomide Pharmacokinetics.
Gomez, D; Li, Y; Liu, L; Palmisano, M; Reyes, J; Wang, X; Zhang, C; Zhou, S, 2019
)
0.51
"Pomalidomide is an immunomodulatory drug, and the dosage of 4 mg per day taken orally on days 1-21 of repeated 28-day cycles has been approved in the European Union and the United States to treat patients with relapsed/refractory multiple myeloma."( In Vivo Assessment of the Effect of CYP1A2 Inhibition and Induction on Pomalidomide Pharmacokinetics in Healthy Subjects.
Hoffmann, M; Li, Y; Liu, L; Palmisano, M; Reyes, J; Wang, X; Zhang, C; Zhou, S, 2018
)
0.48
"Ten Caucasian individuals (6 male, 4 females; mean age 69,3; range 53-81 years) affected by moderate to severe plaque psoriasis (PASI≥10 e/o DLQI≥10 e/O BSA≥10) were treated with apremilast, following dosing regimen of technical data sheet and clinically evaluated both after 12 weeks (T12) and 16 weeks (T16)."( Skin involvement in patients with psoriatic arthritis: preliminary results of treatment with apremilast in real world setting.
Campanati, A; Diotallevi, F; Molinelli, E; Offidani, A; Radi, G, 2019
)
0.51
" Using various dosing schedules, the majority of patients (684/694) received daratumumab at a dose of 16 mg/kg."( Pharmacokinetics and Exposure-Response Analyses of Daratumumab in Combination Therapy Regimens for Patients with Multiple Myeloma.
Belch, A; Capra, M; Clemens, PL; Dimopoulos, MA; Gomez, D; Ho, PJ; Iida, S; Jansson, R; Leiba, M; Medvedova, E; Min, CK; Schecter, J; Sonneveld, P; Sun, YN; Xu, XS; Zhang, L, 2018
)
0.48
"These data support the recommended 16 mg/kg dose of daratumumab and the respective dosing schedules in the POLLUX and CASTOR pivotal studies."( Pharmacokinetics and Exposure-Response Analyses of Daratumumab in Combination Therapy Regimens for Patients with Multiple Myeloma.
Belch, A; Capra, M; Clemens, PL; Dimopoulos, MA; Gomez, D; Ho, PJ; Iida, S; Jansson, R; Leiba, M; Medvedova, E; Min, CK; Schecter, J; Sonneveld, P; Sun, YN; Xu, XS; Zhang, L, 2018
)
0.48
" Among 185 randomly assigned intent-to-treat patients at week 12, a dose-response relationship was observed; APR40 (n = 63), but not APR30 (n = 58), led to statistically significant improvements (vs."( A Phase 2 Randomized Trial of Apremilast in Patients with Atopic Dermatitis.
Chen, M; Estrada, YD; Guttman-Yassky, E; Imafuku, S; Malik, K; Nograles, K; Pavel, AB; Peng, X; Poulin, Y; Shah, N; Simpson, EL; Suarez-Farinas, M; Ungar, B; Wen, HC; Xu, H; Zhou, L, 2019
)
0.51
" Dose titration is recommended during APM treatment due to its tolerability and twice-daily dosing regimen issues."( Preparation of sustained release apremilast-loaded PLGA nanoparticles: in vitro characterization and in vivo pharmacokinetic study in rats.
Alalaiwe, A; Anwer, MK; Ezzeldin, E; Fatima, F; Iqbal, M; Mohammad, M, 2019
)
0.51
" In most cases, they were mild or moderate in severity and tended to resolve over time with continued dosing and without intervention."( [Gastrointestinal side effects of apremilast : Characterization and management].
Beigel, F; Beissert, S; Gerdes, S; Homey, B; Körber, A; Mössner, R; Pinter, A; Radtke, MA; Staubach-Renz, P, 2019
)
0.51
" Pharmacokinetics modeling and noncompartmental analyses showed that weight-based dosing with apremilast 20 mg twice daily in children or apremilast 20 or 30 mg twice daily in adolescents provides exposure (area under the concentration-time curve from time 0 to 12 hours after the dose) that is comparable to that achieved with apremilast 30 mg twice daily in adults."( Pharmacokinetics and safety of apremilast in pediatric patients with moderate to severe plaque psoriasis: Results from a phase 2 open-label study.
Barcellona, C; Becker, EM; de Lucas, R; Fiorillo, L; Hong, Y; Maes, P; Paller, AS; Paris, M; Zhang, W; Zhang, Z, 2020
)
0.56
"This first-time-in-children phase 2 study supports weight-based apremilast dosing for future phase 3 studies of pediatric plaque psoriasis."( Pharmacokinetics and safety of apremilast in pediatric patients with moderate to severe plaque psoriasis: Results from a phase 2 open-label study.
Barcellona, C; Becker, EM; de Lucas, R; Fiorillo, L; Hong, Y; Maes, P; Paller, AS; Paris, M; Zhang, W; Zhang, Z, 2020
)
0.56
" Patients (N = 569) with ≥1 prior line received Rd (lenalidomide, 25 mg, on Days 1-21 of each 28-day cycle; dexamethasone, 40 mg, weekly) ± daratumumab at the approved dosing schedule."( Daratumumab plus lenalidomide and dexamethasone in relapsed/refractory multiple myeloma: extended follow-up of POLLUX, a randomized, open-label, phase 3 study.
Bahlis, NJ; Benboubker, L; Chiu, C; Cook, G; Dimopoulos, MA; Ho, PJ; Kaufman, JL; Kim, K; Krevvata, M; Leiba, M; Moreau, P; Okonkwo, L; Qi, M; Qin, X; San-Miguel, J; Takezako, N; Trivedi, S; Ukropec, J; White, DJ, 2020
)
0.56
"Of the American and European guidelines available for use of apremilast, several organizations are in agreement regarding the dosage of apremilast, but there are significant disagreements concerning matters such as medication indication, pretreatment laboratory testing, and contraindications to therapy."( Comparison of psoriasis guidelines for use of apremilast in the United States and Europe: a critical appraisal and comprehensive review.
Ghamrawi, RI; Ghiam, N; Wu, JJ, 2022
)
0.72
" We evaluated the pharmacokinetics (PK) and safety of lenalidomide and dexamethasone as frontline pre-transplant induction, with doses adjusted at start of each cycle based on creatinine clearance, as per the official dosing guidelines."( An open-label, pharmacokinetic study of lenalidomide and dexamethasone therapy in previously untreated multiple myeloma (MM) patients with various degrees of renal impairment - validation of official dosing guidelines.
Cao, Y; Chen, CI; Chen, E; Chen, H; Kakar, S; Kukreti, V; Lau, A; Le, LW; Levina, O; Paul, H; Prica, A; Reece, DE; Tiedemann, R; Trudel, S, 2020
)
0.56
" The most appropriate delivery and dosing regimens of these therapies for patients at advanced age and frailty status is also unclear."( Optimising the value of immunomodulatory drugs during induction and maintenance in transplant ineligible patients with newly diagnosed multiple myeloma: results from Myeloma XI, a multicentre, open-label, randomised, Phase III trial.
Cairns, DA; Collett, C; Cook, G; Davies, FE; Drayson, MT; Garg, M; Gregory, WM; Jackson, GH; Jenner, MW; Jones, JR; Kaiser, MF; Karunanithi, K; Kishore, B; Lindsay, J; Morgan, GJ; Owen, RG; Pawlyn, C; Russell, NH; Striha, A; Taylor, C; Waterhouse, A; Williams, CD; Wilson, J, 2021
)
0.62
" Previous studies explored addition of weekly cyclophosphamide, but we hypothesized that daily dosing allows for better synergy."( A phase II study of pomalidomide, daily oral cyclophosphamide, and dexamethasone in relapsed/refractory multiple myeloma.
Chan, E; Chari, A; Cho, HJ; Couto, S; Florendo, E; Ip, C; Jagannath, S; Kim-Schulze, S; La, L; Laganà, A; Lau, K; Leshchenko, VV; Madduri, D; Mancia, IS; Melnekoff, DT; Parekh, S; Pierceall, WE; Richter, J; Strumolo, G; Thakurta, A; Thomas, J; Van Oekelen, O; Verina, D; Vishnuvardhan, N; Wang, M; Zarychta, K, 2020
)
0.56
" Here, we investigated the safety and effectiveness of ixazomib dosing schedules."( Safety and Effectiveness of Ixazomib Dose-escalating Strategy in Ixazomib-Lenalidomide-Dexamethasone Treatment for Relapsed/Refractory Multiple Myeloma.
Boku, S; Higai, K; Kagoo, T; Niijima, D; Ogawa, C; Ohashi, Y; Tani, K; Ueno, H; Yachi, Y; Yano, T; Yatabe, M; Yokoyama, A,
)
0.13
"A dose-escalation strategy to optimise ixazomib dosing may reduce treatment interruption due to adverse events without compromising its antitumor activity."( Safety and Effectiveness of Ixazomib Dose-escalating Strategy in Ixazomib-Lenalidomide-Dexamethasone Treatment for Relapsed/Refractory Multiple Myeloma.
Boku, S; Higai, K; Kagoo, T; Niijima, D; Ogawa, C; Ohashi, Y; Tani, K; Ueno, H; Yachi, Y; Yano, T; Yatabe, M; Yokoyama, A,
)
0.13
"This is the first study to characterize PK of pomalidomide in pediatric patients, which supports BSA-based dosing for pediatric patients."( Recurrent or progressive pediatric brain tumors: population pharmacokinetics and exposure-response analysis of pomalidomide.
Benettaib, B; Kassir, N; Li, Y; Ogasawara, K; Palmisano, M; Wang, X; Zhou, S, 2021
)
0.62
"This is the first study to characterize PK of pomalidomide in pediatric patients, which supports BSA-based dosing for pediatric patients."( Recurrent or progressive pediatric brain tumors: population pharmacokinetics and exposure-response analysis of pomalidomide.
Benettaib, B; Kassir, N; Li, Y; Ogasawara, K; Palmisano, M; Wang, X; Zhou, S, 2021
)
0.62
" The drug’s simple dosing schedule with mild side effect profile makes it a practical option for patients as combination therapy."( Review of Apremilast Combination Therapies in the Treatment of Moderate to Severe Psoriasis.
Ivanic, MG; Liao, W; Thatiparthi, A; Walia, S; Wu, JJ, 2021
)
0.62
" Observational studies at our institution found low dosage adjunctive thalidomide safe in treating tuberculous mass lesions and blindness related to optochiasmatic arachnoiditis, with good clinical and radiological response."( The use of thalidomide to treat children with tuberculosis meningitis: A review.
Marceline van Furth, A; Schoeman, JF; Seddon, JA; Solomons, RS; van der Kuip, M; van Toorn, R; Zaharie, SD, 2021
)
1.25
" Preliminary safety data, particularly the occurrence of cytopenias, can be used to guide dosing strategies for future combinations of venetoclax with immunomodulatory agents."( A Phase II Study of Venetoclax in Combination With Pomalidomide and Dexamethasone in Relapsed/Refractory Multiple Myeloma.
Abdallah, AO; Arriola, E; Bowles, KM; Bueno, OF; Coppola, S; Gasparetto, C; Mander, G; Mateos, MV; Morris, L; Ross, JA; Wang, J, 2021
)
0.62
" We aimed to characterize the relationship between serum M-protein kinetics and PFS in the phase 3 ICARIA-MM trial (NCT02990338), and to evaluate an alternative dosing regimen of Isa by simulation."( Joint modelling and simulation of M-protein dynamics and progression-free survival for alternative isatuximab dosing with pomalidomide/dexamethasone.
Ayral, G; Cerou, M; Fau, JB; Gaudel, N; Sebastien, B; Semiond, D; Thai, HT; van de Velde, H; Veyrat-Follet, C, 2022
)
0.72
" Trial simulations were then performed to evaluate whether efficacy is maintained after switching to a monthly dosing regimen."( Joint modelling and simulation of M-protein dynamics and progression-free survival for alternative isatuximab dosing with pomalidomide/dexamethasone.
Ayral, G; Cerou, M; Fau, JB; Gaudel, N; Sebastien, B; Semiond, D; Thai, HT; van de Velde, H; Veyrat-Follet, C, 2022
)
0.72
" Developed models supported the phase III isatuximab dosing regimen selection/confirmation of 10 mg/kg qw/q2w for use in combination with pomalidomide/dexamethasone in patients with RRMM."( Exposure-response analyses for selection/confirmation of optimal isatuximab dosing regimen in combination with pomalidomide/dexamethasone treatment in patients with multiple myeloma.
Brillac, C; Fau, JB; Gaudel-Dedieu, N; Koiwai, K; Nguyen, L; Rachedi, F; Sebastien, B; Semiond, D; Thai, HT; van de Velde, H; Veyrat-Follet, C, 2022
)
0.72
" Twice-weekly maintenance application of topical Cal/BD aerosolized foam has recently been shown to prolong time to remission and is associated with fewer relapses in patients initially treated with standard dosing of the formulation."( The Maintenance Effect of Calcipotriene 0.05% and Betamethasone Dipropionate 0.064% (Cal/BD) Aerosol Foam in Combination With Apremilast.
Kircik, L; Ozyurekoglu, E, 2022
)
0.72
" Upon repeated dosing of Thali@PDA for one week, symptoms of IBD in mice were significantly relieved, and histomorphology of the colitis colons were normalized."( Polydopamine-coated thalidomide nanocrystals promote DSS-induced murine colitis recovery through Macrophage M2 polarization together with the synergistic anti-inflammatory and anti-angiogenic effects.
Bai, Y; Fang, X; Fu, B; Huang, H; Li, X; Ma, C; Meng, Z; Miao, W; Ren, H; Shen, S; Tao, X; Wang, Y; Xu, H; Xu, Y; Yang, J; Yang, Z; Yong, J, 2023
)
1.23
"The largest cohort of monogenic AIDs with the treatment of thalidomide demonstrated that thalidomide can help reduce disease activity and inflammation, reduce the dosage of glucocorticoids, and improve clinical outcomes."( Efficacy and safety of thalidomide in children with monogenic autoinflammatory diseases: a single-center, real-world-evidence study.
Gao, S; Gou, L; Li, J; Ma, M; Song, H; Wang, C; Wang, L; Wang, W; Yu, Z; Zhang, C; Zhong, L; Zhou, Y, 2023
)
1.46
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (2)

ClassDescription
piperidones
phthalimidesA dicarboximide that is phthalimide or derivatives obtained from it by the formal replacement of one or more hydrogens.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (28)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASEHomo sapiens (human)Potency125.89200.003245.467312,589.2998AID2517
RAR-related orphan receptor gammaMus musculus (house mouse)Potency5.95570.006038.004119,952.5996AID1159521
TDP1 proteinHomo sapiens (human)Potency29.09290.000811.382244.6684AID686978
GLI family zinc finger 3Homo sapiens (human)Potency16.78550.000714.592883.7951AID1259369
AR proteinHomo sapiens (human)Potency58.57370.000221.22318,912.5098AID1259243; AID743042
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency39.81070.011212.4002100.0000AID1030
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency0.00100.01237.983543.2770AID1645841
EWS/FLI fusion proteinHomo sapiens (human)Potency0.00370.001310.157742.8575AID1259256
retinoid X nuclear receptor alphaHomo sapiens (human)Potency17.06530.000817.505159.3239AID1159527; AID1159531
farnesoid X nuclear receptorHomo sapiens (human)Potency18.83220.375827.485161.6524AID743220
estrogen nuclear receptor alphaHomo sapiens (human)Potency33.36030.000229.305416,493.5996AID743078
cytochrome P450 2D6Homo sapiens (human)Potency15.48710.00108.379861.1304AID1645840
arylsulfatase AHomo sapiens (human)Potency0.03011.069113.955137.9330AID720538
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency33.58750.035520.977089.1251AID504332
Bloom syndrome protein isoform 1Homo sapiens (human)Potency0.00030.540617.639296.1227AID2364; AID2528
thyroid hormone receptor beta isoform aHomo sapiens (human)Potency0.00110.010039.53711,122.0200AID588545
gemininHomo sapiens (human)Potency0.56230.004611.374133.4983AID624297
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Cereblon isoform 4Magnetospirillum gryphiswaldenseIC50 (µMol)9.25003.53006.31007.8000AID1277063; AID1277066
Cereblon isoform 4Magnetospirillum gryphiswaldenseKi6.13330.64203.94289.6000AID1277067; AID1277070; AID1569040
Bile salt export pumpHomo sapiens (human)IC50 (µMol)1,000.00000.11007.190310.0000AID1449628
Prostaglandin G/H synthase 1Ovis aries (sheep)IC50 (µMol)0.37000.00032.177410.0000AID162144
cAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)IC50 (µMol)500.00000.00001.068010.0000AID158462
Prostaglandin G/H synthase 2Ovis aries (sheep)IC50 (µMol)0.50000.00101.453910.0000AID160735
cAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)IC50 (µMol)500.00000.00001.104010.0000AID158462
cAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)IC50 (µMol)500.00000.00001.465110.0000AID158462
cAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)IC50 (µMol)500.00000.00001.146310.0000AID158462
DNA damage-binding protein 1Homo sapiens (human)IC50 (µMol)15.69000.28601.72773.0000AID1794852; AID1814571
Protein cereblonHomo sapiens (human)IC50 (µMol)21.04500.28601.70663.0000AID1277064; AID1685004; AID1794852; AID1814571
Protein cereblonHomo sapiens (human)Ki15.60501.49006.580010.0000AID1277068; AID1685004
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
DNA damage-binding protein 1Homo sapiens (human)EC50 (µMol)0.03600.00900.02250.0360AID1893698
Protein cereblonHomo sapiens (human)EC50 (µMol)0.03600.00900.03650.0870AID1893698
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
DNA-binding protein IkarosHomo sapiens (human)DC5010.00000.02670.10310.1927AID1769486
Protein cereblonHomo sapiens (human)DC5010.00000.00800.48352.1000AID1769486
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (88)

Processvia Protein(s)Taxonomy
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
cAMP catabolic processcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
signal transductioncAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
G protein-coupled receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
sensory perception of smellcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
regulation of protein kinase A signalingcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
cellular response to xenobiotic stimuluscAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
cAMP-mediated signalingcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
neutrophil homeostasiscAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cAMP catabolic processcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
neutrophil chemotaxiscAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
positive regulation of type II interferon productioncAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
positive regulation of interleukin-2 productioncAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
T cell receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
leukocyte migrationcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cellular response to lipopolysaccharidecAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cellular response to xenobiotic stimuluscAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cellular response to epinephrine stimuluscAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
negative regulation of adenylate cyclase-activating adrenergic receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
regulation of cardiac muscle cell contractioncAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
negative regulation of relaxation of cardiac musclecAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
regulation of calcium ion transmembrane transport via high voltage-gated calcium channelcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cAMP-mediated signalingcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cAMP catabolic processcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
cAMP-mediated signalingcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
regulation of heart ratecAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
cAMP catabolic processcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
positive regulation of heart ratecAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
regulation of release of sequestered calcium ion into cytosol by sarcoplasmic reticulumcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
positive regulation of type II interferon productioncAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
positive regulation of interleukin-2 productioncAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
positive regulation of interleukin-5 productioncAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
negative regulation of peptidyl-serine phosphorylationcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
negative regulation of heart contractioncAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
T cell receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
establishment of endothelial barriercAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
adrenergic receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
regulation of cardiac muscle cell contractioncAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
negative regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathwaycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
regulation of cell communication by electrical coupling involved in cardiac conductioncAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
negative regulation of relaxation of cardiac musclecAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
regulation of calcium ion transmembrane transport via high voltage-gated calcium channelcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
cAMP-mediated signalingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
chromatin organizationDNA-binding protein IkarosHomo sapiens (human)
mesoderm developmentDNA-binding protein IkarosHomo sapiens (human)
lymphocyte differentiationDNA-binding protein IkarosHomo sapiens (human)
erythrocyte differentiationDNA-binding protein IkarosHomo sapiens (human)
negative regulation of DNA-templated transcriptionDNA-binding protein IkarosHomo sapiens (human)
regulation of transcription by RNA polymerase IIDNA-binding protein IkarosHomo sapiens (human)
proteasomal protein catabolic processDNA damage-binding protein 1Homo sapiens (human)
nucleotide-excision repairDNA damage-binding protein 1Homo sapiens (human)
ubiquitin-dependent protein catabolic processDNA damage-binding protein 1Homo sapiens (human)
apoptotic processDNA damage-binding protein 1Homo sapiens (human)
DNA damage responseDNA damage-binding protein 1Homo sapiens (human)
spindle assembly involved in female meiosisDNA damage-binding protein 1Homo sapiens (human)
Wnt signaling pathwayDNA damage-binding protein 1Homo sapiens (human)
protein ubiquitinationDNA damage-binding protein 1Homo sapiens (human)
viral release from host cellDNA damage-binding protein 1Homo sapiens (human)
cellular response to UVDNA damage-binding protein 1Homo sapiens (human)
ectopic germ cell programmed cell deathDNA damage-binding protein 1Homo sapiens (human)
regulation of circadian rhythmDNA damage-binding protein 1Homo sapiens (human)
negative regulation of apoptotic processDNA damage-binding protein 1Homo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic processDNA damage-binding protein 1Homo sapiens (human)
epigenetic programming in the zygotic pronucleiDNA damage-binding protein 1Homo sapiens (human)
positive regulation of viral genome replicationDNA damage-binding protein 1Homo sapiens (human)
positive regulation of gluconeogenesisDNA damage-binding protein 1Homo sapiens (human)
positive regulation of protein catabolic processDNA damage-binding protein 1Homo sapiens (human)
positive regulation by virus of viral protein levels in host cellDNA damage-binding protein 1Homo sapiens (human)
rhythmic processDNA damage-binding protein 1Homo sapiens (human)
negative regulation of developmental processDNA damage-binding protein 1Homo sapiens (human)
biological process involved in interaction with symbiontDNA damage-binding protein 1Homo sapiens (human)
UV-damage excision repairDNA damage-binding protein 1Homo sapiens (human)
regulation of mitotic cell cycle phase transitionDNA damage-binding protein 1Homo sapiens (human)
negative regulation of reproductive processDNA damage-binding protein 1Homo sapiens (human)
DNA repairDNA damage-binding protein 1Homo sapiens (human)
protein ubiquitinationProtein cereblonHomo sapiens (human)
positive regulation of Wnt signaling pathwayProtein cereblonHomo sapiens (human)
negative regulation of protein-containing complex assemblyProtein cereblonHomo sapiens (human)
positive regulation of protein-containing complex assemblyProtein cereblonHomo sapiens (human)
negative regulation of monoatomic ion transmembrane transportProtein cereblonHomo sapiens (human)
locomotory exploration behaviorProtein cereblonHomo sapiens (human)
proteasome-mediated ubiquitin-dependent protein catabolic processProtein cereblonHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (32)

Processvia Protein(s)Taxonomy
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
protein bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
cAMP bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
metal ion bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
calcium channel regulator activitycAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
protein bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cAMP bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
gamma-tubulin bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
transmembrane transporter bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
metal ion bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
metal ion bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
3',5'-cyclic-nucleotide phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
calcium channel regulator activitycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
protein bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
enzyme bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
signaling receptor regulator activitycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
cAMP bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
beta-2 adrenergic receptor bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
transmembrane transporter bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
metal ion bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
ATPase bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
scaffold protein bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
heterocyclic compound bindingcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
DNA bindingDNA-binding protein IkarosHomo sapiens (human)
protein bindingDNA-binding protein IkarosHomo sapiens (human)
protein domain specific bindingDNA-binding protein IkarosHomo sapiens (human)
metal ion bindingDNA-binding protein IkarosHomo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingDNA-binding protein IkarosHomo sapiens (human)
DNA-binding transcription factor activityDNA-binding protein IkarosHomo sapiens (human)
damaged DNA bindingDNA damage-binding protein 1Homo sapiens (human)
DNA bindingDNA damage-binding protein 1Homo sapiens (human)
protein bindingDNA damage-binding protein 1Homo sapiens (human)
protein-macromolecule adaptor activityDNA damage-binding protein 1Homo sapiens (human)
protein-containing complex bindingDNA damage-binding protein 1Homo sapiens (human)
WD40-repeat domain bindingDNA damage-binding protein 1Homo sapiens (human)
cullin family protein bindingDNA damage-binding protein 1Homo sapiens (human)
ubiquitin ligase complex scaffold activityDNA damage-binding protein 1Homo sapiens (human)
protein bindingProtein cereblonHomo sapiens (human)
transmembrane transporter bindingProtein cereblonHomo sapiens (human)
metal ion bindingProtein cereblonHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (37)

Processvia Protein(s)Taxonomy
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
nucleoplasmcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
plasma membranecAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
membranecAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
ruffle membranecAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
perinuclear region of cytoplasmcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
perinuclear region of cytoplasmcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
nucleuscAMP-specific 3',5'-cyclic phosphodiesterase 4AHomo sapiens (human)
centrosomecAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
synaptic vesiclecAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
postsynaptic densitycAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
Z disccAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
dendritic spinecAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
excitatory synapsecAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
gamma-tubulin complexcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
voltage-gated calcium channel complexcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
nucleuscAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
perinuclear region of cytoplasmcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4BHomo sapiens (human)
extracellular spacecAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
ciliumcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
nucleuscAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
perinuclear region of cytoplasmcAMP-specific 3',5'-cyclic phosphodiesterase 4CHomo sapiens (human)
centrosomecAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
plasma membranecAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
apical plasma membranecAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
voltage-gated calcium channel complexcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
calcium channel complexcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
cytosolcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
nucleuscAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
perinuclear region of cytoplasmcAMP-specific 3',5'-cyclic phosphodiesterase 4DHomo sapiens (human)
nucleusDNA-binding protein IkarosHomo sapiens (human)
nucleoplasmDNA-binding protein IkarosHomo sapiens (human)
cytosolDNA-binding protein IkarosHomo sapiens (human)
pericentric heterochromatinDNA-binding protein IkarosHomo sapiens (human)
protein-containing complexDNA-binding protein IkarosHomo sapiens (human)
nucleusDNA damage-binding protein 1Homo sapiens (human)
nucleolusDNA damage-binding protein 1Homo sapiens (human)
chromosome, telomeric regionDNA damage-binding protein 1Homo sapiens (human)
extracellular spaceDNA damage-binding protein 1Homo sapiens (human)
nucleusDNA damage-binding protein 1Homo sapiens (human)
nucleoplasmDNA damage-binding protein 1Homo sapiens (human)
cytoplasmDNA damage-binding protein 1Homo sapiens (human)
Cul4A-RING E3 ubiquitin ligase complexDNA damage-binding protein 1Homo sapiens (human)
extracellular exosomeDNA damage-binding protein 1Homo sapiens (human)
Cul4B-RING E3 ubiquitin ligase complexDNA damage-binding protein 1Homo sapiens (human)
protein-containing complexDNA damage-binding protein 1Homo sapiens (human)
Cul4-RING E3 ubiquitin ligase complexDNA damage-binding protein 1Homo sapiens (human)
site of double-strand breakDNA damage-binding protein 1Homo sapiens (human)
nucleusProtein cereblonHomo sapiens (human)
cytoplasmProtein cereblonHomo sapiens (human)
cytosolProtein cereblonHomo sapiens (human)
membraneProtein cereblonHomo sapiens (human)
perinuclear region of cytoplasmProtein cereblonHomo sapiens (human)
Cul4A-RING E3 ubiquitin ligase complexProtein cereblonHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (269)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1745854NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1745855NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID1893698Displacement of BODIPY FL thalidomide from 6His-tagged CRBN/DDB1 (unknown origin) expressed in baculovirus infected Sf9 insect cells incubated for 1 min under shaking condition followed by 60 mins incubation under dark condition by TR-FRET assay2022ACS medicinal chemistry letters, Aug-11, Volume: 13, Issue:8
SJPYT-195: A Designed Nuclear Receptor Degrader That Functions as a Molecular Glue Degrader of GSPT1.
AID492314Antiinflammatory activity against zymosan A-induced peritonitis in Swiss mouse assessed as inhibition of granulocyte infiltration in to peritoneal cavity at 100 mg/kg, po administered 40 mins before zymosan A challenge measured after 6 hrs relative to con2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID387205Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production pretreated for 3 hrs before LPS challenge assessed after 24 hrs by griess assay2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID1653420Antiinflammatory activity in human monocytes assessed as inhibition of LPS-induced TNFaplha production at 50 uM preincubated for 15 mins followed by LPS addition and measured after 4 hrs by ELISA relative to control2019Bioorganic & medicinal chemistry, 07-01, Volume: 27, Issue:13
Insights of synthetic analogues of anti-leprosy agents.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1179423Antiinflammatory activity against mouse L929 cells assessed as inhibition of LPS-induced TNFalpha production at 15.625 uM after 48 hrs2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Synthesis and evaluation of novel dapsone-thalidomide hybrids for the treatment of type 2 leprosy reactions.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID215086Inhibition of TNF-alpha production from human monocytes upon stimulation with bacterial lipopolysaccharide (LPS) at a concentration of 10 uM1996Journal of medicinal chemistry, Aug-02, Volume: 39, Issue:16
Potent inhibition of tumor necrosis factor-alpha production by tetrafluorothalidomide and tetrafluorophthalimides.
AID492316Antiedematogenic activity in Swiss mouse assessed as inhibition of capsaicin-induced paw edema at 100 umol/kg, po administered 40 mins before capsaicin challenge measured after 30 mins relative to control2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID492315Antiedematogenic activity in Swiss mouse assessed as decrease of capsaicin-induced paw edema weight at 100 umol/kg, po administered 40 mins before capsaicin challenge measured after 30 mins relative to control2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID1769484Drug accumulation in human MOLT-4 cells assessed as intracellular drug accumulation incubated for 4 hrs by LC-MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID387989Toxicity in Swiss albino mouse bearing mouse Ehrlich ascites carcinoma cells assessed as focal necrosis of hepatocytes treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by histopathological analysis2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID309667Inhibition of IL-1-alpha-induced NF-kappaB activation in HeLa cells assessed as blocking of p50/p65 nuclear translocation2007Bioorganic & medicinal chemistry letters, Nov-01, Volume: 17, Issue:21
Inhibitors of NF-kappaB derived from thalidomide.
AID162169Selective index (SI) which is the ratio of IC50 of Prostaglandin G/H synthase 1 / IC50 of Prostaglandin G/H synthase 1 was reported2002Bioorganic & medicinal chemistry letters, Apr-08, Volume: 12, Issue:7
Thalidomide and its analogues as cyclooxygenase inhibitors.
AID1191951Inhibition of BRD4 bromodomain-1 (unknown origin) at 100 uM by europium based LANCE TR-FRET assay2015Bioorganic & medicinal chemistry, Mar-01, Volume: 23, Issue:5
Discovery and structure-activity relationship studies of N6-benzoyladenine derivatives as novel BRD4 inhibitors.
AID1769482Stability in human plasma assessed as half life at 1 uM by LC-MS/MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID301707Inhibition of TNF gene expression in FRT Jurkat TNF reporter cells at 100 uM2007Bioorganic & medicinal chemistry letters, Nov-01, Volume: 17, Issue:21
Synthesis and TNF expression inhibitory properties of new thalidomide analogues derived via Heck cross coupling.
AID387979Cytotoxicity against mouse Ehrlich ascites carcinoma cells assessed as viable cells at 30 uL after 24 hrs by trypan blue exclusion assay2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID387977Cytotoxicity against mouse Ehrlich ascites carcinoma cells assessed as viable cells at 10 uL after 24 hrs by trypan blue exclusion assay2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID215088Inhibition of TNF-alpha production from human monocytes upon stimulation with bacterial lipopolysaccharide (LPS) at a concentration of 200 uM1996Journal of medicinal chemistry, Aug-02, Volume: 39, Issue:16
Potent inhibition of tumor necrosis factor-alpha production by tetrafluorothalidomide and tetrafluorophthalimides.
AID492319Antiinflammatory effect in complete Freund's adjuvant-induced Wistar rat arthritis model assessed as inhibition of paw edema at 100 umol/kg, po daily once administered on day 14 post adjuvant challenge measured on day 21 post adjuvant challenge2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID387976Induction of apoptosis in mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as increase in Fas-L expression treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by immunohistochemical analysis2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID726391Inhibition of IL-2 production in human T cells measured after 2 to 3 days by ELISA2013Bioorganic & medicinal chemistry letters, Jan-01, Volume: 23, Issue:1
Isosteric analogs of lenalidomide and pomalidomide: synthesis and biological activity.
AID540211Fraction unbound in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID492317Antiinflammatory effect in complete Freund's adjuvant-induced Wistar rat arthritis model assessed as inhibition of paw edema at 100 umol/kg, po daily once administered on day 14 post adjuvant challenge measured on day 16 post adjuvant challenge2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID387207Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced TNFalpha synthesis at 10 uM pretreated for 3 hrs before LPS challenge assessed after 24 hrs by ELISA relative to control2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID1317702Anticancer activity against BMOL-T cells assessed as cell growth inhibition up to 100 uM2016European journal of medicinal chemistry, Sep-14, Volume: 120Identification of a thalidomide derivative that selectively targets tumorigenic liver progenitor cells and comparing its effects with lenalidomide and sorafenib.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1179420Antinociceptive effect in mouse assessed as inhibition of acetic acid-induced abdominal constriction at 100 uM/kg, po2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Synthesis and evaluation of novel dapsone-thalidomide hybrids for the treatment of type 2 leprosy reactions.
AID218271The cytotoxicity assessed using human embryonic lung fibroblast WI-38 cells. 1997Journal of medicinal chemistry, Aug-29, Volume: 40, Issue:18
Novel biological response modifiers: phthalimides with tumor necrosis factor-alpha production-regulating activity.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID649077Cytotoxicity against mouse J744 cells after 48 hrs by MTT assay2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID423810Cytotoxicity against human MCF7 cells assessed as cell viability at 100 ug/ml after 72 hrs by MTT assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID1769477Distribution coefficient, logD of compound at 1 mg/ml measured at pH 7.4 by chromatography based LC-UV analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID625967Antiproliferative activity against human HUVEC assessed as tube formation at 195 uM after 24 hrs2011Bioorganic & medicinal chemistry letters, Nov-01, Volume: 21, Issue:21
Stable and orally bio-available pro-drugs of CPS11.
AID387980Antitumor activity against mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days relative to control2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID371658Antiproliferative activity against human EAhy926 cells2009Bioorganic & medicinal chemistry letters, Feb-01, Volume: 19, Issue:3
Preliminary biological evaluations of new thalidomide analogues for multiple sclerosis application.
AID301710Inhibition of TNF gene expression in FRT-Jurkat TNF reporter cells at 1 uM2007Bioorganic & medicinal chemistry letters, Nov-01, Volume: 17, Issue:21
Synthesis and TNF expression inhibitory properties of new thalidomide analogues derived via Heck cross coupling.
AID423811Cytotoxicity against human IM9 cells assessed as cell viability at 100 ug/ml after 72 hrs by MTT assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID521220Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay2007Nature chemical biology, May, Volume: 3, Issue:5
Chemical genetics reveals a complex functional ground state of neural stem cells.
AID1569040Inhibition of MANT-uracil binding to wild-type Magnetospirillum gryphiswaldense CRBN isoform 4 by FRET assay2019Journal of medicinal chemistry, 07-25, Volume: 62, Issue:14
De-Novo Design of Cereblon (CRBN) Effectors Guided by Natural Hydrolysis Products of Thalidomide Derivatives.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID649073Inhibition of NF-kappaB activation expressed in human HT-29 cells assessed as inhibition of TNFalpha-stimulated IL8 release at 400 uM after 24 hrs by flow cytometric analysis relative to control2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID387992Antiproliferative activity against mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as inhibition of Ki67 protein expression treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by immunohistochemical ana2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID471903Cytotoxicity against human ST486 cells by MTT assay2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID257636Inhibitory activity in HUVEC tube formation assay at 100 uM2005Bioorganic & medicinal chemistry letters, Dec-15, Volume: 15, Issue:24
Angiogenesis inhibitors derived from thalidomide.
AID387982Increase in catalase activity per milligram of tissue in mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID1277063Inhibition of MANT-uracil binding to wild type Magnetospirillum gryphiswaldense cereblon isoform 4 by FRET assay2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID1277069Inhibition of MANT-uracil binding to Caenorhabditis elegans CRBN (delta 1 to 15) by Cheng-Prusoff equation analysis2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID340116Antagonist activity at progesterone receptor in human T47D cells assessed as inhibition of progesterone-induced alkaline phosphatase activity at 100 uM2008Bioorganic & medicinal chemistry, Jul-15, Volume: 16, Issue:14
Progesterone receptor antagonists with a 3-phenylquinazoline-2,4-dione/2-phenylisoquinoline-1,3-dione skeleton.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID209214Inhibition of LPS-induced Tumor necrosis factor-alpha production (TNF-alpha) in THP-1 cells1998Bioorganic & medicinal chemistry letters, May-05, Volume: 8, Issue:9
Enhanced potency of perfluorinated thalidomide derivatives for inhibition of LPS-induced tumor necrosis factor-alpha production is associated with a change of mechanism of action.
AID251661Inhibitory activity against tubulin polymerization at 20 uM2005Bioorganic & medicinal chemistry letters, Jan-17, Volume: 15, Issue:2
Tubulin-polymerization inhibitors derived from thalidomide.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID649074Inhibition of NF-kappaB activation expressed in human HT-29 cells assessed as inhibition of TNFalpha-stimulated IL8 release at 200 uM after 24 hrs by flow cytometric analysis relative to control2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID1759151Antiproliferative activity against mouse BMOL-NT cells assessed as cell growth by measuring doubling time at 10 uM measured every 4 hrs for 3 days by IncuCyte zoom live cell analysis (Rvb = 18 to 19 hrs)2021European journal of medicinal chemistry, May-05, Volume: 217In pursuit of a selective hepatocellular carcinoma therapeutic agent: Novel thalidomide derivatives with antiproliferative, antimigratory and STAT3 inhibitory properties.
AID540212Mean residence time in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1816480PROTAC activity at CRBN E3 ligase/EZH2 in PRC2 complex in human WSUDLCL2 cells assessed as reduction in EED level at 10 uM measured after 48 hrs by Western blot analysis
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID423812Cytotoxicity against human HS-Sultan cells assessed as cell viability at 100 ug/ml after 72 hrs by MTT assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID459408Cytotoxicity against human Jurkat T cells assessed as cell death at 100 uM after 24 hrs by flow cytometry2010Bioorganic & medicinal chemistry, Jan-15, Volume: 18, Issue:2
New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.
AID459409Cytotoxicity against human Jurkat T cells assessed as cell death at 10 uM after 24 hrs by flow cytometry2010Bioorganic & medicinal chemistry, Jan-15, Volume: 18, Issue:2
New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.
AID1759152Antiproliferative activity against mouse BMOL-T cells assessed as cell growth by measuring doubling time at 10 uM measured every 4 hrs for 3 days by IncuCyte zoom live cell analysis (Rvb = 14.3 to 15 hrs)2021European journal of medicinal chemistry, May-05, Volume: 217In pursuit of a selective hepatocellular carcinoma therapeutic agent: Novel thalidomide derivatives with antiproliferative, antimigratory and STAT3 inhibitory properties.
AID387978Cytotoxicity against mouse Ehrlich ascites carcinoma cells assessed as viable cells at 20 uL after 24 hrs by trypan blue exclusion assay2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID625966Antiproliferative activity against human ECV304 cells assessed as growth inhibition after 72 hrs by MTT assay2011Bioorganic & medicinal chemistry letters, Nov-01, Volume: 21, Issue:21
Stable and orally bio-available pro-drugs of CPS11.
AID1277066Inhibition of MANT-uracil binding to Magnetospirillum gryphiswaldense cereblon isoform 4 Y101F mutant by FRET assay2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID1769486Protac activity at CRBN/HiBiT-tagged IKZF1 in human MOLT-4 cells assessed as IKZF1 degradation by measuring luminescence by luminescence based HiBiT assay2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID492302Antinociceptive activity in Swiss mouse assessed as inhibition of acetic acid-induced abdominal constrictions at 100 umol/kg, po administered 40 mins before acetic acid challenge measured for 25 mins relative to control2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID81275Tumor necrosis factor-alpha production in human leukemia cell line (HL-60) stimulated with 10 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) at 30 uMolar.1997Journal of medicinal chemistry, Aug-29, Volume: 40, Issue:18
Novel biological response modifiers: phthalimides with tumor necrosis factor-alpha production-regulating activity.
AID471905Cytotoxicity against HUVEC by MTT assay2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID648933Inhibition of TNFalpha-induced NF-kappaB activation expressed in human HT-29 cells coexpressing hrGFP at 100 uM after 24 hrs by propidium iodide staining-based flow cytometric analysis relative to control2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID423806Antiangiogenic activity against VEGF-induced HUVEC assessed as tube length at 100 uM after 11 days after 11 days by BCIP/NBT visualization assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID1769479Efflux ratio of apparent permeability of compound across basolateral to apical side over apical to basolateral side in human Caco-2 cells at 10 uM incubated for 90 mins by LC-MS/MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID1653421Antiinflammatory activity in human monocytes assessed as inhibition of LPS-induced TNFaplha production at 25 uM preincubated for 15 mins followed by LPS addition and measured after 4 hrs by ELISA relative to control2019Bioorganic & medicinal chemistry, 07-01, Volume: 27, Issue:13
Insights of synthetic analogues of anti-leprosy agents.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID726392Antiproliferative activity against human NAMALWA cells assessed as inhibition of [3H]thymidine incorporation after 72 hrs by scintillation counting2013Bioorganic & medicinal chemistry letters, Jan-01, Volume: 23, Issue:1
Isosteric analogs of lenalidomide and pomalidomide: synthesis and biological activity.
AID649070Inhibition of NF-kappaB activation expressed in human HT-29 cells assessed as inhibition of TNFalpha-stimulated IL8 release at 100 uM after 24 hrs by flow cytometric analysis relative to control2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID459413Induction of apoptosis in human Jurkat T cells at 10 uM after 24 hrs by flow cytometry2010Bioorganic & medicinal chemistry, Jan-15, Volume: 18, Issue:2
New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.
AID492312Analgesic activity in Swiss mouse assessed as increase in latency of paw licking at 100 umol/kg, po after 150 mins measured for 60 seconds by hot plate test (Rvb = 5.1 +/- 0.4 seconds)2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID670244Antimycobacterial activity against Mycobacterium tuberculosis H37Ra ATCC 25177 by microbroth dilution method2012Bioorganic & medicinal chemistry, Jul-01, Volume: 20, Issue:13
Synthesis and antimycobacterial activity of some phthalimide derivatives.
AID1404807Inhibition of LPS-induced TNFalpha production in Swiss albino mouse macrophages at 50 uM after 24 hrs by ELISA relative to control2018European journal of medicinal chemistry, Jun-25, Volume: 154Discovery of phenylsulfonylfuroxan derivatives as gamma globin inducers by histone acetylation.
AID459401Inhibition of NF-kappaB-mediated TNF expression in human Jurkat T cells coexpressing GFP reporter gene at 100 uM by flow cytometry2010Bioorganic & medicinal chemistry, Jan-15, Volume: 18, Issue:2
New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.
AID1685004Binding affinity to human CRBN-thalidomide binding domain expressed in Escherichia coli by measuring baseline corrected normalized fluorescence in presence of 0.5% DMSO by MST based assay2021ACS medicinal chemistry letters, Jan-14, Volume: 12, Issue:1
Sweet and Blind Spots in E3 Ligase Ligand Space Revealed by a Thermophoresis-Based Assay.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID387209Antiinflammatory activity in mouse LPS-activated RAW264.7 cells assessed as ROS scavenging activity at 10 uM pretreated for 3 hrs before LPS challenge measured by decrease in fluorescent intensity by confocal microscopy2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID1866020Thermodynamic aqueous solubility of the compound2022Bioorganic & medicinal chemistry, 02-15, Volume: 56Structural modification aimed for improving solubility of lead compounds in early phase drug discovery.
AID387208Antiinflammatory activity in mouse LPS-activated RAW264.7 cells assessed as mean fluorescent intensity of ROS scavenging activity at 10 uM pretreated for 3 hrs before LPS challenge by FACS2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID1814571Displacement of Cy5-O-Len probe from 6XHis-tagged CRBN/DDB1 (unknown origin) incubated in dark for 1 hr by fluorescence polarization assay
AID1816482PROTAC activity at CRBN E3 ligase/EZH2 in PRC2 complex in human WSUDLCL2 cells assessed as reduction in RbAp48 level at 10 uM measured after 48 hrs by Western blot analysis
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1813153Protac activity at CRBN E3 ubiquitin ligase/tyrosinase in human A-375 cells assessed as induction of tyrosinase degradation at 50 uM measured after 24 hrs by immunoblotting analysis2021European journal of medicinal chemistry, Dec-15, Volume: 226Design, synthesis and biological evaluation of tyrosinase-targeting PROTACs.
AID471901Inhibition of okadaic acid-induced TNFalpha production in human HL60 cells at 30 uM after 16 hrs by ELISA relative to control2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID371661Antiangiogenesis activity against MOG peptide, pertussis toxin, Mycobacterium tuberculosis-induced experimental allergic encephalomyelitis C57BL/6J mouse model assessed as inhibition of multiple sclerosis at 100 mg/kg up to 15 days2009Bioorganic & medicinal chemistry letters, Feb-01, Volume: 19, Issue:3
Preliminary biological evaluations of new thalidomide analogues for multiple sclerosis application.
AID492310Analgesic activity in Swiss mouse assessed as increase in latency of paw licking at 100 umol/kg, po after 120 mins measured for 60 seconds by hot plate test (Rvb = 5.6 +/- 0.5 seconds)2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID540213Half life in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID43581Inhibition of beta-lactamase at 100 uM2003Journal of medicinal chemistry, Oct-09, Volume: 46, Issue:21
Identification and prediction of promiscuous aggregating inhibitors among known drugs.
AID423808Antiangiogenic activity against VEGF-induced HUVEC assessed as tube path at 100 uM after 11 days after 11 days by BCIP/NBT visualization assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID387975Antitumor activity against mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as tumor apoptotic index treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by histopathological analysis2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID387981Decrease in lipid peroxidation in mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as malondialdehyde per gram of tissue treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID1277070Inhibition of MANT-uracil binding to Magnetospirillum gryphiswaldense cereblon isoform 4 Y101F mutant by Cheng-Prusoff equation analysis2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID648937Inhibition of TNFalpha-induced NF-kappaB activation expressed in human HT-29 cells coexpressing hrGFP at 200 uM after 24 hrs by propidium iodide staining-based flow cytometric analysis relative to control2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID81272Tumor necrosis factor-alpha production in human leukemia cell line (HL-60) stimulated with 50 nM okadaic acid (OA), at 30 uMolar.1997Journal of medicinal chemistry, Aug-29, Volume: 40, Issue:18
Novel biological response modifiers: phthalimides with tumor necrosis factor-alpha production-regulating activity.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588220Literature-mined public compounds from Kruhlak et al phospholipidosis modelling dataset2008Toxicology mechanisms and methods, , Volume: 18, Issue:2-3
Development of a phospholipidosis database and predictive quantitative structure-activity relationship (QSAR) models.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1179422Antiinflammatory activity against mouse L929 cells assessed as inhibition of LPS-induced TNFalpha production at 125 uM after 48 hrs2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Synthesis and evaluation of novel dapsone-thalidomide hybrids for the treatment of type 2 leprosy reactions.
AID363105Inhibition of TNFalpha release in human whole blood2008Journal of medicinal chemistry, Sep-25, Volume: 51, Issue:18
Recent advances on phosphodiesterase 4 inhibitors for the treatment of asthma and chronic obstructive pulmonary disease.
AID471900Cytotoxicity against human DLD1 cells by MTT assay2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID540210Clearance in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID215085Inhibition of TNF-alpha production from human monocytes upon stimulation with bacterial lipopolysaccharide (LPS) at a concentration of 1 uM1996Journal of medicinal chemistry, Aug-02, Volume: 39, Issue:16
Potent inhibition of tumor necrosis factor-alpha production by tetrafluorothalidomide and tetrafluorophthalimides.
AID540209Volume of distribution at steady state in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID215087Inhibition of TNF-alpha production from human monocytes upon stimulation with bacterial lipopolysaccharide (LPS) at a concentration of 100 uM1996Journal of medicinal chemistry, Aug-02, Volume: 39, Issue:16
Potent inhibition of tumor necrosis factor-alpha production by tetrafluorothalidomide and tetrafluorophthalimides.
AID423807Antiangiogenic activity against VEGF-induced HUVEC assessed as tube joint at 100 uM after 11 days after 11 days by BCIP/NBT visualization assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID471902Enhancement of 12-O-tetradecanoylphorbol-13-acetate-induced TNFalpha production in human HL60 cell at 30 uM after 16 hrs by ELISA relative to control2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID387210Reduction in iNOS expression in LPS-activated mouse RAW264.7 cells at 1 uM pretreated for 3 hrs before LPS challenge assessed after 24 hrs by Western blot2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID387984Antitumor activity against mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as tumor necrosis treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by histopathological analysis relative to control2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID387990Antitumor activity against mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as tumor mitotic index treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by histopathological analysis2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID252627NBT positivity against human leukemia cell line HL-60 at 1*E-5 M2005Bioorganic & medicinal chemistry letters, Jul-01, Volume: 15, Issue:13
Cell differentiation inducers derived from thalidomide.
AID649078Pro-inflammatory activity in NFkappaB-GFP transfected human HT-29 cells at 25 to 400 uM after 24 hrs by propidium iodide staining-based flow cytometric analysis2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1277064Inhibition of MANT-uracil binding to human CRBN (delta 1 to 315) by FRET assay2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID160735Inhibitory activity (RA2) against Prostaglandin G/H synthase 2 was calculated relative to aspirin2002Bioorganic & medicinal chemistry letters, Apr-08, Volume: 12, Issue:7
Thalidomide and its analogues as cyclooxygenase inhibitors.
AID726393Inhibition of TNF-alpha production in LPS-stimulated human PBMC preincubated for 1 hr before LPS challenge measured after 28 to 20 hrs by ELISA2013Bioorganic & medicinal chemistry letters, Jan-01, Volume: 23, Issue:1
Isosteric analogs of lenalidomide and pomalidomide: synthesis and biological activity.
AID459412Induction of apoptosis in human Jurkat T cells at 100 uM after 24 hrs by flow cytometry2010Bioorganic & medicinal chemistry, Jan-15, Volume: 18, Issue:2
New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID468443Inhibition of human FAAH at 1 uM2009Bioorganic & medicinal chemistry letters, Dec-01, Volume: 19, Issue:23
Mining biologically-active molecules for inhibitors of fatty acid amide hydrolase (FAAH): identification of phenmedipham and amperozide as FAAH inhibitors.
AID1449628Inhibition of human BSEP expressed in baculovirus transfected fall armyworm Sf21 cell membranes vesicles assessed as reduction in ATP-dependent [3H]-taurocholate transport into vesicles incubated for 5 mins by Topcount based rapid filtration method2012Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 40, Issue:12
Mitigating the inhibition of human bile salt export pump by drugs: opportunities provided by physicochemical property modulation, in silico modeling, and structural modification.
AID1893697Induction of GSPT1 degradation in PXR knock in human SNU-C4 cells at 10 uM measured after 24 hrs by Western blot analysis relative to control2022ACS medicinal chemistry letters, Aug-11, Volume: 13, Issue:8
SJPYT-195: A Designed Nuclear Receptor Degrader That Functions as a Molecular Glue Degrader of GSPT1.
AID158462Inhibition of PDE4 enzyme from U937 cells1998Bioorganic & medicinal chemistry letters, Oct-06, Volume: 8, Issue:19
Thalidomide analogs and PDE4 inhibition.
AID471899Cytotoxicity against human HT-29 cells by MTT assay2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID1703926Effect on eEF2K expression in human MDA-MB-231 cells at 10 uM measured after 2 hrs by western blot assay2020European journal of medicinal chemistry, Oct-15, Volume: 204Designing an eEF2K-Targeting PROTAC small molecule that induces apoptosis in MDA-MB-231 cells.
AID492306Analgesic activity in Swiss mouse assessed as increase in latency of paw licking at 100 umol/kg, po after 60 mins measured for 60 seconds by hot plate test (Rvb = 4.9 +/- 0.5 seconds)2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID1769481Metabolic stability in human liver microsome assessed as half-life at 1 uM in presence of NADPH incubated up to 60 mins by LC-MS/MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID1653424Cytotoxicity against LPS-induced human monocytes assessed as cell viability at 50 uM by tryphan blue staining based assay relative to control2019Bioorganic & medicinal chemistry, 07-01, Volume: 27, Issue:13
Insights of synthetic analogues of anti-leprosy agents.
AID1317723Growth inhibition of BMOL-NT cells2016European journal of medicinal chemistry, Sep-14, Volume: 120Identification of a thalidomide derivative that selectively targets tumorigenic liver progenitor cells and comparing its effects with lenalidomide and sorafenib.
AID492308Analgesic activity in Swiss mouse assessed as increase in latency of paw licking at 100 umol/kg, po after 90 mins measured for 60 seconds by hot plate test (Rvb = 5.9 +/- 0.8 seconds)2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID492318Antiinflammatory effect in complete Freund's adjuvant-induced Wistar rat arthritis model assessed as inhibition of paw edema at 100 umol/kg, po daily once administered on day 14 post adjuvant challenge measured on day 17 post adjuvant challenge2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID1277068Inhibition of MANT-uracil binding to human CRBN (delta 1 to 315) by Cheng-Prusoff equation analysis2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID215590Inhibition of LPS stimulated Tumor Necrosis Factor-alpha (TNF-alpha) release by human PBMC1998Bioorganic & medicinal chemistry letters, Oct-06, Volume: 8, Issue:19
Thalidomide analogs and PDE4 inhibition.
AID1816478PROTAC activity at CRBN E3 ligase/EZH2 in PRC2 complex in human WSUDLCL2 cells assessed as reduction in SUZ12 level at 10 uM measured after 48 hrs by Western blot analysis
AID387986Toxicity in Swiss albino mouse bearing mouse Ehrlich ascites carcinoma cells assessed as focal degeneration of hepatocytes treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by histopathological analysis2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID387212Reduction in pERK1/2 expression in LPS-activated mouse RAW264.7 cells at 10 uM pretreated for 3 hrs before LPS challenge assessed after 24 hrs by Western blot2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID1569038Inhibition of CRBN-mediated CK1alpha degradation in human OPM2 cells measured after 24 hrs by Western blot analysis2019Journal of medicinal chemistry, 07-25, Volume: 62, Issue:14
De-Novo Design of Cereblon (CRBN) Effectors Guided by Natural Hydrolysis Products of Thalidomide Derivatives.
AID1387863Induction of cereblon-mediated Sirt2 degradation in human HeLa cells at 0.05 to 5 uM after 4 hrs by Western blot method2018Journal of medicinal chemistry, 01-25, Volume: 61, Issue:2
Chemically Induced Degradation of Sirtuin 2 (Sirt2) by a Proteolysis Targeting Chimera (PROTAC) Based on Sirtuin Rearranging Ligands (SirReals).
AID162144Inhibitory activity (RA1) against Prostaglandin G/H synthase 1 was calculated relative to aspirin2002Bioorganic & medicinal chemistry letters, Apr-08, Volume: 12, Issue:7
Thalidomide and its analogues as cyclooxygenase inhibitors.
AID471904Cytotoxicity against human HL60 cells by MTT assay2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.
AID1317703Cytotoxicity against BMOL-NT cells assessed as induction of cell death at 100 uM2016European journal of medicinal chemistry, Sep-14, Volume: 120Identification of a thalidomide derivative that selectively targets tumorigenic liver progenitor cells and comparing its effects with lenalidomide and sorafenib.
AID1858993Cytotoxicity against mouse Ehrlich cells assessed as cell growth inhibition incubated for 3 hrs by trypan blue exclusion assay2022European journal of medicinal chemistry, Jan-05, Volume: 227Role of basic aminoalkyl chains in the lead optimization of Indoloquinoline alkaloids.
AID387211Reduction in iNOS expression in LPS-activated mouse RAW264.7 cells at 10 uM pretreated for 3 hrs before LPS challenge assessed after 24 hrs by Western blot2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID1277067Inhibition of MANT-uracil binding to wild type Magnetospirillum gryphiswaldense cereblon isoform 4 by Cheng-Prusoff equation analysis2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID1769480Kinetic solubility of compound in PBS at 200 uM incubated for 30 mins by LC-MS/MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID648939Cytotoxicity against human HT-29 cells expressing NF-kappaB-hrGFP assessed as highest non-cytotoxic dose for 100% cell survival after 24 hrs by MTT assay2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID1706074Down regulation of NFkappaB p65 expression in LPS/IFNgamma-induced mouse RAW264.7 cells at 10 uM incubated for 20 hrs followed by LPS/IFNgamma stimulation and measured after 4 hrs by Western blot analysis2020European journal of medicinal chemistry, Dec-15, Volume: 208Induced protein degradation of histone deacetylases 3 (HDAC3) by proteolysis targeting chimera (PROTAC).
AID503321Antiproliferative activity against human PC3 cells at 250 nM after 120 hrs by MTT assay relative to DMSO2006Nature chemical biology, Jun, Volume: 2, Issue:6
Identifying off-target effects and hidden phenotypes of drugs in human cells.
AID423805Antiangiogenic activity against VEGF-induced HUVEC assessed as tube area at 100 uM after 11 days by BCIP/NBT visualization assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID648936Inhibition of TNFalpha-induced NF-kappaB activation expressed in human HT-29 cells coexpressing hrGFP at 400 uM after 24 hrs by propidium iodide staining-based flow cytometric analysis relative to control2012Bioorganic & medicinal chemistry, Mar-15, Volume: 20, Issue:6
Discovery of new orally effective analgesic and anti-inflammatory hybrid furoxanyl N-acylhydrazone derivatives.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID120028Compound (0.4 mmol/Kg) was evaluated for its ability to inhibit B16BL6 pulmonary metastasis in mice. The number of lung metastases of treated (T) and nontreated or control (C) is expressed as ratio, T/C.1999Journal of medicinal chemistry, Aug-12, Volume: 42, Issue:16
Synthesis and enantiomeric separation of 2-phthalimidino-glutaric acid analogues: potent inhibitors of tumor metastasis.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID387983Increase in SOD activity per gram of tissue in mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID252970Percent cell proliferation of human leukemia cell line HL-60 at 1*E-5 M2005Bioorganic & medicinal chemistry letters, Jul-01, Volume: 15, Issue:13
Cell differentiation inducers derived from thalidomide.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1179425Antimycobacterial activity against Mycobacterium leprae inoculated in mouse model assessed as mean number of bacilli at 200 mg/kg, po 5 days/week for 4 weeks (Rvb = 3.56 x 10'6 cells)2014Bioorganic & medicinal chemistry letters, Jul-15, Volume: 24, Issue:14
Synthesis and evaluation of novel dapsone-thalidomide hybrids for the treatment of type 2 leprosy reactions.
AID459402Inhibition of NF-kappaB-mediated TNF expression in human Jurkat T cells coexpressing GFP reporter gene at 10 uM by flow cytometry2010Bioorganic & medicinal chemistry, Jan-15, Volume: 18, Issue:2
New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.
AID1769485Drug accumulation in human MOLT-4 cells assessed as intracellular bioavailability by LC-MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID1882261Immunomodulatory activity in human MM cells2022European journal of medicinal chemistry, Feb-05, Volume: 229A review on the treatment of multiple myeloma with small molecular agents in the past five years.
AID1599136Binding affinity to human CRBN (1 to 442 residues)/N-terminal 6His-tagged human DDB1 (1 to 1140 residues) expressed in baculovirus infected BTI-TN-5B1-4 insect cells after 30 mins by cy5 probe based fluorescence polarization assay2019Journal of medicinal chemistry, 06-13, Volume: 62, Issue:11
From Inhibition to Degradation: Targeting the Antiapoptotic Protein Myeloid Cell Leukemia 1 (MCL1).
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID301709Inhibition of TNF gene expression in FRT Jurkat TNF reporter cells at 10 uM2007Bioorganic & medicinal chemistry letters, Nov-01, Volume: 17, Issue:21
Synthesis and TNF expression inhibitory properties of new thalidomide analogues derived via Heck cross coupling.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID106806Inhibition of malate dehydrogenase (MDH) at 400 uM2003Journal of medicinal chemistry, Oct-09, Volume: 46, Issue:21
Identification and prediction of promiscuous aggregating inhibitors among known drugs.
AID1277065Inhibition of MANT-uracil binding to Caenorhabditis elegans CRBN (delta 1 to 15) by FRET assay2016Journal of medicinal chemistry, Jan-28, Volume: 59, Issue:2
A FRET-Based Assay for the Identification and Characterization of Cereblon Ligands.
AID423809Cytotoxicity against human KB cells assessed as cell viability at 100 ug/ml after 72 hrs by MTT assay2009Bioorganic & medicinal chemistry letters, Jul-15, Volume: 19, Issue:14
Synthesis, configurational stability and stereochemical biological evaluations of (S)- and (R)-5-hydroxythalidomides.
AID387991Antiangiogenic activity against mouse Ehrlich ascites carcinoma cells implanted in Swiss albino mouse assessed as inhibition of VEGF expression treated after 7 days post-tumor implantation at 1.25 mM/kg, sc for 5 days by immunohistochemical analysis2008Bioorganic & medicinal chemistry, Nov-15, Volume: 16, Issue:22
Design, synthesis and antitumor evaluation of novel thalidomide dithiocarbamate and dithioate analogs against Ehrlich ascites carcinoma-induced solid tumor in Swiss albino mice.
AID1816476PROTAC activity at CRBN E3 ligase/EZH2 in PRC2 complex in human WSUDLCL2 cells assessed as reduction in EZH2 level at 10 uM measured after 48 hrs by Western blot analysis
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1769483Drug accumulation in human MOLT-4 cells assessed as intracellular unbound fraction incubated for 4 hrs by LC-MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1569045Inhibition of TPA-induced TNFalpha production in human THP1 cells at 3 uM by ELISA relative to control2019Journal of medicinal chemistry, 07-25, Volume: 62, Issue:14
De-Novo Design of Cereblon (CRBN) Effectors Guided by Natural Hydrolysis Products of Thalidomide Derivatives.
AID52790Inhibition of chymotrypsin at 250 uM2003Journal of medicinal chemistry, Oct-09, Volume: 46, Issue:21
Identification and prediction of promiscuous aggregating inhibitors among known drugs.
AID492305Analgesic activity against formalin-induced acute pain in Swiss mouse assessed inhibition of nociception at 100 umol/kg, po administered 40 mins before formalin challenge measured for 15 to 30 mins relative to control2010Bioorganic & medicinal chemistry, Jul-15, Volume: 18, Issue:14
Synthesis and pharmacological evaluation of pyrazine N-acylhydrazone derivatives designed as novel analgesic and anti-inflammatory drug candidates.
AID1769478Apparent permeability in in human Caco-2 cells at 10 uM incubated for 90 mins by LC-MS/MS analysis2021ACS medicinal chemistry letters, Nov-11, Volume: 12, Issue:11
Physicochemistry of Cereblon Modulating Drugs Determines Pharmacokinetics and Disposition.
AID1569044Terminal elimination half life in healthy human at 50 to 400 mg, po at pH 7.42019Journal of medicinal chemistry, 07-25, Volume: 62, Issue:14
De-Novo Design of Cereblon (CRBN) Effectors Guided by Natural Hydrolysis Products of Thalidomide Derivatives.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID387206Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production at 10 uM pretreated for 3 hrs before LPS challenge assessed after 24 hrs by griess assay relative to control2008Bioorganic & medicinal chemistry, Sep-15, Volume: 16, Issue:18
Development and biological evaluation of C(60) fulleropyrrolidine-thalidomide dyad as a new anti-inflammation agent.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347045Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot counterscreen GloSensor control cell line2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347049Natriuretic polypeptide receptor (hNpr1) antagonism - Pilot screen2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347050Natriuretic polypeptide receptor (hNpr2) antagonism - Pilot subtype selectivity assay2019Science translational medicine, 07-10, Volume: 11, Issue:500
Inhibition of natriuretic peptide receptor 1 reduces itch in mice.
AID504836Inducers of the Endoplasmic Reticulum Stress Response (ERSR) in human glioma: Validation2002The Journal of biological chemistry, Apr-19, Volume: 277, Issue:16
Sustained ER Ca2+ depletion suppresses protein synthesis and induces activation-enhanced cell death in mast cells.
AID588349qHTS for Inhibitors of ATXN expression: Validation of Cytotoxic Assay
AID588378qHTS for Inhibitors of ATXN expression: Validation
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1794852Fluorescence thermal melt assay from Article 10.1038/leu.2012.119: \\Cereblon is a direct protein target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide.\\2012Leukemia, Nov, Volume: 26, Issue:11
Cereblon is a direct protein target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
AID1347057CD47-SIRPalpha protein protein interaction - LANCE assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347059CD47-SIRPalpha protein protein interaction - Alpha assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347058CD47-SIRPalpha protein protein interaction - HTRF assay qHTS validation2019PloS one, , Volume: 14, Issue:7
Quantitative high-throughput screening assays for the discovery and development of SIRPα-CD47 interaction inhibitors.
AID1347410qHTS for inhibitors of adenylyl cyclases using a fission yeast platform: a pilot screen against the NCATS LOPAC library2019Cellular signalling, 08, Volume: 60A fission yeast platform for heterologous expression of mammalian adenylyl cyclases and high throughput screening.
AID1347405qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS LOPAC collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347151Optimization of GU AMC qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (9,284)

TimeframeStudies, This Drug (%)All Drugs %
pre-19901408 (15.17)18.7374
1990's576 (6.20)18.2507
2000's2577 (27.76)29.6817
2010's3843 (41.39)24.3611
2020's880 (9.48)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 91.15

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index91.15 (24.57)
Research Supply Index9.32 (2.92)
Research Growth Index4.95 (4.65)
Search Engine Demand Index170.03 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (91.15)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1,385 (14.15%)5.53%
Reviews1,774 (18.12%)6.00%
Case Studies1,511 (15.44%)4.05%
Observational48 (0.49%)0.25%
Other5,071 (51.80%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (408)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Phase III Study to Determine the Role of Ixazomib as an Augmented Conditioning Therapy in Salvage Autologous Stem Cell Transplant (ASCT) and as a Post-ASCT Consolidation and Maintenance Strategy in Patients With Relapsed Multiple Myeloma [NCT03562169]Phase 3406 participants (Anticipated)Interventional2017-03-20Recruiting
Phase III Trial Comparing Treatment With Melphalan+Prednisolon (MP) With Melphalan+Prednisolon+Thalidomide (MPT) for Previously Untreated Elderly Patients With Multiple Myeloma [NCT00934154]Phase 3122 participants (Actual)Interventional2006-03-31Completed
"Twenty-Four-Week, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study of the Effect of Fixed Dose Regimens of Thalidomide and Placebo on CSF and Plasma Biomarkers in Patients With Mild to Moderate Alzheimer's Disease" [NCT01094340]Phase 2/Phase 320 participants (Anticipated)Interventional2010-03-31Recruiting
Thalidomide-Dexamethasone Incorporated Into Double Autologous Stem-Cell Transplantation for Patients Less Than 65 Years of Age With Newly Diagnosed Multiple Myeloma [NCT01341262]Phase 2378 participants (Actual)Interventional2002-03-31Completed
A Phase II Evaluation of Thalidomide (NSC #66847) in the Treatment of Recurrent or Persistent Carcinosarcoma of the Uterus [NCT00025506]Phase 255 participants (Actual)Interventional2001-09-30Completed
Prospective Clinical Study of the Effect of Thalidomide Combined With Megestrol Acetate on Lymphocyte, Inflammatory Factor Regulation and Nutritional Status in Patients With Advanced Malignant Tumors [NCT03777930]Phase 4200 participants (Anticipated)Interventional2018-12-10Not yet recruiting
A Double Blinded Randomized Crossover Phase III Study of Oral Thalidomide Versus Placebo in Patients With Stage D0 Androgen Dependent Prostate Cancer Following Limited Hormonal Ablation [NCT00004635]Phase 3159 participants (Actual)Interventional2000-03-01Completed
Treatment of Refractory Epilepsy With Thalidomide: an Open Trial [NCT01061866]Phase 1/Phase 27 participants (Actual)Interventional2006-06-30Completed
A Randomized Phase II, Open Label, Study of Daratumumab, Weekly Low-Dose Oral Dexamethasone and Cyclophosphamide With or Without Pomalidomide in Patients With Relapsed and Refractory Multiple Myeloma [NCT03215524]Phase 2120 participants (Actual)Interventional2017-10-25Completed
A Single-arm, Open, Prospective, Multi-center Study on Thalidomide Combined With First-line Chemotherapy and Monotherapy for Maintenance Treatment of Liver Metastases From Her2-negative Advanced Gastric Cancer [NCT05198856]Phase 1/Phase 2106 participants (Anticipated)Interventional2022-03-10Not yet recruiting
A Phase III, Multi Center, Randomized, Placebo Controlled Study to Evaluate the Efficacy of the Combination Gefitinib With Thalidomide in Patients With Locally Advanced and Metastatic Non-Small-Cell-Lung-Cancer With EGFR Mutation [NCT02387086]Phase 2/Phase 3380 participants (Anticipated)Interventional2015-05-31Not yet recruiting
Expanded Access for CC-2001 [NCT03723083]0 participants Expanded AccessNo longer available
Anti-Angiogenic Therapy After Autologous Stem Cell Rescue (ASCR) for Pediatric Solid Tumors [NCT01661400]Phase 114 participants (Actual)Interventional2012-10-26Active, not recruiting
A Phase 4, Multicenter, Randomized, Placebo-controlled, Double-blind, Study of the Efficacy and Safety of Apremilast (CC-10004) in Subjects With Moderate Plaque Psoriasis [NCT02425826]Phase 4221 participants (Actual)Interventional2015-04-20Completed
A Phase 3, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Efficacy and Safety Study of Two Doses of Apremilast (CC-10004) in Subjects With Active Psoriatic Arthritis Who Have Not Been Previously Treated With Disease-modifying A [NCT01307423]Phase 3529 participants (Actual)Interventional2010-12-09Completed
A Phase I/II Study of Fludarabine Plus Thalidomide as Frontline Therapy for Newly Diagnosed Patients With Chronic Lymphocytic Leukemia [NCT00096018]Phase 1/Phase 243 participants (Actual)Interventional2002-05-31Completed
A Randomized, Factorial-Design, Phase II Trial of Temozolomide Alone and in Combination With Possible Permutations of Thalidomide, Isotretinoin and/or Celecoxib as Post-Radiation Adjuvant Therapy of Glioblastoma Multiforme [NCT00112502]Phase 2178 participants (Actual)Interventional2005-09-30Completed
Phase II Trial of Neoadjuvant GM-CSF + Thalidomide in High-Risk Patients With Prostate Cancer Undergoing Prostatectomy [NCT00400517]Phase 228 participants (Actual)Interventional2003-03-31Completed
A Phase II Pilot Study Of Thalidomide With Temozolomide In Patients With Relapsed Or Progressive Brain Tumors Or Neuroblastoma [NCT00098865]Phase 215 participants (Actual)Interventional2002-09-30Completed
Sequential High-Dose Melphalan and Busulfan/Cyclophosphamide Followed by Peripheral Blood Progenitor Cell Rescue, Interferon/Thalidomide and Pamidronate for Patients With Multiple Myeloma [NCT00004088]Phase 277 participants (Actual)Interventional1999-04-13Completed
A Phase 1b Multi-Center, Open Label, Dose-Escalation Study to Determine the Maximum Tolerated Dose, Safety, and Anti-Tumor Activity of an Alternative Liquid Formulation of ACY-1215 (Ricolinostat) In Combination With Pomalidomide and Low-Dose Dexamethasone [NCT02189343]Phase 116 participants (Actual)Interventional2014-09-15Completed
A Multicenter, Randomized, Double-blind, Placebo-controlled, Phase II Clinical Study of Thalidomide in the Treatment of Ankylosing Spondylitis [NCT02201043]Phase 2197 participants (Actual)Interventional2013-02-28Completed
Isatuximab, Carfilzomib, Pomalidomide, and Dexamethasone (Isa-KPd) for Patients With Relapsed/Refractory Multiple Myeloma [NCT04883242]Phase 237 participants (Anticipated)Interventional2021-07-29Recruiting
A Study of Thalidomide, Bendamustine and Dexamethasone (BTD) Versus Bortezomib, Bendamustine and Dexamethasone (BBD) in Patients With Renal Failure Defined as a GFR Below 30 Mls/Min [NCT02424851]Phase 231 participants (Actual)Interventional2014-11-30Completed
A Phase II Randomized,Controlled,Open Label,Multicentre Study of Tegafur Combined With Temozolomide Versus Tegafur Combined With Temozolomide and Thalidomide in Subjects With Advanced Extrapancreatic Neuroendocrine Tumor [NCT03204032]Phase 260 participants (Anticipated)Interventional2016-10-31Recruiting
Phase II Trial of Anti-Angiogenic Therapy With RT-PEPC in Patients With Relapsed Mantle Cell Lymphoma [NCT00151281]Phase 225 participants (Actual)Interventional2004-11-30Completed
The Multi-center Clinical Trials of Thalidomide in TI [NCT03184844]Phase 2100 participants (Anticipated)Interventional2017-05-02Recruiting
Ixazomib in Combination With Thalidomide - Dexamethasone in Patients With Relapsed and/or Refractory Multiple Myeloma [NCT02410694]Phase 290 participants (Actual)Interventional2015-04-30Completed
An Open-Label, Single-Arm Phase II Study of Ixazomib, Thalidomide and Dexamethasone in Newly Diagnosed and Treatment-Naive Multiple Myeloma Patients Non-Eligible for Autologous Stem-Cell Transplantation [NCT03608501]Phase 20 participants (Actual)Interventional2019-09-30Withdrawn(stopped due to Business decision (no safety or efficacy concerns))
Phase 2 Study of Daratumumab in Combination With Thalidomide and Dexamethasone in Relapse and / or Refractory Myeloma [NCT03143036]Phase 2100 participants (Anticipated)Interventional2018-05-01Recruiting
The Efficacy and Safety of Thalidomide in Preventing Multi-cycle, Cisplatin-containing CINV: a Pragmatic Randomized Open-label Clinical Trial [NCT03601871]880 participants (Anticipated)Interventional2018-07-12Recruiting
A Phase 4, Multicenter, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study to Evaluate the Efficacy and Safety of Apremilast (CC-10004) in Subjects With Early, Oligoarticular Psoriatic Arthritis Despite Initial Stable Treatment With Either [NCT03747939]Phase 4310 participants (Actual)Interventional2018-12-31Completed
A Phase 3, Multicenter, Randomized, Open-Label Study to Compare the Efficacy and Safety of Pomalidomide, Bortezomib and Low-Dose Dexamethasone Versus Bortezomib and Low-Dose Dexamethasone in Subjects With Relapsed or Refractory Multiple Myeloma [NCT01734928]Phase 3559 participants (Actual)Interventional2013-01-07Completed
A Phase I/II Study of Escalating Doses of Thalidomide in Conjunction With Bortezomib and HIgh Dose Melphalan as a Conditioning Regimen for Autologous Peripheral Blood Stem Cell Transplantation in Patients With Advanced Multiple Myeloma [NCT01242267]Phase 1/Phase 229 participants (Actual)Interventional2010-05-11Completed
An Open-Label, Multicenter, Phase 1b Study of JNJ-54767414 (HuMax CD38) (Anti-CD38 Monoclonal Antibody) in Combination With Backbone Regimens for the Treatment of Subjects With Multiple Myeloma [NCT01998971]Phase 1242 participants (Actual)Interventional2014-02-18Active, not recruiting
Study of Thalidomide With First-line Chemotherapy and as Maintenance Treatment of Advanced Nonsquamous NSCLC With Epidermal Growth Factor Receptor Wild-Type or Unknown Mutation Status: A Multicenter, Randomized, Prospective Clinical Trial [NCT03062800]Phase 2232 participants (Anticipated)Interventional2016-12-31Recruiting
Adherence to Otezla in Patients With Mild Psoriasis [NCT05601492]Early Phase 184 participants (Anticipated)Interventional2023-12-31Not yet recruiting
Phase Ib/II Study of ATG-010 in Combination With Thalidomide and Dexamethasone for Relapsed/Refractory Multiple Myeloma [NCT04891744]Phase 1/Phase 248 participants (Anticipated)Interventional2021-07-06Not yet recruiting
A Pilot, Open-label, Randomized, Two-Way Crossover, Single-Dose Bioequivalence Study of Pomalidomide Under Fasting Condition in Indian Healthy Volunteers [NCT06058689]Phase 110 participants (Anticipated)Interventional2024-09-15Not yet recruiting
A Pilot, Open-label, Randomized, Two-Way Crossover, Single-Dose Bioequivalence Study of Pomalidomide Under Fasting Condition in Chinese Healthy Volunteers. [NCT03424928]Phase 112 participants (Actual)Interventional2018-01-19Completed
Early Response-adapted Intensification of Induction Chemotherapy in Patients With Newly Diagnosed Multiple Myeloma (MM) Who Are Eligible for Autologous Stem Cell Transplantation: Multicenter Phase 2 Study [NCT01114048]Phase 278 participants (Anticipated)Interventional2010-03-31Recruiting
A Phase 3, Prospective, Randomized Clinical Study of VELCADE-Thalidomide-Dexamethasone (VTD) Versus Thalidomide-Dexamethasone (TD) for Previously Untreated Multiple Myeloma (MM) Patients Who Are Candidates to Receive Double Autologous Transplantation [NCT01134484]Phase 3480 participants (Actual)Interventional2006-05-31Active, not recruiting
A Randomized Phase III Study Of Thalidomide And Prednisone As Maintenance Therapy Following Autologous Stem Cell Transplant in Patients With Multiple Myeloma [NCT00049673]Phase 3332 participants (Actual)Interventional2002-10-15Completed
A Phase II Study of Peg-Interferon Alpha-2B (Peg-Intron(TM)) and Thalidomide in Adults With Recurrent High-Grade Gliomas [NCT00047879]Phase 27 participants (Actual)Interventional2002-10-31Completed
S0115, A Phase II Trial Evaluating Modified High Dose Melphalan (100 mg/m) And Autologous Peripheral Blood Stem Cell Supported Transplant (SCT) For High Risk Patients With Multiple Myeloma And/Or Light Chain Amyloidosis (AL Amyloidosis) (A BMT Study) [NCT00064337]Phase 2104 participants (Actual)Interventional2004-01-31Completed
Safety & Efficacy of Thalidomide in Children With Transfusion Dependent Thalassemia: a Quasi Randomized Control Trial in a Tertiary Care Hospital in Bangladesh [NCT06098014]Phase 360 participants (Anticipated)Interventional2023-03-08Recruiting
A Randomized Parallel Phase 2 Study of Elotuzumab Plus Lenalidomide (Elo/Rev) for the Treatment of Serologic Relapse/Progression While on Lenalidomide Maintenance for Multiple Myeloma [NCT03411031]Phase 218 participants (Actual)Interventional2018-10-04Terminated(stopped due to Sponsor no longer providing drug)
Multicenter Non-interventional Study to Investigate Drug Utilization of Pomalidomide in Clinical Practice for the Treatment of Relapsed/Refractory Multiple Myeloma (rrMM) [NCT02555839]150 participants (Anticipated)Observational2015-02-20Active, not recruiting
An Intergroup Phase III Randomized Controlled Trial Comparing Melphalan, Prednisone and Thalidomide (MPT) Versus Melphalan, Prednisone and Lenalidomide (Revlimid(TM))(MPR) in Newly Diagnosed Multiple Myeloma Patients Who Are Not Candidates for High-Dose T [NCT00602641]Phase 3306 participants (Actual)Interventional2008-02-29Active, not recruiting
A Randomized Phase III Study of CC-5013 Plus Dexamethasone Versus CC-5013 Plus Low Dose Dexamethasone in Multiple Myeloma With Thalidomide Plus Dexamethasone Salvage Therapy for Non-Responders [NCT00098475]Phase 3452 participants (Actual)Interventional2004-11-03Active, not recruiting
An Open-Label Phase 2 Study of Lenalidomide (Revlimid) in Combination With Oral Dexamethasone in the Treatment of Previously Untreated, Symptomatic Patients With Chronic Lymphocytic Leukemia (CLL) [NCT01133743]Phase 231 participants (Actual)Interventional2010-05-31Completed
Evaluation of Efficacy and Mechanisms of Topical Thalidomide for Chronic Graft-Versus-Host-Disease Related Stomatitis [NCT00075023]Phase 210 participants (Actual)Interventional2003-12-31Terminated(stopped due to unable to enroll adequate subjects)
A Randomized Phase III Trial of Carboplatin, Paclitaxel and Thoracic Radiotherapy, With or Without Thalidomide, in Patients With Stage III Non-Small Cell Lung Cancer (NSCLC) [NCT00004859]Phase 3589 participants (Actual)Interventional2000-01-31Terminated(stopped due to Trial was stopped early for futility)
Alternative Dosing Scheme of Pomalidomide 4 mg Every Other Day Versus Pomalidomide 2 mg and 4 mg Every Day: Reduction in Costs, Same Efficacy? A PKPD Bioequivalence Pilot Study; the POMAlternative Study [NCT05555329]Phase 412 participants (Anticipated)Interventional2022-12-01Not yet recruiting
A Phase II Study of Daily Alternating Thalidomide and Lenalidomide Therapy Plus Rituximab (ThRiL) as Initial Treatment for Patients With CLL [NCT01125176]Phase 215 participants (Actual)Interventional2012-03-30Completed
Autologous-Allogeneic Tandem Stem Cell Transplantation and Maintenance Therapy With Thalidomide/ DLI for Patients With Multiple Myeloma (MM) and Age < _60 Years: A Phase II-study [NCT00777998]Phase 2221 participants (Actual)Interventional2008-10-14Completed
Myeloma-Developing Regimens Using Genomics (MyDRUG) (Genomics Guided Multi-arm Trial of Targeted Agents Alone or in Combination With a Backbone Regimen) [NCT03732703]Phase 1/Phase 2228 participants (Anticipated)Interventional2019-04-01Recruiting
Thalidomide Plus Dexamethasone as Maintenance Therapy After Autologous Hematopoietic Stem Cell Transplantation for Multiple Myeloma: a Multicenter Phase 3 Randomized Trial [NCT01296503]Phase 3213 participants (Actual)Interventional2003-10-31Completed
A Randomized Phase II Study of Gefitinib Alone Versus Gefitinib Plus Thalidomide for Advanced Non-small Cell Lung Cancer With Epidermal Growth Factor Receptor Activating Mutations [NCT03341494]Phase 2128 participants (Anticipated)Interventional2017-04-01Recruiting
A Phase 2 Study to Evaluate the Efficacy of Bortezomib in Patients With De-novo Waldenstrom's Macroglobulinemia and Lymphoplasmacytic Lymphoma [NCT03335098]Phase 215 participants (Anticipated)Interventional2016-11-21Recruiting
[NCT00006200]Phase 20 participants InterventionalActive, not recruiting
[NCT02870036]Phase 1243 participants (Anticipated)Interventional2016-10-31Recruiting
Thalidomide-Cyclophosphamide-Dexamethasone in Patients < 75 Years or Velcade-Melfalan-Prednisone (V-MP)/Thalidomide-Cyclophosphamide-Dexamethasone in Patients >75 Years, in Refractary or Relapsed Multiple Myeloma [NCT00652041]Phase 440 participants (Anticipated)Interventional2007-01-31Completed
EDOCH Alternating With DHAP Regimen Combined Rituximab or Not to Treat New Diagnosed Younger (Age≤65 Years) Mantle Cell Lymphoma in China: A Multicentre Phase III Trial [NCT02858804]Phase 455 participants (Anticipated)Interventional2016-01-31Recruiting
A Phase II Study Incorporating Bone Marrow Microenvironment (ME) - Co-Targeting Bortezomib Into Tandem Melphalan-Based Autotransplants With DTPACE for Induction/Consolidation and Thalidomide + Dexamethasone for Maintenance [NCT00572169]Phase 3177 participants (Actual)Interventional2006-11-30Active, not recruiting
[NCT02748772]Phase 3148 participants (Anticipated)Interventional2016-01-31Recruiting
Low Dose Chemotherapy (Metronomic Therapy) Versus Best Supportive Care in Progressive and/or Refractory Pediatric Malignancies: a Double Blind Placebo Controlled Randomized Study [NCT01858571]Phase 3108 participants (Actual)Interventional2013-10-31Completed
Phase II Study Using Thalidomide for the Treatment of Amyotrophic Lateral Sclerosis [NCT00140452]Phase 224 participants (Anticipated)Interventional2005-02-28Completed
Phase II Trial of Arsenic Trioxide and Thalidomide in the Treatment of Patients With Refractory Multiple Myeloma [NCT00193544]Phase 240 participants Interventional2002-03-31Completed
Open Label, Phase II Investigation of Thalidomide for the Treatment of Primary Sclerosing Cholangitis [NCT00953615]Phase 21 participants (Actual)Interventional2006-04-30Terminated(stopped due to Lack of enrollment)
A Phase III Study for Patients Relapsing or Progressing After Autologous Transplantation on Total Therapy 2 (TT2, UARK 98-026): Bortezomib, Thalidomide and Dexamethasone Versus Bortezomib, Melphalan, and Dexamethasone [NCT00573391]Phase 35 participants (Actual)Interventional2006-08-31Terminated(stopped due to low accrual)
Randomized Phase 2 Study of Daunorubicin and Cytarabine Liposome + Pomalidomide Versus Daunorubicin and Cytarabine Liposome in Newly Diagnosed AML With MDS-Related Changes [NCT04802161]Phase 278 participants (Anticipated)Interventional2022-08-24Recruiting
A Phase II Study of VAD (Vincristine, Adriamycin, Dexamethasone) Plus Thalidomide (Low Dose) as Frontline Therapy for Newly Diagnosed Patients With Multiple Myeloma (MM) [NCT00054158]Phase 224 participants (Actual)Interventional2004-08-31Completed
Efficacy and Safety of Combination of Hydroxyurea and Low-dose Thalidomide on Hemoglobin Synthesis in Thalassemia Patients [NCT05132270]Phase 2/Phase 3135 participants (Actual)Interventional2020-01-01Completed
Phase 1 Study of the Effects of Huang-Lian-Jie-Du-Tang(HLJDT) on the Survival of Patients With Multiple Myeloma in Maintain Therapy [NCT02467647]Phase 1500 participants (Anticipated)Interventional2015-01-31Recruiting
Study of Pomalidomide in Anal Cancer Precursors (SPACE): a Phase 2 Study of Immunomodulation in People With Persistent HPV-associated High Grade Squamous Intraepithelial Lesions [NCT03113942]Phase 226 participants (Actual)Interventional2017-06-14Active, not recruiting
A Multicenter Phase II Study of Pomalidomide Monotherapy in Kaposi Sarcoma [NCT04577755]Phase 245 participants (Anticipated)Interventional2022-03-18Recruiting
PA-Gemox Regimen Followed by Thalidomide Versus AspaMetDex Regimen in NKTCL Patients:a Randomized, Open-label, Phase 3 Study [NCT02085655]Phase 3264 participants (Anticipated)Interventional2013-04-25Recruiting
The Effect of Thalidomide in Radiation-induced Brain Injury(RI): a Phase II Clinical Trial [NCT03208413]Phase 258 participants (Anticipated)Interventional2017-07-19Recruiting
A Phase I/IIa Trial of VTD-panobinostat Treatment and Panobinostat Maintenance in Relapsed and Relapsed/Refractory Multiple Myeloma Patients [NCT02145715]Phase 1/Phase 254 participants (Anticipated)Interventional2013-01-31Active, not recruiting
Phase II Randomized Study of Docetaxel With or Without Thalidomide in Patients With Androgen-Independent Metastatic Prostate Cancer [NCT00020046]Phase 20 participants Interventional1999-12-31Completed
Irinotecan Plus Thalidomide in Second Line Advanced Gastric Cancer : A Multicenter, Randomized, Controlled and Prospective Trial [NCT02401971]Phase 4900 participants (Anticipated)Interventional2014-08-31Recruiting
A Prospective, Randomized, Double-blind, Placebo-controlled Study of Thalidomide in the Treatment of Refractory Uremic Pruritus [NCT05525234]Phase 440 participants (Anticipated)Interventional2022-09-15Not yet recruiting
A PHASE 2 CLINICAL STUDY OF POMALIDOMIDE (CC-4047) MONOTHERAPY FOR CHILDREN AND YOUNG ADULTS WITH RECURRENT OR PROGRESSIVE PRIMARY BRAIN TUMORS [NCT03257631]Phase 253 participants (Actual)Interventional2017-08-22Completed
A Multicenter, Open Label, Randomized Phase II Study Comparing Daratumumab Combined With Bortezomib-Cyclophosphamide-dexamethasone (Dara-VCd) Versus the Association of Bortezomib-Thalidomide-dexamethasone (VTd) as Pre Transplant Induction and Post Transpl [NCT03896737]Phase 2401 participants (Actual)Interventional2019-04-16Active, not recruiting
The Clinical Efficacy and the Changes of Immune Cells Subsets With Bioagents in Ankylosing Spondylitis Patients [NCT05527444]Phase 4100 participants (Anticipated)Interventional2022-03-15Active, not recruiting
Phase II Trial of Fludarabine & Cyclophosphamide Followed by Thalidomide for Angioimmunoblastic Lymphoma [NCT00958854]Phase 237 participants (Anticipated)Interventional2006-01-31Recruiting
A Randomized, Open-Label, Multi-Center Trial Comparing Thalidomide Plus Dexamethasone (Thal-Dex) Versus DOXIL plusThalidomide Plus Dexamethasone (DOXIL -Thal-Dex) in Subjects With Newly Diagnosed Multiple Myeloma [NCT00097981]Phase 3225 participants (Actual)Interventional2005-01-31Completed
A Phase I/II Study of Sorafenib With Combination of Thalidomide in Advanced or Metastatic Hepatocellular Carcinoma [NCT00971126]Phase 1/Phase 23 participants (Actual)Interventional2009-07-31Terminated(stopped due to Two patients in the first dose level be counted as reaching DLT. DSMB recommend terminated early this trial.)
Phase II Study of Rituximab in Combination With Methotrexate, Doxorubicin, Cyclophosphamide, Leucovorin, Vincristine, Ifosfamide, Etoposide, Cytarabine and Mesna (MACLO/IVAM) in Patients With Previously Untreated Mantle Cell Lymphoma [NCT00450801]Phase 222 participants (Actual)Interventional2004-04-30Completed
Open Label of Thalidomide in Treatment of Women With Chronic Pelvic Pain Associated With Endometriosis [NCT01028781]Phase 19 participants (Actual)Interventional2006-10-31Terminated(stopped due to Difficulty finding eligible participants and lack of funding.)
Doxil® (Pegylated Liposomal Doxorubicin), Dexamethasone Plus Thalidomide (Ddt) in Previously Untreated Multiple Myeloma: A Study Evaluating Efficacy, Toxicity, Harvest Yield and Quality of Life [NCT00222105]Phase 225 participants (Actual)Interventional2002-11-30Completed
A Randomized Study Of Tamoxifen Versus Thalidomide (NSC# 66847) In Patients With Biochemical-Recurrence-Only Epithelial Ovarian Cancer, Cancer Of The Fallopian Tube, And Primary Peritoneal Carcinoma After First Line Chemotherapy [NCT00041080]Phase 3139 participants (Actual)Interventional2003-02-28Completed
Efficacy of Thalidomide in Preventing Chemotherapy-induced Delayed Nausea and Vomiting From Highly Emetogenic Chemotherapy: a Randomized, Multicenter, Double-blind, Placebo-controlled Phase III Trial [NCT02203253]Phase 3642 participants (Actual)Interventional2014-07-31Completed
Thalidomide-Dexamethasone vs Alpha-Interferon-Dexamethasone as Maintenance Therapy After Thalidomide, Dexamethasone and Pegylated Liposomal Doxorubicin Combination for [NCT00633542]Phase 3103 participants (Actual)Interventional2003-06-30Completed
A Randomised, Double-blind, Placebo-controlled Study of Thalidomide in Gastrointestinal Vascular Malformation Related Bleeding [NCT02754960]Phase 20 participants (Actual)Interventional2010-03-31Withdrawn
A Phase 2 Evaluation of Daratumumab-Based Treatment in Newly Diagnosed Multiple Myeloma Patients With Renal Insufficiency [NCT04352205]Phase 225 participants (Anticipated)Interventional2020-05-07Recruiting
[NCT00006198]Phase 20 participants InterventionalActive, not recruiting
The Efficacy and Safety of Chidamide Combined With VDDT Regimen(Vinorelbine,Liposomal Doxorubicin,Dexamethasone and Thalidomide) in Relapse and Refractory Patients With Diffuse Large B Cell Lymphoma [NCT02733380]Phase 220 participants (Anticipated)Interventional2016-05-31Recruiting
A Randomized Phase II, 2-armed Study in Transplant Ineligible (TI) Patients With Newly Diagnosed Multiple Myeloma (NDMM) Comparing Carfilzomib + Thalidomide + Dexamethasone (KTd) Versus Carfilzomib + Lenalidomide + Dexamethasone (KRd) Induction Therapy Wi [NCT02891811]Phase 2124 participants (Actual)Interventional2017-03-10Active, not recruiting
Comparison of Melphalan-Prednisone (MP) to MP Plus Thalidomide in the Treatment of Newly Diagnosed Very Elderly Patients (> 75 Years) With Multiple Myeloma [NCT00644306]Phase 3232 participants (Actual)Interventional2002-04-30Terminated(stopped due to survival advantage demonstrated)
A Phase Ⅳ,Open,Multicenter,Single Arm Study to Evaluate the Efficacy of the Combination Conmana With Thalidomide in Patients With NSCLC(Non-Small-Cell-Lung-Cancer) [NCT02778893]Phase 467 participants (Anticipated)Interventional2016-03-31Recruiting
Randomized Controlled Double-blind Vs. Placebo Multicentre Study on the Safety and Effectiveness of Thalidomide in the Treatment of Refractory Crohn's Disease and Ulcerative Colitis. [NCT00720538]Phase 384 participants (Actual)Interventional2008-08-31Completed
Phase II Study of VDT (VELCADE, Doxil® and Thalidomide) as Frontline Therapy for Patients With Previously Untreated Multiple Myeloma (MM) [NCT00523848]Phase 246 participants (Actual)Interventional2006-06-30Completed
Study of Daratumumab in Combination With Bortezomib (VELCADE), Thalidomide, and Dexamethasone (VTD) in the First Line Treatment of Transplant Eligible Subjects With Newly Diagnosed Multiple Myeloma [NCT02541383]Phase 31,085 participants (Actual)Interventional2015-09-30Active, not recruiting
The AP-GELP Study: A Randomized, Placebo-Controlled Clinical Trial on the Effects of Phosphodiesterase 4-Inhibitor Apremilast in Female Genital Erosive Lichen Planus [NCT03656666]Phase 242 participants (Anticipated)Interventional2019-09-24Active, not recruiting
Multicentre,A Phase II/III Randomized Study of Adjuvant Anti-Angiogenesis Therapy for Patients of High-Risk Oral Cavity Cancer [NCT00934739]Phase 2/Phase 3150 participants (Actual)Interventional2007-06-30Terminated
Phase II Trial of Thalidomide and Doxil® (Doxorubicin HCL Liposome Injection) in Patients With Androgen Independent Prostate Cancer (AIPC) With a Rising PSA While on Chemotherapy [NCT00307294]Phase 240 participants (Actual)Interventional2006-03-31Completed
A Prospective Multicenter Phase 2 Study of FCR/BR Alternating With Ibrutinib in Treatment-naive Patients With Chronic Lymphocytic Leukemia [NCT03980002]Phase 250 participants (Anticipated)Interventional2019-05-15Recruiting
Randomized Phase 3b Study of Three Treatment Regimens in Subjects With Previously Untreated Multiple Myeloma Who Are Not Considered Candidates for High-Dose Chemotherapy and Autologous Stem Cell Transplantation: VELCADE, Thalidomide, and Dexamethasone Ver [NCT00507416]Phase 3502 participants (Actual)Interventional2007-06-30Completed
The Effects of Thalidomide on Symptom Clusters [NCT00379353]Phase 232 participants (Actual)Interventional2006-09-30Completed
A Phase II Study of Thalidomide (THALOMID®), Clarithromycin (BIAXIN®), Lenalidomide(REVLIMID®), and Dexamethasone (DECADRON®) for Subjects With Newly Diagnosed Multiple Myeloma [NCT00538733]Phase 226 participants (Actual)Interventional2007-10-31Completed
A Phase 1, Open Label, Randomized, Two Part Study to Evaluate the Pharmacokinetic Exposure of a Once-Daily (QD) Apremilast Formulation Relative to the Twice-Daily (BID) Reference Immediate Release (IR) Tablet and the Effect of Food on the QD Apremilast Fo [NCT02777554]Phase 1144 participants (Actual)Interventional2016-08-17Completed
Effects of Exercise in Combination With Epoetin Alfa During High-Dose Chemotherapy and Autologous Peripheral Blood Stem Cell Transplantation for Multiple Myeloma [NCT00577096]120 participants (Actual)Interventional2001-10-31Completed
Thalidomide Plus Chemotherapy Versus Chemotherapy Alone: A Phase II Study in Advanced Breast Cancer [NCT02649101]Phase 260 participants (Anticipated)Interventional2015-10-31Recruiting
Thalidomide for the Treatment of Cytopenias of Patients With Low Risk Myelodysplastic Syndromes [NCT00455910]Phase 2112 participants Interventional2003-01-31Completed
An Open-Label Phase IV Study of the Efficacy of Bortezomib-based Combination Therapy the Treatment of Subjects With Multiple Myeloma [NCT02559154]Phase 480 participants (Actual)Interventional2010-07-31Active, not recruiting
Phase Ⅲ Study of Adjuvant Therapy With Thalidomide for Chemoembolization in Advanced Hepatocellular Carcinoma [NCT00921531]Phase 3200 participants (Anticipated)Interventional2009-06-30Recruiting
Phase II Study of Patients With Hormone-Naïve Prostate Cancer With a Rising Prostate Specific Antigen: Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF), Thalidomide Plus Docetaxel [NCT00450008]Phase 29 participants (Actual)Interventional2006-12-31Terminated(stopped due to PI decision)
Phase II Study of Thalidomide in Mastocytosis [NCT00769587]Phase 220 participants (Actual)Interventional2007-06-30Completed
Phase I/II Study of Lenalidomide (Revlimid), Thalidomide, and Dexamethasone in Patients With Relapsed/Refractory Multiple Myeloma [NCT00966693]Phase 1/Phase 277 participants (Actual)Interventional2009-08-25Completed
Low-Dose Thalidomide as Adjuvant Therapy After Radiofrequency Ablation for Hepatocellular Carcinoma [NCT00728078]Phase 2/Phase 3200 participants (Anticipated)Interventional2008-07-31Recruiting
Thalidomide to Chemotherapy Related Nausea and Vomiting in Pancreatic Cancer [NCT06017284]Phase 3100 participants (Anticipated)Interventional2023-11-01Recruiting
The Efficacy and Safety of Thalidomide Combined With Low-dose Hormones in the Treatment of Severe New Coronavirus (COVID-19) Pneumonia: a Prospective, Multicenter, Randomized, Double-blind, Placebo, Parallel Controlled Clinical Study [NCT04273581]Phase 240 participants (Anticipated)Interventional2020-02-18Not yet recruiting
A Phase 3, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Efficacy and Safety Study of Two Doses of Apremilast (CC-10004) in Subjects With Active Psoriatic Arthritis and a Qualifying Psoriasis Lesion [NCT01212770]Phase 3505 participants (Actual)Interventional2010-09-30Completed
Thalidomide Versus Bortezomib in Melphalan Refractory Myeloma [NCT00602511]Phase 3300 participants (Anticipated)Interventional2007-10-31Completed
The Feasibility of Combing THALIDOMIDE and UFUR in the Treatment of Advanced Colorectal Cancer After Oxaliplatin-Contained Chemotherapy [NCT00890188]Phase 234 participants (Anticipated)Interventional2009-01-31Recruiting
Thalomid and Carboplatin for the Treatment of Pediatric Brain Stem Glioma [NCT00179881]Phase 247 participants (Anticipated)Interventional1999-12-31Completed
A Phase II Study of Metronomic and Targeted Anti-angiogenesis Therapy for Children With Recurrent/Progressive Medulloblastoma, Ependymoma and ATRT [NCT01356290]Phase 2100 participants (Anticipated)Interventional2014-04-30Recruiting
A Phase 3, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Efficacy and Safety Study of Two Doses of Apremilast (CC-10004) in Subjects With Active Psoriatic Arthritis [NCT01212757]Phase 3488 participants (Actual)Interventional2010-09-27Completed
Phase III Study of Single Autologous Stem Cell Transplantation Followed by Maintenance Therapy as Front-line Treatment for Myeloma [NCT00892346]Phase 380 participants (Anticipated)Interventional2009-05-31Suspended(stopped due to No avaliability of melphlan in mainland China)
The Efficacy of Thalidomide Plus Cyclophosphamide and Dexamethasone Following by Thalidomide and Prednisone Maintenance Therapy for the Newly Diagnosed Waldenström Macroglobulinemia - a Prospective Multicentre Phase Ⅳ Trial From China [NCT02844309]Phase 444 participants (Anticipated)Interventional2016-05-31Recruiting
A Multicenter Randomized Open Label Phase II Study of Pomalidomide and Dexamethasone in Relapse and Refractory Multiple Myeloma Patients Who Are Progressive and Did Not Achieve at Least a Partial Response to Bortezomib and Lenalidomide [NCT01053949]Phase 284 participants (Actual)Interventional2009-10-31Completed
A Phase 2, Multicenter, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group, Dose Comparison Study of CC-10004 in Subjects With Moderate-to-Severe Plaque-Type Psoriasis [NCT00606450]Phase 2260 participants (Actual)Interventional2006-04-01Completed
A Phase III, Randomized, Open-label, 3-arm Study to Determine the Efficacy and Safety of Lenalidomide(REVLIMID) Plus Low-dose Dexamethasone When Given Until Progressive Disease or for 18 Four-week Cycles Versus the Combination of Melphalan, Prednisone, an [NCT00689936]Phase 31,623 participants (Actual)Interventional2008-08-21Completed
A Phase 2, Single Arm Study to Determine the Safety and Efficacy of Azacitidine, and Thalidomide in Higher Risk Myelodysplastic Syndrome [NCT00704704]Phase 250 participants (Anticipated)Interventional2008-09-30Not yet recruiting
A Phase 1, Open-label Study to Evaluate the Pharmacokinetics of Thalidomide Following Multiple Oral Dosing in Subjects With Multiple Myeloma [NCT01937442]Phase 17 participants (Actual)Interventional2013-11-07Completed
UARK 2006-15: A Phase III Randomized Study of Tandem Transplants With or Without Bortezomib (Velcade) and Thalidomide (Thalomid) to Evaluate Its Effect on Response Rate and Durability of Response in Multiple Myeloma Patients [NCT00574080]Phase 320 participants (Actual)Interventional2006-07-31Terminated(stopped due to low accrual)
Thalidomide for Unresectable Hepatocellular Cancer With Optional Interferon Alpha-2a Upon Disease Progression [NCT00006006]Phase 238 participants (Actual)Interventional2000-08-31Completed
A Phase II Trial of Thalidomide in Patients With Relapsed Chronic Lymphocytic Leukemia [NCT00006226]Phase 241 participants (Anticipated)Interventional2000-09-30Completed
A Phase II Clinical Trial Of Thalidomide, Adramycin And Dexamethasone (TAD) As Initial Therapy For The Treatment Of Multiple Myeloma [NCT00008242]Phase 20 participants Interventional2000-08-31Completed
UARK 2008-03 Phase II Trial for Patients Not Qualifying for TT4 and TT5 Protocols Because of Prior Therapy (No Prior Transplant) [NCT00871013]Phase 2160 participants (Anticipated)Interventional2009-03-31Active, not recruiting
Thalidomide Reduces Arteriovenous Malformation Related Gastrointestinal Bleeding [NCT00389935]Phase 214 participants (Actual)Interventional2006-10-31Completed
Thalidomide for the Treatment of Malnutrition Inflammation Syndrome in Peritoneal Dialysis Patients: A Randomized Control Trial [NCT00390247]Phase 40 participants (Actual)Interventional2007-01-31Withdrawn(stopped due to Fail of applying funding)
Secondary Prophylaxis of Gastrointestinal Bleeding in Cirrhotic Patients Using Thalidomide [NCT00787436]Phase 30 participants (Actual)Interventional2006-05-31Withdrawn
A Phase III Trial of Dexamethasone, Cyclophosphamide, Etoposide, Cisplatin (DCEP) and G-CSF With or Without Thalidomide (NSC #66847) as Salvage Therapy for Patients With Refractory Multiple Myeloma [NCT00005834]Phase 319 participants (Actual)Interventional2000-04-30Terminated(stopped due to poor accrual)
Lenalidomide, Melphalan, Prednisone, and Thalidomide (RMPT) for Relapsed/Refractory Multiple Myeloma [NCT00961467]Phase 244 participants (Actual)Interventional2007-02-28Completed
Phase III Randomized Trial of Interferon-Alfa2b Alone Versus Interferon-Alfa2b Plus Thalidomide in Patients With Previously Untreated Metastatic or Unresectable Renal Cell Carcinoma [NCT00005966]Phase 30 participants Interventional2000-10-31Completed
Phase II Study of Thalidomide (NSC #66847) in Patients With Sarcomas of Gynecologic Origin [NCT00006005]Phase 20 participants Interventional2000-09-30Completed
Evaluation of a TNF-Alpha Modulator for the Treatment of Oral Lesions in HIV/AIDS Patients [NCT00001524]Phase 2110 participants Interventional1996-06-30Completed
A Phase II Study of Tegafur/Uracil(UFUR) Plus Thalidomide for the Treatment of Advanced or Metastatic Hepatocellular Carcinoma (HCC) [NCT00519688]Phase 244 participants (Actual)Interventional2006-07-31Completed
Intensive Dose Temozolomide Treatment or Temozolomide With Thalidomide Treatment in Recurrent Glioblastoma After Standard Therapy:a Randomized Phase II Trial [NCT00521482]Phase 240 participants (Anticipated)Interventional2007-09-30Not yet recruiting
Pharmacogenomic Study to Predict Survival, Best Response and Toxicity in Newly Diagnosed Myeloma Patients Above the Age of 65 Treated With Either a Combination of Melphalan-prednisone-thalidomide or Lenalidomide-dexamethasone [NCT00907452]143 participants (Actual)Interventional2009-07-29Completed
S0833, Modified Total Therapy 3 (TT3) for Newly Diagnosed Patients With Multiple Myeloma (MM): A Phase II SWOG Trial for Patients Aged ≤ 65 Years [NCT01055301]Phase 20 participants (Actual)Interventional2011-07-31Withdrawn(stopped due to lack of accrual)
A Phase II Trial of Combination Therapy With Thalidomide and CPT-11 in Patients With Recurrent Anaplastic Gliomas or Glioblastoma Multiforme [NCT00412542]Phase 278 participants (Actual)Interventional2003-10-31Completed
Anti-Angiogenic Chemotherapy: A Phase II Trial of the Oral 5-Drug Regimen (Thalidomide, Celecoxib, Fenofibrate, Etoposide and Cyclophosphamide) in Patients With Relapsed or Progressive Cancer [NCT00357500]Phase 2101 participants (Actual)Interventional2005-01-31Completed
Multiple Myeloma Treatment With Thalidomide. Three Randomized Studies on Thalidomide as Induction Treatment Before Autotransplant (MY-TAG) or With a Conventional Chemotherapy (MY-DECT) and as Consolidation/Maintenance at Plateau Phase (MY-PLAT). [NCT01070862]Phase 30 participants Interventional2003-05-31Completed
A Phase 2, Prospective, Randomized, Multicenter, Double-blind, Active-control, Parallel-group Study to Determine the Safety of and to Select a Treatment Regimen of CC-4047 (Pomalidomide) Either as Single-agent or in Combination With Prednisone to Study Fu [NCT00463385]Phase 288 participants (Actual)Interventional2007-04-01Completed
Bortezomib + Pegylated Liposomal Doxorubicin (Doxil) + Dexamethasone Followed by Thalidomide + Dexamethasone or Bortezomib + Thalidomide + Dexamethasone for Patients With Symptomatic Untreated High-Risk or Primary Resistant Multiple Myeloma [NCT00458705]Phase 245 participants (Actual)Interventional2006-11-30Completed
The Efficacy and Safety of Thalidomide in the Adjuvant Treatment of Moderate New Coronavirus (COVID-19) Pneumonia: a Prospective, Multicenter, Randomized, Double-blind, Placebo, Parallel Controlled Clinical Study [NCT04273529]Phase 2100 participants (Anticipated)Interventional2020-02-20Not yet recruiting
A Phase II Trial of Thalidomide and Capecitabine in Metastatic Renal Cell Carcinoma [NCT00226980]Phase 230 participants (Anticipated)Interventional2002-10-31Completed
A Phase II Study of Arsenic Trioxide in Combination With Thalidomide, Dexamethasone, and Ascorbic Acid [NCT00227682]Phase 22 participants (Actual)Interventional2004-06-30Terminated(stopped due to Terminated early due to funding suspension by grant sponsor.)
International, Multi-center, Prospective, Double Randomized, Open Phase III Study Evaluating Thalidomide/Dexamethasone Versus Melphalan/Prednisone as Induction Therapy and Thalidomide/Interferon-alpha Versus Interferon-alpha as Maintenance Therapy in Newl [NCT00205751]Phase 2/Phase 3350 participants (Anticipated)Interventional2001-08-31Completed
Efficacy and Safety of Daratumumab in Combination With Bortezomib, Thalidomide, and Dexamethasone Regimens in Newly Diagnosed Multiple Myeloma With Renal Dysfunction in Real-World: A Non-interventional Prospective Multicenter Observational Study [NCT05561049]120 participants (Anticipated)Observational2022-10-01Not yet recruiting
A Phase 3 Study With Randomization to Melphalan/Prednisone/Thalidomide Versus Melphalan/Prednisone/Placebo to Patients With Previously Untreated Multiple Myeloma [NCT00218855]Phase 3363 participants (Actual)Interventional2002-01-31Completed
"A PHASE III STUDY OF VELCADE (BORTEZOMIB) THALIDOMIDE DEXAMETHASONE (VTD) VERSUS VELCADE (BORTEZOMIB) CYCLOPHOSPHAMIDE DEXAMETHASONE (VCD) AS AN INDUCTION TREATMENT PRIOR TO AUTOLOGOUS STEM CELL TRANSPLANTATION IN PATIENTS WITH NEWLY DIAGNOSED MULTIPLE M [NCT01971658]Phase 3358 participants (Actual)Interventional2013-10-31Completed
An Open-label, Randomized Multicenter Investigation of High-dose Dexamethasone Combining Thalidomide Versus High-dose Dexamethasone Mono-therapy for Management of Newly-diagnosed Immune Thrombocytopenia [NCT01976195]Phase 20 participants (Actual)Interventional2013-10-31Withdrawn(stopped due to No eligible patient was enrolled.)
A Phase 1, Double-blind, Four Period Crossover Study to Investigate the Effects of Pomalidomide (CC 4047) on the QT Interval in Healthy Male Subjects [NCT01986894]Phase 172 participants (Actual)Interventional2013-10-18Completed
A Comparative Study of Bortezomib-Thalidomide-Dexamethason and Bortezomib-Cyclophosphamide-Dexamethason in the Treatment of Monoclonal Immunoglobulin Light Chain Amyloidosis: A Prospective Randomized Controlled Trial(BTD-CHINA-TRIAL) [NCT04612582]Phase 470 participants (Anticipated)Interventional2020-01-01Recruiting
Double-blind, Placebo-controlled, Randomized Phase III Trial of Oral Thalidomide in Advanced Hepatocellular Carcinoma With Poor Liver Reserve [NCT00225290]Phase 3230 participants (Anticipated)Interventional2003-02-28Terminated(stopped due to slowly recruitment rate)
A Phase 2, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group Study, To Compare the Efficacy and Safety of Two Doses of Apremilast (CC-10004) in Subjects With Active Rheumatoid Arthritis Who Have Had an Inadequate Response to Methot [NCT01285310]Phase 2237 participants (Actual)Interventional2010-12-09Terminated(stopped due to Study is terminated due to lack of efficacy)
A Phase II Study of Temozolomide, Thalidomide, and Lomustine in the Treatment of Advanced Melanoma [NCT00072345]Phase 20 participants Interventional2003-07-31Completed
An Evaluation of Chronic Thalidomide Administration in Patients Undergoing Chemoembolization for Unresectable Hepatocellular Cancer [NCT00006016]Phase 275 participants (Actual)Interventional2000-05-31Completed
Phase II Evaluation of Temozolomide (SCH52365) and Thalidomide for the Treatment of Recurrent and Progressive Glioblastoma Multiforme [NCT00006358]Phase 244 participants (Actual)Interventional2000-06-13Completed
Thalidomide for Treatment of Oral and Esophageal Aphthous Ulcers and HIV Viremia in Patients With HIV Infection [NCT00000790]Phase 2164 participants InterventionalCompleted
UARK 2007-01, A Phase II Pilot Study of the Combination of Melphalan, Bortezomib, Thalidomide and Dexamethasone (MEL-VTD) and Autologous Transplantation for Patients Relapsing or Progressing After Tandem Transplantation [NCT00577668]Phase 20 participants (Actual)Interventional2007-04-30Withdrawn(stopped due to Poor accrual)
Effects of Thalidomide on Left Ventricular Morphology and Function in Patients With Congestive Heart Failure - The THUNDER Trial [NCT01640639]Phase 4100 participants (Anticipated)Interventional2012-07-31Recruiting
A Phase 3, Randomized, Controlled, Open-label, Multicenter, Safety and Efficacy Study of Dexamethasone Plus MLN9708 or Physicians Choice of Treatment Administered to Patients With Relapsed or Refractory Systemic Light Chain (AL) Amyloidosis [NCT01659658]Phase 3177 participants (Actual)Interventional2012-12-12Terminated(stopped due to Sponsor's decision)
Glutamine Combined With Thalidomide in Preventing Radiation-induced Oral Mucositis in Patients Undergoing radiotherapy-a Multicenter, Open-label, Randomized Controlled Study [NCT06031012]Phase 370 participants (Anticipated)Interventional2023-09-15Not yet recruiting
A Phase 3, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Efficacy and Safety Study of Two Doses of Apremilast (CC-10004) in Subjects With Active Psoriatic Arthritis [NCT01172938]Phase 3504 participants (Actual)Interventional2010-06-02Completed
Usefulness of Adding Thalidomide to Peginterferon and Ribavirin in Patients With Hepatitis C and Resistance to Interferon. Phase II [NCT00856804]Phase 210 participants (Anticipated)Interventional2009-03-31Recruiting
Deciphering Effects of Thalidomide on Red Blood Cells in Transfusion Dependents Beta Thalassemia Patients: A Pharmacodynamics and Pharmacogenetics Analysis [NCT06146478]Phase 3200 participants (Actual)Interventional2022-01-25Completed
Thalidomide in Indolent Non-Hodgkin's Lymphoma: A Feasibility Study [NCT00052416]Phase 10 participants Interventional2002-10-31Completed
A Phase I Pharmacokinetic Interaction Study of Irinotecan (NSC616348) and Thalidomide (NSC66847) in Patients With Advanced Solid Tumors [NCT00062127]Phase 135 participants (Actual)Interventional2003-04-30Completed
S0629, Observational Study of Asymptomatic Waldenstrom's Macroglobulinemia and Phase II Study of Tandem Autologous Transplant and Maintenance Treatment for Patients With Symptomatic Disease [NCT00723658]Phase 20 participants (Actual)Interventional2008-09-30Withdrawn(stopped due to lack of accrual)
Phase 3 Study: The Effect of Thalidomide in Suppression of the Systemic Inflammatory Response Syndrome in Hemodialysis Patients [NCT00529633]Phase 316 participants (Actual)Interventional2007-09-30Terminated(stopped due to Low enrollment -- We could not recruit patients willing to be enrolled)
Multicenter, Randomized Study Comparing the Efficacy and Safety of Two Doses of Thalidomide (100 mg/Day Versus 400 mg/Day) in the Treatment of Subjects With Refractory or Relapsed Multiple Myeloma. [NCT00657488]Phase 2/Phase 3400 participants (Actual)Interventional2001-12-01Completed
A Phase 3 Study of Velcade (Bortezomib) Dexamethasone (VD) Versus Velcade (Bortezomib) Thalidomide Dexamethasone (VTD) as an Induction Treatment Prior to Autologous Stem Cell Transplantation in Patients With Newly Diagnosed Multiple Myeloma [NCT00910897]Phase 3205 participants (Actual)Interventional2008-03-31Active, not recruiting
Treatment of Chronic Cough in Idiopathic Pulmonary Fibrosis With Thalidomide [NCT00600028]Phase 325 participants (Actual)Interventional2007-12-31Completed
UARK 98-025, A Randomized Phase II Trial of Dexamethasone or Dexamethasone in Combination With Thalidomide as Salvage Therapy for Low-Risk Post Transplantation Relapse in Patients With Multiple Myeloma [NCT00083902]Phase 2190 participants Interventional1998-06-30Completed
Risk Adapted Intravenous Melphalan and Adjuvant Thalidomide and Dexamethasone for Untreated Patients With Primary Systemic Amyloidosis [NCT00089167]Phase 20 participants Interventional2002-05-31Completed
A Phase II Trial Of Thalidomide And Procarbazine In Adults With Recurrent/Progressive Gliomas [NCT00079092]Phase 218 participants (Anticipated)Interventional2004-01-01Completed
A Phase 2B, Multicenter, Randomized, Double-Blind, Placebo-Controlled, Dose-Ranging, Efficacy and Safety Study of Apremilast (CC-10004) in Subjects With Moderate-to-Severe Plaque-Type Psoriasis (Core Study) [NCT00773734]Phase 2352 participants (Actual)Interventional2008-09-01Completed
An Open, Non-Comparative Trial to Assess the Efficacy and Safety of Oral Thalidomide (THADO) in Patientswith Hormone-Refractory Prostate Cancer-A PHASE II CLINICAL TRIAL [NCT00201357]Phase 230 participants (Actual)Interventional2002-10-31Completed
Maintenance Therapy With Thalidomide, Dexamethasone and Clarithromycin (Biaxin) Following Autologous/Syngeneic Transplant for Multiple Myeloma [NCT00182663]Phase 230 participants (Anticipated)Interventional2003-06-30Completed
A Phase II Trial of CC-5013 in Patients With Primary Systemic Amyloidosis [NCT00166413]Phase 238 participants (Anticipated)Interventional2005-04-30Completed
A Phase II Study Of Epirubicin And Thalidomide In Unresectable Or Metastatic Hepatocellular Carcinoma [NCT00058487]Phase 212 participants (Anticipated)Interventional2001-12-31Completed
Department of Hematologic Oncology, Sun Yat-sen University Cancer Center, Guangzhou, China [NCT04762745]Phase 1/Phase 256 participants (Anticipated)Interventional2021-02-28Not yet recruiting
A Phase II Study Of Peg-Intron, GM-CSF And Thalidomide In Metastatic Renal Cell Carcinoma [NCT00090870]Phase 210 participants (Actual)Interventional2002-04-30Terminated(stopped due to Pharmaceutical collaborator pulled funding.)
A Pilot Trial of Topical Thalidomide for the Management of Chronic Discoid Lupus Erythematosus [NCT00001680]Phase 217 participants Interventional1997-10-31Completed
Clarithromycin Plus CTd (Cyclophosphamide,Thalidomide and Dexamethasone)Regimen for Patients With Newly Diagnosed Multiple Myeloma:a Phase 3 , Multicenter,Randomized, Open-Label Trial. [NCT02248428]Phase 3130 participants (Anticipated)Interventional2012-04-30Recruiting
A National, Open-Label, Multicenter, Randomized, Comparative Phase III Study of Induction Treatment With Melphalan/Prednisone/Velcade Versus Thalidomide / Prednisone / Velcade and Maintenance Treatment With Thalidomide / Velcade Versus Prednisone / Velcad [NCT00443235]Phase 3260 participants (Anticipated)Interventional2005-03-31Completed
Induced Adult Refractory Active Crohn's Disease Clinical Relieving by Using Thalidomide: A Randomized, Double-blind, Placebo-controlled Multicenter Clinical Study [NCT02956538]Early Phase 172 participants (Anticipated)Interventional2016-10-31Recruiting
A National, Open-Label, Multicenter, Randomized, Comparative Phase III Study of Induction Treatment With VBMCP-VBAD/Velcade Versus Thalidomide / Dexamethasone Versus Velcade / Thalidomide / Dexamethasone Followed by High Dose Intensive Therapy With Autolo [NCT00461747]Phase 3390 participants (Anticipated)Interventional2006-03-31Completed
A Phase II, Open-Label, Single Center Pilot Study to Determine the Safety and Efficacy of THALOMID (Thalidomide) in Patients With Chronic Pancreatitis. [NCT00469703]Phase 210 participants (Anticipated)Interventional2005-08-31Terminated(stopped due to Terminated)
A Phase I Study of Temozolomide, Thalidomide, and Lomustine (TTL) in Patients With Metastatic Melanoma in the Brain [NCT00527657]Phase 117 participants (Actual)Interventional2006-02-09Completed
Phenotypic Personalized Medicine: Systematically Optimized Combination Therapy in Multiple Myeloma Using CURATE.AI [NCT03759093]Phase 2/Phase 320 participants (Anticipated)Interventional2023-09-10Recruiting
A Phase II Trial of Combination Thalidomide Plus Temozolomide in Patients With Metastatic Malignant Melanoma [NCT00104988]Phase 264 participants (Actual)Interventional2005-06-30Completed
Prospective, Open Clinical Trial of Thalidomide in the Treatment of Chronic Radiation Proctitis With Intractable Bleeding [NCT04680195]Phase 262 participants (Anticipated)Interventional2020-12-14Not yet recruiting
A Randomized Phase II Study of Oral Thalidomide in Patients With Hormone-Refractory Prostate Cancer [NCT00001446]Phase 264 participants Interventional1995-09-30Completed
Thalidomide vs. Placebo for Steroid Dependent or Refractory Chronic Graft vs. Host Disease (cGVHD) IND #42782 [NCT00003894]Phase 236 participants (Actual)Interventional1999-03-31Completed
A Phase II, Multi-Center, Open Label Study Of Melphalan, Prednisone, Thalidomide And Bortezomib In Advanced And Refractory Multiple Myeloma Patients [NCT00358020]Phase 230 participants Interventional2004-11-30Completed
Efficacy of Thalidomide in the Treatment of Severe Recurrent Epistaxis in Hereditary Hemorrhagic Telangiectasia (HHT) [NCT01485224]Phase 231 participants (Actual)Interventional2011-11-30Completed
A Phase 1, Open-Label, Randomized Three-Period, Six-Sequence Crossover Study In Healthy Adult Subjects To Evaluate The Bioavailablity Of An Oral Suspension Formulation Relative To The Tablet Formulation Of Apremilast And To Assess The Effect Of Food On Th [NCT02641353]Phase 134 participants (Actual)Interventional2016-01-05Completed
Frontline Thalidomide for Amyloidosis Involving Myocardium: Investigation of Organ Reversing Capacity of Lenalidomide [NCT02966522]Phase 230 participants (Anticipated)Interventional2016-10-31Recruiting
A Phase I Trial Using Combination Irinotecan and Thalidomide for Recurrent CNS Tumors. [NCT00251797]Phase 110 participants (Actual)Interventional2000-03-31Completed
T Cell Immunity in Collagen Biosynthesis of Scleroderma [NCT00418132]Phase 130 participants (Actual)Interventional2000-08-31Terminated(stopped due to Study terminated early due to difficulties in subject recruitment)
Open-Label Study of Thalidomide for Chronic Prostatitis/Chronic Pelvic Pain [NCT00301405]Phase 29 participants (Actual)Interventional2006-03-31Terminated(stopped due to Study closed. Difficult enrollment of patients with prostatitis.)
UARK 99-016, A Phase II Trial of Combination Bisphosphonate and Anti-Angiogenesis Therapy With Pamidronate and Thalidomide in Patients With Multiple Myeloma and Poor Hematopoietic Stem Cell Reserve [NCT00083408]Phase 220 participants Interventional1998-03-31Completed
UARK 98-018, A Randomized Phase II Trial of DCEP or DCEP in Combination With Thalidomide as Salvage Therapy for Post Transplantation Relapse in Patients With Multiple Myeloma [NCT00083681]Phase 2180 participants Interventional1998-06-30Completed
Evaluation of TNF-Alpha Modulator for Clinical and Molecular Indicators of Analgesic Effect [NCT00121563]Phase 290 participants Interventional2005-07-31Completed
Use of Thalidomide in Chronic Uveitis [NCT00314665]Phase 415 participants Interventional2004-01-31Terminated
UARK 98-035, A Phase III Study of D.T. PACE Versus High Dose Melphalan and Autologous Transplant in Patients With Previously Treated Multiple Myeloma [NCT00083876]Phase 3500 participants Interventional1998-09-30Completed
A Phase II Trial With VELCADE® (PS-341), Cytoxan (Cyclophosphamide), Dexamethasone and Thalomid® (VEL-CTD) in Previously Untreated Multiple Myeloma Patients [NCT00438841]Phase 243 participants (Anticipated)Interventional2006-08-31Active, not recruiting
Randomised, Controlled, Open-labelled, Multi-centre Comparison of Thalidomide Versus High-dose Dexamethasone for the Treatment of Relapsed Refractory Multiple Myeloma [NCT00452569]Phase 3499 participants (Actual)Interventional2006-02-01Completed
Phase II Study of Docetaxel and Thalidomide as a Second-Line Treatment for Non-Small Cell Lung Cancer [NCT00114192]Phase 237 participants (Anticipated)Interventional2004-06-30Completed
"Phase II Study of the Combination of Low-Dose Thalidomide, Prednisone, and Oral Cyclophosphamide (TPC) in the Therapy of Myelofibrosis With Myeloid Metaplasia (MMM)" [NCT00445900]Phase 222 participants (Anticipated)Interventional2004-10-31Completed
Study of Efficacy of PAD-regimen(Bortezomib,Pirarubicin and Dexamethasone) and TAD-regimen(Thalidomide,Pirarubicin and Dexamethasone) in Newly Diagnosed Multiple Myeloma,Influence in Concentration of Bone Metabolites,and the Relations With Different Cytog [NCT01249690]Phase 4100 participants (Anticipated)Interventional2010-06-30Recruiting
MAGNETISMM-1 A PHASE I, OPEN LABEL STUDY TO EVALUATE THE SAFETY, PHARMACOKINETIC, PHARMACODYNAMIC AND CLINICAL ACTIVITY OF ELRANATAMAB (PF-06863135), A B-CELL MATURATION ANTIGEN (BCMA) - CD3 BISPECIFIC ANTIBODY, AS A SINGLE AGENT AND IN COMBINATION WITH I [NCT03269136]Phase 1101 participants (Actual)Interventional2017-11-29Active, not recruiting
A Phase II Multicenter Study of Pomalidomide Monotherapy in HIV-Positive Individuals With Kaposi Sarcoma (KS) in Sub-Saharan Africa (SSA) [NCT03601806]Phase 226 participants (Actual)Interventional2021-04-26Active, not recruiting
A Phase II Study of Dexamethasone (DECADRON®), Thalidomide (THALOMID®), and Lenalidomide (REVLIMID®) for Subjects With Relapsed or Refractory Multiple Myeloma [NCT00538824]Phase 25 participants (Actual)Interventional2007-12-31Terminated(stopped due to low enrollment)
A Phase II Trial For High-Risk Myeloma Evaluating Accelerating and Sustaining Complete Remission (AS-CR) by Applying Non-Host-Exhausting and Timely Dose-Reduced Mel-80-CFZ-TD-Pace Transplant(s) With Interspersed Mel-20-CFZ-TD-Pace With CFZ-RD and CFZ-D Ma [NCT02128230]Phase 220 participants (Actual)Interventional2014-06-10Terminated(stopped due to Low enrollment and Futility as determined by Amgen's Carfilzomib NASCR program.)
University of Arkansas (UARK 2001-12), A Phase III Study of DTPACE Followed by Tandem Transplant With MEL 200 Versus MEL/DTPACE Hybrid and DTPACE Consolidation in Patients With Active Multiple Myeloma [NCT00083915]Phase 397 participants (Actual)Interventional2001-06-30Completed
A Phase 2, Open-label, Investigator-Initiated Study to Evaluate the Safety and Efficacy of Apremilast in Subjects With Recalcitrant Contact or Atopic Dermatitis [NCT00931242]Phase 210 participants (Actual)Interventional2009-06-30Completed
A Phase II Study of Thalidomide in Combination With Temodar in Patients With Metastatic Neuroendocrine Tumors [NCT00165230]Phase 232 participants Interventional2002-05-31Completed
Phase II Study of Pegylated Interferon and Thalidomide in Pretreated Metastatic Malignant Melanoma [NCT00238329]Phase 232 participants (Anticipated)Interventional2001-01-31Completed
[NCT00222053]Phase 3800 participants (Actual)Interventional2000-04-30Completed
Induction Therapy With TCD Regimen (Thalidomide, Cyclophosphamide, Dexamethasone) Followed by Autologous Stem Cell Transplantation in Newly Diagnosed Multiple Myeloma Patients [NCT00349115]Phase 243 participants (Anticipated)Interventional2006-06-30Recruiting
A Pilot Study to Evaluate the Efficacy and Safety of Apremilast in Patients of Chronic and Recurrent Erythema Nodosum Leprosum [NCT04822909]Phase 410 participants (Actual)Interventional2019-09-15Completed
Phase II Multicenter Clinical Trial to Investigate the Efficacy and Safety of Bendamustine, Dexamethasone and Thalidomide in R/R MM Pts After Treatment With Lenalidomide and Bortezomib or Which Are Ineligible to One of These Drugs [NCT01526694]Phase 230 participants (Actual)Interventional2012-07-31Completed
Risk-adapted Therapy for AL Amyloidosis [NCT01527032]Phase 20 participants Interventional2002-09-30Completed
A Phase I, Placebo-Controlled, Dose-Escalation Study of the Safety, Tolerability, and Pharmacokinetics of Thalidomide in Subjects With HIV-1 Infection [NCT00000812]Phase 136 participants InterventionalCompleted
Iberoamerican Phase III International Study, Open, Multicenter, Randomized, Comparative of Thalidomide / Cyclophosphamide / Dexamethasone Versus Thalidomide / Dexamethasone Versus Thalidomide / Melphalan / Prednisone as Induction Therapy Followed by Maint [NCT01532856]Phase 364 participants (Actual)Interventional2007-01-31Active, not recruiting
Further Evaluation of Thalidomide's Ability to Potentiate the Immune Response to HIV-Infected Patients [NCT00002174]20 participants InterventionalCompleted
A Pilot Study of G-CSF to Disrupt the Bone Marrow Microenvironment in Bortezomib-, Carfilzomib-, or IMID-Refractory Multiple Myeloma [NCT01537861]Early Phase 17 participants (Actual)Interventional2012-06-30Terminated(stopped due to Unexpected toxicity (2 early deaths))
A Phase II Clinical Trial on VEGF Expression Interfered by Thalidomide Combined With Concurrent Chemoradiotherapy in Esophageal Cancer [NCT01551641]Phase 2180 participants (Anticipated)Interventional2012-01-31Recruiting
Randomised Comparisons, in Myeloma Patients of All Ages, of Thalidomide, Lenalidomide, Carfilzomib and Bortezomib Induction Combinations, and of Lenalidomide and Combination Lenalidomide Vorinostat as Maintenance (Myeloma XI) [NCT01554852]Phase 34,420 participants (Actual)Interventional2010-05-31Active, not recruiting
A Randomized Phase II Dose Finding Study Of Thalidomide And Prednisone As Maintenance Therapy Following Autologous Stem Cell Transplant In Patients With Multiple Myeloma [NCT00006890]Phase 267 participants (Actual)Interventional2000-07-12Completed
UARK 2005-01, A Phase III Study of Velcade, Thalidomide, and Dexamethasone (VTD) With or Without Adriamycin® in Relapsed/Refractory Patients [NCT00111748]Phase 3180 participants (Anticipated)Interventional2005-02-28Completed
Phase II Study of Arsenic Trioxide, Ascorbic Acid, Dexamethasone, and Thalidomide in Patients With Previously Untreated High-Risk or Relapsed or Refractory Multiple Myeloma [NCT00112879]Phase 20 participants (Actual)InterventionalWithdrawn
A PHASE II STUDY OF ORAL THALIDOMIDE FOR PATIENTS WITH HIV INFECTION AND KAPOSI'S SARCOMA [NCT00019123]Phase 20 participants Interventional1996-04-30Completed
Long-Term Assessment of Thalidomide and Hydroxyurea Combination Therapy in β-Thalassemia Patients [NCT06153784]Phase 2/Phase 3603 participants (Actual)Interventional2020-07-07Completed
Randomized Phase II Study of Thalidomide Versus Thalidomide Plus Fludarabine for Patients With Chronic Lymphocytic Leukemia Previously Treated With Fludarabine [NCT00009984]Phase 270 participants (Actual)Interventional2002-03-31Terminated
Blood and Marrow Transplant Clinical Research Network [NCT00023530]0 participants Interventional2001-09-30Completed
Phase II Study of Carboplatin, Irinotecan, and Thalidomide in Patients With Advanced Non-Small Cell Lung Cancer [NCT00025285]Phase 246 participants (Actual)Interventional2001-11-01Completed
Submyeloablative Allogeneic Blood Stem Cell Transplantation With HLA Identical Donor Lymphocyte Infusions From Matched Related and Matched Unrelated Donors for Treatment of Metastatic Renal Cell Carcinoma [NCT00025519]Phase 20 participants (Actual)Interventional2001-06-30Withdrawn
Phase II Study of Low-Dose Interferon Alfa 2B (Schering Plough) Plus Thalidomide (Celgene) for Patients With Resected High-Risk Soft Tissue Sarcoma [NCT00026416]Phase 20 participants Interventional2001-10-31Active, not recruiting
Phase II Trial of Thalidomide for Therapy of Radioiodine-Unresponsive Papillary and Follicular Thyroid Carcinomas and Medullary Thyroid Carcinomas [NCT00026533]Phase 20 participants Interventional2001-06-30Completed
Interferon Alpha In Combination With Thalidomide In The Treatment Of Metastatic Renal Cell Carcinoma A Randomized Phase II Study [NCT00027664]Phase 290 participants (Anticipated)Interventional2001-02-28Active, not recruiting
A Randomized, Multi-Center, Double-Blind, Placebo-Controlled Trial Assessing The Safety And Efficacy Of Thalidomide (THALOMID) For The Treatment Of Anemia In Red Blood Cell Transfusion-Dependent Patients With Myelodysplastic Syndromes [NCT00030550]Phase 20 participants Interventional2001-09-30Completed
A Phase II Study of Combination Therapy of a Protracted Oral Schedule of Temozolomide and Thalidomide as First-Line or Subsequent Therapy for Patients With Metastatic, Locally Advanced or Unresectable Leiomyosarcoma [NCT00033709]Phase 20 participants Interventional2002-03-31Active, not recruiting
Thalidomide for Multiple Myeloma [NCT00038233]Phase 327 participants (Actual)Interventional1999-05-31Completed
A Phase II Clinical And Biologic Study Of The Combination Of Low Dose Interferon-Alpha And Thalidomide (NSC #66847) For Patients With Relapsed Or Refractory Low-Grade Follicular Lymphoma [NCT00015912]Phase 235 participants (Actual)Interventional2001-07-31Terminated(stopped due to Administratively complete.)
Phase II Study of Thalidomide in the Treatment of Myelodysplastic Syndromes in Adults: A Clinical and Biologic Study [NCT00015990]Phase 229 participants (Actual)Interventional2001-04-30Completed
Phase II Trial of Thalidomide in Patients With Ovarian Cancer [NCT00016224]Phase 20 participants Interventional2001-01-31Completed
A Phase II, Pharmacologic and Biologic Study of Escalating Doses of Thalidomide (NSC #66847) Administered Orally Once a Day in Combination With a Fixed Dose of SU5416 (NSC #696819) in Patients With Metastatic Melanoma [NCT00017316]Phase 235 participants (Actual)Interventional2001-03-31Completed
A Randomized Trial of Interleukin-2 With or Without a Tumor Necrosis Factor Antagonist in Patients With HIV-1 Infection [NCT00001475]Phase 285 participants Interventional1995-06-30Completed
Trial Of Oral Thalidomide, Celecoxib, Etoposide And Cyclophosphamide In Adult Patients With Relapsed Or Progressive Malignant Gliomas [NCT00047281]Phase 20 participants Interventional2004-03-31Completed
Phase II Study of Fludarabine, Carboplatin, and Topotecan With Thalidomide for Patients With Relapsed/Refractory or High Risk Acute Myelogenous Leukemia, Chronic Myeloid Leukemia and Advanced Myelodysplastic Syndromes [NCT00053287]Phase 242 participants (Actual)Interventional2002-09-30Completed
A Phase II Study Of Temozolomide And Thalidomide In Patients With Metastatic Melanoma In The Brain [NCT00072163]Phase 250 participants (Actual)Interventional2003-10-31Completed
An Open Protocol For The Compassionate Use of Thalidomide For Patients With Advanced Or Refractory Malignancies [NCT00081757]Phase 1/Phase 2250 participants Interventional1998-09-30Completed
A Phase II Trial Combining Estramustine, Docetaxel And Thalidomide In Patients With Androgen-Independent Metastatic Prostate Cancer [NCT00083005]Phase 260 participants (Anticipated)Interventional2004-03-31Completed
UARK 99-006, A Phase II Pilot Study of Anti-Angiogenesis Therapy Using Thalidomide in Patients With Waldenstrom's Macroglobulinemia [NCT00083707]Phase 240 participants Interventional1999-01-31Completed
A Phase I/II Trial of Combination Therapy With 5-Fluorouracil, Interferon-an Interleukin-2, and Thalidomide for Metastatic, Advanced or Recurrent Renal Cell Carcinoma. [NCT00277017]Phase 1/Phase 215 participants (Actual)Interventional2000-09-30Completed
Hepatocellular Carcinoma Family of Tumours In Children / Adolescents and Young Adults [NCT00276705]Phase 247 participants (Anticipated)Interventional2005-06-30Active, not recruiting
A Pilot Study of Thalidomide as an Inhibitor of Angiogenesis in the Treatment of Myelofibrosis With Myeloid Metaplasia (MMM) [NCT00015821]Phase 243 participants (Anticipated)Interventional2000-05-31Completed
Phase II Randomized Study of Monoclonal Antibody VEGF in Patients With Unresectable Advanced Renal Cell Cancer [NCT00019539]Phase 20 participants Interventional1998-11-30Completed
A Phase II Trial of Thalidomide (NSC #66847, IND #48832) for Patients With Relapsed or Refractory Low Grade Non-Hodgkin's Lymphoma [NCT00022581]Phase 245 participants (Anticipated)Interventional2001-07-31Completed
A Phase II Evaluation of Thalidomide (NSC #66847, IND 48832) in the Treatment of Recurrent of Persistent Endometrial Carcinoma [NCT00025467]Phase 260 participants (Actual)Interventional2001-09-30Completed
Evaluation of Interferon Alpha-2b and Thalidomide in Patients With Disseminated Malignant Melanoma, Phase II [NCT00026520]Phase 20 participants Interventional2001-11-30Completed
A Tolerance and Efficacy Trial of Preoperative Thalidomide Treatment Followed by Radical Retropubic Prostatectomy (RRP) in Select Patients With Locally Advanced Prostate Cancer [NCT00038181]Phase 218 participants (Actual)Interventional2000-10-05Completed
A Phase II Study Of Thalidomide And CPT-11 (IRINOTECAN) Following Radiotherapy For Glioblastoma Multiforme [NCT00039468]Phase 226 participants (Actual)Interventional2002-03-31Completed
Phase I Pharmacokinetic Trial of Thalidomide and Docetaxel: A Regimen Based on Anti-Angiogenic Therapeutic Principles [NCT00049296]Phase 126 participants (Actual)Interventional2002-07-31Completed
A Phase II Study Of Genasense In Combination With Thalidomide And Dexamethasone In Relapsed And Refractory Multiple Myeloma [NCT00049374]Phase 20 participants Interventional2002-09-30Completed
Phase II Randomized Trial of Bevacizumab Versus Bevacizumab and Thalidomide for Relapsed/Refractory Multiple Myeloma [NCT00022607]Phase 20 participants Interventional2002-01-31Completed
A Phase II Study on the Effectiveness of Thalomid (Thalidomide) Combined With Procrit (Erythropoietin) for the Treatment of Anemia in Patients With Low and Intermediate Risk-1 (IPSS Score Less Than or Equal to 1.5) Myelodysplastic Syndromes [NCT00053001]Phase 20 participants Interventional2001-06-30Completed
A Phase II Evaluation of Thalidomide (NSC #66847) in the Treatment of Recurrent or Persistent Leiomyosarcoma of the Uterus [NCT00025220]Phase 260 participants (Actual)Interventional2001-09-30Completed
Pharmacologic T Cell Costimulation In HIV Disease [NCT00053430]Phase 240 participants (Actual)Interventional2001-04-30Completed
Phase II Trial Of Thalidomide In Patients With Low Grade Neuroendocrine Tumors (Carcinoid and Islet Cell Cancers) [NCT00027638]Phase 20 participants Interventional2001-03-31Completed
A Randomized Phase III Study On The Effect Of Thalidomide Combined With Adriamycin, Dexamethasone (AD) And High Dose Melphalan In Patients With Multiple Myeloma [NCT00028886]Phase 3450 participants (Anticipated)Interventional2001-03-31Active, not recruiting
A Multicenter, Randomized, Parallel-group , Double Blind, Placebo-controlled Study of Combination Thalidomide Plus Dexamethasone Therapy vs. Dexamethasone Therapy Alone as Induction Therapy for Previously Untreated Subjects With Multiple Myeloma [NCT00057564]Phase 3470 participants (Actual)Interventional2003-02-28Completed
A Phase III Study of Conventional Radiation Therapy Plus Thalidomide (NSC#66847) Versus Conventional Radiation Therapy for Multiple Brain Metastases [NCT00033254]Phase 3332 participants (Actual)Interventional2002-03-31Completed
A Randomized Phase III Trial Of Thalidomide (NSC # 66847) Plus Dexamethasone Versus Dexamethasone In Newly Diagnosed Multiple Myeloma [NCT00033332]Phase 30 participants Interventional2002-04-30Completed
Thalidomide-Dexamethasone for Multiple Myeloma [NCT00038090]Phase 2/Phase 383 participants (Actual)Interventional2000-06-30Completed
Phase I/II Study of Paclitaxel, Estramustine Phosphate and Thalidomide for Patients With Metastatic Androgen-Independent Prostate Carcinoma (AI-PCa) [NCT00038246]Phase 1/Phase 240 participants (Actual)Interventional2000-10-31Completed
Thalidomide fOr the Prevention of Restenosis After Coronary ArtERy Stent Implantation - The TOP RACER Trial [NCT01638078]Phase 4100 participants (Anticipated)Interventional2014-01-31Not yet recruiting
Phase II Trial of Thalidomide in Refractory/Relapsed Diffuse Large B-Cell Lymphoma and Hodgkin's Disease [NCT00209014]Phase 22 participants (Actual)Interventional2003-07-31Terminated(stopped due to Celgene unable to continue funds.)
Thalidomide, Cyclophosphamide, Oral Idarubicin and Dexamethasone (T-CID) as Induction Therapy and a Randomized Trial of Thalidomide vs Thalidomide Plus Oral Idarubicin as Maintenance Therapy in Patients With Multiple Myeloma [NCT00124813]Phase 280 participants (Anticipated)Interventional2002-08-31Recruiting
A Phase II Clinical Trial of Taxotere, Emcyt and Thalidomide (TET) for the Treatment of Hormone-Refractory Prostate Cancer [NCT00046826]Phase 20 participants Interventional2001-09-30Completed
Phase II Study Of Temozolomide, Thalidomide And Celecoxib In Patients With Newly Diagnosed Glioblastoma Multiforme In The Post-Radiation Setting [NCT00047294]Phase 20 participants Interventional2001-04-30Completed
A Phase II Study Of Whole-Brain Radiation Therapy With Thalidomide And Temozolomide In Patients With Newly Diagnosed Brain Metastases [NCT00049361]Phase 20 participants Interventional2004-01-01Completed
[NCT00050843]Phase 3220 participants Interventional2001-08-31Completed
UARK 2001-37, A Phase I Exploratory Study of Combination PS-341 and Thalidomide in Refractory Multiple Myeloma [NCT00083460]Phase 186 participants (Actual)Interventional2001-12-31Completed
A Pilot Clinical and Mechanistic Study of Radiotherapy Plus Thalidomide in Locally Advanced Hepatocellular Carcinoma [NCT00155272]Phase 1/Phase 219 participants Interventional2005-03-31Recruiting
UARK 2000-46, A Phase II Study of Tumor Antigen-Pulsed Autologous Dendritic Cell Vaccination Administrated Subcutaneously or Intranodally in Multiple Myeloma Patients [NCT00083538]Phase 240 participants (Actual)Interventional2001-02-28Completed
UARK 98-003, A Phase II Pilot Study of Anti-Angiogenesis Therapy Using Thalidomide in Patients With Multiple Myeloma [NCT00083577]Phase 2250 participants Interventional1998-02-28Completed
UARK, 98-032, Thalidomide Anti-Angiogenesis Therapy of Relapsed or Refractory Leukemia [NCT00083694]Phase 225 participants Interventional1998-08-31Completed
A Phase I/II, Multi-Center, Open Label Study of Melphalan, Prednisone, Thalidomide and Defibrotide in Advanced and Refractory Multiple Myeloma Patients [NCT00406978]Phase 1/Phase 224 participants (Actual)Interventional2006-02-28Completed
Treatment of Idiopathic Pulmonary Fibrosis With Thalidomide [NCT00162760]Phase 219 participants Interventional2003-10-31Completed
Phase II Trial of Daily Thalidomide in Extensive Stage Small Cell Lung Cancer Patients Achieving a Complete or Partial Response to Induction Chemotherapy [NCT00053300]Phase 230 participants (Actual)Interventional2002-08-31Completed
A Phase II Trial of Capecitabine and Thalidomide in Previously Treated Metastatic Colorectal Carcinoma [NCT00165217]Phase 237 participants Interventional2001-11-30Completed
Anti-Angiogenic Chemotherapy: A Phase II Trial of Thalidomide, Celecoxib, Etoposide and Cyclophosphamide in Patients With Relapsed or Progressive Cancer [NCT00165451]Phase 220 participants (Actual)Interventional2001-06-30Completed
Phase II Study of Thalidomide in Combination With Capecitabine in Patients With Metastatic Breast Cancer [NCT00193102]Phase 240 participants (Anticipated)Interventional2001-04-30Terminated
A Phase III Randomized, Double Blind, Placebo Controlled Trial Of Carboplatin/Etoposide With Or Without Thalidomide In Small Cell Lung Cancer (Study 12) [NCT00061919]Phase 3724 participants (Actual)Interventional2003-04-30Completed
A Phase I/II Assessment of Combination Immuno-Oncology Drugs Elotuzumab, Anti-LAG-3 (BMS-986016) and Anti-TIGIT (BMS-986207) [NCT04150965]Phase 1/Phase 214 participants (Actual)Interventional2020-06-30Active, not recruiting
A Pilot Study Of Hycamtin (Topotecan) And Thalomid (Thalidomide) In Patients With Recurrent Malignant Gliomas [NCT00014443]Phase 25 participants (Anticipated)Interventional2000-08-31Terminated(stopped due to Poor enrollment)
A Phase III Randomized Trial of Thalidomide Plus Zoledronic Acid Versus Zoledronic Acid Alone in Patients With Early Stage Multiple Myeloma [NCT00432458]Phase 368 participants (Actual)Interventional2003-07-31Completed
Bioequivalence of Three Different Tablet Formulations of 30 mg of Apremilast (EU-sourced Otezla® vs. US-sourced Otezla® vs. Japan-sourced Otezla®) Administered in Healthy Male and Female Subjects in the Fasted State as Well as (for EU-sourced Otezla® vs. [NCT04811573]Phase 120 participants (Actual)Interventional2021-03-31Terminated(stopped due to due to company decision)
Randomized, Open, Parallel Group Study for the Evaluation of an Oral Dose of 100 mg Thalidomide and Subsequent Dose Escalation of 400 mg Thalidomide in Combination With Riluzole in Patients With Amyotrophic Lateral Sclerosis (ALS) [NCT00231140]Phase 240 participants Interventional2005-12-31Terminated
Phase III, Prospective, Open Label, Multicenter, Randomized Trial of Melphalan, Prednisone and Thalidomide Versus Melphalan and Prednisone as First Line Therapy in Myeloma Patients Aged >65. [NCT00232934]Phase 3400 participants Interventional2002-01-31Completed
An International, Multicenter, Non-Randomized, Open-Labeled Study to Evaluate the Efficacy of Lower Dose Dexamethasone/Thalidomide and Higher Frequency ZOMETA(TM) in the Treatment of Previously Untreated Patients With Multiple Myeloma [NCT00263484]Phase 256 participants (Actual)Interventional2005-12-31Completed
Prospective Study of the Use of Thalidomide in Patients With Arachnoiditis [NCT00284505]Phase 23 participants (Anticipated)Interventional2005-07-31Completed
Trial of Thalidomide, a- Interferon +/- Octreotide in Patients With Unresectable Hepatocellular Carcinoma [NCT00250796]Phase 212 participants (Actual)Interventional2000-09-30Completed
A Phase I Study of Arsenic Trioxide and Ascorbic Acid (ATO/AA) in Combination With Low Dose Velcade-Thalidomide-Dexamethasone (VTD) in Relapsed/Refractory Multiple Myeloma (MM) [NCT00258245]Phase 15 participants (Actual)Interventional2005-05-31Completed
A Phase II Trial of Combination Therapy With Thalidomide, Arsenic Trioxide, Dexamethasone, and Ascorbic Acid (TADA) in Patients With Chronic Idiopathic Myelofibrosis or Overlap Myelodysplastic/Myeloproliferative Disorders [NCT00274820]Phase 215 participants (Actual)Interventional2005-10-31Completed
2015-12: A Phase II Study Exploring the Use of Early and Late Consolidation/Maintenance With Anti-CD38 (Protein) Monoclonal Antibody to Improve Progression Free Survival in Patients With Newly Diagnosed Multiple Myeloma [NCT03004287]Phase 250 participants (Anticipated)Interventional2017-07-01Active, not recruiting
Randomized Controlled Trial of Thalidomide vs Placebo in Skin Sarcoidosis [NCT00305552]Phase 340 participants (Actual)Interventional2005-02-28Completed
A Phase 1, Multicenter, Open Label, Dose-escalation Study to Determine the Maximum Tolerated Dose for the Combination of Pomalidomide (POM), Bortezomib (BTZ) and Low-Dose Dexamethasone (LDDEX) in Subjects With Relapsed or Refractory Multiple Myeloma (MM) [NCT01497093]Phase 134 participants (Actual)Interventional2012-02-15Completed
A Phase 2, Randomized Study of VELCADE® (Bortezomib), Dexamethasone, and Thalidomide Versus VELCADE® (Bortezomib), Dexamethasone, Thalidomide, and Cyclophosphamide in Subjects With Previously Untreated Multiple Myeloma Who Are Candidates for Autologous Tr [NCT00531453]Phase 298 participants (Actual)Interventional2007-10-31Completed
Evaluation of Ruxolitinib And Thalidomide Combination as a Therapy for Patients With Myelofibrosis [NCT03069326]Phase 230 participants (Actual)Interventional2017-02-27Active, not recruiting
Efficacy and Safety of Low Dose Thalidomide in Transfusion Dependent Thalassemia Patients of Pakistan [NCT03651102]Phase 2/Phase 3654 participants (Actual)Interventional2018-01-01Completed
Industry Alliance Platform Trial to Assess the Efficacy and Safety of Multiple Candidate Agents for the Treatment of COVID-19 in Hospitalized Patients [NCT04590586]Phase 3515 participants (Actual)Interventional2020-11-24Completed
ANGIOCOMB Antiangiogenic Therapy for Pediatric Patients With Diffuse Brain Stem and Thalamic Tumors [NCT01756989]Phase 250 participants (Anticipated)Interventional2005-01-31Completed
The Efficacy of Thalidomide Plus Prednisone and Methotrexate for the Symptomatic Large Granular Lymphocytic Leukemia - a Prospective Multicenter Clinical Trial From China [NCT04453345]Phase 2/Phase 342 participants (Anticipated)Interventional2013-05-20Recruiting
UARK 2008-02, A Phase II Trial for High-risk Myeloma Evaluation Accelerating and Sustaining Complete Remission (AS-CR) by Applying Non-host-exhausting and Timely Dose-reduced MEL-80-VRD-PACE Tandem Transplants [NCT00869232]Phase 290 participants (Actual)Interventional2008-10-31Active, not recruiting
A Phase 2 Trial of Daily Alternating Thalidomide and Lenalidomide Plus Rituximab (ThRiL) for Patients With Previously Treated Waldenstrom Macroglobulinemia [NCT01779167]Phase 24 participants (Actual)Interventional2012-06-30Terminated(stopped due to Slow Accrual)
Comparison of Melphalan-Prednisone(MP),MP-THALIDOMIDE,and Autologous Stem Cell Transplantation in the Treatment of Newly Diagnosed Elderly Patients With Multiple Myeloma. [NCT00367185]Phase 3500 participants Interventional2000-05-31Completed
Phase II Study of Thalidomide and Rituximab in Waldenstrom's Macroglobulinemia [NCT00142116]Phase 225 participants (Actual)Interventional2003-05-31Completed
A Phase II, Parallel Group, Randomized, Placebo-Controlled Study of the Safety and Efficacy of Thalidomide in Reducing Weight Loss in Adults With HIV Wasting Syndrome [NCT00002127]Phase 275 participants InterventionalCompleted
Pilot Study of Thalidomide for Sjogren's Syndrome [NCT00001599]Phase 228 participants Interventional1997-05-31Completed
Compassionate Use Study of Two Dose Levels of Thalidomide in Adults With HIV Wasting Syndrome [NCT00002157]0 participants InterventionalCompleted
A Pilot Study of Thalidomide to Overcome Lenalidomide Resistance in Patients Suffering Biochemical Progression on Maintenance Therapy After Autologous Hematopoietic Stem Cell Transplantation for Multiple Myeloma [NCT01927718]10 participants (Actual)Interventional2014-01-31Terminated(stopped due to Poor Response Rate)
A Phase 1 Multi-Center, Open-Label, Dose-Escalation Study to Determine the Pharmacokinetics and Safety of Pomalidomide When Given in Combination With Low Dose Dexamethasone in Subjects With Relapsed or Refractory Multiple Myeloma and Impaired Renal Functi [NCT01575925]Phase 125 participants (Actual)Interventional2012-06-01Completed
A Phase I/II Trial of Cyclophosphamide, Carfilzomib, Thalidomide and Dexamethasone (CYCLONE) in Patients With Newly Diagnosed Active Multiple Myeloma [NCT01057225]Phase 1/Phase 264 participants (Actual)Interventional2010-03-31Completed
The Study of the Optimal Treatment Strategy for Patients With Gastrointestinal Bleeding Due to Gastrointestinal Vascular Malformation: a Randomized, Double Blind, Placebo Controlled Study [NCT02301949]Phase 20 participants (Actual)Interventional2015-12-31Withdrawn
A Phase-3, Multi-Center, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study to Compare Efficacy and Safety of Pomalidomide in Subjects With Myeloproliferative Neoplasm-Associated Myelofibrosis and Red Blood Cell-Transfusion-Dependence [NCT01178281]Phase 3267 participants (Actual)Interventional2010-09-08Completed
Long-term Follow-up and/or Continued Thalidomide (THALOMID®) Maintenance Therapy for Patients Enrolled on Clinical Trial 20030165 [NCT02507336]Phase 22 participants (Actual)Interventional2015-11-24Completed
Placebo-Controlled Trial of Safety and Efficacy of Thalidomide in Patients With Infections Due to Mycobacterium and/or HIV [NCT00002104]Phase 10 participants InterventionalCompleted
A Study to Investigate the Potential of Thalidomide Treatment to Enhance Immune Responses in HIV-Infected Individuals Who Are Receiving Highly Active Antiretroviral Therapy. [NCT00002392]12 participants InterventionalCompleted
A Phase II Study of Thalidomide and Cyclophosphamide in Patients With Recurrent or Refractory Malignancies [NCT00003754]Phase 20 participants Interventional1998-09-30Completed
A Phase II Study of Thalidomide in Recurrent and Metastatic Squamous Cell Carcinoma of the Head and Neck [NCT00003850]Phase 247 participants (Actual)Interventional1999-04-30Completed
A Randomized Study Comparing Carboplatin and Thalidomide With Carboplatin Alone in Patients With Stage Ic - IV Ovarian Cancer [NCT00004876]Phase 230 participants (Anticipated)Interventional1999-08-31Completed
[NCT00004276]Phase 250 participants Interventional1990-09-30Completed
[NCT00004450]60 participants Interventional1998-08-31Completed
Thalidomide, Cyclophosphamide and Dexamethasone for Adult Patients With Recurrent/Refractory Langerhans Cell Histiocytosis: A Single Arm, Single Center, Prospective Phase 2 Study [NCT04120519]Phase 220 participants (Anticipated)Interventional2019-10-10Recruiting
Thalidomide in the Treatment of Chronic Plaque Psoriasis. [NCT01891019]Phase 221 participants (Actual)Interventional2003-04-30Completed
A Trial of Tandem Autologous Stem Cell Transplants +/- Post Second Autologous Transplant Maintenance Therapy vs Single Autologous Stem Cell Transplant Followed by Matched Sibling Non-myeloablative Allogeneic Stem Cell Transplant for Patients With Multiple [NCT00075829]Phase 3710 participants (Actual)Interventional2003-12-31Completed
UARK 98-026, Total Therapy II - A Phase III Study for Newly Diagnosed Multiple Myeloma Evaluating Anti-Angiogenesis With Thalidomide and Post-Transplant Consolidation Chemotherapy [NCT00083551]Phase 3668 participants (Actual)Interventional1998-08-31Completed
A Phase II Trial of Docetaxel, Thalidomide, Prednisone and Bevacizumab in Patients With Androgen-Independent Prostate Cancer [NCT00089609]Phase 273 participants (Actual)Interventional2005-04-19Completed
A Phase II Trial Of Thalidomide/Dexamethasone Induction Followed By Tandem Melphalan Transplant And Prednisone/Thalidomide Maintenance (A BMT Study) [NCT00040937]Phase 2147 participants (Actual)Interventional2002-06-30Completed
S0417 A Phase II Study of Bortezomib (Velcade™, PS-341), Thalidomide, and Dexamethasone in Patients With Refractory Multiple Myeloma [NCT00124579]Phase 27 participants (Actual)Interventional2005-08-31Terminated(stopped due to poor accrual)
A Multicentre, Randomized Phase III Study of Thalidomide Maintenance Treatment in Patients With Diffuse Large B-cell Lymphoma [NCT03016000]Phase 3226 participants (Anticipated)Interventional2017-07-26Recruiting
Phase II Trial of Neoadjuvant Therapy With Carboplatin and Gemcitabine With Thalidomide in Patients With Stage II and IIIA Non-Small Cell Lung Cancer [NCT00281827]Phase 222 participants (Actual)Interventional2002-05-31Terminated(stopped due to Due to drug unavailability)
A Phase 1, Open-Label, Two-Part Study to Evaluate the Pharmacokinetics of Pomalidomide (CC-4047) in Hepatically Impaired Male Subjects [NCT01835561]Phase 132 participants (Actual)Interventional2013-03-01Completed
Superiority of the Triple Combinations of Bortezomib, Cyclophosphamide and Dexamethasone (VCD) Versus Cyclophosphamide, Thalidomide and Dexamethasone (CTD) in Patients With Newly Diagnose Multiple Myeloma, Eligible for Transplantation [NCT03402295]Phase 3311 participants (Actual)Interventional2009-06-15Completed
Safety and Efficacy of Pyrotinib Combined With Thalidomide in Advanced Non-Small-Cell Lung Cancer With HER2 Exon 20 Insertions: A Prospective, Single-arm, Open-label Phase II Study [NCT04382300]Phase 239 participants (Anticipated)Interventional2020-06-30Recruiting
Thalidomide in Inducing and Maintaining Remission of Crohn's Disease [NCT02501291]Phase 247 participants (Actual)Interventional2013-01-31Completed
UARK 98-036, A Phase II Trial of Combination Bisphosphonate and Anti-Angiogenesis Therapy With Pamidronate and Thalidomide in Patients With Smoldering/Indolent Myeloma [NCT00083382]Phase 283 participants (Actual)Interventional1998-12-31Completed
A Randomized Controlled Study of Velcade (Bortezomib) Plus Thalidomide Plus Dexamethasone Compared to Thalidomide Plus Dexamethasone for the Treatment of Myeloma Patients Progressing or Relapsing After Autologous Transplantation [NCT00256776]Phase 3269 participants (Actual)Interventional2005-07-31Terminated
PS-341 (Bortezomib, Velcade®), Adriamycin and Dexamethasone (PAD) Combination Therapy Followed by Thalidomide With Dexamethasone (Thal/Dex) for Relapsed or Refractory Multiple Myeloma [NCT00319865]Phase 247 participants Interventional2005-11-30Recruiting
A Phase II Trial of Oral Thalidomide as an Adjuvant Agent Following Metastasectomy in Patients With Recurrent Colorectal Cancer [NCT00019747]Phase 239 participants (Actual)Interventional1999-08-31Terminated(stopped due to DSMB recommended closure of the protocol due to slow accrual.)
[NCT00384800]Phase 241 participants (Anticipated)Interventional2006-09-30Recruiting
A Phase I/II Study of Temozolamide and Thalidomide in the Treatment of Advanced Melanoma [NCT00005815]Phase 1/Phase 20 participants Interventional1999-12-31Completed
A Phase 2, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Efficacy and Safety Study of Apremilast (CC-10004) in Subjects With Moderate to Severe Atopic Dermatitis [NCT02087943]Phase 2191 participants (Actual)Interventional2014-06-30Completed
A Single Arm Open Labeled Multicentre Phase 1b Dose Escalation Study of Carfilzomib Taken in Combination With Thalidomide and Dexamethasone in Relapsed AL Amyloidosis [NCT02545907]Phase 1/Phase 210 participants (Actual)Interventional2017-09-14Completed
A MULTIARM, OPEN LABEL, RANDOMIZED PHASE II STUDY OF MLN9708 PLUS ORAL DEXAMETHASONE or PLUS ORAL CYCLOPHOSPHAMIDE AND DEXAMETHASONE or PLUS ORAL THALIDOMIDE AND DEXAMETHASONE FOLLOWED BY MAINTENANCE WITH MLN9708 IN NEWLY DIAGNOSED ELDERLY MULTIPLE MYELOM [NCT02586038]Phase 2175 participants (Anticipated)Interventional2015-10-31Active, not recruiting
A PHASE III, MULTI-CENTER, RANDOMIZED OPEN LABEL STUDY OF VELCADE, MELPHALAN, PREDNISONE AND THALIDOMIDE (V-MPT) Versus VELCADE, MELPHALAN, PREDNISONE (V-MP) IN ELDERLY UNTREATED MULTIPLE MYELOMA PATIENTS [NCT01063179]Phase 3511 participants (Actual)Interventional2006-05-31Completed
Phase II Trial of Thalidomide (Thalidomide Pharmion) in Patients With Advanced or Relapsed Lymphoma of the Mucosa Associated Lymphoid Tissue (MALT) [NCT00373646]Phase 28 participants (Actual)Interventional2006-06-30Completed
Thalidomide, Cyclophosphamide and Prednisone in Newly Diagnosed Multicentric Castleman's Disease: a Prospective, Single-center, Single-arm, Phase-II Pilot Trial [NCT03043105]Phase 225 participants (Actual)Interventional2017-01-01Active, not recruiting
Phase 2a Single-Arm Safety Study of Elotuzumab in Combination With Thalidomide and Dexamethasone in Subjects With Relapsed and/or Refractory Multiple Myeloma [NCT01632150]Phase 251 participants (Actual)Interventional2012-05-31Completed
An Open-label, Randomised Trial of Bortezomib Consolidation (With Thalidomide and Prednisolone) Vs Thalidomide and Prednisolone Alone in Previously Untreated Subjects With Multiple Myeloma After Receiving Bortezomib, Cyclophosphamide, Dexamethasone (VCD) [NCT01539083]Phase 3256 participants (Actual)Interventional2012-01-13Completed
A Phase II Randomized,Controlled,Open Label,Multicentre Study of Tegafur Combined With Temozolomide Versus Tegafur Combined With Temozolomide and Thalidomide in Subjects With Advanced Pancreatic Neuroendocrine Tumor [NCT03204019]Phase 260 participants (Anticipated)Interventional2016-10-31Recruiting
Selinexor in Combination With Immunomodulator to Treat Relapsed/Refractory Multiple Myeloma Patients [NCT04941937]Phase 290 participants (Anticipated)Interventional2022-01-27Recruiting
A Randomized, Multicenter, Double-Blind, Placebo-Controlled Study of Efficacy of Thalidomide for Refractory Small Intestinal Bleeding From Vascular Malformation [NCT02707484]Phase 3150 participants (Actual)Interventional2016-04-30Completed
Biochemotherapy With Temozolomide, Velban, Cisplatin, Interleukin-2, Interferon-alpha and Thalidomide for Metastatic Melanoma With Optional Intrathecal Interleukin-2 Treatment [NCT00505635]Phase 25 participants (Actual)Interventional2007-03-31Terminated(stopped due to Slow accrual)
[NCT02998827]90 participants (Anticipated)Interventional2016-11-30Enrolling by invitation
The Phase II Clinical Trials of Thalidomide in NTDT [NCT02995707]Phase 230 participants (Anticipated)Interventional2016-09-30Recruiting
TACTIC: a Phase II Study of TAS-102 Monotherapy and Thalidomide Plus TAS-102 as Third-line Therapy and Beyond in Patients With Advanced Colorectal Carcinoma [NCT05266820]Phase 2120 participants (Anticipated)Interventional2021-10-01Recruiting
Phase II Trial of Adjuvant Thalidomide Following Cytoreductive Surgery and Intraperitoneal Hyperthermic Chemotherapy for Peritoneal Carcinomatosis or Adenomucinosis From Colorectal/Appendiceal Cancer [NCT00310076]Phase 229 participants (Actual)Interventional2002-10-31Completed
Long-term Effects of Thalidomide for Recurrent Gastrointestinal Bleeding Due to Vascular Malformation : An Open-label, Randomized, Parallel Controlled Study [NCT00964496]Phase 255 participants (Actual)Interventional2004-11-30Completed
Tandem Autotransplantation for Multiple Myeloma in Participants With Less Than 12 Months of Preceding Therapy, Incorporating Velcade (Bortezomib) With the Transplant Chemotherapy and During Maintenance [NCT01548573]Phase 219 participants (Actual)Interventional2012-05-31Terminated(stopped due to Met study stopping rules)
Adjuvant Therapy With Thalidomide After Curative Resection of Hepatocellular Carcinoma.: a Randomized Controlled Trial [NCT01924624]140 participants (Anticipated)Interventional2013-07-31Recruiting
VELCADE (Bortezomib) and Thalidomide in Newly Diagnosed Patients With Multiple Myeloma [NCT00287872]Phase 230 participants (Actual)Interventional2004-09-30Completed
Phase III Randomized Trial of Thalidomide/Dexamethasone vs VAD as Induction Chemotherapy for Newly Diagnosed Myeloma Patients and Evaluation of the Effects of Zoledronate on Chemotherapy Induced Apoptosis and Antigen Presentation. [NCT00215943]Phase 390 participants (Actual)Interventional2003-06-30Terminated(stopped due to Poor accrual, changes in management of newly diagnosed myeloma patients, new drugs/more effective regimens.)
Single Autologous Transplant Followed by Consolidation and Maintenance for Participants ≥ 65 Years of Age Diagnosed With Multiple Myeloma or a Related Plasma Cell Malignancy [NCT01849783]Phase 241 participants (Actual)Interventional2013-04-04Completed
A Phase II Study of Maintenance Treatment With Sequential Bortezomib, Thalidomide and Dexamethasone Following Autologous Peripheral Blood Stem Cell Transplant in Patients With Multiple Myeloma [NCT00792142]Phase 245 participants (Actual)Interventional2008-01-16Completed
A Phase II, Prospective, Open Label Study (PO-MMM-PI-0011) to Determine the Safety and Efficacy of Pomalidomide (CC-4047) in Subjects With Primary, Post Polycythemia Vera, or Post Essential Thrombocythemia Myelofibrosis (PMF; Post-PV MF, or Post-ET MF) [NCT00946270]Phase 270 participants (Actual)Interventional2009-07-22Completed
A Pilot Phase II Study of Pre-Operative Radiation Therapy and Thalidomide (IND 48832; NSC 66847) for Low Grade Primary Soft Tissue Sarcoma or Pre-Operative MAID/Thalidomide/Radiation Therapy for High/Intermediate Grade Primary Soft Tissue Sarcoma of the E [NCT00089544]Phase 223 participants (Actual)Interventional2004-06-17Terminated
Relevance of Monitoring Blood Levels Compared to Salivar Levels of Drugs Used in Rheumatic Autoimmune Diseases: Adherence and Understanding the Possible Underlying Mechanisms Involved in Effectiveness and in Adverse Effects [NCT03122431]Phase 493 participants (Actual)Interventional2017-06-05Completed
Single Arm, Multicentre Study of Carfilzomib in Combination With Thalidomide and Dexamethasone (CaTD) in Patients With Relapsed and/or Refractory Multiple Myeloma (RRMM) [NCT03140943]Phase 2100 participants (Anticipated)Interventional2017-09-13Recruiting
UARK 2013-13, Total Therapy 4B - Formerly 2008-01 - A Phase III Trial for Low Risk Myeloma Ages 65 and Under: A Trial Enrolling Subjects to Standard Total Therapy 3 (S-TT3) [NCT00734877]Phase 3382 participants (Actual)Interventional2008-07-31Active, not recruiting
[NCT01274403]Phase 2130 participants (Actual)InterventionalCompleted
An Randomized, Open-label, Phase III Study Comparing Thalidomide Combined With R-CHOP and R-CHOP in Newly Diagnosed Double-expressor Diffuse Large B-Cell Lymphoma Patients [NCT03318835]Phase 3162 participants (Anticipated)Interventional2017-08-22Recruiting
A Phase 2B, Multicenter, Randomized, Double-Blind, Placebo-Controlled, Efficacy and Safety Study of Two Doses of Apremilast (CC-10004) In Japanese Subjects With Moderate-To-Severe Plaque-Type Psoriasis [NCT01988103]Phase 2254 participants (Actual)Interventional2013-07-09Completed
A Phase 2 Study Incorporating Bone Marrow Microenvironment (ME) Co-Targeting Bortezomib Into Tandem Melphalan-Based Autotransplants With DT PACE for Induction/Consolidation and Thalidomide + Dexamethasone for Maintenance [NCT00081939]Phase 2303 participants (Actual)Interventional2004-01-31Completed
Thalidomide, a Novel Immunological Treatment to Modify the Natural History of Paediatric Crohn's Disease: a New Proposal From a Well-established Paediatric Research Network [NCT03221166]Phase 39 participants (Actual)Interventional2018-02-27Terminated(stopped due to Difficulty in recruiting subjects who meet the inclusion/exclusion criteria)
A Phase 1, Open-Label, Single Center Study to Evaluate the Pharmacokinetics of Prototype Modified-Release Formulations Of Apremilast (CC-10004) in Healthy Male Subjects [NCT02236988]Phase 180 participants (Actual)Interventional2014-01-07Completed
A PHASE 3, MULTICENTER, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED, PARALLEL-GROUP STUDY TO EVALUATE THE EFFICACY AND SAFETY OF APREMILAST (CC-10004) IN THE TREATMENT OF ACTIVE ANKYLOSING SPONDYLITIS [NCT01583374]Phase 3490 participants (Actual)Interventional2012-05-02Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00004088 (2) [back to overview]Three-year Overall Survival
NCT00004088 (2) [back to overview]Progression-free Survival
NCT00004635 (2) [back to overview]The Number of Participants With Adverse Events
NCT00004635 (2) [back to overview]Time to Progression
NCT00004859 (3) [back to overview]Response Rate at Best Response to Treatment
NCT00004859 (3) [back to overview]Time to Disease Progression
NCT00004859 (3) [back to overview]Overall Survival Time
NCT00025506 (5) [back to overview]Overall Survival
NCT00025506 (5) [back to overview]Progression Free Survival
NCT00025506 (5) [back to overview]Progression-free Survival (PFS) > 6 Months
NCT00025506 (5) [back to overview]Tumor Response
NCT00025506 (5) [back to overview]Frequency and Severity of Adverse Effects as Assessed by Common Toxicity Criteria (CTC) v2.0
NCT00040937 (2) [back to overview]Overall Survival
NCT00040937 (2) [back to overview]Assess Toxicity of Thalidomide/Dexamethasone as a Pre-transplant Induction Regimen.
NCT00041080 (1) [back to overview]Median Progression-free Survival
NCT00047879 (1) [back to overview]The Number of Participants With Adverse Events
NCT00064337 (2) [back to overview]Overall Survival
NCT00064337 (2) [back to overview]Hematologic Response
NCT00075023 (1) [back to overview]Mean Percentage Change in Total Surface Area of Oral Ulceration.
NCT00075829 (8) [back to overview]Overall Survival (OS) for High Risk
NCT00075829 (8) [back to overview]Interval From First to Second Transplantation
NCT00075829 (8) [back to overview]Cumulative Incidence of Treatment Related Mortality (TRM)
NCT00075829 (8) [back to overview]Cumulative Incidence of Progression/Relapse
NCT00075829 (8) [back to overview]Overall Survival (OS) for Standard Risk
NCT00075829 (8) [back to overview]Incidences of Graft Versus Host Disease (GVHD)
NCT00075829 (8) [back to overview]Incidences of Chronic GVHD
NCT00075829 (8) [back to overview]Progression-Free Survival (PFS)
NCT00081939 (1) [back to overview]Percentage of Participants With Progression-Free Survival (PFS) at 3 Years From Initiation of Study Treatment
NCT00083382 (1) [back to overview]Best Response
NCT00083551 (1) [back to overview]Overall Survival
NCT00089544 (1) [back to overview]Treatment Delivery With Compliance Defined as Receiving at Least 95% of the Pre-operative Protocol Dose of RT, All 3 Cycles of MAID (if Applicable), and Receive Thalidomide on 75% of the Days During Radiation
NCT00089609 (6) [back to overview]Number of Participants Who Had a Prostate-specific Antigen (PSA) Response
NCT00089609 (6) [back to overview]Number of Participants Who Died After a Follow Up of 34 Months Following Treatment
NCT00089609 (6) [back to overview]Number of Participants With a Significant Increase in Circulating Apoptotic Endothelial Cell (CAEC) Level
NCT00089609 (6) [back to overview]Number of Participants With Adverse Events
NCT00089609 (6) [back to overview]Disease Progression by Clinical and Radiographic Criteria Without the Use of Prostate-Specific Antigen (PSA)
NCT00089609 (6) [back to overview]Time to Progression Using Bubley Criteria
NCT00096018 (2) [back to overview]Overall Responders (Complete and Partial Response)
NCT00096018 (2) [back to overview]Duration of Response
NCT00097981 (7) [back to overview]Transplantation: Number of Participants Who Underwent Transplantation (Peripheral Stem Cell / Bone Marrow)
NCT00097981 (7) [back to overview]Time to Progression
NCT00097981 (7) [back to overview]Time to 1st Response
NCT00097981 (7) [back to overview]Overall Survival: Number of Participants Died Due to Any Cause
NCT00097981 (7) [back to overview]Complete Response Rate: Number of Participants Who Achieved a Complete Response
NCT00097981 (7) [back to overview]Engraftment: Number of Participants Who Underwent Engraftment
NCT00097981 (7) [back to overview]Overall Response: Number of Participants Who Achieved a Complete Response (CR) or Partial Response (PR)
NCT00098475 (2) [back to overview]Proportion of Patients With Objective Response (First Phase, Step 1)
NCT00098475 (2) [back to overview]Proportion of Patients With Objective Response (First Phase, Step 2)
NCT00098865 (3) [back to overview]Overall Survival
NCT00098865 (3) [back to overview]Therapy Completion Rate
NCT00098865 (3) [back to overview]Overall Response
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Thalidomide Arms Versus no Thalidomide Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Celecoxib Arms Versus no Celecoxib Arms
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Celecoxib Arms Versus no Celecoxib Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Thalidomide Arms Versus no Thalidomide Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) of Individual Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Doublet Versus Triplet Therapy
NCT00112502 (10) [back to overview]Median Overall Survival (OS) Comparison of Doublet Versus Triplet Therapy
NCT00112502 (10) [back to overview]Overall Survival of Individual Arms
NCT00112502 (10) [back to overview]Median Progression-Free Survival (PFS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms
NCT00124579 (3) [back to overview]Overall Response Rate Complete Remission (CR), Remission (R), and Partial Remission (PR).
NCT00124579 (3) [back to overview]Progression-Free Survival
NCT00124579 (3) [back to overview]Toxicity Evaluation
NCT00142116 (2) [back to overview]Time to Progression
NCT00142116 (2) [back to overview]Objective Response Rate
NCT00151281 (4) [back to overview]Asses the Toxicity Profiles
NCT00151281 (4) [back to overview]Dynamic Levels of Plasma VEGF
NCT00151281 (4) [back to overview]The Quality of Life (QoL) of Patients Receiving RT-PEPC Treatment
NCT00151281 (4) [back to overview]Overall Survival and Progression Free Survival
NCT00215943 (4) [back to overview]Number of Participants With Progression Free Survival (PFS), by Treatment Arm
NCT00215943 (4) [back to overview]Overall Survival (OS), by Treatment Arm
NCT00215943 (4) [back to overview]Response Rates of VAD vs. Thalidomide/Dexamethasone
NCT00215943 (4) [back to overview]Number of Participants With Adverse Events, by Group
NCT00222105 (2) [back to overview]Overall Response Rate
NCT00222105 (2) [back to overview]Toxicity
NCT00256776 (2) [back to overview]Median Time to Progression (TTP)
NCT00256776 (2) [back to overview]Progression Free Survival
NCT00281827 (6) [back to overview]Number of Patients Alive at 1 Year (Survival)
NCT00281827 (6) [back to overview]Number of Patients Reporting Clinical Response
NCT00281827 (6) [back to overview]Number of Patients Disease-free at 2 Years
NCT00281827 (6) [back to overview]Number of Patients Disease-free at 1 Year
NCT00281827 (6) [back to overview]Number of Patients Alive at 56 Months (End of Study)
NCT00281827 (6) [back to overview]Number of Patients Alive at 2 Years (Survival)
NCT00287872 (3) [back to overview]Clinical Response to Treatment
NCT00287872 (3) [back to overview]Peripheral Motor and Sensory Neuropathy (Grade 2 and Higher)
NCT00287872 (3) [back to overview]The Time to Response
NCT00307294 (4) [back to overview]Overall Survival
NCT00307294 (4) [back to overview]Time to Progression
NCT00307294 (4) [back to overview]Response Rate
NCT00307294 (4) [back to overview]Best Overall PSA Response
NCT00310076 (3) [back to overview]Progression Free Survival
NCT00310076 (3) [back to overview]Time to Progression
NCT00310076 (3) [back to overview]Number of Events of Toxicity Graded 3 and 4
NCT00357500 (4) [back to overview]27-Week Overall Survival
NCT00357500 (4) [back to overview]27-Week Progression-Free Survival
NCT00357500 (4) [back to overview]Best Response
NCT00357500 (4) [back to overview]Therapy Completion Rate
NCT00379353 (8) [back to overview]Change in Body Composition as Measured by Body Mass Index (BMI)
NCT00379353 (8) [back to overview]Change in Serum Cytokines and Receptors
NCT00379353 (8) [back to overview]Change in Symptoms as Measured by Edmonton Symptom Assessment Scale (ESAS)
NCT00379353 (8) [back to overview]Functional Assessment of Anorexia/Cachexia Therapy (FAACT)
NCT00379353 (8) [back to overview]Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F)
NCT00379353 (8) [back to overview]Hospital Anxiety and Depression Scale (HADS) HADS-A (Anxiety)
NCT00379353 (8) [back to overview]Hospital Anxiety and Depression Scale (HADS) HADS-D (Depression)
NCT00379353 (8) [back to overview]Pittsburgh Sleep Quality Index (PSQI)
NCT00400517 (4) [back to overview]Proportion of Patients P0 at Surgery
NCT00400517 (4) [back to overview]Time to Clinical Progression
NCT00400517 (4) [back to overview]Proportion of Patients With Negative Surgical Margins
NCT00400517 (4) [back to overview]Prostate-specific Antigen Response
NCT00412542 (1) [back to overview]Number of Participants Progression Free at 6 Months With Malignant Gliomas
NCT00432458 (6) [back to overview]Number of Participants With Severe (Grade 3, 4 or 5) Adverse Events
NCT00432458 (6) [back to overview]Time to Treatment Failure
NCT00432458 (6) [back to overview]Time to Disease Progression (TTP)
NCT00432458 (6) [back to overview]Number of Participants With a Confirmed Response (Complete Response [CR], Very Good Partial Response [VGPR] or Partial Response [PR]) on Two Consecutive Evaluations at Least 2 Weeks Apart in the First 12 Months of Treatment
NCT00432458 (6) [back to overview]12-month Progression-free Survival (PFS)
NCT00432458 (6) [back to overview]Duration of Response (Complete Response, Partial Response, and Very Good Partial Response)
NCT00450801 (4) [back to overview]Progression-free Survival Rate
NCT00450801 (4) [back to overview]Overall Survival Rate
NCT00450801 (4) [back to overview]Response Rate
NCT00450801 (4) [back to overview]Number of Patients Experiencing Adverse Events.
NCT00458705 (1) [back to overview]Disease Response
NCT00463385 (10) [back to overview]Percentage of Participants With Clinical Response by Baseline JAK2 Assessment
NCT00463385 (10) [back to overview]Change From Baseline in Hemoglobin Concentration for Responders
NCT00463385 (10) [back to overview]Change From Baseline in Hemoglobin Concentration for Non-Responders
NCT00463385 (10) [back to overview]Time to the First Clinical Response
NCT00463385 (10) [back to overview]Duration of First Clinical Response
NCT00463385 (10) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Anemia (FACT-An) Subscale and Total Scores
NCT00463385 (10) [back to overview]Percentage of Participants With a Clinical Response Within the First 12 Cycles of Treatment
NCT00463385 (10) [back to overview]Number of Participants With Adverse Events (AEs)
NCT00463385 (10) [back to overview]Percentage of Participants With a Clinical Response Within the First 6 Cycles of Treatment
NCT00463385 (10) [back to overview]Change From Baseline in Likert Abdominal Pain Scale
NCT00505635 (1) [back to overview]Time to Progression (TTP)
NCT00507416 (8) [back to overview]Change From Baseline in EORTC QLQ-C30 - Global Health Status
NCT00507416 (8) [back to overview]Overall Survival
NCT00507416 (8) [back to overview]Percentage of Participants With a Complete Response
NCT00507416 (8) [back to overview]Progression Free Survival (PFS)
NCT00507416 (8) [back to overview]Time to Alternative Therapy
NCT00507416 (8) [back to overview]Percentage of Participants With an Overall Response
NCT00507416 (8) [back to overview]Percentage of Participants With a Complete Response or a Very Good Partial Response
NCT00507416 (8) [back to overview]Duration of Response
NCT00523848 (3) [back to overview]Complete Response Rate
NCT00523848 (3) [back to overview]Overall Response Rate (Complete and Partial)
NCT00523848 (3) [back to overview]Time to Disease Progression
NCT00529633 (2) [back to overview]Difference in Serum Albumin
NCT00529633 (2) [back to overview]Difference in Serum CRP
NCT00531453 (2) [back to overview]Percent of Participants Achieving Overall Combined Complete Response (CR) Following High-dose Chemotherapy (HDT)/Stem Cell Transplantation (SCT)
NCT00531453 (2) [back to overview]Percent of Particpants Achieving Overall Combined Complete Response (CR) Following Induction
NCT00538733 (4) [back to overview]Event Free Survival
NCT00538733 (4) [back to overview]Progression Free Survival
NCT00538733 (4) [back to overview]Effect of Drug Combination on Multiple Myeloma
NCT00538733 (4) [back to overview]Median Time to Maximum Response
NCT00538824 (1) [back to overview]Effect of Drug Combination on Multiple Myeloma
NCT00577096 (10) [back to overview]Number of Platelet Transfusions Needed to Maintain Adequate Number of Platelets. (Long Term)
NCT00577096 (10) [back to overview]Number of Red Blood Cell Transfusions Needed to Maintain Hemoglobin Levels (Long Term)
NCT00577096 (10) [back to overview]Hemoglobin Levels Before Chemotherapy and During Transplantation Period (Long Term)
NCT00577096 (10) [back to overview]Total Number of Days of Stem Cell Collection (Short Term)
NCT00577096 (10) [back to overview]Number of Stem Cell Collection Attempts (Short Term)
NCT00577096 (10) [back to overview]Number of Stem Cell Collection Attempts (Long Term)
NCT00577096 (10) [back to overview]Number of Red Blood Cell Transfusions Needed to Maintain Hemoglobin Levels (Short Term)
NCT00577096 (10) [back to overview]Number of Platelet Transfusions Needed to Maintain Adequate Number of Platelets.(Short Term)
NCT00577096 (10) [back to overview]Hemoglobin Levels Before Chemotherapy and During Transplantation Period (Short Term)
NCT00577096 (10) [back to overview]Total Number of Days of Stem Cell Collection (Long Term)
NCT00600028 (2) [back to overview]Efficacy of Thalidomide in Suppressing the Chronic Cough of Idiopathic Pulmonary Fibrosis Using the Cough Quality of Life Questionnaire.
NCT00600028 (2) [back to overview]Efficacy of Thalidomide in Suppressing the Chronic Cough of Idiopathic Pulmonary Fibrosis Using the Visual Analog Scale of Cough and the St. George Respiratory Questionnaire.
NCT00602641 (4) [back to overview]Progression-Free Survival (PFS)
NCT00602641 (4) [back to overview]Very Good Partial Response (VGPR) Rate
NCT00602641 (4) [back to overview]Change in Functional Assessment of Cancer Therapy-Neurotoxicity Trial Outcome Index (FACT-Ntx TOI) Score From Baseline to Cycle 12
NCT00602641 (4) [back to overview]Overall Survival
NCT00689936 (43) [back to overview]Kaplan-Meier Estimates of PFS Based on the Response Assessment by the Investigator At the Time of Final Analysis
NCT00689936 (43) [back to overview]Kaplan-Meier Estimates of Progression-free Survival (PFS) Based on the Response Assessment by the Independent Review Adjudication Committee (IRAC)
NCT00689936 (43) [back to overview]Percentage of Participants With a Myeloma Response by Adverse Risk Cytogenetic Risk Category Based on IRAC Review.
NCT00689936 (43) [back to overview]Percentage of Participants With a Myeloma Response by Favorable Hyperdiploidy Risk Cytogenetic Risk Category Based on IRAC Review
NCT00689936 (43) [back to overview]Percentage of Participants With a Myeloma Response by Normal Risk Cytogenetic Risk Category Based on IRAC Review
NCT00689936 (43) [back to overview]Percentage of Participants With a Myeloma Response by Uncertain Risk Cytogenetic Risk Category Based on IRAC Review
NCT00689936 (43) [back to overview]Percentage of Participants With an Objective Response After Second-line Anti-myeloma Treatment at the Time of Final Analysis
NCT00689936 (43) [back to overview]Percentage of Participants With an Objective Response Based on Investigator Assessment at Time of Final Analysis
NCT00689936 (43) [back to overview]Percentage of Participants With an Objective Response Based on IRAC Review
NCT00689936 (43) [back to overview]Time to First Response Based on the Investigator Assessment at the Time of Final Analysis
NCT00689936 (43) [back to overview]Time to First Response Based on the Review by the IRAC
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Appetite Loss Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Cognitive Functioning Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Constipation Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Diarrhea Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Dyspnea Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Emotional Functioning Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Fatigue Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Financial Difficulties Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Insomnia Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Nausea/Vomiting Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Pain Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Physical Functioning Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Role Functioning Domain
NCT00689936 (43) [back to overview]Change From Baseline in the EORTC QLQ-C30 Social Functioning Domain
NCT00689936 (43) [back to overview]Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Cancer (EORTC QLQ-C30) Global Health Status Domain
NCT00689936 (43) [back to overview]Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Body Image Scale
NCT00689936 (43) [back to overview]Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Disease Symptoms Scale
NCT00689936 (43) [back to overview]Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Future Perspective Scale
NCT00689936 (43) [back to overview]Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Side Effects Treatment Scale
NCT00689936 (43) [back to overview]Change From Baseline in the European Quality of Life-5 Dimensions (EQ-5D) Health Utility Index Score
NCT00689936 (43) [back to overview]Number of Participants With Adverse Events (AEs) During the Active Treatment Phase
NCT00689936 (43) [back to overview]Shift From Baseline to Most Extreme Postbaseline Value in Absolute Neutrophil Count During the Active Treatment Phase
NCT00689936 (43) [back to overview]Shift From Baseline to Most Extreme Postbaseline Value in Hemoglobin During the Active Treatment Phase
NCT00689936 (43) [back to overview]Shift From Baseline to Most Extreme Postbaseline Value in Platelet Count During the Active Treatment Phase.
NCT00689936 (43) [back to overview]Shift From Baseline to Most Extreme Postbaseline Value in Creatinine Clearance (CrCl) During the Active Treatment Phase
NCT00689936 (43) [back to overview]Kaplan Meier Estimates for Time to Second-line Anti-myeloma Treatment (AMT)
NCT00689936 (43) [back to overview]Kaplan Meier Estimates of Duration of Myeloma Response as Determined by an Investigator Assessment at Time of Final Analysis
NCT00689936 (43) [back to overview]Kaplan Meier Estimates of Duration of Myeloma Response as Determined by the IRAC
NCT00689936 (43) [back to overview]Kaplan Meier Estimates of Overall Survival at the Time of Final Analysis (OS)
NCT00689936 (43) [back to overview]Kaplan Meier Estimates of Time to Second Line Therapy AMT at the Time of Final Analysis
NCT00689936 (43) [back to overview]Kaplan Meier Estimates of Time to Treatment Failure (TTF)
NCT00689936 (43) [back to overview]Kaplan Meier Estimates of Time to Treatment Failure (TTF) at the Time of Final Analysis
NCT00773734 (97) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAE) in the Apremilast Exposure Period
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Physical Component Summary Score at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Physical Component Summary Score at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Physical Component Summary Score at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in PASI Score at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in PASI Score at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in PASI Score at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 2 Years
NCT00773734 (97) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAE) in the Placebo Controlled Phase
NCT00773734 (97) [back to overview]LTE Study: Percent Change From Baseline in PASI Score at 4 Years
NCT00773734 (97) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAE) in the Apremilast Exposure Period
NCT00773734 (97) [back to overview]Time to Loss of 50% of the PASI Response During the Observational Follow-up Phase Relative to the End of Treatment (Participants Who Had at Least a PASI-50 Response at the End of Treatment Phase)
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 2 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 18 Months
NCT00773734 (97) [back to overview]Core Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 24
NCT00773734 (97) [back to overview]Core Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 16
NCT00773734 (97) [back to overview]Core Study: Area Under the Plasma Concentration-time Curve (AUC0-8)
NCT00773734 (97) [back to overview]Core Study: Area Under the Plasma Concentration-time Curve (AUC0-8)
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 4 Years
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 2 Years
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at Week 32
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 3 Years
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 2 Years
NCT00773734 (97) [back to overview]Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2 Physical Component Summary Score at Week 24
NCT00773734 (97) [back to overview]Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2; Mental Component Summary Score at Week 16
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 3 Years
NCT00773734 (97) [back to overview]Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2; Mental Component Summary Score at Week 24
NCT00773734 (97) [back to overview]Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2; Physical Component Summary Score at Week 16
NCT00773734 (97) [back to overview]Core Study: Peak; (Maximum) Plasma Concentration (Cmax) of Apremilast
NCT00773734 (97) [back to overview]Core Study: Peak; (Maximum) Plasma Concentration (Cmax) of Apremilast
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at Week 40
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at Week 52
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 32
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 40
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 52
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 32
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 40
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 52
NCT00773734 (97) [back to overview]Core Study: Percent Change From Baseline in PASI Score at Week 16
NCT00773734 (97) [back to overview]Core Study: Percent Change From Baseline in the Percent of Affected Body Surface Area (BSA) During the Active Treatment Phase at Week 24
NCT00773734 (97) [back to overview]Core Study: Percent Change From Baseline in the Percent of Affected Body Surface Area (BSA) During the Placebo Controlled Phase
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in PASI Score at Week 16
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 24
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in PASI Score at Week 24
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in Psoriasis Area and Severity Index (PASI) at Week 16
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a 90% Improvement (Response) From Baseline in the PASI Score at Week 16
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 24
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 24
NCT00773734 (97) [back to overview]Core Study: Percentage of Participants With a Static Physician Global Assessment (sPGA) Greater Than 2 at Baseline Who Achieved a Score of 0 or 1 at Week 16
NCT00773734 (97) [back to overview]Core Study: Time to Achieve a PASI-50 Response During the Placebo Controlled Phase
NCT00773734 (97) [back to overview]Core Study: Time to Achieve a PASI-75 Response During the Placebo Controlled Phase
NCT00773734 (97) [back to overview]Core Study: Time to Maximum Plasma Concentration of Drug (Tmax)
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score at Week 40
NCT00773734 (97) [back to overview]Core Study: Time to Maximum Plasma Concentration of Drug (Tmax)
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 32
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 40
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 52
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Mental Component Summary Score at Week 32
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Mental Component Summary Score at Week 40
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Mental Component Summary Score at Week 52
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score (PCS) at Week 32
NCT00773734 (97) [back to overview]Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score at Week 52
NCT00773734 (97) [back to overview]Extension Study: Percent Change From Baseline in the Affected BSA at Week 32
NCT00773734 (97) [back to overview]Extension Study: Percent Change From Baseline in the Affected BSA at Week 40
NCT00773734 (97) [back to overview]Extension Study: Percent Change From Baseline in the Affected BSA at Week 52
NCT00773734 (97) [back to overview]Extension Study: Percent Change in PASI Score at Week 32
NCT00773734 (97) [back to overview]Extension Study: Percent Change in PASI Score at Week 40
NCT00773734 (97) [back to overview]Extension Study: Percent Change in PASI Score at Week 52
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 32
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 40
NCT00773734 (97) [back to overview]Extension Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 52
NCT00773734 (97) [back to overview]LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 18 Months
NCT00773734 (97) [back to overview]LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 4 Years
NCT00773734 (97) [back to overview]Core Study: Percent Change From Baseline in PASI Score at Week 24
NCT00773734 (97) [back to overview]LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 18 Months
NCT00792142 (3) [back to overview]One Year Overall Survival
NCT00792142 (3) [back to overview]One Year Progression-free Survival (PFS)
NCT00792142 (3) [back to overview]Number of Participants With Adverse Events
NCT00931242 (3) [back to overview]Number of Patients Achieving an Improvement (Decrease) in IGA (Investigator Global Assessment) by Two or More Points
NCT00931242 (3) [back to overview]Number of Patients Achieving 50% Reduction in Eczema Area and Severity Index (EASI) Score at Week 12 in Reference to Week 0
NCT00931242 (3) [back to overview]Number of Patients Achieving 75% Reduction in Eczema Area and Severity Index (EASI) Score at Week 12 in Reference to Week 0
NCT00946270 (1) [back to overview]Number of Participants With Best Overall Response
NCT00964496 (7) [back to overview]Change From Baseline in Total Transfused Red Cell Requirements at 12 Months
NCT00964496 (7) [back to overview]Participants Dependent on Blood Transfusions
NCT00964496 (7) [back to overview]Participants Whose Rebleeds Decreased From Baseline by ≥ 50% at 12 Months
NCT00964496 (7) [back to overview]Cessation of Bleeding
NCT00964496 (7) [back to overview]Change From Baseline in Bleeding Duration at 12 Months
NCT00964496 (7) [back to overview]Change From Baseline in Bleeding Episodes at 12 Months
NCT00964496 (7) [back to overview]Change From Baseline in Hemoglobin (Hb) Level at 12 Months
NCT00966693 (7) [back to overview]Progression Free Survival
NCT00966693 (7) [back to overview]Number of Participants With Dose Limitations Toxicities of the Combination of Lenalidomide and Thalidomide and Dexamethasone (LTD) in Patients With Relapsed/Refractory Multiple Myeloma (RRMM)
NCT00966693 (7) [back to overview]Incidence of Adverse Events
NCT00966693 (7) [back to overview]Time to Best Response
NCT00966693 (7) [back to overview]Time to Progression
NCT00966693 (7) [back to overview]Complete Response(CR) and Very Good Partial Response(VGPR)
NCT00966693 (7) [back to overview]Time to Next Therapy
NCT01057225 (11) [back to overview]Time to Treatment Failure
NCT01057225 (11) [back to overview]Survival Time (Phase II)
NCT01057225 (11) [back to overview]Stem Cell Collection and Engraftment (Phase II)
NCT01057225 (11) [back to overview]Progression-free Survival (Phase II)
NCT01057225 (11) [back to overview]Progression Free Survival (12 Month)
NCT01057225 (11) [back to overview]Progession Free Survival (24 Month)
NCT01057225 (11) [back to overview]Overall Survival (24 Month)
NCT01057225 (11) [back to overview]Overall Survival (12 Month)
NCT01057225 (11) [back to overview]Maximum Tolerated Dose (Phase I)
NCT01057225 (11) [back to overview]Complete Response (Phase II)
NCT01057225 (11) [back to overview]Percentage of Patients Who Have at Least a Confirmed Very Good Partial Response (Phase II)
NCT01061866 (1) [back to overview]Change From Baseline in the Mean Number of Daily Seizures at 1 Year.
NCT01125176 (5) [back to overview]Duration of Response
NCT01125176 (5) [back to overview]Time to Response
NCT01125176 (5) [back to overview]Progression Free Survival
NCT01125176 (5) [back to overview]Overall Survival
NCT01125176 (5) [back to overview]Overall Response Rate as Defined as the Number of Patients Who Experience a Response (Complete or Partial) to Treatment at the Time of Best Response
NCT01172938 (53) [back to overview]Percentage of Participants With a ACR 70 Response at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With a Modified PsARC Response at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With an ACR 20 Response at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With an ACR 50 Response at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With an ACR 50 Response at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants With an ACR 70 Response at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants With an ACR 70 Response at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants With Good or Moderate EULAR Response at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 52
NCT01172938 (53) [back to overview]Number of Participants With Adverse Events During the Apremilast-Exposure Period
NCT01172938 (53) [back to overview]Number of Participants With Adverse Events During the Placebo-Controlled Period
NCT01172938 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 16
NCT01172938 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants With a ACR 20 Response at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants With a ACR 50 Response at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 24
NCT01172938 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in SF-36 Physical Function at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in the CDAI Score at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in the Dactylitis Severity Score at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in the DAS28 at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in the FACIT-Fatigue Scale Score at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24
NCT01172938 (53) [back to overview]Change From Baseline in the Patient Assessment of Pain at Week 52
NCT01172938 (53) [back to overview]Change From Baseline in the SF-36 Physical Functioning Domain at Week 52
NCT01172938 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 16
NCT01172938 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52
NCT01178281 (9) [back to overview]China Extension: Number of Participants Achieving a Hemoglobin Increase of ≥ 15 g/L Compared to Baseline for ≥ 84 Consecutive Days
NCT01178281 (9) [back to overview]Duration of RBC-Transfusion Independence
NCT01178281 (9) [back to overview]Overall Survival
NCT01178281 (9) [back to overview]Percentage of Participants Who Achieved RBC-Transfusion Independence
NCT01178281 (9) [back to overview]Time to RBC-Transfusion Independence
NCT01178281 (9) [back to overview]Change From Baseline in EuroQoL-5D (EQ-5D) Health Index Score
NCT01178281 (9) [back to overview]Change From Baseline in EuroQoL-5D (EQ-5D) Visual Analog Scale
NCT01178281 (9) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Anemia (FACT-An) Total Score
NCT01178281 (9) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAE)
NCT01212757 (53) [back to overview]Percentage of Participants With an ACR 70 Response at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants With Good or Moderate EULAR Response at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 52
NCT01212757 (53) [back to overview]Number of Participants With Treatment Emergent Adverse Events During the Placebo-Controlled Phase
NCT01212757 (53) [back to overview]Number of Participants With TEAEs During the Apremilast-Exposure Period
NCT01212757 (53) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in the CDAI Score at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in the Dactylitis Severity Score at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in the DAS28 at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in the FACIT-Fatigue Scale Score at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16
NCT01212757 (53) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24
NCT01212757 (53) [back to overview]Change From Baseline in the Patient Assessment of Pain at Week 52
NCT01212757 (53) [back to overview]Change From Baseline in the SF-36 Physical Functioning Scale Score at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants With a ACR 20 Response at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants With a ACR 50 Response at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants With a ACR 70 Response at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With a Modified PsARC Response at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16
NCT01212757 (53) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With an ACR 20 Response at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With an ACR 50 Response at Week 24
NCT01212757 (53) [back to overview]Percentage of Participants With an ACR 50 Response at Week 52
NCT01212757 (53) [back to overview]Percentage of Participants With an ACR 70 Response at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With Good or Moderate EULAR Response at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With an ACR 70 Response at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants With an ACR 70 Response at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With an ACR 50 Response at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants With an ACR 50 Response at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With an ACR 20 Response at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants With an ACR 20 Response at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With a ACR 50 Response at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants With a Modified PsARC Response at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants With a ACR 70 Response at Week 24
NCT01212770 (56) [back to overview]Number of Participants With Treatment Emergent Adverse Events During the Apremilast Exposure Period
NCT01212770 (56) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs) During the Placebo-Controlled Phase
NCT01212770 (56) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 16
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a ≥ 75% Improvement in Psoriasis Area and Severity Index Score (PASI75) at Week 52
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a ≥ 75% Improvement in Psoriasis Area and Severity Index Score (PASI75) at Week 24
NCT01212770 (56) [back to overview]Percentage of Participants Achieving a ≥ 75% Improvement in Psoriasis Area and Severity Index Score (PASI75) at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in the SF-36 Physical Functioning Scale Score at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in the Patient Assessment of Pain at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in the FACIT-Fatigue Scale Score at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in the DAS28 at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in the Dactylitis Severity Score at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in the CDAI Score at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52
NCT01212770 (56) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24
NCT01212770 (56) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16
NCT01212770 (56) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16
NCT01242267 (4) [back to overview]Treatment Free Interval/PFS
NCT01242267 (4) [back to overview]Toxicity Assessment
NCT01242267 (4) [back to overview]Maximum Tolerated Dose of Thalidomide
NCT01242267 (4) [back to overview]Complete Response (CR) and Very Good Partial Response (VgPR) Rate
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the High Sensitivity C-Reactive Protein (CRP) at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Tender Joint Count at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Tender Joint Count at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve an Improvement of at Least 4 Units From Baseline in the Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Swollen Joint Count at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Swollen Joint Count at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Swollen Joint Count at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Subject Global Assessment of Disease Activity at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Subject Global Assessment of Disease Activity at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Subject Global Assessment of Disease Activity at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Subject Assessment of Pain at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Subject Assessment of Pain at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Subject Assessment of Pain at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Physician Global Assessment of Disease Activity at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Physician Global Assessment of Disease Activity at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Physician Global Assessment of Disease Activity at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the High Sensitivity C-Reactive Protein (CRP) at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the High Sensitivity C-Reactive Protein (CRP) at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) Score at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) Score at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Health Assessment Questionnaire - Disability Index (HAQ-DI) Score at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in Erythrocyte Sedimentation Rate (ESR) at Week 52
NCT01285310 (60) [back to overview]Percentage Change From Baseline in Erythrocyte Sedimentation Rate (ESR) at Week 24
NCT01285310 (60) [back to overview]Percentage Change From Baseline in Erythrocyte Sedimentation Rate (ESR) at Week 16
NCT01285310 (60) [back to overview]Change From Baseline in the Medical Outcome Study Short Form 36-item (SF-36) Physical Functioning Domain at Week 52
NCT01285310 (60) [back to overview]Change From Baseline in the Medical Outcome Study Short Form 36-item (SF-36) Physical Functioning Domain at Week 24
NCT01285310 (60) [back to overview]Change From Baseline in the Medical Outcome Study Short Form 36-item (SF-36) Physical Functioning Domain at Week 16
NCT01285310 (60) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24
NCT01285310 (60) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16
NCT01285310 (60) [back to overview]Change From Baseline in the FACIT-Fatigue Scale Score at Week 52
NCT01285310 (60) [back to overview]Change From Baseline in the Disease Activity Score 28 (DAS 28) Using CRP at Week 52
NCT01285310 (60) [back to overview]Change From Baseline in the Clinical Disease Activity Index (CDAI) at Week 52
NCT01285310 (60) [back to overview]Change From Baseline in the Clinical Disease Activity Index (CDAI) at Week 24
NCT01285310 (60) [back to overview]Change From Baseline in the Clinical Disease Activity Index (CDAI) at Week 16
NCT01285310 (60) [back to overview]Percentage Change From Baseline in the Tender Joint Count at Week 52
NCT01285310 (60) [back to overview]Change From Baseline in Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve an Improvement of ≥ 0.22 Units From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 24
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 50% Improvement (ACR 50) Response at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve Low Disease Activity or Remission Based on the Clinical Disease Activity Index (CDAI) ≤ 10 at Week 24
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 50% Improvement (ACR 50) Response at Week 24
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 50% Improvement (ACR 50) Response at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 20% Improvement (ACR 20) Response at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 20% Improvement (ACR 20) Response at Week 24
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 20% Improvement (ACR 20) Response at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve the European League Against Rheumatism (EULAR) Response Criteria Using CRP at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve the European League Against Rheumatism (EULAR) Response Criteria Using CRP at Week 24
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve the European League Against Rheumatism (EULAR) Response Criteria Using CRP at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve an Improvement of ≥ 0.22 Units From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve an Improvement of at Least 4 Units From Baseline in the Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve an Improvement of at Least 4 Units From Baseline in the Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve Low Disease Activity or Remission Based on the Clinical Disease Activity Index (CDAI) ≤ 10 at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve Low Disease Activity or Remission Based on the Clinical Disease Activity Index (CDAI) ≤ 10 at Week 16
NCT01285310 (60) [back to overview]Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52
NCT01285310 (60) [back to overview]Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 24
NCT01285310 (60) [back to overview]Change From Baseline in Disease Activity Score 28 (DAS28) Using CRP at Week 24
NCT01285310 (60) [back to overview]Change From Baseline in Disease Activity Score 28 (DAS28) (Using C-Reactive Protein) (CRP) at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 70% Improvement (ACR 70) Response at Week 52
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 70% Improvement (ACR 70) Response at Week 24
NCT01285310 (60) [back to overview]Percentage of Participants Who Achieve an Improvement of ≥ 0.22 Units From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 16
NCT01285310 (60) [back to overview]Percentage of Participants With an American College of Rheumatology 70% Improvement (ACR 70) Response at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With a ACR 50 Response at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With a ACR 50 Response at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With a ACR 20 Response at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With ≥ 20% Improvement in Maastricht Ankylosing Spondylitis Entheses Score at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants Achieving a MASES Score of Zero at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in the SF-36v2 Physical Functioning Scale Score at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in the Participants Assessment of Pain Using the Visual Analog Scale at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in the FACIT-Fatigue Scale Score at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With an ACR 50 Response at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in the Disease Activity Score (DAS28) After 16 Weeks of Treatment
NCT01307423 (53) [back to overview]Change From Baseline in the DAS28 at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in the Dactylitis Severity Score at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in the CDAI Score at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in Patient's Assessment of Pain at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in Participants Assessment of Pain at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index [HAQ-DI]) at Week 24
NCT01307423 (53) [back to overview]Number of Participants With Treatment Emergent Adverse Events During the Placebo Controlled Phase
NCT01307423 (53) [back to overview]Number of Participants With Treatment Emergent Adverse Events During the Apremilast Exposure Period
NCT01307423 (53) [back to overview]Percentage of Participants With Pre-existing Enthesopathy Whose MASES Improves From Baseline to 0 at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With Pre-existing Enthesopathy Whose Maastricht Ankylosing Spondylitis Entheses Score Improves to 0 at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With Pre-existing Dactylitis Whose Dactylitis Severity Score Improves to 0 at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With Pre-existing Dactylitis Whose Dactylitis Severity Score Improves From Baseline to 0 at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With Pre-existing Dactylitis Whose Dactylitis Severity Score Improves From Baseline by ≥ 1 at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With MASES Improvement ≥ 20% at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With Good or Moderate EULAR Response at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With an ACR 70 Response at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With an ACR 20 Response at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16
NCT01307423 (53) [back to overview]Percentage of Participants With a Modified PsARC Response at Week 52
NCT01307423 (53) [back to overview]Percentage of Participants With a ACR 70 Response at Week 24
NCT01307423 (53) [back to overview]Percentage of Participants With a ACR 70 Response at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire- Disability Index [HAQ-DI]) at Week 16
NCT01307423 (53) [back to overview]Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52
NCT01307423 (53) [back to overview]Change From Baseline in Disease Activity Score (DAS 28) at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 24
NCT01307423 (53) [back to overview]Change From Baseline in Dactylitis Severity Score at Week 16
NCT01539083 (8) [back to overview]Overall Survival (OS)
NCT01539083 (8) [back to overview]Disease-free Survival (DFS)
NCT01539083 (8) [back to overview]Consolidation Phase: Percentage of Participants With Complete Response (CR) and Very Good Partial Response (VGPR) at Month 12
NCT01539083 (8) [back to overview]Consolidation Phase: Change From Baseline in FACT/GOG-NTX Total Score at the End of the Consolidation Phase
NCT01539083 (8) [back to overview]Consolidation Phase: Percentage of Participants With Stringent Complete Response (sCR) at Months 3, 6, 9 and 12
NCT01539083 (8) [back to overview]Consolidation Phase: Percentage of Participants With Complete Response (CR) at Months 3, 6, 9 and 12
NCT01539083 (8) [back to overview]Consolidation Phase: Change From Baseline in AQOL-6D Scores at the End of the Consolidation Phase
NCT01539083 (8) [back to overview]Progression Free Survival (PFS)
NCT01548573 (4) [back to overview]Event-Free Survival (EFS)
NCT01548573 (4) [back to overview]Identification of Drug Resistant Genes
NCT01548573 (4) [back to overview]Number of Grade 3 Non-hematologic and Grade 4 Hematologic Serious Adverse Events Associated With the Addition of Bortezomib, Thalidomide, and Dexamethasone Into Autologous Transplant Regimens.
NCT01548573 (4) [back to overview]Overall Survival
NCT01583374 (10) [back to overview]Number of Participants With Treatment Emergent Adverse Events During the Apremilast Exposure Period
NCT01583374 (10) [back to overview]Percentage of Participants Who Achieved an Assessment of SpondyloArthritis International Society 20 (ASAS 20) Response at Week 16
NCT01583374 (10) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs) During the Placebo Controlled Phase
NCT01583374 (10) [back to overview]Change From Baseline in the Radiographic Score Using the Modified Stoke Ankylosing Spondylitis Spine Score (m-SASSS) at Week 104 and Week 260
NCT01583374 (10) [back to overview]Percentage of Participants Who Achieved an Assessment of SpondyloArthritis International Society 20 (ASAS) Response at Week 24
NCT01583374 (10) [back to overview]Change From Baseline in Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) at Week 24
NCT01583374 (10) [back to overview]Change From Baseline in Bath Ankylosing Spondylitis Functional Index (BASFI) at Week 24
NCT01583374 (10) [back to overview]Change From Baseline in Bath Ankylosing Spondylitis Metrology Index-Linear (BASMI-Linear) at Week 24
NCT01583374 (10) [back to overview]Change From Baseline in the Ankylosing Spondylitis Quality of Life (ASQoL) Summary Score at Week 24
NCT01583374 (10) [back to overview]Change From Baseline in the Physical Component Summary Score (PCS) of Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) at Week 24
NCT01632150 (4) [back to overview]Percentage of All Participants Who Received Treatment Without Cyclophosphamide and Had Grade 3 or Higher Nonhematologic Adverse Events (AEs)
NCT01632150 (4) [back to overview]Percentage of Participants Who Received Treatment Including Cyclophosphamide and Had Grade 3 or Higher Nonhematologic Adverse Events (AEs)
NCT01632150 (4) [back to overview]Percentage of All Participants Who Received Treatment Including Cyclophosphamide and Had 1 Dose Reduction or Discontinued Due to an Adverse Event
NCT01632150 (4) [back to overview]Percentage of All Participants Who Received Treatment Without Cyclophosphamide and Had 1 Dose Reduction or Discontinued Due to an Adverse Event
NCT01659658 (21) [back to overview]Number of Hospitalizations
NCT01659658 (21) [back to overview]2-Year Vital Organ (Heart or Kidney) Deterioration and Mortality Rate
NCT01659658 (21) [back to overview]Percentage of Participants With Overall Hematologic Response
NCT01659658 (21) [back to overview]Percentage of Participants With Complete Hematologic Response
NCT01659658 (21) [back to overview]Percentage of Participants With Best Vital Organ (Cardiac and/or Kidney) Response
NCT01659658 (21) [back to overview]Overall Survival
NCT01659658 (21) [back to overview]EuroQol 5-Dimension 3-Level (EQ-5D-3L) Visual Analogue Scale Score
NCT01659658 (21) [back to overview]Duration of Hematologic Response
NCT01659658 (21) [back to overview]Change From Baseline in SF-36 Physical Component Summary Score at Week 28 of the PFS Follow-up
NCT01659658 (21) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-Ntx) Score at Week 28 of the PFS Follow-up
NCT01659658 (21) [back to overview]Change From Baseline in Amyloidosis Symptom Scale Total Score at Week 28 of the PFS Follow-up
NCT01659658 (21) [back to overview]Change From Baseline in 36-item Short Form General Health Survey (SF-36) Mental Component Summary Score at Week 28 of the PFS Follow-up
NCT01659658 (21) [back to overview]Hematologic Disease Progression Free Survival
NCT01659658 (21) [back to overview]Plasma Concentration of Ixazomib
NCT01659658 (21) [back to overview]Progression Free Survival (PFS)
NCT01659658 (21) [back to overview]Number of Participants in Each Category of the EuroQol 5-Dimensional (EQ-5D) Questionnaire Score
NCT01659658 (21) [back to overview]Vital Organ Progression Free Survival
NCT01659658 (21) [back to overview]Time to Vital Organ (Heart or Kidney) Deterioration and Mortality Rate
NCT01659658 (21) [back to overview]Time To Treatment Failure (TTF)
NCT01659658 (21) [back to overview]Time To Subsequent Anticancer Treatment
NCT01659658 (21) [back to overview]Number of Participants With Serious Adverse Events (SAEs)
NCT01734928 (6) [back to overview]Duration of Response by Independent Response Adjudication Committee (IRAC)
NCT01734928 (6) [back to overview]Number of Participants With Grade 3-4 Treatment Emergent Adverse Events (TEAE)
NCT01734928 (6) [back to overview]Number of Participants With Grade 5 Treatment Emergent Adverse Events (TEAE)
NCT01734928 (6) [back to overview]Overall Survival (OS)
NCT01734928 (6) [back to overview]Progression Free Survival by Independent Response Adjudication Committee (IRAC)
NCT01734928 (6) [back to overview]Overall Response Rate by Independent Response Adjudication Committee (IRAC)
NCT01779167 (1) [back to overview]Number of Patients Who Demonstrate a Response (Complete, Partial, Minor) to Treatment
NCT01849783 (4) [back to overview]Percentage of Participants With Serious Treatment-Related Complications
NCT01849783 (4) [back to overview]Percentage of Participants Able to Complete Full Course Therapy
NCT01849783 (4) [back to overview]Median Progression Free Survival (mPFS)
NCT01849783 (4) [back to overview]Mean Change in Quality-Of-Life Indicators Post-Transplant
NCT01927718 (1) [back to overview]Number of Participants With Response
NCT01988103 (10) [back to overview]Percent Change From Baseline in the Psoriasis Affected Body Surface Area (BSA) at Week 16
NCT01988103 (10) [back to overview]Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at Week 16
NCT01988103 (10) [back to overview]Change From Baseline in Pruritus Visual Analogue Scale 100-mm (VAS) at Week 16
NCT01988103 (10) [back to overview]Change From Baseline in Mental Component Summary (MCS) Score of the Medical Outcome Study Short Form 36-item (SF-36) Health Survey Version 2.0 at Week 16
NCT01988103 (10) [back to overview]Number of Participants With Adverse Events (AE) in the Placebo Controlled Phase
NCT01988103 (10) [back to overview]Number of Participants With Adverse Events (AE) in the During the Apremilast-exposure Period
NCT01988103 (10) [back to overview]Percentage of Participants Who Achieved a Static Physician's Global Assessment (sPGA) Score of Clear (0) or Almost Clear (1) With at Least 2 Point Reduction From Baseline to Week 16
NCT01988103 (10) [back to overview]Percentage of Participants Who Achieved a 75% Improvement (Response) From Baseline in the Psoriasis Area and Severity Index (PASI-75) at Week 16
NCT01988103 (10) [back to overview]Percentage of Participants Who Achieved a 50% Improvement From Baseline (Response) Reduction in the PASI-50 at Week 16
NCT01988103 (10) [back to overview]Percent Change From Baseline in the Psoriasis Area and Severity Index (PASI) Score
NCT02087943 (6) [back to overview]Percentage Change From Baseline in the Eczema Area and Severity Index (EASI) Score at Week 12.
NCT02087943 (6) [back to overview]Percentage of Participants Who Achieved a Score of 0 (Cleared) or 1 (Almost Cleared) and at Least a 2-point Reduction From Baseline in a Static Physician's Global Assessment of Acute Signs (sPGA-A) at Week 12.
NCT02087943 (6) [back to overview]Percentage of Participants Who Achieved at Least a 50% Reduction From Baseline in the EASI Score (EASI 50) at Week 12
NCT02087943 (6) [back to overview]The Percentage Change From Baseline in the Average Weekly Pruritus Numerical Rating Scale (NRS) Score at Week 4
NCT02087943 (6) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs) During the Placebo Controlled Period
NCT02087943 (6) [back to overview]Number of Participants With TEAEs During the Apremilast Exposure Period
NCT02128230 (1) [back to overview]The Remission Rate for Participants With High-risk Myeloma
NCT02236988 (39) [back to overview]Group 2: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast
NCT02236988 (39) [back to overview]Group 2: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast
NCT02236988 (39) [back to overview]Group 2: Half-life of Apremilast in Terminal Phase (T1/2)
NCT02236988 (39) [back to overview]Group 2: Observed Maximum Plasma Concentration (Cmax) of Apremilast
NCT02236988 (39) [back to overview]Group 2: Relative Bioavailability of Apremilast Test Formulations Relative to Reference
NCT02236988 (39) [back to overview]Group 2: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose
NCT02236988 (39) [back to overview]Group 2: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast
NCT02236988 (39) [back to overview]Group 3: Apparent Total Plasma Clearance (CL/F) of Apremilast
NCT02236988 (39) [back to overview]Group 3: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast
NCT02236988 (39) [back to overview]Group 3: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast
NCT02236988 (39) [back to overview]Group 3: Half-life of Apremilast in Terminal Phase (T1/2)
NCT02236988 (39) [back to overview]Group 3: Observed Maximum Plasma Concentration (Cmax) of Apremilast
NCT02236988 (39) [back to overview]Group 3: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose
NCT02236988 (39) [back to overview]Group 3: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast
NCT02236988 (39) [back to overview]Group 4: Apparent Total Plasma Clearance (CL/F) of Apremilast
NCT02236988 (39) [back to overview]Group 4: Apparent Total Volume of Distribution (Vz/F) of Apremilast
NCT02236988 (39) [back to overview]Group 4: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast
NCT02236988 (39) [back to overview]Group 4: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast
NCT02236988 (39) [back to overview]Group 4: Half-life of Apremilast in Terminal Phase (T1/2)
NCT02236988 (39) [back to overview]Group 4: Observed Maximum Plasma Concentration (Cmax) of Apremilast
NCT02236988 (39) [back to overview]Group 4: Relative Bioavailability of Apremilast Test Formulations Relative to Reference
NCT02236988 (39) [back to overview]Group 4: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose
NCT02236988 (39) [back to overview]Group 4: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast
NCT02236988 (39) [back to overview]Group 1: Number of Participants With Treatment-emergent Adverse Events
NCT02236988 (39) [back to overview]Group 2: Number of Participants With Treatment-emergent Adverse Events
NCT02236988 (39) [back to overview]Group 3: Number of Participants With Treatment-emergent Adverse Events
NCT02236988 (39) [back to overview]Group 4: Number of Participants With Treatment-emergent Adverse Events
NCT02236988 (39) [back to overview]Group 3: Relative Bioavailability of Apremilast Test Formulations Relative to Reference
NCT02236988 (39) [back to overview]Group 1: Apparent Total Plasma Clearance (CL/F) of Apremilast
NCT02236988 (39) [back to overview]Group 1: Apparent Total Volume of Distribution (Vz/F) of Apremilast
NCT02236988 (39) [back to overview]Group 1: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast
NCT02236988 (39) [back to overview]Group 1: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast
NCT02236988 (39) [back to overview]Group 1: Half-life of Apremilast in Terminal Phase (T1/2)
NCT02236988 (39) [back to overview]Group 1: Observed Maximum Plasma Concentration (Cmax) of Apremilast
NCT02236988 (39) [back to overview]Group 1: Relative Bioavailability of Apremilast Test Formulations Relative to Reference
NCT02236988 (39) [back to overview]Group 1: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose
NCT02236988 (39) [back to overview]Group 1: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast
NCT02236988 (39) [back to overview]Group 2: Apparent Total Plasma Clearance (CL/F) of Apremilast
NCT02236988 (39) [back to overview]Group 2: Apparent Total Volume of Distribution (Vz/F) of Apremilast
NCT02424851 (5) [back to overview]Overall Survival
NCT02424851 (5) [back to overview]Renal Response After Two Cycles of Trial Treatment
NCT02424851 (5) [back to overview]Quality of Life Measured by the EQ-5D-3L Questionnaire at Baseline and 1 Month Follow up
NCT02424851 (5) [back to overview]Haematological and Non-haematological Toxicity in Both Treatment Arms
NCT02424851 (5) [back to overview]Number of Participants With >50% Reduction From Baseline in Serum Free Light Chain
NCT02425826 (15) [back to overview]Percentage of Participants Who Achieved at Least a 75% Improvement (Response) in the Psoriasis Area and Severity Index (PASI)-75 From Baseline at Week 16
NCT02425826 (15) [back to overview]Percentage of Participants With Scalp Psoriasis Who Achieved a Clear (0) or Minimal (1) on Scalp Physician's Global Assessment (ScPGA) Scale at Week 16.
NCT02425826 (15) [back to overview]Mean Change From Baseline in Pruritus Visual Analog Scale (VAS)
NCT02425826 (15) [back to overview]Number of Participants Who Experienced Treatment-emergent Adverse Events (TEAEs) During the Apremilast-Exposure Phase
NCT02425826 (15) [back to overview]Percentage of Participants With Scalp Psoriasis Who Were Initially Randomized to Apremilast and Maintained the Scalp Physician's Global Assessment (ScPGA) Response From Week 16 to Week 52.
NCT02425826 (15) [back to overview]Treatment Satisfaction Questionnaire for Medication (TSQM) Version II at Week 16
NCT02425826 (15) [back to overview]Percentage of Participants Who Achieved a sPGA Score of Clear (0) or Almost Clear (1) at Week 16 From Baseline
NCT02425826 (15) [back to overview]Percentage of Participants Who Achieved a Clear (0) or Very Mild (1) on Patient Global Assessment (PtGA) Scale at Week 16 From Baseline
NCT02425826 (15) [back to overview]Mean Percentage Change From Baseline in the Product of BSA (%) x sPGA at Week 52
NCT02425826 (15) [back to overview]Mean Percentage Change From Baseline in the Product of BSA (%) and the sPGA Which is Considered as the Total Psoriasis Severity Index at Week 16
NCT02425826 (15) [back to overview]Mean Percentage Change From Baseline in Psoriasis Area Severity Index Score (PASI) at Week 16
NCT02425826 (15) [back to overview]Mean Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at Week 16
NCT02425826 (15) [back to overview]Treatment Satisfaction Questionnaire for Medication (TSQM) Version II at Week 52
NCT02425826 (15) [back to overview]Number of Participants Who Experienced Treatment-Emergent Adverse Events (TEAEs) During the Placebo Controlled Phase
NCT02425826 (15) [back to overview]Percentage of Participants Who Achieved at Least a 50% Improvement (Response) in the Psoriasis Area and Severity Index (PASI)-50 From Baseline at Week 16.
NCT02545907 (10) [back to overview]Number of Participants With Dose-Limiting Toxicities as Assessed by Reported Data
NCT02545907 (10) [back to overview]Number of Patients Experiencing Dose Delays Based on Reported Data.
NCT02545907 (10) [back to overview]Compliance Profile of KTD Based on Reported Chemotherapy Compliance Data.
NCT02545907 (10) [back to overview]Number of Patients Progression-free at 6 Months Based on Reported Data.
NCT02545907 (10) [back to overview]Number of Patients Withdrawing From Treatment Based on Reported Data.
NCT02545907 (10) [back to overview]Clonal Response Rate Within 3 Months, at 3 Months, Within 6 Months and at 6 Months as Determined by Paraprotein and Free Light Chain Assessment.
NCT02545907 (10) [back to overview]Time to Amyloidotic Organ Response Based on Reported Data.
NCT02545907 (10) [back to overview]Time to Maximum Response Based on Reported Data.
NCT02545907 (10) [back to overview]Number of Deaths at 6 Months Based on Reported Data.
NCT02545907 (10) [back to overview]Number of Participants Experiencing Grade 3 or 4 Toxicity as Assessed by CTCAE v4.0.
NCT02641353 (10) [back to overview]Area Under the Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) for Apremilast
NCT02641353 (10) [back to overview]Lag Time (Tlag) of Apremilast
NCT02641353 (10) [back to overview]Maximum Observed Plasma Concentration (Cmax) of Apremilast
NCT02641353 (10) [back to overview]Relative Bioavailability (F) of Apremilast Oral Suspension Formulation
NCT02641353 (10) [back to overview]Number of Participants With Treatment-emergent Adverse Events
NCT02641353 (10) [back to overview]Area Under the Concentration-time Curve From Time Zero to Infinity (AUC0-∞) for Apremilast
NCT02641353 (10) [back to overview]Time to Maximum Observed Plasma Concentration (Tmax) of Apremilast
NCT02641353 (10) [back to overview]Terminal Elimination Half-life (T1/2) of Apremilast
NCT02641353 (10) [back to overview]Apparent Clearance of Apremilast From Plasma After Extravascular Administration (CL/F)
NCT02641353 (10) [back to overview]Apparent Volume of Distribution of Apremilast During the Terminal Phase (Vz/F)
NCT02777554 (6) [back to overview]Part 2: Peak Maximum Plasma Concentration (Cmax) of Apremilast
NCT02777554 (6) [back to overview]Part 2: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Observable Concentration (AUC0-t) of Apremilast
NCT02777554 (6) [back to overview]Part 2: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast
NCT02777554 (6) [back to overview]Part 1: Peak Maximum Plasma Concentration (Cmax) of Apremilast
NCT02777554 (6) [back to overview]Part 1: Area Under the Concentration-time Curve From Time Zero to 24 Hours Postdose (AUC0-24) of Apremilast
NCT02777554 (6) [back to overview]Number of Participants With Treatment-emergent Adverse Events
NCT03043105 (6) [back to overview]Overall Survival
NCT03043105 (6) [back to overview]Progression-free Survival
NCT03043105 (6) [back to overview]Number of Participants With Treatment-related Serious Adverse Events as Assessed by CTCAE v4.0 ( ≥3 Grade)
NCT03043105 (6) [back to overview]Change in SF-36 Score
NCT03043105 (6) [back to overview]Number of Participants With Treatment-related Adverse Events as Assessed by CTCAE v4.0 ( ≥1 Grade)
NCT03043105 (6) [back to overview]Number of Patients With Durable Tumor and Symptomatic Response
NCT03122431 (2) [back to overview]Serum Levels of Thalidomide
NCT03122431 (2) [back to overview]Serum Levels of Hydroxycloroquine
NCT03257631 (7) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT03257631 (7) [back to overview]Percentage of Participants With an Objective Response or Long-term Stable Disease
NCT03257631 (7) [back to overview]Kaplan-Meier Estimate of Duration of Response
NCT03257631 (7) [back to overview]Percentage of Participants With Long-term Stable Disease
NCT03257631 (7) [back to overview]Kalan-Meier Estimate of Overall Survival
NCT03257631 (7) [back to overview]Kaplan-Meier Estimate of Progression-Free Survival (PFS)
NCT03257631 (7) [back to overview]Percentage of Participants Who Achieved an Objective Response
NCT03411031 (3) [back to overview]Minimum Response (MR)
NCT03411031 (3) [back to overview]Overall Response
NCT03411031 (3) [back to overview]Percentage of Participants With Progression Free Survival (PFS)
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Percentage of Participants Who Died Before or on Day 29
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Percentage of Participants Who Died Before or on Day 29
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Percentage of Participants With a ≥ 2-point Improvement From Baseline or Fit for Discharge on the Clinical Severity Status 8-Point Ordinal Scale at Day 29
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Time to Confirmed Clinical Recovery Without Rehospitalization Through Day 29
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Percentage of Participants Who Achieved Sustained Clinical Recovery
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Percentage of Participants Who Died Before or on Day 29
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Time to Confirmed Clinical Recovery Without Rehospitalization Through Day 29
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Percentage of Participants With a ≥ 2-point Improvement From Baseline or Fit for Discharge on the Clinical Severity Status 8-Point Ordinal Scale at Day 29
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Clinical Severity Status 8-Point Ordinal Scale Score at Days 8, 15, and 29
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Clinical Severity Status 8-Point Ordinal Scale Score at Days 8, 15, and 29
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Percentage of Participants Who Achieved Oxygen-Free Recovery at Day 29
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Percentage of Participants Who Achieved Sustained Clinical Recovery
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Percentage of Participants With a ≥ 2-point Improvement From Baseline or Fit for Discharge on the Clinical Severity Status 8-Point Ordinal Scale at Day 29
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Time to Confirmed Clinical Recovery Without Rehospitalization Through Day 29
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Percentage of Participants Who Achieved Oxygen-Free Recovery at Day 29
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Percentage of Participants Who Achieved Clinical Recovery by Days 8, 15, and 29
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Number of Participants With Treatment-emergent Adverse Events
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Percentage of Participants Who Achieved Clinical Recovery by Days 8, 15, and 29
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Number of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Percentage of Participants Who Achieved Clinical Recovery at Days 8, 15, and 29
NCT04590586 (24) [back to overview]Apremilast Sub-protocol: Number of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT04590586 (24) [back to overview]Zilucoplan Sub-protocol: Clinical Severity Status 8-Point Ordinal Scale Score at Days 8, 15, and 29
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Percentage of Participants Who Achieved Oxygen-Free Recovery at Day 29
NCT04590586 (24) [back to overview]Lanadelumab Sub-protocol: Percentage of Participants Who Achieved Sustained Clinical Recovery
NCT04811573 (3) [back to overview]Area Under the Concentration-time Curve of Apremilast in Plasma Over the Time Interval From 0 to the Last Quantifiable Data Point (AUC0-tz)
NCT04811573 (3) [back to overview]Area Under the Concentration-time Curve of Apremilast in Plasma Over the Time Interval From 0 Extrapolated to Infinity (AUC0-∞)
NCT04811573 (3) [back to overview]Maximum Measured Concentration of Apremilast in Plasma (Cmax)

Three-year Overall Survival

Kaplan-Meier estimate at three years post-first transplant of survival. Outcome is death or alive at follow-up (censored). 95 percent confidence interval of the point estimate is calculated using Greenwood's variance. (NCT00004088)
Timeframe: Estimate reported at three years after day 0 of the first cycle of infusion of cells of the tandem transplant.

Interventionproportion of participants (Number)
HD Chemo Followed by PBPC Rescue0.662

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Progression-free Survival

"Kaplan-Meier estimate at three years post-first transplant of survival. Event of interest is the first of Death or Progression. Censoring is Alive in Continuous Complete Remission at date of last follow-up.~95 percent confidence interval of the point estimate is calculated using Greenwood's variance." (NCT00004088)
Timeframe: Estimate reported at three years after day 0 of the first cycle of infusion of cells of the tandem transplant.

Interventionproportion of participants (Number)
HD Chemo Followed by PBPC Rescue0.456

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The Number of Participants With Adverse Events

Here are the total number of participants with adverse events. For the detailed list of adverse events see the adverse event module. (NCT00004635)
Timeframe: Date treatment consent signed to date off study, approximately 60 months

InterventionParticipants (Count of Participants)
Thalidomide117
Placebo98

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Time to Progression

Time to progression is defined as follows: if the PSA returns to baseline (defined as the PSA value prior to starting leuprolide or goserelin) or increases to the absolute value of 5 ng/ml. (NCT00004635)
Timeframe: 36 months

Interventionmonths (Median)
Thalidomide15
Placebo9.6

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Response Rate at Best Response to Treatment

Proportion of patients with complete or partial response using the Response Evaluation Criteria In Solid Tumors (RECIST) v1.0. Complete response is defined as the complete disappearance of all clinically detectable malignant disease for at least 4 weeks. Partial response is defined as greater than or equal to 50% decrease in tumor size for at least 4 weeks without increase in size of any area of known malignant disease of greater than 25%, or appearance of new areas of malignant disease. (NCT00004859)
Timeframe: every other month until 24 months from study entry, every 3 months for year 3, every 4 months for the 4th year and every 6 months for the 5th year

InterventionProportion of participants (Number)
Arm A (Paclitaxel + Carboplatin + Radiation )0.35
Arm B (Paclitaxel + Carboplatin + Radiation + Thalidomide)0.38

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Time to Disease Progression

Time to disease progression is defined as the time from randomization to documented disease progression or to death without progression. Patients without documented progression or death reported were censored at the time of the last documented disease evaluation. Progression is defined, using the Response Evaluation Criteria In Solid Tumors (RECIST), as a measurable increase in the smallest dimension of any target or non-target lesion, or the appearance of new lesions, since baseline. (NCT00004859)
Timeframe: every other month until 24 months from study entry, every 3 months for year 3, every 4 months for the 4th year and every 6 months for the 5th year

InterventionMonths (Median)
Arm A (Paclitaxel + Carboplatin + Radiation )7.4
Arm B (Paclitaxel + Carboplatin + Radiation + Thalidomide)7.8

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Overall Survival Time

Survival time is defined as time from study entry to death from any cause (NCT00004859)
Timeframe: every other month until 24 months from study entry, then every 3 months for year 3, every 4 months for year 4 and every 6 months for year 5

InterventionMonths (Median)
Arm A (Paclitaxel + Carboplatin + Radiation )15.3
Arm B (Paclitaxel + Carboplatin + Radiation + Thalidomide)16.0

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Overall Survival

The observed length of life from entry into the study to death or the date of last contact. (NCT00025506)
Timeframe: From study entry to death or last contact, up to 5 years.

Interventionmonths (Median)
Thalidomide5.9

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Progression Free Survival

Progression is defined according to RECIST v1.0 as at least a 20% increase in the sum of LD target lesions taking as reference the smallest sum LD recorded since study entry, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, global deterioration in health status attributable to the disease requiring a change in therapy without objective evidence of progression, or unequivocal progression of existing non-target lesions. (NCT00025506)
Timeframe: Every other cycle until progression or death, up to 5 years.

Interventionmonths (Median)
Thalidomide1.91

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Progression-free Survival (PFS) > 6 Months

Progression is defined according to RECIST v1.0 as at least a 20% increase in the sum of LD target lesions taking as reference the smallest sum LD recorded since study entry, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, global deterioration in health status attributable to the disease requiring a change in therapy without objective evidence of progression, or unequivocal progression of existing non-target lesions. (NCT00025506)
Timeframe: Every other cycle for 6 months

Interventionpercentage of participants (Number)
Thalidomide17.8

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Tumor Response

RECIST 1.0 defines complete response as the disappearance of all target lesions and non-target lesions and no evidence of new lesions documented by two disease assessments at least 4 weeks apart. Partial response is defined as at least a 30% decrease in the sum of longest dimensions (LD) of all target measurable lesions taking as reference the baseline sum of LD. There can be no unequivocal progression of non-target lesions and no new lesions. Documentation by two disease assessments at least 4 weeks apart is required. In the case where the ONLY target lesion is a solitary pelvic mass measured by physical exam, which is not radiographically measurable, a 50% decrease in the LD is required. These patients will have their response classified according to the definitions stated above. Complete and partial responses are included in the objective tumor response rate. (NCT00025506)
Timeframe: For those patients whose disease can be evaluated by physical examination, response was assessed prior to each 28-day cycle. CT scan or MRI if used to follow lesion for measurable disease every other cycle. (average = 4 months)

Interventionpercentage of participants (Number)
Thalidomide4.4

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Frequency and Severity of Adverse Effects as Assessed by Common Toxicity Criteria (CTC) v2.0

(NCT00025506)
Timeframe: Each cycle during treatment and 30 days after the last treatment (average 4 months)

,,,,
InterventionParticipants (Count of Participants)
NauseaVomitingConstipationAnorexiaFatigueNeutropeniaThrombocytopeniaAnemiaCardiovascularNeuropathy (sensory)Other neurologicDermatologicMetabolicPain
Grade 03136274222414422312731394038
Grade 1446251199122434
Grade 2649115309256202
Grade 341303004116021
Grade 400000001200000

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Overall Survival

(NCT00040937)
Timeframe: 4-7 years

Interventionproportion surviving at 4 years (Number)
Treatment Arm.64

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Assess Toxicity of Thalidomide/Dexamethasone as a Pre-transplant Induction Regimen.

To assess Grade 3-5 AE related to thalidomide/dexamethasone when administered as a pre-transplant induction regimen. (NCT00040937)
Timeframe: Induction

InterventionParticipants (Number)
Induction/PBSC Mobilization2

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Median Progression-free Survival

(NCT00041080)
Timeframe: from enrollment onto the study until first disease progression or death due to any cause

Interventionmonths (Median)
Grp - 13.2
Grp - 24.5

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The Number of Participants With Adverse Events

Here are the total number of participants with adverse events. For the detailed list of adverse events see the adverse event module. (NCT00047879)
Timeframe: 4 months

InterventionParticipants (Number)
Glioblastoma Multiforme Stratum4
Anaplastic Glioma Stratum2

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Overall Survival

Time from initial registration until death or date of last contact, whichever occurs first, for up to 5 years from the date of the last patient registration. (NCT00064337)
Timeframe: 5 years from initial registration, or until death, whichever occurred earlier, on average, about 4.5 years

InterventionMonths (Median)
Treatment68

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Hematologic Response

(NCT00064337)
Timeframe: Until off study

InterventionParticipants (Count of Participants)
Treatment8

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Mean Percentage Change in Total Surface Area of Oral Ulceration.

Mean percentage change in total surface area of oral ulceration (NCT00075023)
Timeframe: baseline to 4 weeks

Interventionpercentage change (Mean)
Thalidomide Gel-66
Placebo-59

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Overall Survival (OS) for High Risk

The event is death from any cause, patients alive at the time of last observation are considered censored. (NCT00075829)
Timeframe: Year 3

Interventionpercentage of participants (Number)
Auto-Auto High Risk67
Auto-Allo High Risk59

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Interval From First to Second Transplantation

Upon recovery from the first autograft, but at least 60 days (preferably between 60-120 days) after the first autograft, patients will receive a second transplant according to treatment assignments. (NCT00075829)
Timeframe: Year 1

Interventiondays (Median)
Auto-Auto Standard Risk98
Auto-Allo Standard Risk105
Auto-Auto High Risk101
Auto-Allo High Risk111

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Cumulative Incidence of Progression/Relapse

Patients are considered experiencing an event when they progress. Deaths without progression are considered as a competing risk. Patients initiating non-protocol anti-myeloma therapy are considered to have progressed on this protocol. (NCT00075829)
Timeframe: Year 3

Interventionpercentage of patients (Number)
Auto-Auto Standard Risk50
Auto-Allo Standard Risk46
Auto-Auto High Risk57
Auto-Allo High Risk38

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Overall Survival (OS) for Standard Risk

The event is death from any cause, patients alive at the time of last observation are considered censored. (NCT00075829)
Timeframe: Years 1, 2, and 3

,
Interventionpercentage of patients (Number)
1 year2 years3 years
Auto-Allo Standard Risk918577
Auto-Auto Standard Risk958980

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Incidences of Graft Versus Host Disease (GVHD)

Incidence and severity of GVHD will be scored according to the BMT clinical trials network Manual of Procedures. (NCT00075829)
Timeframe: Day 100

Interventionpercentage of patients (Number)
Grades II-IVGrades III-IV
Auto-Allo Standard Risk269

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Incidences of Chronic GVHD

Incidence and severity of chronic GVHD will be scored according to the BMT clinical trials network Manual of Procedures. (NCT00075829)
Timeframe: Years 1 and 2

Interventionpercentage of patients (Number)
1 year2 years
Auto-Allo Standard Risk4754

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Progression-Free Survival (PFS)

Patients are considered a failure for this endpoint if they die or if they progress or relapse. (NCT00075829)
Timeframe: Year 3

Interventionpercentage of patients (Number)
Auto-Auto Standard Risk46
Auto-Allo Standard Risk43
Auto-Auto High Risk33
Auto-Allo High Risk40

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Percentage of Participants With Progression-Free Survival (PFS) at 3 Years From Initiation of Study Treatment

In patients with no confirmed Partial Response, Near Complete Response, or Complete Response, progression was defined as a >25% increase from baseline in myeloma protein production or other signs of disease progression such as hypercalcemia, etc. (NCT00081939)
Timeframe: 3 years

Interventionpercentage of participants (Number)
Study Treatment77

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Best Response

"Best response to study treatment as defined by protocol-specific response criteria:~Complete Response (CR) = absence of urine and serum M-components by immunofixation; bone marrow should be adequately cellular (>20%) with <1% monoclonal plasma cells by DNA-clg flow cytometry; serum calcium level must be normal; no new bone lesions nor enlargement of existing lesions; Normalization of serum concentrations of normal immunoglobulins is not required for CR. Partial Response (PR) = Reduction by > 75% in serum myeloma protein production; Decrease in monoclonal marrow plasmacytosis to <5%; Decrease in Bence-Jones proteinuria by >90%; No new lytic bone lesions or soft tissue plasmacytoma.~Treatment Failures/Progressive Disease (PD) = Such patients do not fulfill the above criteria and/or have new lytic lesions (but not compression fractures), hypercalcemia, or other new manifestations of disease." (NCT00083382)
Timeframe: 2 years

Interventionparticipants (Number)
Treatment Failure/Progressive DiseasePartial ResponseComplete Response
Thalidomide + Bisphosphonate561710

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Overall Survival

Overall Survival at six years after initiating protocol therapy (NCT00083551)
Timeframe: 6 Years

Interventionpercentage of participants (Number)
Thalidomide65
No Thalidomide58

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Treatment Delivery With Compliance Defined as Receiving at Least 95% of the Pre-operative Protocol Dose of RT, All 3 Cycles of MAID (if Applicable), and Receive Thalidomide on 75% of the Days During Radiation

Was to be estimated using a binomial distribution and accompanied by the associated 95% confidence interval. Due to early study closure, this endpoint could not be fully evaluated per the protocol plan. (NCT00089544)
Timeframe: Duration of treatment (which can continue up to approximately 15 months).

,
Interventionparticipants (Number)
Not CompliantCompliant
Cohort A (Chemotherapy, Radiation, Thalidomide, Surgery)510
Cohort B (Thalidomide, Radiation, Surgery)25

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Number of Participants Who Had a Prostate-specific Antigen (PSA) Response

PSA response was assessed by the PSA Consensus Criteria. PSA decline is defined as a decline in PSA of at least 50% with no other evidence of disease progression. (NCT00089609)
Timeframe: 21.6 months

InterventionParticipants (Count of Participants)
Main Cohort - Prostate Cancer52

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Number of Participants Who Died After a Follow Up of 34 Months Following Treatment

From on study date to date of death at 34 months. (NCT00089609)
Timeframe: 34 months

InterventionParticipants (Count of Participants)
Main Cohort - Prostate Cancer38

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Number of Participants With a Significant Increase in Circulating Apoptotic Endothelial Cell (CAEC) Level

"The assay utilized has no standard curve. Categorizing patients with ≥ 75% PSA decline in one group and < PSA decline in another group, every patient is their own control with comparison of CAEC at baseline vs. 6 weeks (after two cycles of treatment). Blood is drawn from the patient and a million viable mononuclear cells are counted and then it is determined how many CAECs are in the specimen. The cell count is then compared from baseline to post 2 cycles of treatment. Thus, significant increase is dependent upon this comparison and varies between patients." (NCT00089609)
Timeframe: Baseline and at 6 weeks (after two cycles of treatment)

InterventionParticipants (Count of Participants)
Main Cohort - Particpants With ≥75% PSA Decline14
Main Cohort - Particpants With <75% PSA Decline0

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Number of Participants With Adverse Events

Here is the number of participants with adverse events. For a detailed list of adverse events see the adverse event module. (NCT00089609)
Timeframe: 37 months

InterventionParticipants (Count of Participants)
Main Cohort - Prostate Cancer60
Expansion Cohort - Prostate Cancer13

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Disease Progression by Clinical and Radiographic Criteria Without the Use of Prostate-Specific Antigen (PSA)

Clinical and radiographic response was measured by the Response Evaluation Criteria in Solid Tumors (RECIST) Criteria. Complete response (CR) is disappearance of all target lesions. Partial response (PR) is at least a 30% decrease in the sum of the longest diameter (LD) of target lesions. taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. Stable disease (SD) is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking s reference the smallest sum LD since the treatment started. Progressive disease (PD) is at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded or the appearance of one or more new lesions. (NCT00089609)
Timeframe: up to 34 months

InterventionParticipants (Count of Participants)
Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)
Main Cohort - Prostate Cancer219111

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Time to Progression Using Bubley Criteria

Time to disease progression was based on the Prostate-Specific Antigen (PSA) Working Group 1 Criteria (Bubley Criteria) and standard Response Evaluation Criteria in Solid Tumors (RECIST) for measurable disease. Per the criteria, investigators report at a minimum a PSA decline of at least 50% and this must be confirmed by a second PSA value 4 or more weeks later. Patients may not demonstrate clinical or radiographic evidence of disease progression during this time period. (NCT00089609)
Timeframe: up to 40 months

InterventionMonths (Median)
Main Cohort - Prostate Cancer18.3

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Overall Responders (Complete and Partial Response)

Criteria for response were based on the Revised National Cancer Institute-sponsored Working Group Guidelines for response, which includes clinical, hematologic, and bone marrow features (Cheson, B.D., et al., National Cancer Institute-sponsored Working Group guidelines for chronic lymphocytic leukemia: revised guidelines for diagnosis and treatment. Blood. 1996;87:4990-97.) (NCT00096018)
Timeframe: 4 weeks, every 3 months for 2 years, and then every 4 months for 2 years

Interventionparticipants (Number)
Phase I - Dose Escalation8
Phase II18

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Duration of Response

(NCT00096018)
Timeframe: 4 weeks, every 3 months for 2 years, and then every 4 months for 2 years

Interventionmonths (Mean)
Phase I - Dose Escalation43.3
Phase II30.0

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Transplantation: Number of Participants Who Underwent Transplantation (Peripheral Stem Cell / Bone Marrow)

(NCT00097981)
Timeframe: From randomization until death or as assessed up to 2 years post last participant last treatment visit

InterventionParticipants (Number)
Thalidomide + Dexamethasone30
DOXIL + Thalidomide + Dexamethasone28

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Time to Progression

Time to progression is the interval between the date of randomization until disease progression or death due to progression. (NCT00097981)
Timeframe: From randomization until death or as assessed up to 2 years post last participant last treatment visit

InterventionDays (Median)
Thalidomide + Dexamethasone584
DOXIL + Thalidomide + Dexamethasone408

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Time to 1st Response

Time to first response was defined as the interval from date of randomization to date of achieving a partial response (PR) or better according to the current European Group for Blood and Marrow Transplantation (EBMT) criteria. According to EBMT criteria, PR is defined as not all CR criteria + 50 percentage or more reduction in serum monoclonal paraprotein. (NCT00097981)
Timeframe: From Cycle 2 until 28 days following completion of treatment

InterventionDays (Median)
Thalidomide + Dexamethasone44
DOXIL + Thalidomide + Dexamethasone58

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Overall Survival: Number of Participants Died Due to Any Cause

(NCT00097981)
Timeframe: From randomization until death or as assessed up to 2 years post last participant last treatment visit

InterventionParticipants (Number)
Thalidomide + Dexamethasone21
DOXIL + Thalidomide + Dexamethasone22

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Complete Response Rate: Number of Participants Who Achieved a Complete Response

Complete response rate to study medication is defined as number of participants who acheived complete response by the local investigator according to the current European Group for Blood and Marrow Transplantation (EBMT) criteria. According to EBMT criteria, CR is defined as the absence of serum and urine monoclonal paraprotein + plus no increase in size or number of lytic bone lesions. Complete response was assessed at the beginning of every treatment cycle prior to treatment, starting at Cycle 2. (NCT00097981)
Timeframe: From Cycle 2 until 28 days following completion of treatment

InterventionParticipants (Number)
Thalidomide + Dexamethasone5
DOXIL + Thalidomide + Dexamethasone8

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Engraftment: Number of Participants Who Underwent Engraftment

Engraftment is the process of transplanted stem cells reproducing new cells. (NCT00097981)
Timeframe: From randomization until death or as assessed up to 2 years post last participant last treatment visit

InterventionParticipants (Number)
Thalidomide + Dexamethasone25
DOXIL + Thalidomide + Dexamethasone25

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Overall Response: Number of Participants Who Achieved a Complete Response (CR) or Partial Response (PR)

Overall response to study medication is defined as number of participants who acheived a complete response (CR) or partial response (PR) by the local investigator according to the current European Group for Blood and Marrow Transplantation (EBMT) criteria. According to EBMT criteria, CR is defined as the absence of serum and urine monoclonal paraprotein + plus no increase in size or number of lytic bone lesions; and PR is defined as not all CR criteria + 50 percentage or more reduction in serum monoclonal paraprotein. (NCT00097981)
Timeframe: From Cycle 2 until 28 days following completion of treatment

InterventionParticipants (Number)
Thalidomide + Dexamethasone81
DOXIL + Thalidomide + Dexamethasone76

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Proportion of Patients With Objective Response (First Phase, Step 1)

"Objective response is defined as either complete response (CR) or partial response (PR). Patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow are considered to have CR. PR requires all the following: (1) ≥50% reduction in the level of the serum monoclonal paraprotein. (2) Reduction in 24-hour urinary light chain excretion either by ≥90% or to <200 mg. (3)For patients with non-secretory (or oligosecretory) myeloma only, a ≥50% reduction in plasma cells in a bone marrow aspirate and on trephine biopsy must be documented. (4)50% reduction in size of soft tissue plasmacytoma (by radiography or clinical examination). (5) No increase in the number or size of lytic bone lesions (development of a compression fracture does not exclude response).~As the expansion phase was a substudy terminated early with only 7 patients enrolled, the clinical results presented are mainly for the first phase only." (NCT00098475)
Timeframe: Assessed every 4 weeks for 16 weeks during Step 1

InterventionProportion of patients (Number)
Arm I (Lenalidomide, Dexamethasone)0.79
Arm II (Lenalidomide, Low-dose Dexamethasone)0.683

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Proportion of Patients With Objective Response (First Phase, Step 2)

"Objective response is defined as either complete response (CR) or partial response (PR). Patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow are considered to have CR. PR requires all the following: (1) ≥50% reduction in the level of the serum monoclonal paraprotein. (2) Reduction in 24-hour urinary light chain excretion either by ≥90% or to <200 mg. (3)For patients with non-secretory (or oligosecretory) myeloma only, a ≥50% reduction in plasma cells in a bone marrow aspirate and on trephine biopsy must be documented. (4)50% reduction in size of soft tissue plasmacytoma (by radiography or clinical examination). (5) No increase in the number or size of lytic bone lesions (development of a compression fracture does not exclude response).~As the expansion phase was a substudy terminated early with only 7 patients enrolled, the clinical results presented are mainly for the first phase only." (NCT00098475)
Timeframe: Assessed every 4 weeks for 16 weeks during Step 2

InterventionProportion of patients (Number)
Arm I (Lenalidomide, Dexamethasone)0
Arm II (Lenalidomide, Low-dose Dexamethasone)0

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Overall Survival

Time from registration to death. Patients alive at last follow-up were censored. (NCT00098865)
Timeframe: Assessed after treatment discontinued every 3 months up to 2 years.

Interventionmonths (Median)
Thalidomide and Temozolomide12.8

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Therapy Completion Rate

Feasibility in this study was defined as completion of 6 months of thalidomide with temozolomide therapy. The corresponding therapy completion rate is defined as the proportion of patients who completed 6 months of therapy. (NCT00098865)
Timeframe: 6 months

Interventionproportion of participants (Number)
Thalidomide and Temozolomide.40

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Overall Response

"Overall response is the best response during 6 months of therapy measured by radiographic response.~Complete Response (CR): Disappearance of all detectable tumors by imaging, if initially positive, as well as 2 consecutively negative CSF cytologic examinations (if the initial cytology was positive).~Partial Response (PR): > 50% reduction in the sum of the products of the maximum perpendicular diameter of all measurable lesions; or 2 consecutively negative CSF cytologies and a < 50% reduction in tumor size.~Stable Disease (SD): < 50% reduction in the sum of the products of the maximum perpendicular diameters of all measurable lesions, and persistently negative or positive CSF cytology Progressive Disease (PD): > 25% increase in the size of any measurable lesion, the appearance of a new radiographically demonstrable lesion, or the conversion of negative CSF cytology to positive, as confirmed by at least one repeat CSF cytology" (NCT00098865)
Timeframe: Assessed every 8 weeks while on treatment and every 3 months for one year off-study

Interventionparticipants (Number)
Partial ResponseStable DiseaseProgressive DiseaseUnevaluable
Thalidomide and Temozolomide1941

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Median Overall Survival (OS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms

Isotretinoin versus not Isotretinoin analysis: We compared the median OS outcome of participants in arms IV, V, VII and VIII, versus participants in arms I, II, III and VI. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Isotretinoin: Arm IV, Arm V, Arm VII and ARM VIII17.1
No Isotretinoin: Arm I, Arm II, Arm III and ARM VI19.9

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Median Overall Survival (OS) Comparison of Thalidomide Arms Versus no Thalidomide Arms

Thalidomide versus not Thalidomide analysis: We compared the median OS outcome of participants in arms II, VI, VII and VIII, versus participants in arms I, III, IV and V. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Thalidomide: Arm II, Arm VI, Arm VII and Arm VIII18.3
No Thalidomide: Arm I, Arm III, Arm IV and Arm V17.4

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Median Progression-Free Survival (PFS) Comparison of Celecoxib Arms Versus no Celecoxib Arms

Celecoxib versus not Celecoxib analysis: We compared the median PFS outcome of participants in arms III, V, VI and VIII, versus participants in arms I, II, IV and VII. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Celecoxib: Arm III, Arm V, Arm VI and Arm VIII8.3
No Celecoxib: Arm I, Arm II, Arm IV and Arm VII7.4

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Median Overall Survival (OS) Comparison of Celecoxib Arms Versus no Celecoxib Arms

Celecoxib versus not Celecoxib analysis: We compared the median OS outcome of participants in arms III, V, VI and VIII, versus participants in arms I, II, IV and VII. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Celecoxib: Arm III, Arm V, Arm VI and Arm VIII20.2
No Celecoxib: Arm I, Arm II, Arm IV and Arm VII17.1

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Median Progression-Free Survival (PFS) Comparison of Thalidomide Arms Versus no Thalidomide Arms

Thalidomide versus not Thalidomide analysis: Comparison of median PFS outcome of participants in arms II, VI, VII and VIII, versus participants in arms I, III, IV and V. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up, up to one year (12 study cycles).

Interventionmonths (Median)
Thalidomide: Arm II, Arm VI, Arm VII and Arm VIII7.6
No Thalidomide: Arm I, Arm III, Arm IV and Arm V8.7

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Median Progression-Free Survival (PFS) of Individual Arms

Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Arm I: TMZ10.5
Arm II: TMZ + Thalidomide7.7
Arm III: TMZ + Celecoxib13.4
Arm IV: TMZ + Isotretinoin6.5
Arm V: TMZ + Isotretinoin + Celecoxib11.6
Arm VI: TMZ + Thalidomide + Celecoxib7.9
Arm VII: TMZ + Thalidomide + Isotretinoin6.2
Arm VIII: TMZ + Thalidomide + Isotretinoin + Celecoxib5.8

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Median Progression-Free Survival (PFS) Comparison of Doublet Versus Triplet Therapy

Doublet (2 agents) versus Triplet (3 agents) therapy analysis: We compared the median PFS outcome of participants in arms II, III, IV, versus participants in arms V, VI and VII. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Doublet (2 Agents): Arm II, Arm III and Arm IV8.3
Triplet (3 Agents): Arm V, Arm VI and Arm VII8.2

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Median Overall Survival (OS) Comparison of Doublet Versus Triplet Therapy

Doublet (2 agents) versus Triplet (3 agents) therapy analysis: We compared the median OS outcome of participants in arms II, III, IV, versus participants in arms V, VI and VII. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Doublet (2 Agents): Arm II, Arm III and Arm IV17.0
Triplet (3 Agents): Arm V, Arm VI and Arm VII20.1

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Overall Survival of Individual Arms

Overall Survival (OS) was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Arm I: TMZ21.2
Arm II: TMZ + Thalidomide17.4
Arm III: TMZ + Celecoxib18.1
Arm IV: TMZ + Isotretinoin11.7
Arm V: TMZ + Isotretinoin + Celecoxib23.1
Arm VI: TMZ + Thalidomide + Celecoxib20.2
Arm VII: TMZ + Thalidomide + Isotretinoin17.9
Arm VIII: TMZ + Thalidomide + Isotretinoin + Celecoxib18.5

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Median Progression-Free Survival (PFS) Comparison of Isotretinoin Arms Versus no Isotretinoin Arms

Isotretinoin versus not Isotretinoin analysis: We compared the median PFS outcome of participants in arms IV, V, VII and VIII, versus participants in arms I, II, III and VI. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.

Interventionmonths (Median)
Isotretinoin: Arm IV, Arm V, Arm VII and Arm VIII6.6
No Isotretinoin: Arm I, Arm II, Arm III and Arm VI9.1

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Overall Response Rate Complete Remission (CR), Remission (R), and Partial Remission (PR).

"Responses are defined as follows:~Complete Remission: Absence of bone marrow or blood findings of multiple myeloma. This includes disappearance of all evidence of serum and urine M-proteins on immunofixation electrophoresis studies. Normalization of serum concentrations of normal immunoglobulins is not required for CR. There must also be no evidence of increasing anemia. Bone marrow cellularity must be ≥ 20% with plasma cells ≤ 5%.~Remission: A ≥ 75% reduction in the serum M-protein, and if a urine M-protein (Bence-Jones protein) is present, either a ≥ 90% reduction in this protein, or a urine M-protein < 0.2gm/day. Bone marrow plasma cells must be ≤ 5%.~Partial Remission: A ≥ 50% reduction in the serum M-protein, and if present, a ≥ 50% reduction in the urine M-protein (Bence-Jones protein). Bone marrow plasma cells must not be increased from baseline level." (NCT00124579)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Bortezomib With Thalidomide and Dexamethasone14

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Progression-Free Survival

From date of initial registration to date of progression/relapse of disease (> 25% increase from baseline in myeloma protein production or other signs of disease progression such as hypercalcemia, etc.) or death from any cause, whichever came first, up to 5 years (NCT00124579)
Timeframe: about 12-18 months

InterventionMonths (Median)
Bortezomib With Thalidomide and Dexamethasone8

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Toxicity Evaluation

To evaluate the qualitative and quantitative toxicities associated with this regimen. (NCT00124579)
Timeframe: From date of protocol therapy start to date of protocol therapy end, i.e., up to about 3.5 years

InterventionParticipants (Number)
Albumin, serum-low (hypoalbuminemia)Allergy/Immunology-OtherBilirubin (hyperbilirubinemia)Edema: limbExtremity-lower (gait/walking)Fatigue (asthenia, lethargy, malaise)HemoglobinInf (clin/microbio) w/Gr 3-4 neuts - LungLeukocytes (total WBC)LymphopeniaMuscle weakness, not d/t neuropathy - Extrem-lowerMuscle weakness, not d/t neuropathy - body/generalNeuropathy: motorNeuropathy: sensoryNeutrophils/granulocytes (ANC/AGC)Platelets
Bortezomib + Thal/Dex1111111111111121

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Time to Progression

Time to disease progression (TTP) was calculated from the start of therapy using the Kaplan-Meier method. (NCT00142116)
Timeframe: 49.1 months

Interventionmonths (Median)
TTP for all evaluable patientsTTP for responding patientsTTP for previously treated patientsTTP for previously untreated patients
Thalidomide and Rituximab34.838.715.2536.04

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Objective Response Rate

Response determinations were made using modified consensus panel criteria from the Third International Workshop on WM, and response rates were determined on an evaluable basis. A complete response was defined as having resolution of all symptoms, normalization of serum IgM levels with complete disappearance of IgM paraprotein by immunofixation, and resolution of any adenopathy or splenomegaly. Patients achieving a partial response and a minor response were defined as achieving a more than or equal to 50% and more than or equal to 25% reduction in serum IgM levels, respectively. Patients with stable disease were defined as having less than 25% change in serum IgM levels, in the absence of new or increasing adenopathy or splenomegaly and/or other progressive signs or symptoms of WM. Progressive disease was defined as a greater than 25% increase in serum IgM level occurred from the lowest attained response value or progression of clinically significant disease-related symptom(s). (NCT00142116)
Timeframe: 3 years

Interventionparticipants (Number)
Complete ResponsePartial ResponseMinor ResponseStable Disease
All WM Patients11527

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Asses the Toxicity Profiles

Toxicities were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events, version 3.0. (NCT00151281)
Timeframe: 38 months

InterventionParticipants (Count of Participants)
Grade 3 or 4 neutropeniaAnemiaThrombocytopeniaFatigueConstipationCoughNauseaNeuropathyDyspneaRash
RT-PEPC Drug Therapy141422141413131110

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Dynamic Levels of Plasma VEGF

Stromal angiogenesis was assessed using blood vascular and perivascular markers, including VEGFR-1, VEGFR-2, CD34, and a-SMA, as well as lymphatic vascular markers ofVEGFR-3, podoplanin, and Lyve-1. (NCT00151281)
Timeframe: 38 months

Interventionpg/mL (Median)
RT-PEPC Drug Therapy109.5

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The Quality of Life (QoL) of Patients Receiving RT-PEPC Treatment

"QoL assessments were obtained with version 3 of the Functional Assessment of Cancer Therapy-General (FACT-G) instrument. The FACT-G is comprised of four subscales: physical well-being (7-items, score range 0-28), social/family well-being (7-items, score range 0-28), emotional well-being (6-items, score range 0-24), and functional well-being (7-items, score range 0-28). Users of the FACT-G are able to generate an overall score and four subscale scores with ranges and distributions that are sample-specific. All questions in the FACT-G use a 5-point rating scale (0 = Not at all to 4 = Very much) A higher number indicates a better Quality of Life, and has a possible range of 0-108 points.~ANOVA was used to compare the difference in the means of total score among the different time points (baseline, every 2M until 6M, and every 6M until PD). The mean of the total FACT-G scores at baseline and mean of total score at all timepoints (using ANOVA) are reported below." (NCT00151281)
Timeframe: baseline, every 2 months until Month 6, and every 6 months until disease progression

InterventionFACT-G score (Mean)
Mean FACT-G Score at baselineMean Total FACT-G Score between all time points
RT-PEPC Drug Therapy83.389.4

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Overall Survival and Progression Free Survival

measured by overall Response Rate (ORR), which includes Complete response and partial response. (NCT00151281)
Timeframe: 38 months

Interventionpercentage of patients (Number)
Study Treatment Arm73

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Number of Participants With Progression Free Survival (PFS), by Treatment Arm

"Number of participants with PFS for thalidomide/Dexamethasone vs. VAD with respect to progression free survival in newly diagnosed MM. Progressive Disease (PD): (for patients not in CR) Requires one or more of the following; > 25% increase in the level of serum monoclonal paraprotein, which must also be an absolute increase of at least 5 g/L and confirmed on a repeat investigation.~> 25% increase in 24-hour urinary light chain excretion, which must also be an absolute increase of at least 200mg and confirmed on a repeat investigation.~>25% increase in plasma cells in a bone marrow aspirate, which also must be an absolute increase of at least 10%. Definite increase in the size of existing lytic lesions or plasmacytomas. Development of new bone lesions or plasmacytomas (except compression fractures). Development of hypercalcemia (corrected calcium > 11.5 mg/dL not attributable to other causes)." (NCT00215943)
Timeframe: 4 Months

Interventionparticipants (Number)
Active Comparator: VAD Treatment2
Active Comparator: Thalidomide and Dexamethasone Treatment1

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Overall Survival (OS), by Treatment Arm

"Median OS for thalidomide/Dexamethasone participants vs. VAD participants. Months from On Study to Expired/Last Date Known Alive.~Investigators had planned to accrue 176 participants to calculate median overall survival." (NCT00215943)
Timeframe: Up to 10 Years

Interventionmonths (Median)
Active Comparator: VAD Treatment57
Active Comparator: Thalidomide and Dexamethasone Treatment56.5

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Response Rates of VAD vs. Thalidomide/Dexamethasone

Blade (15) criteria for remission in multiple myeloma was used to assess response. Complete Response (CR)includes: Disappearance of the original monoclonal protein from the blood and urine on at least two determinations for a minimum of 6 weeks by immunofixation studies. Partial Response (PR) includes: At least a 50% reduction in the level of serum monoclonal protein for at least two determinations 6 weeks apart. Minimal Response (MR)includes: At least a 25% to 49% reduction in the level of serum monoclonal protein for at least 2 determinations 2 weeks apart. (NCT00215943)
Timeframe: End of Cycle 4 - 4 Months per Participant

,
Interventionparticipants (Number)
Complete ResponsePartial ResponseMinimal Response
Active Comparator: Thalidomide and Dexamethasone Treatment1162
Active Comparator: VAD Treatment196

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Number of Participants With Adverse Events, by Group

Number of participants with toxicities of Thalidomide/Dexamethasone vs. VAD as induction regimens in newly diagnosed multiple myeloma (MM). (NCT00215943)
Timeframe: 4 Years, 7 Months

,
Interventionparticipants (Number)
Serious Adverse Events (SAEs)Adverse Events (AEs)
Active Comparator: Thalidomide and Dexamethasone Treatment137
Active Comparator: VAD Treatment036

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Overall Response Rate

Response rate after completion of first cycle. Measured as the proportion of subjects who have a partial response (PR) or complete response (CR), represented as the overall response rate (ORR). SWOG/IBMTR (Southwest Oncology Group/International Blood and Marrow Transplant Research) criteria utilized to determine multiple myeloma response rates. (NCT00222105)
Timeframe: At End of Cycle 1, 28 Days

Interventionpercentage of participants (Number)
Arm 195

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Toxicity

Count of Participants with adverse events. (NCT00222105)
Timeframe: End of study, up to 12 months

InterventionParticipants (Count of Participants)
Arm 110

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Median Time to Progression (TTP)

(NCT00256776)
Timeframe: 3 year

Interventionmonths (Median)
Thal + Dex + Velcade19.5
Thal + Dex13.8

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Progression Free Survival

(NCT00256776)
Timeframe: 3 year

Interventionmonths (Median)
Thal + Dex + Velcade18.3
Thal + Dex13.6

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Number of Patients Alive at 1 Year (Survival)

Participants who were alive at one year from date of enrollment . (NCT00281827)
Timeframe: 12 Months

InterventionParticipants (Number)
Intent-to-Treat21

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Number of Patients Reporting Clinical Response

Objective clinical response measuring using tumor assessments: Complete Response (CR) = disappearance of all target and non-target lesions and normalization of tumor marker level, if applicable. Pathological Complete Response (PCR) = No viable tumor cells in specimen determined by light microscopy. Partial Response (PR) = at least 30% decrease in the sum of longest diameter of target lesions from baseline. Progressive Disease (PD) = at least 20% increase in the sum of longest diameters of target lesions from baseline or new lesions. Stable Disease (SD) = Neither PR or PD. (NCT00281827)
Timeframe: At end of 3 -21 day cycles of treatment

InterventionParticipants (Number)
Complete ResponsePathological Complete ResponsePartial ResponseStable DiseaseProgressive Disease
Evaluable Patients001442

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Number of Patients Disease-free at 2 Years

Calculated from date of enrollment to date of recurrence or death, whichever came first (NCT00281827)
Timeframe: 2 Years

InterventionParticipants (Number)
Intent-To-Treat8

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Number of Patients Disease-free at 1 Year

Calculated from date of enrollment to date of recurrence or death, whichever came first (NCT00281827)
Timeframe: 1 year

InterventionParticipants (Number)
Intent-to-Treat14

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Number of Patients Alive at 56 Months (End of Study)

Patients alive from date of enrollment to date of death or censored at date of last contact (Overall Survival). (NCT00281827)
Timeframe: Up to 56 months

InterventionParticipants (Number)
Intent-to-Treat8

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Number of Patients Alive at 2 Years (Survival)

Participants who were alive at 2 years from date of enrollment. (NCT00281827)
Timeframe: 24 Months

InterventionParticipants (Number)
Intent-to-Treat16

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Clinical Response to Treatment

Clinical evaluations of disease response were determined with each cycle. Bone marrow biopsies were done at baseline and at study termination. Clinical responses were defined by the International Myeloma Working Group criteria: Stringent Complete Response (SCR), CR and normal free light chain ratio and no clonal cells in bone marrow; Complete Response (CR), Negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤ 5% plasma cells in bone marrow; Very Good Partial Response (VGPR), Serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥ 90% reduction in serum M-protein and urine M-protein level < 100 mg/24 hours; Partial Response (PR), ≥ 50% reduction of serum M-Protein and reduction in urinary M-protein by ≥ 90% or to < 200 mg/24 hours. Objective response is defined as a best overall response of SCR, CR, VGPR, or PR. (NCT00287872)
Timeframe: 1-6 months

Interventionpercentage of participants (Number)
Bortezomib and Thalidomide81.5

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Peripheral Motor and Sensory Neuropathy (Grade 2 and Higher)

Neuropathy was monitored using Total Neuropathy Score reduced (TNSr). (NCT00287872)
Timeframe: 1-6 months

Interventionparticipants (Number)
Bortezomib and Thalidomide19

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The Time to Response

(NCT00287872)
Timeframe: 1-6 months

Interventionmonths (Median)
Bortezomib and Thalidomide2

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Overall Survival

(NCT00307294)
Timeframe: 36 months

Interventionmonths (Median)
Thalidomide and Doxil12

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Time to Progression

Time from start of treatment until the disease progression per RECIST criteria. (NCT00307294)
Timeframe: Up to 18 months

Interventionmonths (Median)
Thalidomide and Doxil3.7

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Response Rate

The number of patients experiencing a response to treatment, per RECIST criteria / total number of patients evaluable for response. (NCT00307294)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
Thalidomide and Doxil9.3

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Best Overall PSA Response

PSA response as stable disease or progressive disease, per Prostate-Specific Antigen Working Group criteria. (NCT00307294)
Timeframe: 4 weeks

Interventionpercentage of patients (Number)
Stable diseaseProgressive Disesase
Thalidomide and Doxil48.843.7

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Progression Free Survival

(NCT00310076)
Timeframe: 60 months after treatment

Interventionyears (Median)
Chemo Therapy Followed by Thalidomide0.775

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Time to Progression

Time to progression after surgery was recorded. (NCT00310076)
Timeframe: 9 hours

Interventionyears (Median)
Chemo Therapy Followed by Thalidomide0.775

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Number of Events of Toxicity Graded 3 and 4

Adverse events with Common Toxicity Criteria grades of 3 and 4 are reported (NCT00310076)
Timeframe: up to 60 months

Interventionnumber of events (Number)
Grade 3Grade 4
Chemo Therapy Followed by Thalidomide174

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27-Week Overall Survival

27-week overall survival is the probability of patients remaining alive at 27-weeks from study entry estimated using with Kaplan-Meier methods. (NCT00357500)
Timeframe: Assessed every 9 weeks on treatment and annually until death or initiation of new therapy, up to 27 weeks.

InterventionProbability (Number)
5-drug Metronomic Antiangiogenic Regimen0.61

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27-Week Progression-Free Survival

27-week progression-free survival is the probability of patients remaining alive and progression-free at 27-weeks from study entry estimated using Kaplan-Meier methods. As appropriate for tumor type and location, gadolinium-enhanced MRI and other imaging modalites were used to assess response. Progressive disease was defined as >/=25% increase in product of diameters, development of new areas of disease, or disease-attributable clinical deterioration or death, progressive disease. For patients with leukemia PD was defined as >/=25% or >/=5,000 cells/mm3 increase in number of circulating cells, development of extramedullary disease, or other clinical evidence of progression. (NCT00357500)
Timeframe: Assessed every 9 weeks on treatment and annually until death or initiation of new therapy, up to 27 weeks.

InterventionProbability (Number)
5-drug Metronomic Antiangiogenic Regimen0.31

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Best Response

As appropriate for tumor type and location, gadolinium-enhanced MRI and other imaging modalites were used to assess response. Best response was regarded as best response at any single assessment. Response was defined as follows: complete resolution of all demonstrable tumor, complete response (CR); >/=50% decrease in the product of the 2 maximum perpendicular diameters relative to the baseline evaluation, partial response (PR); <50% decrease and <25% increase in product of diameters, stable disease (SD); and >/=25% increase in product of diameters, development of new areas of disease, or disease-attributable clinical deterioration or death, progressive disease (PD). For patients with leukemia PD was defined as >/=25% or >/=5,000 cells/mm3 increase in number of circulating cells, development of extramedullary disease, or other clinical evidence of progression. (NCT00357500)
Timeframe: Assessed at study entry, every 9 weeks on treatment and at treatment discontinuation, up to 27 weeks.

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive DiseaseNot Evaluable
5-drug Metronomic Antiangiogenic Regimen11236471

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Therapy Completion Rate

Proportion of patients alive at 27 weeks without progressive disease (PD) and having tolerated therapy. As appropriate for tumor type and location, gadolinium-enhanced MRI and other imaging modalites were used to assess response. Progressive disease was defined as >/=25% increase in product of diameters, development of new areas of disease, or disease-attributable clinical deterioration or death, progressive disease. For patients with leukemia PD was defined as >/=25% or >/=5,000 cells/mm3 increase in number of circulating cells, development of extramedullary disease, or other clinical evidence of progression. (NCT00357500)
Timeframe: 27 weeks

Interventionproportion of patients (Number)
5-drug Metronomic Antiangiogenic Regimen.25

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Change in Body Composition as Measured by Body Mass Index (BMI)

BMI, commonly used to measure overweight and obesity, is a measure of body fat based on a person's weight and height. (NCT00379353)
Timeframe: Baseline to Day 29

Interventionkg/m^2 (Median)
Thalidomide (Baseline)21.1
Thalidomide (Day 15)21.2
Thalidomide (Day 29)23.4
Placebo (Baseline)22.3
Placebo (Day 15)23.7
Placebo (Day 29)22.1

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Change in Serum Cytokines and Receptors

Cytokines Levels of IL-1β and its receptor IL RA, IL-6 its receptor IL-6R, and TNF-α and its receptors (i.e. tumor necrosis factor receptor (TNFR)) of TNFR1, TNFR2, IL-10, IL-8(serum) measured at baseline, Days 15 and 29. Multiplex bead Immunoassay used to measure serum/plasma levels of IL-1, IL-6, TNF-α, IL-10, IL-8 and their receptors where assay sensitivity for the cytokines was 3-6 pg/mL. Serum IL-10, IL-1β, IL-1RA, IL-6R, sTNF-RI, sTNF-R2 were also analyzed using an enzyme-linked immunosorbent assay device. Lowering cytokine levels can decrease fatigue, increase appetite and decrease anxiety and depression. (NCT00379353)
Timeframe: Baseline to Day 15

,,,
Interventionpg/mL (Median)
IL-6IL-1bIL1RATumor necrosis factor -a (TNF-a)IL-17IL-8IL-6RTumor necrosis factor receptor 1 (TNFR1)Tumor necrosis factor receptor 2 (TNFR2)IL10
Placebo (Baseline)76.40.8357921.212.07139.913567.467886788.22.83
Placebo (Day 15)-6.510.57102.36.2411-3.710059.799.4-107.82.6
Thalidomide (Baseline)54.10.5267718.23.236.162642007.287882.58
Thalidomide (Day 15)850.67290.76.49.22.125446-77.275.42.58

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Change in Symptoms as Measured by Edmonton Symptom Assessment Scale (ESAS)

ESAS assessment of appetite (symptom) where the severity at the time of assessment is rated from 0 to 10 on a numerical scale; with 0 meaning that the symptom is absent and 10 that it is the worst possible severity. Evaluated at baseline [± 3 days], 2 weeks[± 3 days] and 4 weeks [± 3 days] (NCT00379353)
Timeframe: Baseline to Day 29

,,,,,
Interventionunits on a scale (Median)
PainFatigueAppetiteDepression
Placebo (Baseline)36.56.52.5
Placebo (Day 15)6.5532
Placebo (Day 29)2.555.52
Thalidomide (Baseline)3766
Thalidomide (Day 15)35.54.51.5
Thalidomide (Day 29)4572

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Functional Assessment of Anorexia/Cachexia Therapy (FAACT)

12-item symptom-specific subscale of the FACT-G designed to measure participants' additional concerns about their anorexia/cachexia during the previous 7 days. Participant rates concerns from 0 to 4 (0= not at all, 4= very much), combined are the 12 items subscales for a total of 0 to 48 where the higher number would represent greater concern. (NCT00379353)
Timeframe: Baseline to Day 29

,
Interventionunits on a scale (Median)
BaselineDay 15Day 29
Group 1: Thalidomide22.53225
Group 2: Placebo22.52827

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Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F)

The FACIT-F consists of 27 general quality of life questions divided into 4 domains (physical, social, emotional and functional), plus a 13-item fatigue subscore. The participant rates the intensity of fatigue and its related symptoms on a scale of 0-4 (0= not at all, 4= very much) where the 13-item fatigue subscore totals are combined for a total of 0 to 52, with the higher number representing greater fatigue. (NCT00379353)
Timeframe: Baseline to Day 29

,
Interventionunits on a scale (Median)
BaselineDay 15Day 29
Group 1: Thalidomide2124.516
Group 2: Placebo202424

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Hospital Anxiety and Depression Scale (HADS) HADS-A (Anxiety)

The HADS is a self-report rating scale of 14 items on a 4-point Likert scale (range 0-3). It is designed to measure anxiety and depression (7 items for each subscale). The total score is the sum of the 14 items, and for each subscale the score is the sum of the respective seven items (ranging from 0-21). The higher the score The higher the score, the more likely the patient is showing signs of anxiety and as a result may benefit from a counseling/supportive session. (NCT00379353)
Timeframe: Baseline to Day 29

,
Interventionunits on a scale (Median)
BaselineDay 15Day 29
Group 1: Thalidomide996
Group 2: Placebo746.5

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Hospital Anxiety and Depression Scale (HADS) HADS-D (Depression)

The HADS is a self-report rating scale of 14 items on a 4-point Likert scale (range 0-3). It is designed to measure anxiety and depression (7 items for each subscale). The total score is the sum of the 14 items, and for each subscale the score is the sum of the respective seven items (ranging from 0-21). The higher the score, the more likely the patient is showing signs of depression and as a result may benefit from a counseling/supportive session. (NCT00379353)
Timeframe: Baseline to Day 29

,
Interventionunits on a scale (Median)
BaselineDay 15Day 29
Group 1: Thalidomide1088
Group 2: Placebo88.56.59

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Pittsburgh Sleep Quality Index (PSQI)

PSQI measures the quality and patterns of sleep. It differentiates poor from good sleep by measuring subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. A participant indicates how frequently each item was experienced on a scale from 0 to 3. The 7 component scores are then summed to obtain a global sleep score that can range from 0 to 21. A score of >/= 5 indicates poor sleepers. (NCT00379353)
Timeframe: Baseline to Day 29

,
Interventionunits on a scale (Median)
BaselineDay 15Day 29
Group 1: Thalidomide9.510.58
Group 2: Placebo118.58

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Proportion of Patients P0 at Surgery

Pathologic Complete Response is defined as complete eradication of tumor. (NCT00400517)
Timeframe: 8 weeks

InterventionParticipants (Count of Participants)
GM-CSF Injections and Oral Thalidomide0

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Time to Clinical Progression

Time to progression. WIth a median follow up of 32 months (12-51 months), 5 of 26 patients developed biochemical failure. (NCT00400517)
Timeframe: 32 months

InterventionParticipants (Count of Participants)
GM-CSF Injections and Oral Thalidomide5

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Proportion of Patients With Negative Surgical Margins

Presence or Absence of prostate cancer tissue at the sites of surgical resection. This is done by reviewing the entire specimen resected at the time or Radical Prostatectomy. (NCT00400517)
Timeframe: 8 Weeks

InterventionParticipants (Count of Participants)
GM-CSF Injections and Oral Thalidomide0

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Prostate-specific Antigen Response

Number of subjects that achieved a PSA decline while on therapy. Any PSA decline while on treatment, compared with baseline PSA prior to study entry. (NCT00400517)
Timeframe: 8 weeks

InterventionParticipants (Count of Participants)
GM-CSF Injections and Oral Thalidomide22

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Number of Participants Progression Free at 6 Months With Malignant Gliomas

Progression-free Survival (PFS) measured as number of participants that are alive and progression-free at 6 months. (NCT00412542)
Timeframe: 6 Months

Interventionparticipants (Number)
Participants With Recurrent Malignant Gliomas24

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Number of Participants With Severe (Grade 3, 4 or 5) Adverse Events

"Adverse events were graded according to the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 2.~Description of Grades:~Grade 1: Mild Grade 2: Moderate Grade 3: Severe Grade 4: Life-threatening Grade 5: Death" (NCT00432458)
Timeframe: During treatment (up to 5 years)

Interventionparticipants (Number)
Arm I: Thal/ZLD17
Arm II: ZLD13

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Time to Treatment Failure

Time to treatment failure (TTF) was defined as the time from randomization to the date at which the patient was removed from (protocol) treatment due to disease progression, unacceptable toxicity, participant refusal or death. The median TTF with 95% CI was estimated using the Kaplan Meier method (NCT00432458)
Timeframe: time from randomization to treatment failure (up to 5 years)

Interventionmonths (Median)
Arm I: Thal/ZLD16.5
Arm II: ZLD11.1

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Time to Disease Progression (TTP)

Time to disease progression (TTP) was defined as the time from randomization to the earliest documentation of disease progression. Participants were followed for a maximum of 5 years from registration. The median OS with 95% CI was estimated using the Kaplan Meier method, a two-sided (stratified) log-rank test was calculated. (NCT00432458)
Timeframe: randomization to progression (up to 5 years)

Interventionyears (Median)
Arm I: Thal/ZLD2.4
Arm II: ZLD1.2

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Number of Participants With a Confirmed Response (Complete Response [CR], Very Good Partial Response [VGPR] or Partial Response [PR]) on Two Consecutive Evaluations at Least 2 Weeks Apart in the First 12 Months of Treatment

"Response is defined as follows:~CR: Complete disappearance of M-protein from serum & urine on immunofixation, <5% plasma cells in bone marrow (BM)~VGPR: >=90% reduction in serum M-component; Urine M-Component <100 mg per 24 hours; <=5% plasma cells in BM~PR: >= 50% reduction in serum M-Component and/or Urine M-Component >= 90% reduction or <200 mg per 24 hours; or >= 50% decrease in difference between involved and uninvolved FLC levels" (NCT00432458)
Timeframe: 12 months

Interventionparticipants (Number)
Arm I: Thal/ZLD13
Arm II: ZLD0

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12-month Progression-free Survival (PFS)

PFS at 12 months is a dichotomized outcome indicating whether or not a participant was progression free (and alive) at 12 months from the date of randomization. (NCT00432458)
Timeframe: 12 months

Interventionparticipants (Number)
Arm I: Thal/ZLD30
Arm II: ZLD18

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Duration of Response (Complete Response, Partial Response, and Very Good Partial Response)

Duration of response (DOR) is defined as the time from first documentation of response (CR, VGPR or PR) to disease progression. The median DOR with 95% CI was estimated using the Kaplan Meier method (NCT00432458)
Timeframe: time from start of response to progression (up to 5 years)

Interventionyears (Median)
Arm I: Thal/ZLD3.3

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Progression-free Survival Rate

Percentage of participants achieving progression-free survival at 1, 3 and 5 years after the start of protocol therapy, based upon the International Working Group Response Criteria for Non-Hodgkin's Lymphoma (NHL). Progression is defined as a ≥ 50% increase from nadir in the product of the two largest perpendicular diameters (PPD-size) of any previously identified abnormal node, or appearance of any new lesion. (NCT00450801)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
1 year progression-free survival3 year progression-free survival5-year progression-free survival
R-MACLO-IVAM-T917869

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Overall Survival Rate

Percentage of participants who are alive up to five years after receipt of protocol therapy. (NCT00450801)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
1-year rate overall survival Rate2-year overall survival Rate3-year overall survival rate4-year overall survival rate5-year overall survival rate
R-MACLO-IVAM-T9696968787

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Response Rate

Percentage of participants achieving complete response (CR) to protocol therapy according to International Working Group Response Criteria for Non-Hodgkin's Lymphoma (NHL) using the CT imaging method. Patients were classified by best tumor response; CR was defined as normalization of the lactate dehydrogenase (LDH), complete disappearance of disease-related symptoms and lymph nodes, and clearance of lymphoma from involved organs; complete response unconfirmed (CRu) as a residual lymph node greater than 1.5 cm in greatest transverse diameter that had regressed by more than 75% or an indeterminate bone marrow examination; partial response (PR) as greater than 50% reduction in the involved lymph nodes, or disappearance of the involved lymph nodes but persistent bone marrow involvement; relapse/progression as new or increased lymph nodes, organomegaly, or reappearance of bone marrow involvement. (NCT00450801)
Timeframe: Up to 5 years

Interventionpercentage of participants (Number)
R-MACLO-IVAM-T100

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Number of Patients Experiencing Adverse Events.

Number of patients experiencing adverse events during the course of protocol therapy. (NCT00450801)
Timeframe: Up to 5 years

Interventionparticipants (Number)
R-MACLO Cycles22
R-IVAM Cycles22
Thalidomide Therapy19

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Disease Response

The response of myeloma to BDDTD will be assessed by standard electrophoretic and immunofixation tests of blood and urine for a monoclonal protein (M protein), and bone marrow aspirate and biopsy. These tests will be performed at enrollment and at the conclusion of therapy. (NCT00458705)
Timeframe: 2 years

Interventionparticipants (Number)
Complete ResponseNear Complete ResponsePartial ResponseStable DiseaseProgression of DiseaseVery Good Partial Response
Combination Therapy10810237

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Percentage of Participants With Clinical Response by Baseline JAK2 Assessment

Percentage of participants who achieved a clinical response, presented by participants with positive and negative janus kinase 2 (JAK2) V617F mutation results at Baseline. (NCT00463385)
Timeframe: Up to 336 days

Interventionpercentage of participants (Number)
Prednisone, Positive JAK246.2
Pomalidomide 2 mg, PositiveJAK227.3
Pomalidomide 2 mg + Prednisone, Positive JAK230.0
Pomalidomide 0.5 mg + Prednisone, Positive JAK266.7
Prednisone, Negative JAK250.0
Pomalidomide 2 mg, Negative JAK228.6
Pomalidomide 2 mg + Prednisone, Negative JAK212.5
Pomalidomide 0.5 mg + Prednisone, Negative JAK225.0

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Change From Baseline in Hemoglobin Concentration for Responders

Change from Baseline in hemoglobin for participants with a clinical response within the first 6 cycles of treatment. (NCT00463385)
Timeframe: Baseline, Cycle 6 (168 days)

Interventiong/dL (Median)
Prednisone1.4
Pomalidomide 2 mg2.0
Pomalidomide 0.5 mg + Prednisone-0.1

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Change From Baseline in Hemoglobin Concentration for Non-Responders

Change from Baseline in hemoglobin for participants without a clinical response within the first 6 cycles of treatment. (NCT00463385)
Timeframe: Baseline, Cycle 6 (168 days)

Interventiong/dL (Median)
Prednisone1.2
Pomalidomide 2 mg0.1
Pomalidomide 2 mg + Prednisone-0.8
Pomalidomide 0.5 mg + Prednisone0.5

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Time to the First Clinical Response

"The time to the first clinical response achieved within 168 days after the first study drug dosing date was calculated for participants who achieved a clinical response as:~Start date of the first clinical response - the first study drug date +1.~A clinical responder was defined as either:~A baseline red blood cell (RBC)-transfusion-dependent participant with a ≥ 56 consecutive day RBC transfusion-free period after the first dose of study drug, or~A baseline RBC-transfusion-independent participant with an increase in hemoglobin of 2.0 g/dL or more from baseline for ≥ 56 consecutive days in the absence of RBC transfusions, or~A participant with either a ≥ 50% reduction in palpable splenomegaly of a spleen that was ≥ 10 cm at baseline or a spleen that was palpable at > 5 cm and became not palpable." (NCT00463385)
Timeframe: Up to 168 days

Interventionweeks (Median)
Prednisone0.3
Pomalidomide 2 mg8.0
Pomalidomide 2 mg + Prednisone10.1
Pomalidomide 0.5 mg + Prednisone1.2

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Duration of First Clinical Response

"For RBC-transfusion-dependent patients, duration of response was calculated as the last day of response - first day of response +1, where the last day of response was the date of the first RBC-transfusion administrated at or more than 56 days after the response started. For patients who did not receive a subsequent transfusion after the response started, the end date of response was censored at the day of last hemoglobin assessment.~For RBC-transfusion-independent patients, the duration of response was calculated as the last day of response - first day of response +1, where the last day of response was the earlier of the date of a hemoglobin increase of < 2.0 g/dL and the date of a RBC transfusion at ≥ 56 days after the response started. For patients whose hemoglobin measurements were always ≥ 2.0 g/dL and never received a RBC transfusion after response started, the end date of the response was censored at the date of last hemoglobin measurement.~Kaplan-Meier methodology was used." (NCT00463385)
Timeframe: Up to 40 months

Interventionmonths (Median)
Prednisone3.7
Pomalidomide 2 mgNA
Pomalidomide 2 mg + Prednisone6.0
Pomalidomide 0.5 mg + Prednisone10.6

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Change From Baseline in Functional Assessment of Cancer Therapy-Anemia (FACT-An) Subscale and Total Scores

"The FACT-An comprises the four subscales of the 27-item FACT-General Scale (FACT-G), Physical Well-being, Social/Family Well-being, Emotion Well-being, Functional Well-Being, and the Additional Concerns Anemia subscale. Questions are rated on a scale from 0 to 4, where higher scores indicate more impact on quality of life.~Physical Well-being consists of 7 questions, the subscale score ranges from 0-28;~Social/Family Well-being consists of 7 questions, the subscale score ranges from 0-28;~Emotion Well-being consists of 6 questions, the subscale score ranges from 0-24;~Functional Well-Being consists of 7 questions, the subscale score ranges from 0-28;~Anemia subscale consists of 20 questions, the subscale score ranges from 0-80;~Total FACT-An score ranges from 0-188." (NCT00463385)
Timeframe: Baseline and Cycle 6 (168 days).

,,,
Interventionunits on a scale (Mean)
Physical Well-Being subscaleSocial/Family Well-Being subscaleEmotional Well-Being subscaleFunctional Well-Being subscaleAnemia subscaleTotal FACT-An score
Pomalidomide 0.5 mg + Prednisone2.30.91.72.55.811.4
Pomalidomide 2 mg0.4-1.90.0-2.12.31.6
Pomalidomide 2 mg + Prednisone5.31.7-0.32.719.327.3
Prednisone0.61.91.30.91.22.3

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Percentage of Participants With a Clinical Response Within the First 12 Cycles of Treatment

"A clinical responder was defined as either:~A baseline red blood cell (RBC)-transfusion-dependent participant with a ≥ 56 consecutive day RBC transfusion-free period after the first dose of study drug, or~A baseline RBC-transfusion-independent participant with an increase in hemoglobin of 2.0 g/dL or more from baseline for ≥ 56 consecutive days in the absence of RBC transfusions, or~A participant with either a ≥ 50% reduction in palpable splenomegaly of a spleen that was ≥ 10 cm at baseline or a spleen that was palpable at > 5 cm and became not palpable.~Participants who discontinued the study early without achieving clinical response were counted as non-responders." (NCT00463385)
Timeframe: Up to 336 days

Interventionpercentage of participants (Number)
Prednisone50.0
Pomalidomide 2 mg18.2
Pomalidomide 2 mg + Prednisone18.2
Pomalidomide 0.5 mg + Prednisone45.5

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Number of Participants With Adverse Events (AEs)

"A serious AE (SAE) was defined as any AE which resulted in death or was life-threatening, required or prolonged inpatient hospitalization, resulted in persistent or significant disability/incapacity, was a congenital anomaly/birth defect, or constituted an important medical event (events that may have jeopardized the patient or required intervention to prevent one of the outcomes listed above).~The severity of AEs were graded according to National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE, Version 3.0) or according to the following scale:~Grade 1 = Mild; Grade 2 = Moderate; Grade 3 = Severe; Grade 4 = Life-threatening; Grade 5 = Death.~The Investigator determined the relationship between study drug and the occurrence of an AE as Not Related or Related (since the study was double-blinded, a patient receiving only prednisone could have an AE that was judged as related to pomalidomide, and vice-versa)." (NCT00463385)
Timeframe: From date of the first dose of the study drug until discontinuation or the data cut-off date (up to approximately 45 months).

,,,
Interventionparticipants (Number)
At least one AEAt least one AE related to pomalidomideAt least one AE related to prednisoneAt least one Grade 3-4 AEAt least one Grade 3-4 AE related to pomalidomideAt least one Grade 3-4 AE related to prednisoneAt least one SAEAt least one SAE related to pomalidomideAt least one SAE related to prednisoneAE leading to discontinuation of pomalidomideAE leading to discontinuation of prednisoneAE leading to a dose reduction of pomalidomideAE leading to a dose interruption of pomalidomideAE leading to a dose interruption of prednisone
Pomalidomide 0.5 mg + Prednisone21155156383361173
Pomalidomide 2 mg21171014721063117298
Pomalidomide 2 mg + Prednisone18161113116118552196
Prednisone201510106564475052

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Percentage of Participants With a Clinical Response Within the First 6 Cycles of Treatment

"A clinical responder was defined as either:~A baseline red blood cell (RBC)-transfusion-dependent participant with a ≥ 56 consecutive day RBC transfusion-free period after the first dose of study drug, or~A baseline RBC-transfusion-independent participant with an increase in hemoglobin of 2.0 g/dL or more from baseline for ≥ 56 consecutive days in the absence of RBC transfusions, or~A participant with either a ≥ 50% reduction in palpable splenomegaly of a spleen that was ≥ 10 cm at baseline or a spleen that was palpable at > 5 cm and became not palpable.~Participants who discontinued the study early without achieving clinical response were counted as non-responders." (NCT00463385)
Timeframe: Up to 168 days

Interventionpercentage of participants (Number)
Prednisone55.0
Pomalidomide 2 mg23.5
Pomalidomide 2 mg + Prednisone21.1
Pomalidomide 0.5 mg + Prednisone47.6

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Change From Baseline in Likert Abdominal Pain Scale

Participants rated abdominal discomfort or pain over the previous week on a scale from zero to ten, where zero is no discomfort or pain and ten is the worst pain imaginable. (NCT00463385)
Timeframe: Baseline and Cycle 6 (168 days)

Interventionunits on a scale (Mean)
Prednisone0.3
Pomalidomide 2 mg-1.0
Pomalidomide 2 mg + Prednisone0.3
Pomalidomide 0.5 mg + Prednisone-0.1

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Time to Progression (TTP)

TTP defined as the time from date of first dose of study medication to first documentation of objective tumor progression in days. Response evaluation by Response Evaluation Criteria in Solid Tumors (RECIST) done following 2 cycles and 3 cycles. Progression is defined, using RECIST, as a measurable increase in the smallest dimension of any target or non-target lesion, or the appearance of new lesions, since baseline. (NCT00505635)
Timeframe: Following two 21 day cycles until disease progression

Interventiondays (Geometric Mean)
Biochemotherapy With Temozolomide93.2

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Change From Baseline in EORTC QLQ-C30 - Global Health Status

"The European Organisation for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact).~The EORTC QLQ-C30 Global Health Status/QOL Scale is scored between 0 and 100, where higher scores indicate better Global Health Status/QOL. Negative changes from baseline indicate deterioration in QOL or functioning and positive changes indicate improvement." (NCT00507416)
Timeframe: Baseline and Day 1 of Cycles 3, 5, 7, 9, 11 and 13

,,
Interventionunits on a scale (Mean)
Cycle 3, Day 1 (n=129, 115, 125)Cycle 5, Day 1 (n=114, 98, 107)Cycle 7, Day 1 (n=89, 79, 84)Cycle 9, Day 1 (n=87, 66, 67)Cycle 11, Day 1 (n=71, 61, 65)Cycle 13, Day 1 (n=67, 52, 61)
Bortezomib and Dexamethasone1.3-4.9-3.3-4.2-11.6-10.2
Bortezomib, Melphalan and Prednisone2.0-0.4-4.7-1.02.81.0
Bortezomib, Thalidomide, and Dexamethasone-4.4-6.1-8.6-8.1-7.9-8.5

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Overall Survival

Overall survival is defined as the time between randomization and death. Participants still alive at the cutoff date or lost to follow-up were censored at the date of last contact. (NCT00507416)
Timeframe: From randomization until death. Median follow-up time was 43 months.

Interventionmonths (Median)
Bortezomib and Dexamethasone49.8
Bortezomib, Thalidomide, and Dexamethasone51.5
Bortezomib, Melphalan and Prednisone53.1

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Percentage of Participants With a Complete Response

Participants with a best overall response of complete response, defined as negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% plasma cells in bone marrow. Response was assessed by the Investigator using the IMWG uniform response criteria. (NCT00507416)
Timeframe: Response assessed every other cycle, for up to 13 cycles (49 weeks).

Interventionpercentage of participants (Number)
Bortezomib and Dexamethasone3
Bortezomib, Thalidomide, and Dexamethasone4
Bortezomib, Melphalan and Prednisone4

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Progression Free Survival (PFS)

"PFS is defined as the time from randomization to disease progression or death, whichever occurs first. Participants who did not progress and were still alive at the cut-off date were censored at the date of last contact. Response was assessed by the Investigator using the International Myeloma Working Group (IMWG) uniform response criteria.~Progressive disease requires 1 of the following:~Increase of ≥ 25% from nadir in:~Serum M-component (absolute increase ≥ 0.5 g/dl)~Urine M-component (absolute increase ≥ 200 mg/24 hours)~In patients without measurable serum and urine M-protein levels the difference between involved and uninvolved free light chain (FLC) levels (absolute increase > 100 mg/dl)~Bone marrow plasma cell percentage (absolute % ≥ 10%)~Development of new or increase in the size of existing bone lesions or soft tissue plasmacytomas.~Development of hypercalcemia (corrected serum calcium > 11.5 mg/dl) attributed solely to plasma cell proliferative disease" (NCT00507416)
Timeframe: From randomization until disease progression. Median follow-up time was 43 months.

Interventionmonths (Median)
Bortezomib and Dexamethasone14.7
Bortezomib, Thalidomide, and Dexamethasone15.4
Bortezomib, Melphalan and Prednisone17.3

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Time to Alternative Therapy

Time to alternative therapy is defined as the time between randomization and alternative therapy. Participants who did not receive alternative therapy were censored at the time of last contact. (NCT00507416)
Timeframe: From randomization until alternative therapy. Median follow-up time was 43 months.

Interventionmonths (Median)
Bortezomib and Dexamethasone19.7
Bortezomib, Thalidomide, and Dexamethasone24.5
Bortezomib, Melphalan and Prednisone19.0

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Percentage of Participants With an Overall Response

"Overall response defined as a best overall response of complete response (CR), very good partial response (VGPR) or partial response (PR), assessed by the Investigator using the IMWG uniform response criteria.~CR: Negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% plasma cells in bone marrow.~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥ 90% reduction in serum M-protein plus urine M-protein level <100 mg per 24 hours (h).~PR requires 1 of the following:~≥50% reduction of serum M-protein and 24-h urinary M-protein by ≥ 90% or to <200 mg/24 h, or~If M-protein not measurable, a ≥50% decrease in the difference between involved and uninvolved FLC levels, or~If FLC not measurable, a ≥ 50% reduction in plasma cells, provided baseline bone marrow plasma cell percentage was ≥30%.~If present at baseline, a ≥50% reduction in the size of soft tissue plasmacytomas is also required." (NCT00507416)
Timeframe: Response assessed every other cycle for up to 13 cycles (49 weeks).

Interventionpercentage of participants (Number)
Bortezomib and Dexamethasone73
Bortezomib, Thalidomide, and Dexamethasone80
Bortezomib, Melphalan and Prednisone70

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Percentage of Participants With a Complete Response or a Very Good Partial Response

"Complete response is defined by negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas, and <5% plasma cells in bone marrow.~Very good partial response is defined by serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine M-protein level <100 mg per 24 hours.~Response was assessed by the Investigator using the IMWG uniform response criteria." (NCT00507416)
Timeframe: Response assessed every other cycle for up to 13 cycles (49 weeks).

Interventionpercentage of participants (Number)
Bortezomib and Dexamethasone37
Bortezomib, Thalidomide, and Dexamethasone51
Bortezomib, Melphalan and Prednisone41

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Duration of Response

Duration of response is defined in participants with an overall response as the time between first documentation of response and disease progression. Responders without disease progression were censored at the last clinical assessment of response. (NCT00507416)
Timeframe: From first documented response until disease progression. Median follow-up time was 43 months.

Interventionmonths (Median)
Bortezomib and Dexamethasone18.3
Bortezomib, Thalidomide, and Dexamethasone22.4
Bortezomib, Melphalan and Prednisone19.8

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Complete Response Rate

(NCT00523848)
Timeframe: Every 3 months

Interventionpercentage of participants (Number)
VDT: VELCADE, Doxil and Low-dose Thalidomide22.50

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Overall Response Rate (Complete and Partial)

(NCT00523848)
Timeframe: Every 3 months

Interventionpercentage of participants (Number)
VDT: VELCADE, Doxil and Low-dose Thalidomide77.50

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Time to Disease Progression

(NCT00523848)
Timeframe: Every 3 monthsntil the date of first documented progression or date of death from any cause, whichever came first

Interventionmonths (Median)
VDT: VELCADE, Doxil and Low-dose Thalidomide27.8

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Difference in Serum Albumin

"Serum albumin in treated patient and control (no drug) patients were tabulated once weekly for week #1-4 , then once every 4 weeks thereafter at week# 8, 12, 16, 20, 24 to see changes of health status. Final data collected at week 28 -- to ensure patient safety" (NCT00529633)
Timeframe: 28 weeks total

,
Interventiong/dL of Albumin (Number)
week 1week 2week 3week 4week 8week 12week 16week 20week 24week 28
Placebo3.73.53.44.03.64.14.03.83.93.9
Thalidomide3.43.73.53.63.83.63.52.93.63.5

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Difference in Serum CRP

"Serum CRP in treated patient and control (no drug) patients were tabulated once weekly for week #1-4 , then once every 4 weeks thereafter at week# 8, 12, 16, 20, 24 to see changes of health status. Final data collected at week 28 -- to ensure patient safety" (NCT00529633)
Timeframe: 28 weeks total

,
InterventionMg/L CRP (Number)
week 1week 2week 3week 4week 8week 12week 16week 20week 24week 28
Placebo1.762.071.762.292.872.873.411.926.013.93
ThalidomideNANANANANANANANANANA

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Percent of Participants Achieving Overall Combined Complete Response (CR) Following High-dose Chemotherapy (HDT)/Stem Cell Transplantation (SCT)

"Percent of Participants Achieving Overall Combined Complete Response (CR) (CR w/normalized serum κ:λ ratio + CR + Near Complete Response (nCR)) following stem cell transplantation.~CR criteria: negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow.~κ:λ ratio: normal free light chain (FLC) ratio~nCR criteria: positive immunofixation analysis of serum or urine as the only evidence of disease; disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow." (NCT00531453)
Timeframe: all data included in clinical database as of 10 April 2009

Interventionpercentage of participants (Number)
Three Drug Regimen (VDT)76
Four Drug Regimen (VDTC)78

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Percent of Particpants Achieving Overall Combined Complete Response (CR) Following Induction

"Percent of Particpants Achieving Overall combined complete response (CR w/normalized serum κ:λ ratio + CR + near complete response (nCR)) following induction therapy.~CR criteria: negative immunofixation on the serum and urine, disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow.~κ:λ ratio: normal free light chain (FLC) ratio~nCR criteria: positive immunofixation analysis of serum or urine as the only evidence of disease; disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow." (NCT00531453)
Timeframe: all data included in clinical database as of 10 April 2009

Interventionpercentage of participants (Number)
Three Drug Regimen (VDT)51
Four Drug Regimen (VDTC)44

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Event Free Survival

(NCT00538733)
Timeframe: from baseline to the time of first event that lead to removal from study (defined as progression, death, withdrawal of consent, or removal for toxicity)

Interventionmonths (Median)
T-BiRD Therapy (All Patients)21.5

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Progression Free Survival

"Progression determined using International Myeloma Working Group criteria, as defined below.~An increase of > 25% from lowest response value one or more of the following:~Serum M-component and/or (the absolute increase must be > 0.5 g/dL)*~Urine M-component and/or (the absolute increase must be > 200 mg/24 h)~Only in patients without measurable serum and urine M-protein levels; the difference between involved and uninvolved FLC levels. The absolute increase must be > 10 mg/dL~Bone marrow plasma cell percentage; the absolute percentage must be > 10%~Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas~Development of hypercalcaemia (corrected serum calcium > 11.5 mg/dL or 2.65 mmol/L) that can be attributed solely to the plasma cell proliferative disorder *if starting serum M protein is greater then 5 g/dL, absolute increase of 1g/dL is sufficient to determine relapse." (NCT00538733)
Timeframe: From start of treatment, to the date of first progression

Interventionmonths (Median)
T-BiRD Therapy (All Patients)35.6

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Effect of Drug Combination on Multiple Myeloma

Objective response rate, defined according to the International Myeloma Working Group (IMWG) criteria as greater then or equal to a Partial Response (PR). The best response was recorded. The IMWG criteria can be found here: imwg.myeloma.org/international-myeloma-working-group-imwg-uniform-response-criteria-for-multiple-myeloma/ (NCT00538733)
Timeframe: This was collected from patients for their duration on study treatment. Only the best response was recorded. Best responses were reported at any point of the study, from start of treatment up until removal of study, which occurred up to 57.4 cycles

Interventionparticipants (Number)
sCR (stringent complete response)VGPR (very good partial response)PR (partial response)SD (stable disease)
T-BiRD Therapy (All Patients)2995

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Median Time to Maximum Response

Median Time to maximum response, reported in cycles of treatment. One cycle = 28 days. (NCT00538733)
Timeframe: from baseline to cycle with maximum response

Interventioncycles (Median)
T-BiRD Therapy (All Patients)4

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Effect of Drug Combination on Multiple Myeloma

The maximum response for all patients that were treated on study. Maximum response was assessed using the International myeloma working group (IMWG) guidelines for response. http://imwg.myeloma.org/international-myeloma-working-group-imwg-uniform-response-criteria-for-multiple-myeloma/ (NCT00538824)
Timeframe: The best response for all patients at any point were assessed for patients that were treated on study, from start of treatment up to 20 weeks

Interventionparticipants (Number)
partial response (PR)minimal response (MR)progression of disease
DexTR (All Patients)212

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Number of Platelet Transfusions Needed to Maintain Adequate Number of Platelets. (Long Term)

(NCT00577096)
Timeframe: up to 30 weeks

InterventionPlatelet Transfusions (Mean)
Usual Care3.6
Exercise2.0

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Number of Red Blood Cell Transfusions Needed to Maintain Hemoglobin Levels (Long Term)

The targeted hemoglobin level for each participant was 10-12 g/dl. This is the number of red blood cell (RBC) transfusions administered to participants, as part of the investigational therapy algorithm, in an attempt to alleviate the anemia caused by multiple myeloma and high-dose chemotherapy. The numbers of RBC and platelet transfusions were obtained from the University of Arkansas for Medical Sciences blood bank. (NCT00577096)
Timeframe: up to 30 weeks

InterventionRBC Transfusions (Mean)
Usual Care1.8
Exercise1.0

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Hemoglobin Levels Before Chemotherapy and During Transplantation Period (Long Term)

Hemoglobin Levels were measured at baseline, before peripheral blood stem cell transplantation (PBSCT), during PBSCT and at hospital discharge. (NCT00577096)
Timeframe: up to 30 weeks

,
Interventiong/dl (Mean)
BaselineBefore TransplantationDuring TransplanationAt Discharge
Exercise11.712.010.811.0
Usual Care11.512.010.810.9

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Total Number of Days of Stem Cell Collection (Short Term)

(NCT00577096)
Timeframe: up to 15 weeks

InterventionDays (Mean)
Usual Care5.3
Exercise4.0

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Number of Stem Cell Collection Attempts (Short Term)

(NCT00577096)
Timeframe: up to 15 weeks

InterventionStem Cell Collection Attempts (Mean)
Usual Care1.4
Exercise1.1

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Number of Stem Cell Collection Attempts (Long Term)

(NCT00577096)
Timeframe: up to 30 weeks

InterventionStem Cell Collection Attempts (Mean)
Usual Care1.3
Exercise1.1

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Number of Red Blood Cell Transfusions Needed to Maintain Hemoglobin Levels (Short Term)

The targeted hemoglobin level for each participant was 10-12 g/dl. This is the number of red blood cell (RBC) transfusions administered to participants, as part of the investigational therapy algorithm, in an attempt to alleviate the anemia caused by multiple myeloma and high-dose chemotherapy. The numbers of RBC and platelet transfusions were obtained from the University of Arkansas for Medical Sciences blood bank. (NCT00577096)
Timeframe: up to 15 weeks

InterventionRBC Transfusions (Mean)
Usual Care2.3
Exercise1.8

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Number of Platelet Transfusions Needed to Maintain Adequate Number of Platelets.(Short Term)

(NCT00577096)
Timeframe: up to 15 weeks

InterventionPlatelet transfusions (Mean)
Usual Care3.1
Exercise2.3

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Hemoglobin Levels Before Chemotherapy and During Transplantation Period (Short Term)

Hemoglobin Levels were measured at baseline, before peripheral blood stem cell transplantation (PBSCT), During PBSCT and at hospital discharge. (NCT00577096)
Timeframe: up to 15 weeks

,
Interventiong/dl (Mean)
BaselineBefore transplantationDuring transplantationAt discharge
Exercise11.611.010.410.6
Usual Care12.110.810.110.6

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Total Number of Days of Stem Cell Collection (Long Term)

(NCT00577096)
Timeframe: up to 30 weeks

InterventionDays (Mean)
Usual Care4.9
Exercise4.5

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Efficacy of Thalidomide in Suppressing the Chronic Cough of Idiopathic Pulmonary Fibrosis Using the Cough Quality of Life Questionnaire.

"The primary endpoint, suppression of cough was measured by the Cough Quality of Life Questionnaire (CQLQ) to measure the effect of interventions on cough-specific quality of life.~CQLQ consist of 28 questions about cough and its effects using Likert-like 4-point scales, with lower scores indicating less effect of cough on health related quality of life.~CQLQ scale ranges from 28 to 112 ( The lower the value, the higher the quality of life, 28 is considered the best)." (NCT00600028)
Timeframe: 6 months

Interventionunits on a scale (Mean)
Arm Thalidomide 1st, Placebo 2nd (Intervention Thalidomide)47.3
Arm Thalidomide 1st, Placebo 2nd (Intervention Placebo)55.2
Arm Placebo 1st, Thalidomide 2nd (Intervention Placebo)61.6
Arm Placebo 1st, Thalidomide 2nd (Intervention Thalidomide)44.5

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Efficacy of Thalidomide in Suppressing the Chronic Cough of Idiopathic Pulmonary Fibrosis Using the Visual Analog Scale of Cough and the St. George Respiratory Questionnaire.

"The secondary endpoint, suppression of cough was measured by the visual analog scale of cough (VAS) was significantly lower during treatment with thalidomide than placebo.~Secondary endpoints were Cough VAS - the visual analog scale of cough evaluates the severity of cough in patients with IPF.~Visual analog scale of cough ranges from 0 to 100 (0 is considered the best).~St. George Respiratory Questionnaire helps to evaluate cough-specific and respiratory quality of life in patients with IPF.~St. George Respiratory Questionnaire score ranges from 0 to 100 (0 is considered the best)." (NCT00600028)
Timeframe: 6 months

,,,
Interventionunits on a scale (Mean)
Severity of cough (VAS Score)Quality of life (SGRQ Score)
Arm Placebo 1st, Thalidomide 2nd (Intervention Placebo)6858.8
Arm Placebo 1st, Thalidomide 2nd (Intervention Thalidomide)17.840.7
Arm Thalidomide 1st, Placebo 2nd (Intervention Placebo)65.954.7
Arm Thalidomide 1st, Placebo 2nd (Intervention Thalidomide)30.346.4

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Progression-Free Survival (PFS)

PFS is defined as the time from randomization to the earlier of progression or death of any cause. (NCT00602641)
Timeframe: Assessed every 3 months for 2 years, then every 6 months for 3 years, then annually for 10 years from the date of randomization.

Interventionmonths (Median)
Arm I (MPT-T)21.0
Arm II (mPR-R)18.7

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Very Good Partial Response (VGPR) Rate

Response evaluation was based on the International Myeloma Working Group (IMWG) response criteria. VGPR rate was defined as patients achieving at least VGPR which include patients who achieving complete response (CR) and VGPR. CR refers to patients who have complete disappearance of an M-protein and no evidence of myeloma in the bone marrow. VGPR refers to patients who meet the following criteria: Serum and urine M-component detectable by immunofixation but not on electrophoresis; Or 90% or greater reduction in serum M-component plus urine M-component <100 mg per 24 hours; If the serum and urine M protein are unmeasurable and the immunoglobulin free light chain parameter is being used to measure response, a ≥ 90% decrease in the difference between involved and uninvolved free light chain (FLC) levels is required in place of the M protein criteria. (NCT00602641)
Timeframe: Assessed every cycle (1 cycle=28 days) for the first 12 cycles, and then every 2 cycles while on treatment. Post treatment assessed every 3 months < 2 years from study entry, every 6 months if 2-5 years, every 12 months if 6-10 years from study entry.

Interventionproportion of participants (Number)
Arm I (MPT-T)0.247
Arm II (mPR-R)0.316

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Change in Functional Assessment of Cancer Therapy-Neurotoxicity Trial Outcome Index (FACT-Ntx TOI) Score From Baseline to Cycle 12

A combined scale was used to assess the quality of life (QOL) comprising of the well established and validated functional well-being (FWB) and physical well-being (PWB) components of FACT-G version 4 (14 questions), which will address the physical and functional well-being of multiple myeloma patients plus the FACT-neurotoxicity (NTX, 11 questions), which will evaluate symptoms of neurotoxicity. This pooled scale is referred to as the FACT Ntx TOI. The FACT-Ntx TOI has 25 items and the score ranges from 0 (worst possible outcome) to 100 (best possible outcome). (NCT00602641)
Timeframe: Administered at registration, the beginning of cycle 7 d1, the end of cycle 12 d28, then at the end of cycle 18, 24, and 38 d28. For patients who discontinue treatment early, assessed at time of discontinuation and at the next quarterly follow-up visit.

Interventionunits on a scale (Mean)
Arm I (MPT-T)-2.8
Arm II (mPR-R)3.3

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Overall Survival

Overall survival was defined as time from randomization to death from any cause. (NCT00602641)
Timeframe: Assessed every 3 months for 2 years, then every 6 months for 3 years, then annually for 10 years from the date of randomization.

Interventionmonths (Median)
Arm I (MPT-T)52.6
Arm II (mPR-R)47.7

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Kaplan-Meier Estimates of PFS Based on the Response Assessment by the Investigator At the Time of Final Analysis

PFS was calculated as the time from randomization to the first documented PD or death due to any cause during the study, which ever occurred first based on the International Myeloma Working Group Uniform Response criteria (IMWG). Those who withdrew for any reason or received another anti-myeloma therapy without documented PD were censored on the date of their last response assessment, prior to receiving any other anti-myeloma therapy. Censoring rules for PFS: - No baseline assessments and no progression or death documented within the 2 scheduled assessments; Death within the lst two assessments without any adequate response assessment; Progression documented between scheduled assessments; Death between adequate assessments; no progression; study discontinuations for reasons other than PD or death; new anti-myeloma started prior to PD; death or PD after an extended lost to follow-up time period (2 or more missed scheduled assessment's). (NCT00689936)
Timeframe: From date of randomization to date of data cut-off date of 21 January 2016; median follow-up for all participants was 17.7 months

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)26.0
Lenalidomide and Dexamethasone Rd1821.0
Melphalan + Prednisone + Thalidomide (MPT)21.9

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Kaplan-Meier Estimates of Progression-free Survival (PFS) Based on the Response Assessment by the Independent Review Adjudication Committee (IRAC)

PFS was calculated as the time from randomization to the first documented PD or death due to any cause during the study, which ever occurred first based on the International Myeloma Working Group Uniform Response criteria (IMWG). Those who withdrew for any reason or received another anti-myeloma therapy without documented PD were censored on the date of their last response assessment, prior to receiving any other anti-myeloma therapy. Censoring rules for PFS: - No baseline assessments and no progression or death documented within the 2 scheduled assessments; Death within the lst two assessments without any adequate response assessment; Progression documented between scheduled assessments; Death between adequate assessments; no progression; study discontinuations for reasons other than PD or death; new anti-myeloma started prior to PD; death or PD after an extended lost to follow-up time period (2 or more missed scheduled assessment's). (NCT00689936)
Timeframe: From date of randomization until the data cut-off date of 24 May 2013. Median follow-up time for all participants was 17.1 months.

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)25.5
Lenalidomide and Dexamethasone Rd1820.7
Melphalan + Prednisone + Thalidomide (MPT)21.2

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Percentage of Participants With a Myeloma Response by Adverse Risk Cytogenetic Risk Category Based on IRAC Review.

Participants were placed in adverse and non-adverse cytogenetic risk categories at baseline and response rates evaluated. Adverse Risk: t(4;14), t(14;16), del(13q) or monosomy 13, del(17p), 1q gain Favorable Hyperdiploidy: : t(11;14), gains of 5/9/15; Normal: a normal result, gains other than 5/9/15, IgH deletion Uncertain risk: probes used for analysis cannot place participant in any of the other risk categories. Objective response = best overall response including CR, VGPR or PR based on the IRAC Review; A CR is negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPRis serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

InterventionPercentage of participants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)70.0
Lenalidomide and Dexamethasone Rd1869.7
Melphalan + Prednisone + Thalidomide (MPT)58.2

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Percentage of Participants With a Myeloma Response by Favorable Hyperdiploidy Risk Cytogenetic Risk Category Based on IRAC Review

Participants were placed in adverse and non-adverse cytogenetic risk categories at baseline and response rates evaluated. Adverse Risk: t(4;14), t(14;16), del(13q) or monosomy 13, del(17p), 1q gain Favorable Hyperdiploidy: : t(11;14), gains of 5/9/15; Normal: a normal result, gains other than 5/9/15, IgH deletion Uncertain risk: probes used for analysis cannot place participant in any of the other risk categories. Objective response = best overall response including CR, VGPR or PR based on the IRAC Review; A CR is negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPRis serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionpercentage of participants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)80.4
Lenalidomide and Dexamethasone Rd1881.6
Melphalan + Prednisone + Thalidomide (MPT)70.6

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Percentage of Participants With a Myeloma Response by Normal Risk Cytogenetic Risk Category Based on IRAC Review

Participants were placed in adverse and non-adverse cytogenetic risk categories at baseline and response rates evaluated. Adverse Risk: t(4;14), t(14;16), del(13q) or monosomy 13, del(17p), 1q gain Favorable Hyperdiploidy: : t(11;14), gains of 5/9/15; Normal: a normal result, gains other than 5/9/15, IgH deletion Uncertain risk: probes used for analysis cannot place participant in any of the other risk categories. Objective response = best overall response including CR, VGPR or PR based on the IRAC Review; A CR is negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPRis serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionpercentage of particpants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)80.4
Lenalidomide and Dexamethasone Rd1874.8
Melphalan + Prednisone + Thalidomide (MPT)61.0

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Percentage of Participants With a Myeloma Response by Uncertain Risk Cytogenetic Risk Category Based on IRAC Review

Participants were placed in adverse and non-adverse cytogenetic risk categories at baseline and response rates evaluated. Adverse Risk: t(4;14), t(14;16), del(13q) or monosomy 13, del(17p), 1q gain Favorable Hyperdiploidy: : t(11;14), gains of 5/9/15; Normal: a normal result, gains other than 5/9/15, IgH deletion Uncertain risk: probes used for analysis cannot place participant in any of the other risk categories. Objective response = best overall response including CR, VGPR or PR based on the IRAC Review; A CR is negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPRis serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionpercentage of participants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)60.5
Lenalidomide and Dexamethasone Rd1876.8
Melphalan + Prednisone + Thalidomide (MPT)57.5

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Percentage of Participants With an Objective Response After Second-line Anti-myeloma Treatment at the Time of Final Analysis

Objective response according to IMWG Uniform Response Criteria was defined as a best overall response including a complete response (CR), very good partial response (VGPR) or partial response (PR) based on the IRAC Review. A CR is defined s: negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPR is serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is: ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment; data cut-off date of 21 January 2016; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionpercentage of participants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)46.2
Lenalidomide and Dexamethasone Rd1853.1
Melphalan + Prednisone + Thalidomide (MPT)45.7

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Percentage of Participants With an Objective Response Based on Investigator Assessment at Time of Final Analysis

Objective response according to IMWG Uniform Response Criteria was defined as a best overall response including a complete response (CR), very good partial response (VGPR) or partial response (PR) based on the IRAC Review. A CR is defined s: negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPR is serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is: ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 21 January 2016; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionpercentage of participants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)80.7
Lenalidomide and Dexamethasone Rd1878.6
Melphalan + Prednisone + Thalidomide (MPT)67.5

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Percentage of Participants With an Objective Response Based on IRAC Review

Objective response according to IMWG Uniform Response Criteria was defined as a best overall response including a complete response (CR), very good partial response (VGPR) or partial response (PR) based on the IRAC Review. A CR is defined as: negative serum and urine on immunofixation, disappearance of any soft tissue plasmacytomas and ≤5% plasma cells in BM; A VGPR is serum and urine M-protein detectable by immunofixation but not on electrophoresis or ≥90% reduction in serum M-protein and urine M-protein level <100 mg/24 hours; A PR is: ≥50% reduction of serum M-Protein and reduction in urinary M-protein by ≥90% or to <200 mg/24 hours. If present at baseline a ≥50% reduction in size of soft tissue plasmacytomas. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionpercentage of participants (Number)
Lenalidomide and Low-Dose Dexamethasone (Rd)75.1
Lenalidomide and Dexamethasone Rd1873.4
Melphalan + Prednisone + Thalidomide (MPT)62.3

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Time to First Response Based on the Investigator Assessment at the Time of Final Analysis

The time to first myeloma response was defined as the time from randomization to the time when the response criteria for at least a PR was first met based on the IMWG criteria assessed by the investigator. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 21 January 2016; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm.

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)1.8
Lenalidomide and Dexamethasone Rd181.8
Melphalan + Prednisone + Thalidomide (MPT)2.8

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Time to First Response Based on the Review by the IRAC

The time to first myeloma response was defined as the time from randomization to the time when the response criteria for at least a PR was first met based on the IMWG criteria. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)1.8
Lenalidomide and Dexamethasone Rd181.8
Melphalan + Prednisone + Thalidomide (MPT)2.8

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Change From Baseline in the EORTC QLQ-C30 Appetite Loss Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Appetite Loss Scale is scored between 0 and 100, with a high score indicating a higher level of appetite loss. Negative change from Baseline values indicate improvement in appetite and positive values indicate worsening of appetite. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd182.9-3.3-8.6-6.4-5.1-7.5
Lenalidomide and Low-Dose Dexamethasone (Rd)1.3-5.9-9.8-7.3-8.1-1.0
Melphalan + Prednisone + Thalidomide (MPT)1.0-6.2-13.5-10.5-12.2-2.6

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Change From Baseline in the EORTC QLQ-C30 Cognitive Functioning Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Cognitive Functioning Scale is scored between 0 and 100, with a high score indicating better functioning/support. Negative change from Baseline values indicate deterioration in functioning and positive values indicate improvement. (NCT00689936)
Timeframe: Cycle 1 Day 1, (Baseline) then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-1.71.80.9-1.2-2.8-2.6
Lenalidomide and Low-Dose Dexamethasone (Rd)-1.2-0.7-0.9-1.6-2.2-4.9
Melphalan + Prednisone + Thalidomide (MPT)-1.8-1.5-0.3-0.6-0.7-7.1

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Change From Baseline in the EORTC QLQ-C30 Constipation Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Constipation Scale is scored between 0 and 100, with a high score indicating a higher level of constipation. Negative change from Baseline values indicate improvement in constipation and positive values indicate worsening of constipation. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd186.30.0-5.1-5.2-5.9-7.5
Lenalidomide and Low-Dose Dexamethasone (Rd)8.31.8-2.4-2.4-4.5-7.9
Melphalan + Prednisone + Thalidomide (MPT)18.413.96.83.70.0-2.2

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Change From Baseline in the EORTC QLQ-C30 Diarrhea Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Diarrhea Scale is scored between 0 and 100, with a high score indicating a higher level of diarrhea. Negative change from Baseline values indicate improvement in diarrhea and positive values indicate worsening of diarrhea. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd182.33.46.09.110.96.4
Lenalidomide and Low-Dose Dexamethasone (Rd)3.83.78.211.814.810.8
Melphalan + Prednisone + Thalidomide (MPT)-0.6-2.4-2.2-2.5-1.7-0.5

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Change From Baseline in the EORTC QLQ-C30 Dyspnea Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Dyspnoea Scale is scored between 0 and 100, with a high score indicating a higher level of symptoms. Negative change from Baseline values indicate improvement in symptoms and positive values indicate worsening symptoms. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd183.6-1.9-2.9-1.62.90.8
Lenalidomide and Low-Dose Dexamethasone (Rd)0.9-0.8-2.3-3.5-1.8-1.0
Melphalan + Prednisone + Thalidomide (MPT)4.22.00.1-1.60.47.8

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Change From Baseline in the EORTC QLQ-C30 Emotional Functioning Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Emotional Functioning Scale is scored between 0 and 100, with a high score indicating better functioning/support. Negative change from Baseline values indicate deterioration in functioning and positive values indicate improvement. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd180.13.95.84.93.13.7
Lenalidomide and Low-Dose Dexamethasone (Rd)0.63.84.64.65.82.6
Melphalan + Prednisone + Thalidomide (MPT)1.02.15.55.15.1-0.0

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Change From Baseline in the EORTC QLQ-C30 Fatigue Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Fatigue Scale is scored between 0 and 100, with a high score indicating a higher level of symptoms. Negative change from Baseline values indicate improvement in symptoms and positive values indicate worsening symptoms. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd184.4-3.4-5.9-2.30.1-1.6
Lenalidomide and Low-Dose Dexamethasone (Rd)2.6-2.5-3.7-4.3-3.10.3
Melphalan + Prednisone + Thalidomide (MPT)2.8-1.8-4.5-3.9-4.32.7

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Change From Baseline in the EORTC QLQ-C30 Financial Difficulties Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Financial Difficulties Scale is scored between 0 and 100, with a high score indicating a higher level of financial difficulties. Negative change from Baseline values indicate improvement in financial difficulties and positive values indicate worsening of financial difficulties. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-0.3-0.4-0.31.61.80.5
Lenalidomide and Low-Dose Dexamethasone (Rd)2.11.91.40.42.01.9
Melphalan + Prednisone + Thalidomide (MPT)0.51.90.71.10.45.0

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Change From Baseline in the EORTC QLQ-C30 Insomnia Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Insomnia Scale is scored between 0 and 100, with a high score indicating a higher level of symptoms. Negative change from Baseline values indicate improvement in symptoms and positive values indicate worsening symptoms. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd183.2-1.3-1.91.11.4-1.6
Lenalidomide and Low-Dose Dexamethasone (Rd)2.10.2-1.2-1.0-0.5-5.2
Melphalan + Prednisone + Thalidomide (MPT)-10.5-8.9-11.6-9.6-6.0-4.5

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Change From Baseline in the EORTC QLQ-C30 Nausea/Vomiting Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Nausea/Vomiting Scale is scored between 0 and 100, with a high score indicating a higher level of symptoms. Negative change from Baseline values indicate improvement in symptoms and positive values indicate worsening symptoms. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-0.5-2.5-4.0-3.6-2.7-4.2
Lenalidomide and Low-Dose Dexamethasone (Rd)1.8-1.1-1.3-2.2-2.30.4
Melphalan + Prednisone + Thalidomide (MPT)4.0-1.2-3.9-3.9-3.91.0

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Change From Baseline in the EORTC QLQ-C30 Pain Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Pain Scale is scored between 0 and 100, with a high score indicating a higher level of symptoms. Negative change from Baseline values indicate improvement in symptoms and positive values indicate worsening symptoms. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-4.4-13.1-16.1-14.7-12.4-7.9
Lenalidomide and Low-Dose Dexamethasone (Rd)-5.4-13.4-14.4-14.0-14.4-8.0
Melphalan + Prednisone + Thalidomide (MPT)-7.8-12.1-13.4-14.3-14.7-6.0

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Change From Baseline in the EORTC QLQ-C30 Physical Functioning Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Physical Functioning Scale is scored between 0 and 100, with a high score indicating better functioning/support. Negative change from Baseline values indicate deterioration in functioning and positive values indicate improvement. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-1.44.77.67.46.83.0
Lenalidomide and Low-Dose Dexamethasone (Rd)-1.73.44.75.06.9-0.1
Melphalan + Prednisone + Thalidomide (MPT)-0.92.25.36.98.3-0.1

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Change From Baseline in the EORTC QLQ-C30 Role Functioning Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Role Functioning Scale is scored between 0 and 100, with a high score indicating better functioning/support. Negative change from Baseline values indicate deterioration in functioning and positive values indicate improvement. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-4.66.38.69.49.13.8
Lenalidomide and Low-Dose Dexamethasone (Rd)-2.72.46.37.88.0-0.3
Melphalan + Prednisone + Thalidomide (MPT)-2.44.18.211.814.5-1.0

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Change From Baseline in the EORTC QLQ-C30 Social Functioning Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used in clinical research to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Social Functioning Scale is scored between 0 and 100, with a high score indicating better functioning/support. Negative change from Baseline values indicate deterioration in functioning and positive values indicate improvement. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-2.22.05.23.83.22.7
Lenalidomide and Low-Dose Dexamethasone (Rd)-4.30.74.02.94.2-1.2
Melphalan + Prednisone + Thalidomide (MPT)-1.42.43.45.86.0-3.5

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Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Cancer (EORTC QLQ-C30) Global Health Status Domain

The European Organization for Research and Treatment of Cancer (EORTC) Core Quality of Life (QOL) questionnaire (EORTC QLQ-C30) is a 30-question tool used to assess the overall quality of life in cancer patients. It consists of 15 domains: 1 global health status (GHS) scale, 5 functional scales (Physical, Role, Cognitive, Emotional, Social), and 9 symptom scales/items (Fatigue, Nausea and Vomiting, Pain, Dyspnea, Sleep Disturbance, Appetite Loss, Constipation, Diarrhea, Financial Impact). The EORTC QLQ-C30 Global Health Status/QOL scale is scored between 0 and 100, with a high score indicating better Global Health Status/QOL. Negative change from Baseline values indicate deterioration in QOL or functioning and positive values indicate improvement. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Study discontinuation
Lenalidomide and Dexamethasone Rd18-1.34.75.43.25.75.0
Lenalidomide and Low-Dose Dexamethasone (Rd)0.44.85.94.86.4-0.1
Melphalan + Prednisone + Thalidomide (MPT)1.04.36.16.54.80.3

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Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Body Image Scale

EORTC QLQ-MY20 is a validated questionnaire to assess the overall quality of life in patients with multiple myeloma. EORTC QLQ-MY20 includes four scales: disease symptoms, treatment side-effects, future perspective, and body image. Questions used a 4-point scale (from 1 'Not at All' to 4 'Very Much'). Scores were averaged, and transformed to a 0-100 scale; for the body image scale, a higher score indicates a better body image. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-1.50.81.5-0.4-0.31.8
Lenalidomide and Low-Dose Dexamethasone (Rd)-4.5-1.7-1.4-1.4-2.3-5.6
Melphalan + Prednisone + Thalidomide (MPT)-1.6-3.0-2.8-2.6-1.1-5.6

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Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Disease Symptoms Scale

EORTC QLQ-MY20 is a validated questionnaire to assess the overall quality of life in patients with multiple myeloma. EORTC QLQ-MY20 includes four scales: disease symptoms, treatment side-effects, future perspective, and body image. Questions used a 4-point scale (from 1 'Not at All' to 4 'Very Much'). Scores were averaged, and transformed to a 0-100 scale; a higher score indicates more severe disease symptom(s). (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-4.1-10.0-9.9-8.7-6.2-4.5
Lenalidomide and Low-Dose Dexamethasone (Rd)-4.0-9.1-8.8-7.8-8.7-3.5
Melphalan + Prednisone + Thalidomide (MPT)-4.4-7.0-7.9-6.5-7.9-3.7

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Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Future Perspective Scale

EORTC QLQ-MY20 is a validated questionnaire to assess the overall quality of life in patients with multiple myeloma. EORTC QLQ-MY20 includes four scales: disease symptoms, treatment side-effects, future perspective, and body image. Questions used a 4-point scale (from 1 'Not at All' to 4 'Very Much'). Scores were averaged, and transformed to a 0-100 scale; for the future perspective scale, a higher score indicates a better perspective of the future. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd183.99.212.312.111.78.8
Lenalidomide and Low-Dose Dexamethasone (Rd)4.78.59.810.812.75.8
Melphalan + Prednisone + Thalidomide (MPT)3.36.38.010.09.53.2

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Change From Baseline in the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire for Patients With Multiple Myeloma (EORTC QLQ-MY20) Side Effects Treatment Scale

EORTC QLQ-MY20 is a validated questionnaire to assess the overall quality of life in patients with multiple myeloma. EORTC QLQ-MY20 includes four scales: disease symptoms, treatment side-effects, future perspective, and body image. Questions used a 4-point scale (from 1 'Not at All' to 4 'Very Much'). Scores were averaged, and transformed to a 0-100 scale; a higher score represents a more severe overall side effect of treatment. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd184.01.2-0.41.22.3-1.0
Lenalidomide and Low-Dose Dexamethasone (Rd)2.51.01.71.92.20.6
Melphalan + Prednisone + Thalidomide (MPT)5.63.52.94.74.33.8

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Change From Baseline in the European Quality of Life-5 Dimensions (EQ-5D) Health Utility Index Score

EQ-5D is a self-administered questionnaire that assesses health-related quality of life. The EQ-5D descriptive health profile comprises five dimensions of health (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression). Each dimension has 3 levels of response: No problem (1), some problems (2), and extreme problems (3). A unique EQ-5D health state is defined by combining one level from each of the five dimensions into a single utility index score. EQ-5D index values range from -0.59 to 1.00 where higher EQ-5D scores represent better health status. A positive change from baseline score indicates improvement in health status and better health state. (NCT00689936)
Timeframe: Cycle 1 Day 1 (Baseline), then Months 1, 3, 6, 12, 18 and Discontinuation visit

,,
Interventionunits on a scale (Mean)
Month 1Month 3Month 6Month 12Month 18Discontinuation Visit
Lenalidomide and Dexamethasone Rd18-0.00.10.10.10.10.0
Lenalidomide and Low-Dose Dexamethasone (Rd)0.00.10.10.10.10.0
Melphalan + Prednisone + Thalidomide (MPT)0.00.10.10.10.10.0

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Number of Participants With Adverse Events (AEs) During the Active Treatment Phase

A TEAE is any AE occurring or worsening on or after the first treatment of any study drug, and within 30 days after the last dose of the last study drug. Severity grades according to Common Terminology Criteria for Adverse Events v3.0 (CTCAE) on a 1-5 scale: Grade 1= Mild AE, Grade 2= Moderate AE, Grade 3= Severe AE, Grade 4= Life-threatening or disabling AE, Grade 5=Death related to AE. A serious AE is any AE occurring at any dose that: • Results in death; • Is life-threatening; • Requires or prolongs existing inpatient hospitalization; • Results in persistent or significant disability/incapacity; • Is a congenital anomaly/birth defect; • Constitutes an important medical event. (NCT00689936)
Timeframe: From first dose of study drug through 28 days following the discontinuation visit from active treatment phase; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

,,
InterventionParticipants (Number)
≥ 1 adverse event (AE)≥ 1 grade (Gr) 3 or 4 AE≥ 1 grade (Gr) 5 AE≥ 1 serious adverse event (SAE)≥ 1 AE related to Lenalidomide/Dex/Mel/Pred/Thal≥ 1 AE related to Lenalidomide≥ 1 AE related to dexamethasone≥ 1 AE related to melphalan≥ 1 AE related to prednisone≥ 1 AE related to thalidomide≥1 AE related to Lenalidomide/Dex or Mel/Pred/Thal≥ 1 Gr 3 or 4 AE related to Len/Dex/Mel/Pred/Thal≥ 1 grade 3 or 4 AE related to Lenalidomide≥ 1 grade 3 or 4 AE related to dexamethasone≥ 1 grade 3 or 4 AE related to melphalan≥ 1 grade 3 or 4 AE related to prednisone≥ 1 grade 3 or 4 AE related to Thalidomide≥1Gr 3 or 4 AE related to Len/Dex or Mel/Pred/Thal≥ 1 Grade 5 AE related to Len/Dex/Mel/Pred/Thal≥ 1 Grade 5 AE related to Lenalidomide≥ 1 Grade 5 AE related to Dexamethasone≥ 1 Grade 5 AE related to melphalan≥ 1 Grade 5 AE related to prednisone≥ 1 Grade 5 AE related to Thalidomide≥1 Grade 5 AE related to Len/Dex or Mel/Pred/Thal≥1 SAE related to Len/Dex/Mel/Pred/Thal≥1 SAE related to Lenalidomide≥1 SAE related to dexamethasone≥1 SAE related to melphalan≥1 SAE related to prednisone≥1 SAE related to thalidomide≥1 SAE related to Len/Dex or Mel/Pred/Thal≥1AE leading to Len/Dex/Mel/Pred/Thal Withdrawal≥1 AE leading to Lenalidomide withdrawal≥1 AE leading to dexamethasone withdrawal≥1 AE leading to melphalan withdrawal≥1 AE leading to prednisone withdrawal≥1 AE leading to Thalidomide withdrawal≥1AE leading to Len/DexOR Mel/Pred/Thal Withdrawal≥1AE leading to Len/Dex/Mel/Pred/Thal reduction≥1 AE leading to Lenalidomide reduction≥1 AE leading to dexamethasone reduction≥1 AE leading to melphalan reduction≥1 AE leading to prednisone reduction≥1 AE leading to thalidomide reduction≥1AE leading to Len/Dex or Mel/Pred/Thal reduction≥1 AE leading to Rd or MPT interruption≥1 AE leading to Lenalidomide interruption≥1 AE leading to dexamethasone interruption≥1 AE leading to melphalan interruption≥1 AE leading to prednisone interruption≥1 AE leading to Thalidomide interruption≥1 AE leading to Len and Dex or MPT interruption
Lenalidomide and Dexamethasone Rd1853643336308501481410000269326290177000104119700051581309700064109931040008421415511800020321301280000241
Lenalidomide and Low-Dose Dexamethasone (Rd)5294535035950648242900026937334222900013117121600011195165130000951571091520009627920317000030368353319000290
Melphalan + Prednisone + Thalidomide (MPT)53948038270527004413264931454230030711831649100065521420075629427153008378146713480019947254241900328324388249

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Shift From Baseline to Most Extreme Postbaseline Value in Absolute Neutrophil Count During the Active Treatment Phase

Neutrophil counts was assessed for participants from baseline grade to most extreme severity grade using the NCI CTCAE v 3.0 grading scale. (NCT00689936)
Timeframe: Randomization to end of treatment or the data cut off of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

,,
Interventionparticipants (Number)
Normal Baseline Grade to Normal Postbaseline GradeNormal Baseline Grade to Grade 1 postbaselineNormal Baseline Grade to Grade 2 postbaselineNormal Baseline Grade to Grade 3 postbaselineNormal Baseline Grade to Grade 4 postbaselineGrade 1 Baseline to Normal postbaselineGrade1 Baseline to Grade 1 postbaselineGrade 1 Baseline to Grade 2 postbaselineGrade 1 Baseline to Grade 3 postbaselineGrade 1 Baseline to Grade 4 postbaselineGrade 2 Baseline to normal postbaselineGrade 2 Baseline to Grade 1 postbaselineGrade 2 Baseline to Grade 2 postbaselineGrade 2 Baseline to Grade 3 postbaselineGrade 2 Baseline to Grade 4 postbaselineGrade 3 Baseline to Normal postbaselineGrade 3 Baseline to Grade 1 postbaselineGrade 3 Baseline to Grade 2 postbaselineGrade 3 Baseline to Grade 3 postbaselineGrade3 Baseline to Grade 4 postbaselineGrade 4 Baseline to Normal postbaseline GradeGrade 4 Baseline to Grade 1 postbaseline GradeGrade 4 Baseline to Grade 2 postbaselineGrade 4 Baseline Grade to Grade 3 postbaselineGrade 4 Baseline to Grade 4 postbaseline
Lenalidomide and Dexamethasone Rd181338510971306111530401111850012200000
Lenalidomide and Low-Dose Dexamethasone (Rd)103961217021781725911141890022001000
Melphalan + Prednisone + Thalidomide (MPT)3779128141452211202101721100000100000

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Shift From Baseline to Most Extreme Postbaseline Value in Hemoglobin During the Active Treatment Phase

Hemoglobin was assessed for participants from baseline grade to most extreme severity grade using the NCI CTCAE v 3.0 grading scale. (NCT00689936)
Timeframe: Randomization to end of treatment or the data cut off of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

,,
Interventionparticipants (Number)
Normal Baseline Grade to Normal Postbaseline GradeNormal Baseline Grade to Grade 1 postbaselineNormal Baseline Grade to Grade 2 postbaselineNormal Baseline Grade to Grade 3 postbaselineNormal Baseline Grade to Grade 4 postbaselineGrade 1 Baseline to Normal postbaselineGrade 1 Baseline to Grade 1 postbaselineGrade1 Baseline to Grade 2 postbaselineGrade 1 Baseline to Grade 3 postbaselineGrade 1 Baseline to Grade 4 postbaselineGrade 2 Baseline to normal postbaselineGrade 2 Baseline to Grade 1 postbaselineGrade 2 Baseline to Grade 2 postbaselineGrade 2 Baseline to Grade 3 postbaselineGrade 2 Baseline to Grade 4 postbaselineGrade 3 Baseline to Normal postbaselineGrade 3 Baseline to Grade 1 postbaselineGrade 3 Baseline to Grade 2 postbaselineGrade 3 Baseline to Grade 3 postbaselineGrade 3 Baseline to Grade 4 postbaselineGrade 4 Baseline to Normal postbaselineGrade 4 Baseline to Grade 1 postbaselineGrade 4 Baseline to Grade 2 postbaselineGrade 4 Baseline to Grade 3 postbaselineGrade 4 Baseline to Grade 4 postbaseline
Lenalidomide and Dexamethasone Rd18103081001261231750121354190148300011
Lenalidomide and Low-Dose Dexamethasone (Rd)639800010612825208125484001210500001
Melphalan + Prednisone + Thalidomide (MPT)92541001101232040141334711001010200102

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Shift From Baseline to Most Extreme Postbaseline Value in Platelet Count During the Active Treatment Phase.

Improvement in platelets was assessed for participants from baseline grade to most extreme severity grade using the NCI CTCAE v 3.0 grading scale. (NCT00689936)
Timeframe: Randomization to end of treatment or the data cut off of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

,,
Interventionparticipants (Number)
Normal Baseline Grade to Normal Postbaseline GradeNormal Baseline Grade to Grade 1 postbaselineNormal Baseline Grade to Grade 2 postbaselineNormal Baseline Grade to Grade 3 postbaselineNormal Baseline Grade to Grade 4 postbaselineGrade1 Baseline to Normal postbaseline GradeGrade 1 Baseline to Grade 1 postbaselineGrade 1 Baseline to Grade 2 postbaselineGrade 1 Baseline to Grade 3 postbaselineGrade 1 Baseline to Grade 4 postbaselineGrade 2 Baseline to normal postbaseline GradeGrade 2 Baseline to Grade 1 postbaselineGrade 2 Baseline to Grade 2 postbaselineGrade 2 Baseline to Grade 3 postbaselineGrade 2 Baseline to Grade 4 postbaselineGrade 3 Baseline to Normal postbaseline GradeGrade 3 Baseline to Grade 1 postbaselineGrade 3 Baseline to Grade 2 postbaselineGrade 3 Baseline to Grade 3 postbaselineGrade 3 Baseline to Grade 4 postbaseline
Lenalidomide and Dexamethasone Rd1819721130125338191210132000001
Lenalidomide and Low-Dose Dexamethasone (Rd)19721624154134151020033100002
Melphalan + Prednisone + Thalidomide (MPT)16520827311165171010212200110

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Shift From Baseline to Most Extreme Postbaseline Value in Creatinine Clearance (CrCl) During the Active Treatment Phase

Renal function was assessed for participants from baseline to the most extreme value in creatinine clearance calculated using the Cockcroft-Gault estimation. (NCT00689936)
Timeframe: Randomization to end of treatment or the data cut off of 24 May 2013; median duration of treatment was 80.2 weeks in the Rd arm; 72 weeks in the Rd18 arm and 67.1 weeks in the MPT arm

,,
Interventionparticipants (Number)
CrCl< 30 mL/min to CrCl< 30 mL/minCrCl < 30 mL/min to CrCl ≥ 30 but < 50 mL/minCrCl < 30 mL/min to CrCl ≥ 50 but < 80 mL/minCrCl< 30 mL/min to ≥ 80 mL/minCrCl≥ 30 but < 50 mL/min to < 30 mL/minCrCl ≥ 30 but < 50 mL/min to CrCl ≥ 30 but < 50 mLCrCl ≥ 30 but < 50 mL/min to CrCl ≥ 50 but < 80 mLCrCl ≥ 30 but < 50 mL/min to ≥ 80 mL/minCrCl ≥ 50 but < 80 mL to CrCl< 30 mL/minCrCl ≥ 50 but < 80 mL to CrCl ≥ 30 but < 50 mL/minCrCl ≥ 50 but < 80 mL to CrCl ≥ 50 but < 80 mL/minCrCl ≥ 50 but < 80 mL to ≥ 80 mL/minCrCl ≥ 80 mL/min to CrCl< 30 mL/minCrCl ≥ 80 mL/min to CrCl ≥ 30 but < 50 mL/minCrCl ≥ 80 mL/min to CrCl ≥ 50 but < 80 mL/minCrCl ≥ 80 mL/min to CrCl ≥ 80 mL/min
Lenalidomide and Dexamethasone Rd18171482241551201130991010114
Lenalidomide and Low-Dose Dexamethasone (Rd)15187213767904112107006109
Melphalan + Prednisone + Thalidomide (MPT)1919500416520410297009121

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Kaplan Meier Estimates for Time to Second-line Anti-myeloma Treatment (AMT)

Time to second-line anti-myeloma therapy was defined as time from randomization to the start of another non-protocol anti-myeloma therapy. (NCT00689936)
Timeframe: From date of randomization until the data cut-off of 24 May 2013; median follow-up for all participants was 23.0 months

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)39.1
Lenalidomide and Dexamethasone Rd1828.5
Melphalan + Prednisone + Thalidomide (MPT)26.7

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Kaplan Meier Estimates of Duration of Myeloma Response as Determined by an Investigator Assessment at Time of Final Analysis

Duration of response was defined as the duration from the time when the response criteria were first met for CR or VGPR or PR based on IMWG criteria until the first date the response criteria were met for progressive disease or until the participant died from any cause, whichever occurred first. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment; data cut-off date of 21 January 2016; median follow-up for responders was 19.9 months

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)31.5
Lenalidomide and Dexamethasone Rd1821.5
Melphalan + Prednisone + Thalidomide (MPT)22.1

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Kaplan Meier Estimates of Duration of Myeloma Response as Determined by the IRAC

Duration of response was defined as the duration from the time when the response criteria were first met for CR or VGPR or PR based on IMWG criteria until the first date the response criteria were met for progressive disease or until the participant died from any cause, whichever occurred first. (NCT00689936)
Timeframe: Disease response was assessed every 28 days until end of treatment or the data cut-off date of 24 May 2013; median follow-up for responders was 20.1 months

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)35.0
Lenalidomide and Dexamethasone Rd1822.1
Melphalan + Prednisone + Thalidomide (MPT)22.3

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Kaplan Meier Estimates of Overall Survival at the Time of Final Analysis (OS)

Overall survival was defined as the time between randomization and death. Participants, who died, regardless of the cause of death, were considered to have had an event. All participants who were lost to follow-up prior to the end of the trial or who were withdrawn from the trial were censored at the time of last contact. Participants who were still being treated were censored at the last available date the participant was known to be alive. (NCT00689936)
Timeframe: From date of randomization to date of data cut-off date of 21 January 2016; median follow-up for all participants was 48.3 months

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)59.1
Lenalidomide and Dexamethasone Rd1862.3
Melphalan + Prednisone + Thalidomide (MPT)49.1

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Kaplan Meier Estimates of Time to Second Line Therapy AMT at the Time of Final Analysis

Time to second-line anti-myeloma therapy is defined as time from randomization to the start of another non-protocol anti-myeloma therapy. Those who do not receive another anti-myeloma therapy were censored at the last assessment or follow-up visit known to have received no new therapy. (NCT00689936)
Timeframe: From date of randomization until the data cut-off of date 21 January 2016; median follow-up for all participants was 23.0 months

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)36.7
Lenalidomide and Dexamethasone Rd1828.5
Melphalan + Prednisone + Thalidomide (MPT)26.7

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Kaplan Meier Estimates of Time to Treatment Failure (TTF)

TTF is defined as the time between the randomization and discontinuation of study treatment for any reason, including disease progression (determined by IRAC based on the IMWG response criteria), treatment toxicity, start of another anti-myeloma therapy (AMT) or death. (NCT00689936)
Timeframe: From date of randomization until the data cut-off of 24 May 2013; median follow-up for all participants was 16.1 months.

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)16.9
Lenalidomide and Dexamethasone Rd1817.2
Melphalan + Prednisone + Thalidomide (MPT)14.1

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Kaplan Meier Estimates of Time to Treatment Failure (TTF) at the Time of Final Analysis

TTF is defined as the time between the randomization and discontinuation of study treatment for any reason, including disease progression (determined by the investigators assessment based on the IMWG response criteria), treatment toxicity, start of another anti-myeloma therapy (AMT) or death. (NCT00689936)
Timeframe: From date of randomization until the data cut-off date of 21 January 2016; median follow up for all participants was 16.1 months.

Interventionmonths (Median)
Lenalidomide and Low-Dose Dexamethasone (Rd)16.9
Lenalidomide and Dexamethasone Rd1817.2
Melphalan + Prednisone + Thalidomide (MPT)14.1

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Number of Participants With Treatment Emergent Adverse Events (TEAE) in the Apremilast Exposure Period

An AE was any noxious, unintended, or untoward medical occurrence, that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly/birth defect, or is a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. An AE is a treatment emergent AE if the AE start date is on or after the date of the first dose of study drug and no later than 28 days after the last dose. (NCT00773734)
Timeframe: Week 0-88; up to data cut off of 21 July 2011

,,
Interventionparticipants (Number)
Any treatment emergent AEAny drug-related TEAEAny severe TEAEAny serious TEAEAny serious drug-related≥ 1 TEAE leading to drug interruption≥ 1 TEAE leading to drug withdrawal≥ 1 TEAE leading to death
Apremilast 10mg BID6723310350
Apremilast 20mg BID973198111110
Apremilast 30 mg BID1104513609150

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score at 18 Months

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionunits on a scale (Mean)
Apremilast 20mg BID10.2

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Physical Component Summary Score at 4 Years

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionunits on a scale (Mean)
Apremilast 10mg BID1.4
Placebo-Apremilast 20mg BID2.0
Apremilast 20mg BID-4.1
Placebo-Apremilast 30 mg BID10.2
Apremilast 30 mg BID9.4

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Physical Component Summary Score at 3 Years

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionunits on a scale (Mean)
Apremilast 10mg BID6.6
Placebo-Apremilast 20mg BID1.0
Apremilast 20mg BID-0.1
Placebo-Apremilast 30 mg BID4.4
Apremilast 30 mg BID4.2

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Physical Component Summary Score at 2 Years

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionunits on a scale (Mean)
Apremilast 10mg BID4.1
Placebo-Apremilast 20mg BID3.7
Apremilast 20mg BID1.0
Placebo-Apremilast 30 mg BID2.4
Apremilast 30 mg BID5.0

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 4 Years

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionunits on a scale (Mean)
Apremilast 10mg BID-1.1
Placebo-Apremilast 20mg BID4.1
Apremilast 20mg BID-1.0
Placebo-Apremilast 30 mg BID17.6
Apremilast 30 mg BID1.2

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 3 Years

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionunits on a scale (Mean)
Apremilast 10mg BID6.0
Placebo-Apremilast 20mg BID-2.7
Apremilast 20mg BID3.6
Placebo-Apremilast 30 mg BID2.1
Apremilast 30 mg BID2.4

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 2 Years

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionunits on a scale (Mean)
Apremilast 10mg BID5.0
Placebo-Apremilast 20mg BID2.0
Apremilast 20mg BID5.2
Placebo-Apremilast 30 mg BID4.5
Apremilast 30 mg BID0.2

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LTE Study: Change From Baseline in the Medical Outcome Study Short Form, SF-36, Version 2; Mental Component Summary Score at 18 Months

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionunits on a scale (Mean)
Apremilast 20mg BID-2.8

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LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 4 Years

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionunits on a scale (Mean)
Apremilast 10mg BID-6.0
Placebo-Apremilast 20mg BID-9.0
Apremilast 20mg BID-3.5
Placebo-Apremilast 30 mg BID-7.0
Apremilast 30 mg BID-10.3

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LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 2 Years

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercent change (Median)
Apremilast 10mg BID-60.5
Placebo-Apremilast 20 mg BID-66.2
Apremilast 20mg BID-75.0
Apremilast 30 mg BID-41.5
Placebo-Apremilast 30 mg BID-77.4

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LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 3 Years

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionpercent change (Median)
Apremilast 10mg BID-85.7
Placebo-Apremilast 20 mg BID-63.4
Apremilast 20mg BID-60.9
Placebo-Apremilast 30 mg BID-52.2
Apremilast 30 mg BID-81.0

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LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 4 Years

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercent change (Median)
Apremilast 10mg BID-75.0
Placebo-Apremilast 20 mg BID-50.6
Apremilast 20mg BID-73.5
Placebo-Apremilast 30 mg BID-75.0
Apremilast 30 mg BID-91.9

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LTE Study: Percent Change From Baseline in PASI Score at 18 Months

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercent change (Mean)
Apremilast 10mg BID-71.8
PBO-Apremilast 20mg BID-60.5
Apremilast 20mg BID-65.3
PBO-Apremilast 30 mg BID-50.0
Apremilast 30 mg BID-77.3

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LTE Study: Percent Change From Baseline in PASI Score at 2 Years

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercent change (Mean)
Apremilast 10mg BID-57.8
PBO-Apremilast 20mg BID-64.5
Apremilast 20mg BID-65.9
PBO-Apremilast 30 mg BID-46.0
Apremilast 30 mg BID-78.4

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LTE Study: Percent Change From Baseline in PASI Score at 3 Years

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionpercent change (Mean)
Apremilast 10mg BID-87.7
PBO-Apremilast 20mg BID-69.0
Apremilast 20mg BID-48.8
PBO-Apremilast 30 mg BID-48.0
Apremilast 30 mg BID-80.0

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LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 3 Years

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 148 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionpercentage of participants (Number)
Apremilast 10mg BID20.0
Placebo-Apremilast 20mg BID0.0
Apremilast 20mg BID10.0
Placebo-Apremilast 30 mg BID0.0
Apremilast 30 mg BID20.0

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LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 18 Months

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercent change (Mean)
Apremilast 10mg BID-71.1
Placebo-Apremilast 20 mg BID-73.9
Apremilast 20mg BID-74.2
Placebo-Apremilast 30 mg BID-44.2
Apremilast 30 mg BID-76.7

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LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 2 Years

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercent change (Mean)
Apremilast 10mg BID-64.7
Placebo-Apremilast 20 mg BID-66.2
Apremilast 20mg BID-74.5
Placebo-Apremilast 30 mg BID-24.7
Apremilast 30 mg BID-74.5

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LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 3 Years

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionpercent change (Mean)
Apremilast 10mg BID-86.1
Placebo-Apremilast 20 mg BID-63.4
Apremilast 20mg BID-58.4
Placebo-Apremilast 30 mg BID-39.1
Apremilast 30 mg BID-78.5

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LTE Study: Percent Change From Baseline in the Percent of the Affected Body Surface Area (BSA) at 4 Years

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercent change (Mean)
Apremilast 10mg BID-75.0
Placebo-Apremilast 20 mg BID-50.6
Apremilast 20mg BID-72.4
Placebo-Apremilast 30 mg BID-75.0
Apremilast 30 mg BID-86.1

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LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 18 Months

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercentage of participants (Number)
Apremilast 10mg BID100.0
Placebo-Apremilast 20mg BID50.0
Apremilast 20mg BID70.0
Placebo-Apremilast 30 mg BID50.0
Apremilast 30 mg BID100

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LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 2 Years

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID60.0
Placebo-Apremilast 20mg BID50.0
Apremilast 20mg BID50.0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID90.0

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Number of Participants With Treatment Emergent Adverse Events (TEAE) in the Placebo Controlled Phase

An AE was any noxious, unintended, or untoward medical occurrence, that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly/birth defect, or is a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. An AE is a treatment emergent AE if the AE start date is on or after the date of the first dose of study drug and no later than 28 days after the last dose. (NCT00773734)
Timeframe: Week 0 to Week 16; up to data cut off of 21 July 2011

,,,
Interventionparticipants (Number)
Any treatment emergent AEAny drug-related TEAEAny severe TEAEAny serious TEAEAny serious drug-related≥ 1 TEAE leading to drug interruption≥ 1 TEAE leading to drug withdrawal≥ 1 TEAE leading to death
Apremilast 10mg BID5920100320
Apremilast 20mg BID6723530380
Apremilast 30 mg BID72325406120
Placebo5711320451

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LTE Study: Percent Change From Baseline in PASI Score at 4 Years

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercent change (Mean)
Apremilast 10mg BID-82.5
PBO-Apremilast 20mg BID-52.0
Apremilast 20mg BID-54.3
PBO-Apremilast 30 mg BID-80.0
Apremilast 30 mg BID-85.0

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Number of Participants With Treatment Emergent Adverse Events (TEAE) in the Apremilast Exposure Period

An AE was any noxious, unintended, or untoward medical occurrence, that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly/birth defect, or is a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. An AE is a treatment emergent AE if the AE start date is on or after the date of the first dose of study drug and no later than 28 days after the last dose. (NCT00773734)
Timeframe: Week 0 to 6 years of study treatment; maximum duration of exposure was 314.6 weeks

,,
Interventionparticipants (Number)
Any treatment emergent AEAny drug-related TEAEAny severe TEAEAny serious TEAEAny serious drug-related≥ 1 TEAE leading to drug interruption≥ 1 TEAE leading to drug withdrawal≥ 1 TEAE leading to death
Apremilast 10mg BID6723420350
Apremilast 20mg BID9732109111110
Apremilast 30 mg BID11146146010160

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Time to Loss of 50% of the PASI Response During the Observational Follow-up Phase Relative to the End of Treatment (Participants Who Had at Least a PASI-50 Response at the End of Treatment Phase)

Time to loss of response was modified to be 50% loss in the PASI response observed at the end of treatment for participants who achieved at least a PASI-50 at the end of treatment. This definition was changed since participants may have already lost their maximal PASI response prior to enrollment into the Observation Follow-up Phase. Included all participants that enrolled into the observational follow-up phase after the treatment phase. (NCT00773734)
Timeframe: Up to 4 weeks after the last dose

Interventionweeks (Median)
Apremilast 10mg BIDNA
Apremilast 20mg BIDNA
Apremilast 30 mg BIDNA
Placebo-Apremilast 20mg BIDNA
Placebo-Apremilast 30 mg BID5.3

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LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 4 Years

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercentage of participants (Number)
Apremilast 10mg BID20.0
Placebo-Apremilast 20 mg BID0.0
Apremilast 20mg BID0.0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID30.0

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LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 3 Years

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease (NCT00773734)
Timeframe: Week 0 and month 36

Interventionpercentage of participants (Number)
Apremilast 10mg BID60.0
Placebo-Apremilast 20 mg BID0.0
Apremilast 20mg BID0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID30.0

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LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 2 Years

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID20.0
Placebo-Apremilast 20 mg BID0.00
Apremilast 20mg BID10.0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID40.0

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LTE Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at 18 Months

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercentage of participants (Number)
Apremilast 10mg BID60.0
Placebo-Apremilast 20 mg BID0.0
Apremilast 20mg BID20.0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID60.0

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LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 4 Years

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 196 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercentage of participants (Number)
Apremilast 10mg BID0.0
Placebo-Apremilast 20mg BID0.0
Apremilast 20mg BID0.0
Placebo-Apremilast 30 mg BID0.0
Apremilast 30 mg BID20.0

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LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 3 Years

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionpercentage of participants (Number)
Apremilast 10mg BID60.0
Placebo-Apremilast 20mg BID50.0
Apremilast 20mg BID30.0
Placebo-Apremilast 30 mg BID50.0
Apremilast 30 mg BID60.0

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LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 2 Years

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 100 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID0.0
Placebo-Apremilast 20mg BID0
Apremilast 20mg BID10.0
Placebo-Apremilast 30 mg BID0.0
Apremilast 30 mg BID30.0

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LTE Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at 18 Months

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 76 of the long-term extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercentage of participants (Number)
Apremilast 10mg BID0.0
Placebo-Apremilast 20mg BID0.0
Apremilast 20mg BID10.0
Placebo-Apremilast 30 mg BID0.0
Apremilast 30 mg BID30.0

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Core Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 24

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionunits on a scale (Mean)
Apremilast 10mg BID-3.4
Apremilast 20mg BID-6.2
Apremilast 30 mg BID-4.9
Placebo-Apremilast (APR) 20 mg BID-6.4
Placebo-Apremilast 30 mg BID-5.4

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Core Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 16

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo BID-1.9
Apremilast 10mg BID-3.2
Apremilast 20mg BID-5.9
Apremilast 30 mg BID-4.4

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Core Study: Area Under the Plasma Concentration-time Curve (AUC0-8)

Area under the concentration versus time curve from time 0 (pre-dose) to 8 hours, calculated using the linear trapezoid rule. (NCT00773734)
Timeframe: Week 14; Predose, 0.5, 1, 2, 3, 4, and 8 hours after the morning dose of apremilast

Interventionng*h/mL (Geometric Mean)
Apremilast 10mg BID1008
Apremilast 20mg BID1591
Apremilast 30 mg BID3467

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Core Study: Area Under the Plasma Concentration-time Curve (AUC0-8)

Area under the concentration versus time curve from time 0 (pre-dose) to 8 hours, calculate using the linear trapezoid rule. (NCT00773734)
Timeframe: Week 24

Interventionng*h/mL (Geometric Mean)
Apremilast 10mg1200
Apremilast 20mg1257
Apremilast 30 mg3477

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LTE Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at 4 Years

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercentage of participants (Number)
Apremilast 10mg BID40.0
Placebo-Apremilast 20mg BID25.0
Apremilast 20mg BID20.0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID40.0

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LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 18 Months

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercentage of participants (Number)
Apremilast 10mg BID60.0
Placebo-Apremilast 20mg BID0.0
Apremilast 20mg BID40.0
Placebo-Apremilast 30 mg BID0.0
Apremilast 30 mg BID50.0

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LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 2 Years

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID20.0
Placebo-Apremilast 20mg BID0.0
Apremilast 20mg BID30.0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID50.0

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Extension Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at Week 32

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score at Week 32 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionpercentage of participants (Number)
Apremilast 10mg BID27.7
Apremilast 20mg BID38.0
Apremilast 30 mg BID46.6
Placebo-Apremilast 20mg BID33.3
Placebo-Apremilast 30 mg BID55.6

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LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 3 Years

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionunits on a scale (Mean)
Apremilast 10mg BID-11.7
Placebo-Apremilast 20mg BID-3.0
Apremilast 20mg BID-4.2
Placebo-Apremilast 30 mg BID-2.0
Apremilast 30 mg BID-6.0

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LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 2 Years

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Month 24

Interventionunits on a scale (Mean)
Apremilast 10mg BID-5.2
Placebo-Apremilast 20mg BID-13.5
Apremilast 20mg BID-5.9
Placebo-Apremilast 30 mg BID-1.8
Apremilast 30 mg BID-6.8

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Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2 Physical Component Summary Score at Week 24

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionunits on a scale (Mean)
Apremilast 10mg BID1.1
Apremilast 20mg BID2.3
Apremilast 30 mg BID1.0
PBO-Apremilast 20mg BID2.5
PBO-Apremilast 30 mg BID2.7

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Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2; Mental Component Summary Score at Week 16

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo BID-0.6
Apremilast 10mg BID2.8
Apremilast 20mg BID2.9
Apremilast 30 mg BID3.0

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LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 3 Years

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 36

Interventionpercentage of participants (Number)
Apremilast 10mg BID60.0
Placebo-Apremilast 20mg BID25.0
Apremilast 20mg BID10.0
Placebo-Apremilast 30 mg BID0.0
Apremilast 30 mg BID30.0

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Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2; Mental Component Summary Score at Week 24

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionunits on a scale (Mean)
Apremilast 10mg BID2.8
Apremilast 20mg BID3.9
Apremilast 30 mg BID2.9
PBO-Apremilast 20mg BID2.8
PBO-Apremilast 30 mg BID0.5

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Core Study: Change From Baseline in the Medical Outcome Study Short Form 36-Item Health Survey (SF-36), Version 2; Physical Component Summary Score at Week 16

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to week 16

Interventionunits on a scale (Least Squares Mean)
Placebo BID0.7
Apremilast 10mg BID1.3
Apremilast 20mg BID2.1
Apremilast 30 mg BID0.8

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Core Study: Peak; (Maximum) Plasma Concentration (Cmax) of Apremilast

The maximum observed plasma concentration of apremilast observed at Week 14 (steady-state Cmax) (NCT00773734)
Timeframe: Week 14; Predose, 0.5, 1, 2, 3, 4, and 8 hours after the morning dose of apremilast

Interventionng/mL (Geometric Mean)
Apremilast 10mg BID209
Apremilast 20mg BID298
Apremilast 30 mg BID637

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Core Study: Peak; (Maximum) Plasma Concentration (Cmax) of Apremilast

The maximum observed plasma concentration of apremilast observed at Week 24 (steady-state Cmax) (NCT00773734)
Timeframe: Week 24

Interventionng/mL (Geometric Mean)
Apremilast 10mg BID238
Apremilast 20mg BID236
Apremilast 30 mg BID670

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Extension Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at Week 40

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score at Week 40 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionpercentage of participants (Number)
Apremilast 10mg BID21.3
Apremilast 20mg BID28.0
Apremilast 30 mg BID34.5
Placebo-Apremilast 20mg BID37.0
Placebo-Apremilast 30 mg BID44.4

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Extension Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at Week 52

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score at Week 52. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionpercentage of participants (Number)
Apremilast 10mg BID14.9
Apremilast 20mg BID22.0
Apremilast 30 mg BID36.2
Placebo-Apremilast 20mg BID37.0
Placebo-Apremilast 30 mg BID33.3

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Extension Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 32

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 32 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionpercentage of participants (Number)
Apremilast 10mg BID10.6
Apremilast 20mg BID14.0
Apremilast 30 mg BID19.0
Placebo-Apremilast 20mg BID18.5
Placebo-Apremilast 30 mg BID25.9

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Extension Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 40

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 40 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionpercentage of participants (Number)
Apremilast 10mg BID8.5
Apremilast 20mg BID14.0
Apremilast 30 mg BID17.2
Placebo-Apremilast 20mg BID18.5
Placebo-Apremilast 30 mg BID22.2

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Extension Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 52

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 52 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionpercentage of participants (Number)
Apremilast 10mg BID4.3
Apremilast 20mg BID10.0
Apremilast 30 mg BID13.8
Placebo-Apremilast 20mg BID14.8
Placebo-Apremilast 30 mg BID11.1

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Extension Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 32

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease. (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionpercentage of participants (Number)
Apremilast 10mg BID23.4
Apremilast 20mg BID26
Apremilast 30 mg BID44.8
Placebo-Apremilast 20mg BID33.3
Placebo-Apremilast 30 mg BID59.3

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Extension Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 40

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less disease. (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionpercentage of participants (Number)
Apremilast 10mg BID23.4
Apremilast 20mg BID18.0
Apremilast 30 mg BID29.3
Placebo-Apremilast 20mg BID29.6
Placebo-Apremilast 30 mg BID37.0

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Extension Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 52

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease. (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionpercentage of participants (Number)
Apremilast 10mg BID12.8
Apremilast 20mg BID10.0
Apremilast 30 mg BID22.4
Placebo-Apremilast 20mg BID33.3
Placebo-Apremilast 30 mg BID22.2

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Core Study: Percent Change From Baseline in PASI Score at Week 16

The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score. (NCT00773734)
Timeframe: Week 0 to Week 16

InterventionPercent change (Least Squares Mean)
Placebo BID-20.3
Apremilast 10mg BID-34.0
Apremilast 20mg BID-45.4
Apremilast 30 mg BID-53.2

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Core Study: Percent Change From Baseline in the Percent of Affected Body Surface Area (BSA) During the Active Treatment Phase at Week 24

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionpercent change (Mean)
Apremilast 10mg BID-28.1
Apremilast 20mg BID-40.6
Apremilast 30 mg BID-54.0
Placebo-Apremilast 20 mg BID-52.5
Placebo-Apremilast 30 mg BID-54.2

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Core Study: Percent Change From Baseline in the Percent of Affected Body Surface Area (BSA) During the Placebo Controlled Phase

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Week 16

Interventionpercent change (Least Squares Mean)
Placebo BID-8.0
Apremilast 10mg BID-28.3
Apremilast 20mg BID-38.0
Apremilast 30 mg BID-50.4

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Core Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in PASI Score at Week 16

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score at Week 16. The improvement in PASI score was used as a measure of efficacy The PASI score was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 16

Interventionpercentage of participants (Number)
Placebo BID25.0
Apremilast 10mg BID38.2
Apremilast 20mg BID47.1
Apremilast 30 mg BID60.2

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Core Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 24

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score at Week 24. The improvement in PASI score was used as a measure of efficacy. The PASI score was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID38.2
Apremilast 20mg49.4
Apremilast 30 mg BID65.9
Placebo-Apremilast 20mg BID61.8
PBO-Apremilast 30 mg BID75.0

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Core Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in PASI Score at Week 24

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score at Week 24. The improvement in PASI score was used as a measure of efficacy.The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head,trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID18.0
Apremilast 20mg BID26.4
Apremilast 30 mg BID39.8
PBO-Apremilast 20mg BID41.2
PBO-Apremilast 30 mg BID44.4

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Core Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in Psoriasis Area and Severity Index (PASI) at Week 16

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score at Week 16. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 and Week 16

Interventionpercentage of participants (Number)
Placebo BID5.7
Apremilast 10mg BID11.2
Apremilast 20mg BID28.7
Apremilast 30 mg BID40.9

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Core Study: Percentage of Participants Who Achieved a 90% Improvement (Response) From Baseline in the PASI Score at Week 16

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 16. The improvement in PASI score was used as a measure of efficacy. The PASI score was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 16

Interventionpercentage of participants (Number)
Placebo BID1.1
Apremilast 10mg BID4.5
Apremilast 20mg BID9.2
Apremilast 30 mg BID11.4

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Core Study: Percentage of Participants Who Achieved a 90% Improvement (Response) in the PASI Score at Week 24

PASI-90 response is the percentage of participants who achieved at least a 90% reduction (improvement) from baseline in PASI score at Week 24. The improvement in PASI score was used as a measure of efficacy..The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionpercentage of participants (Number)
Apremilast 10mg4.5
Apremilast 20mg8.0
Apremilast 30 mg14.8
PBO-Apremilast 20mg BID14.7
Placebo-Apremilast 30 mg BID16.7

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Core Study: Percentage of Participants Who Achieved a Static Physician Global Assessment (sPGA) Score of 0 or 1 at Week 24

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease (NCT00773734)
Timeframe: Week 0 and Week 24

Interventionpercentage of participants (Number)
Apremilast 10mg BID13.5
Apremilast 20mg BID24.1
Apremilast 30 mg BID34.1
Placebo-Apremilast 20 mg BID41.2
Placebo-Apremilast 30 mg BID50.0

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Core Study: Percentage of Participants With a Static Physician Global Assessment (sPGA) Greater Than 2 at Baseline Who Achieved a Score of 0 or 1 at Week 16

The sPGA was a measure of psoriasis disease severity at the time of evaluation by the investigator. It does not compare assessments across visits or rely on investigator recall of prior disease severity. The sPGA was a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examined all of the lesions on the participant and assigned a score ranging from 0 to 5 for thickness, erythema and degree of scaling . Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equaled the overall sPGA score. Fractional values for the sPGA were rounded to the next highest integer (eg, a score of 3.5 was rounded to 4, 3.4 was rounded to 3). A lower sPGA score was associated with less severe disease (NCT00773734)
Timeframe: Week 0 to Week 16

Interventionpercentage of participants (Number)
Placebo12.6
Apremilast 10mg10.5
Apremilast 20mg25.0
Apremilast 30 mg33.7

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Core Study: Time to Achieve a PASI-50 Response During the Placebo Controlled Phase

For PASI-50 responders in the placebo-controlled period weeks 0-16, time to achieve PASI-50 was defined as the time interval, inclusive between the date of randomization (day 1) and the date of the first assessment where PASI-50 was achieved. (NCT00773734)
Timeframe: Week 0 to 16

Interventionweeks (Median)
Placebo BID6.5
Apremilast 10mg BID5.9
Apremilast 20mg BID6.0
Apremilast 30 mg BID4.3

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Core Study: Time to Achieve a PASI-75 Response During the Placebo Controlled Phase

For PASI-75 responders in the placebo-controlled period Weeks 0-16, time to achieve PASI-75 was defined as the time interval, inclusive between the date of randomization (day 1) and the date of the first assessment where PASI-75 is achieved. (NCT00773734)
Timeframe: Weeks 0 to 16

Interventionweeks (Median)
Placebo BID8.1
Apremilast 10mg BID10.0
Apremilast 20mg BID11.9
Apremilast 30 mg BID6.3

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Core Study: Time to Maximum Plasma Concentration of Drug (Tmax)

Time to achieve maximum plasma concentration (Cmax) observed at Week 14 (Time to achieve steady-state Tmax) (NCT00773734)
Timeframe: Week 14; Predose, 0.5, 1, 2, 3, 4, and 8 hours after the morning dose of apremilast

Interventionhours (Median)
Apremilast 10mg BID2.00
Apremilast 20mg BID2.00
Apremilast 30 mg BID1.00

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Extension Study: Change From Baseline in Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score at Week 40

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionunits on a scale (Mean)
Apremilast 10mg BID-0.2
Apremilast 20mg BID1.6
Apremilast 30 mg BID1.7
Placebo-Apremilast 20mg BID3.2
Placebo-Apremilast 30 mg BID1.8

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Core Study: Time to Maximum Plasma Concentration of Drug (Tmax)

Time to achieve maximum plasma concentration (tmax) observed at Week 24 (Time to achieve steady-state Tmax) (NCT00773734)
Timeframe: Week 24

Interventionhours (Median)
Apremilast 10mg BID1.00
Apremilast 20mg BID1.50
Apremilast 30 mg BID1.00

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Extension Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 32

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionunits on a scale (Mean)
Apremilast 10mg BID-6.5
Apremilast 20mg BID-7.5
Apremilast 30 mg BID-6.0
Placebo-Apremilast 20mg BID-8.1
Placebo-Apremilast 30 mg BID5.5

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Extension Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 40

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionunits on a scale (Mean)
Apremilast 10mg BID-5.5
Apremilast 20mg BID-6.6
Apremilast 30 mg BID-6.4
Placebo-Apremilast 20mg BID-7.1
Placebo-Apremilast 30 mg BID-5.9

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Extension Study: Change From Baseline in Dermatology Life Quality Index (DLQI) at Week 52

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionunits on a scale (Mean)
Apremilast 10mg BID-5.8
Apremilast 20mg BID-6.1
Apremilast 30 mg BID-5.6
Placebo-Apremilast 20mg BID-6.8
Placebo-Apremilast 30 mg BID-4.9

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Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Mental Component Summary Score at Week 32

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionunits on a scale (Mean)
Apremilast 10mg BID5.2
Apremilast 20mg BID3.8
Apremilast 30 mg BID2.9
Placebo-Apremilast 20mg BID4.6
Placebo-Apremilast 30 mg BID2.8

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Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Mental Component Summary Score at Week 40

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionunits on a scale (Mean)
Apremilast 10mg BID5.4
Apremilast 20mg BID4.8
Apremilast 30 mg BID1.7
Placebo-Apremilast 20mg BID2.9
Placebo-Apremilast 30 mg BID3.8

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Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Mental Component Summary Score at Week 52

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionunits on a scale (Mean)
Apremilast 10mg BID5.1
Apremilast 20mg BID4.1
Apremilast 30 mg BID2.4
Placebo-Apremilast 20mg BID4.7
Placebo-Apremilast 30 mg BID3.4

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Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score (PCS) at Week 32

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value. (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionunits on a scale (Mean)
Apremilast 10mg BID1.4
Apremilast 20mg BID2.6
Apremilast 30 mg BID1.8
Placebo-Apremilast 20mg BID3.1
Placebo-Apremilast 30 mg BID1.5

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Extension Study: Change From Baseline in the Medical Outcome Study Short Form,SF-36, Version 2; Physical Component Summary Score at Week 52

The SF-36 was a 36-item general health status instrument and consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better health. Two overall summary scores were obtained - a Physical Component Summary score (PCS) and a Mental Component Summary score (MCS). Scores from the 8 scales, PCS and MCS were transformed to the norm-based scores using weights from U.S. general population, with 50 as the average and 10 as the standard deviation, higher scores indicating better health. For norm based scores, change from baseline were calculated for the 8 scales and the two summary scales, where change = visit value - baseline value.. (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionunits on a scale (Mean)
Apremilast 10mg BID1.2
Apremilast 20mg BID1.2
Apremilast 30 mg BID2.0
Placebo-Apremilast 20mg BID3.4
Placebo-Apremilast 30 mg BID0.3

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Extension Study: Percent Change From Baseline in the Affected BSA at Week 32

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionpercent change (Mean)
Apremilast 10mg BID-47.1
Apremilast 20mg BID-65.1
Apremilast 30 mg BID-75.3
Placebo-Apremilast 20mg BID-62.6
Placebo-Apremilast 30 mg BID-66.7

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Extension Study: Percent Change From Baseline in the Affected BSA at Week 40

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionpercent change (Mean)
Apremilast 10mg BID-55.4
Apremilast 20mg BID-65.4
Apremilast 30 mg BID-74.3
Placebo-Apremilast 20mg BID-66.2
Placebo-Apremilast 30 mg BID-68.0

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Extension Study: Percent Change From Baseline in the Affected BSA at Week 52

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionpercent change (Mean)
Apremilast 10mg BID-53.1
Apremilast 20mg BID-58.3
Apremilast 30 mg BID-67.3
Placebo-Apremilast 20mg BID-67.4
Placebo-Apremilast 30 mg BID-64.9

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Extension Study: Percent Change in PASI Score at Week 32

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionpercent change (Mean)
Apremilast 10mg BID-51.0
Apremilast 20mg BID-63.1
Apremilast 30 mg BID-72.7
Placebo-Apremilast 20mg BID-64.0
Placebo-Apremilast 30 mg BID-69.2

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Extension Study: Percent Change in PASI Score at Week 40

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionpercent change (Mean)
Apremilast 10mg BID-55.9
Apremilast 20mg BID-63.3
Apremilast 30 mg BID-71.1
Placebo-Apremilast 20mg BID-64.5
Placebo-Apremilast 30 mg BID-71.7

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Extension Study: Percent Change in PASI Score at Week 52

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionpercent change (Mean)
Apremilast 10mg BID-55.1
Apremilast 20mg BID-58.9
Apremilast 30 mg BID-65.3
Placebo-Apremilast 20mg BID-62.7
Placebo-Apremilast 30 mg BID-62.0

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Extension Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 32

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score at Week 32 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 32

Interventionpercentage of participants (Number)
Apremilast 10mg BID57.4
Apremilast 20mg BID72.0
Apremilast 30 mg BID86.2
Placebo-Apremilast 20mg BID74.1
Placebo-Apremilast 30 mg BID74.1

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Extension Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 40

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score at Week 16 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 40

Interventionpercentage of participants (Number)
Apremilast 10mg BID48.9
Apremilast 20mg BID62.0
Apremilast 30 mg BID82.8
Placebo-Apremilast 20mg BID63.0
Placebo-Apremilast 30 mg BID66.7

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Extension Study: Percentage of Participants Who Achieved a 50% Improvement (Response) in the PASI Score at Week 52

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score at Week 52 of the extension study. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Week 52

Interventionpercentage of participants (Number)
Apremilast 10mg BID42.6
Apremilast 20mg BID48.0
Apremilast 30 mg BID72.4
Placebo-Apremilast 20mg BID55.6
Placebo-Apremilast 30 mg BID48.1

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LTE Study: Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at 18 Months

The DLQI was a validated, self-administered, 10-item questionnaire that measures the impact of skin disease on subjects' quality of life, based on recall over the past week. Domains include symptoms, feelings, daily activities, social, leisure, work or studying, personal relationships and treatment. Each question on the extent of the impact of skin disease was answered on a scale of 0 (not at all) to 3 (very much); the total DLQI score ranged from 0 to 30. A DLQI score greater than 10 is indicative of severe psoriasis. (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionunits on a scale (Mean)
Apremilast 20mg BID-6.5

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LTE Study: Percentage of Participants Who Achieved a 75% Improvement (Response) in the PASI Score at 4 Years

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). (NCT00773734)
Timeframe: Week 0 to Month 48

Interventionpercentage of participants (Number)
Apremilast 10mg BID40.0
Placebo-Apremilast 20mg BID0.0
Apremilast 20mg BID0
Placebo-Apremilast 30 mg BID25.0
Apremilast 30 mg BID30.0

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Core Study: Percent Change From Baseline in PASI Score at Week 24

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling were scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions was scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The total qualitative score (sum of erythema, thickness, and scaling scores) was multiplied by the degree of involvement for each anatomic region and then multiplied by a constant. The values for each anatomic region were summed to yield the PASI score (NCT00773734)
Timeframe: Week 0 to Week 24

Interventionpercent change (Mean)
Apremilast 10mg BID-36.3
Apremilast 20mg BID-46.5
Apremilast 30 mg BID-56.8
PBO-Apremilast 20mg BID-61.7
PBO-Apremilast 30 mg BID-61.7

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LTE Study: Median Percent Change From Baseline in the Affected Body Surface Area (BSA) at 18 Months

"The overall BSA affected by psoriasis was estimated by comparison of the size of the affected area to the palm area of the participant's hand (entire palmar surface or handprint), which equates to approximately 1% of total BSA." (NCT00773734)
Timeframe: Week 0 to Month 18

Interventionpercent change (Median)
Apremilast 10mg BID-78.6
Placebo-Apremilast 20 mg BID-73.9
Apremilast 20mg BID-73.3
Placebo-Apremilast 30 mg BID-49.2
Apremilast 30 mg BID-86.4

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One Year Overall Survival

One year overall survival estimated using the product-limit method of Kaplan and Meier. Defined as the percentage of patients alive at year one after starting treatment. (NCT00792142)
Timeframe: From date of treatment initiation until death from any cause, assessed up to one year.

Interventionpercentage of participants (Number)
Treatment (Stem Cell Transplant, Maintenance Treatment)95

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One Year Progression-free Survival (PFS)

"PFS estimated using the product-limit method of Kaplan and Meier. Defined as the percentage of patients progression-free at year one after starting treatment.~International Myeloma Working Group uniform response criteria for disease progression:~Increase of > 25% from baseline in Serum M-component and/or (the absolute increase must be > 0.5 g/dl); Urine M-component and/or (the absolute increase must be > 200 mg/24 h; Only in patients without measurable serum and urine M-protein levels:~the difference between involved and uninvolved FLC levels. The absolute increase must be >l0mg/dl.~Bone marrow plasma cell percentage: the absolute % must be > 10%C; Definite development of new bone lesions or soft tissue plasmacytomas.~or definite increase in the size of existing bone lesions or soft tissue plasmacytomas Development of hypercalcemia (corrected serum calcium >11.5 mg/dl or 2.65 mmol/l) that can be attributed solely to the plasma cell proliferative disorder." (NCT00792142)
Timeframe: From start of treatment initiation until disease progression, relapse or death from any cause, assessed up to 1 year.

Interventionpercentage of participants (Number)
Treatment (Stem Cell Transplant, Maintenance Treatment)88

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Number of Participants With Adverse Events

All grade 3 and above treatment-related adverse events (AEs) during bortezomib/dexamethasone treatment cycles. (NCT00792142)
Timeframe: After 4 months of maintenance therapy

InterventionParticipants (Count of Participants)
LeukopeniaLymphopeniaNeutropeniaThrombocytopeniaCataractFatigueUpper respiratory infectionAnxietyPain in extremitySinus bradycardiaHyperglycemiaHypophosphatemia
Treatment (Stem Cell Transplant, Maintenance Treatment)1132112111143

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Number of Patients Achieving an Improvement (Decrease) in IGA (Investigator Global Assessment) by Two or More Points

Improvement in IGA (Investigator Global Assessment) by two or more points on a five point scale, with 0 being no disease activity and 5 being maximum disease activity, at week 12 (NCT00931242)
Timeframe: 12 weeks

Interventionparticipants (Number)
Apremilast2

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Number of Patients Achieving 50% Reduction in Eczema Area and Severity Index (EASI) Score at Week 12 in Reference to Week 0

EASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, edema, lichenification, and excoriations/erosions are scored on a scale of 0 (none) to 3 (severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 to 6. The total qualitative score is multiplied by the degree of involvement for each anatomic region and then multiplied by a constant and summed to yield the EASI score. (NCT00931242)
Timeframe: 12 weeks

Interventionparticipants (Number)
Apremilast2

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Number of Patients Achieving 75% Reduction in Eczema Area and Severity Index (EASI) Score at Week 12 in Reference to Week 0

EASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, edema, lichenification, and excoriations/erosions are scored on a scale of 0 (none) to 3 (severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 to 6. The total qualitative score is multiplied by the degree of involvement for each anatomic region and then multiplied by a constant and summed to yield the EASI score. (NCT00931242)
Timeframe: 12 weeks

Interventionparticipants (Number)
Apremilast1

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Number of Participants With Best Overall Response

Primary endpoint is best overall response. An evaluable subject classified as a treatment success for the primary endpoint if the subject's best overall response is clinical improvement (CI) as determined by International Working Group Criteria over the first 6 cycles of study treatment. International Working Group (IWG) consensus criteria for treatment response in myelofibrosis - Clinical improvement (CI) in anemia 1/ A minimum 20g/L increase in hemoglobin level or 2. becoming transfusion independent for at least 8 week duration. (NCT00946270)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Group 1 CC-40470
Group 23
Group 3 CC-4047 + Prednisone6

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Change From Baseline in Total Transfused Red Cell Requirements at 12 Months

Change of total transfused red cell requirements at 12 months after randomization from one year before baseline in transfusion dependent patients (NCT00964496)
Timeframe: baseline and 12 months

Interventionmilliliter (Mean)
Thalidomide Group-1585.71
Iron-controlled Group-28.57

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Participants Dependent on Blood Transfusions

Numbers of participants dependent on blood transfusions (NCT00964496)
Timeframe: 52 months

Interventionparticipants (Number)
Thalidomide Group3
Iron-controlled Group13

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Participants Whose Rebleeds Decreased From Baseline by ≥ 50% at 12 Months

The primary end point was defined as the patients whose rebleeds decreased from baseline by ≥ 50% at 12 months. Reduction of rebleeds = [(total bleeding episode at 12 months - total bleeding episodes at a year before randomization)/total bleeding episodes at a year before randomization(baseline)]*100%. Rebleeding was defined based on a positive fecal occult blood test (FOBT) (monoclonal colloidal gold color technology) at any visit after treatment. (NCT00964496)
Timeframe: baseline and 12 months

Interventionparticipants (Number)
Thalidomide Group20
Iron-controlled Group1

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Cessation of Bleeding

The cessation of bleeding was defined as repeated negative faecal occult blood test (FOBT) (monoclonal colloidal gold color technology) during our observation period. Rebleeding was defined based on a positive FOBT at any visit after treatment. (NCT00964496)
Timeframe: 52 months

Interventionparticipants (Number)
Thalidomide Group13
Iron-controlled Group0

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Change From Baseline in Bleeding Duration at 12 Months

The change from baseline in bleeding duration at 12 months (NCT00964496)
Timeframe: baseline and 12 months

Interventiondays (Mean)
Thalidomide Group5.2
Iron-controlled Group0.8

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Change From Baseline in Bleeding Episodes at 12 Months

The Change from baseline in bleeding episodes at 12 months (NCT00964496)
Timeframe: baseline and 12 months

Interventionbleeding episodes (Mean)
Thalidomide Group-9.36
Iron-controlled Group1.41

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Change From Baseline in Hemoglobin (Hb) Level at 12 Months

The change from baseline in average hemoglobin (Hb) level(tested every month) at 12 months. (NCT00964496)
Timeframe: baseline and 12 months

Interventiong/L (Mean)
Thalidomide Group3.06
Iron-controlled Group-0.01

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Progression Free Survival

Estimated using the method of Kaplan and Meier. Comparison of time-to-event endpoints by important subgroups was made using the log-rank test. Cox proportional hazard regression will be employed for multivariate analysis on time-to-event outcomes. (NCT00966693)
Timeframe: Up to 9 years

InterventionMonths (Mean)
RTD (Cohort 1, Phase 1)32.74
RTD (Cohort 2, Phase 1)9.04
RTD (Cohort 3, Phase 1)14.61
RTD (Cohort 2, Phase 2)10.02

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Number of Participants With Dose Limitations Toxicities of the Combination of Lenalidomide and Thalidomide and Dexamethasone (LTD) in Patients With Relapsed/Refractory Multiple Myeloma (RRMM)

To determine the dose limitations toxicities of the combination of lenalidomide and thalidomide and dexamethasone (LTD) in patients with relapsed/refractory multiple myeloma (RRMM). (NCT00966693)
Timeframe: After one 28-day cycle

InterventionParticipants (Count of Participants)
RTD (Cohort 1, Phase 1)1
RTD (Cohort 2, Phase 1)0
RTD (Cohort 3, Phase 1)3
RTD (Cohort 2, Phase 2)0

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Incidence of Adverse Events

Linear regression was utilized to assess the effect of patient prognostic factors on the toxicity rate. (NCT00966693)
Timeframe: Up to 9 years

InterventionParticipants (Count of Participants)
RTD (Cohort 1, Phase 1)0
RTD (Cohort 2, Phase 1)0
RTD (Cohort 3, Phase 1)2
RTD (Cohort 2, Phase 2)10

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Time to Best Response

Estimated using the method of Kaplan and Meier. Comparison of time-to-event endpoints by important subgroups was made using the log-rank test. Cox proportional hazard regression will be employed for multivariate analysis on time-to-event outcomes. (NCT00966693)
Timeframe: Up to 9 years

Interventionmonths (Mean)
RTD (Cohort 1, Phase 1)19
RTD (Cohort 2, Phase 1)5
RTD (Cohort 3, Phase 1)5.16
RTD (Cohort 2, Phase 2)3.3

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Time to Progression

Time to Progression was estimated using Kaplan Meier analysis. (NCT00966693)
Timeframe: Up to 9 years

InterventionMonths (Mean)
RTD (Cohort 1, Phase 1)32.74
RTD (Cohort 2, Phase 1)9.04
RTD (Cohort 3, Phase 1)14.61
RTD (Cohort 2, Phase 2)10.02

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Complete Response(CR) and Very Good Partial Response(VGPR)

To determine the best overall response (CR+VGPR+PR) of the lenalidomide, thalidomide, dexamethasone combination based on IMWG criteria at nadir. (NCT00966693)
Timeframe: Evaluated each 28-day cycle and nadir of criteria is considered best overall response (median time to best response for this study was 2 cycles (range for best overall response was 1-21 cycles).

,,,
InterventionParticipants (Count of Participants)
Partial RemissionProgressive DiseaseVery Good Partial RemissionMinimal Residual DiseaseStringent Complete RemissionNon EvaluableStable Disease
RTD (Cohort 1, Phase 1)2000010
RTD (Cohort 2, Phase 1)0230000
RTD (Cohort 2, Phase 2)13689377
RTD (Cohort 3, Phase 1)2211030

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Time to Treatment Failure

The time from the date of registration to the date at which the patient is removed from treatment due to progression, adverse events, or refusal. If the patient is considered to be a major treatment violation or is taken off study as a non-protocol failure, the patient will be censored on the date they were removed from treatment. The distribution of time to treatment failure will be estimated using the method of Kaplan-Meier (NCT01057225)
Timeframe: From baseline to end of active treatment

Interventionmonths (Number)
Arm INA

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Survival Time (Phase II)

Survival time is defined as the time from registration to death due to any cause. The distribution of survival time will be estimated using the method of Kaplan-Meier (NCT01057225)
Timeframe: From baseline to death

Interventionmonths (Median)
All Treated PatientsNA

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Stem Cell Collection and Engraftment (Phase II)

For patients going on to stem cell collection, the total number of CD34 positive cells collected per collection, days to platelets over 20,000 without transfusion and ANC over 1000 will be recorded. If a patient fails to collect adequate stem cells for transplant, this will be recorded as such. The number of patients with successful stem cell mobilization are reported. (NCT01057225)
Timeframe: Following the first 4 courses of treatment

Interventionparticipants (Number)
All Treated Patients42

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Progression-free Survival (Phase II)

"PFS was defined as the time from registration to progression or death due to any cause. Progression was defined as any one or more of the following:~• Increase of 25% from lowest confirmed response in: Serum M-component (absolute increase must be ≥ 0.5 g/dl)c Urine M-component (absolute increase must be ≥ 200 mg/24 hour) If at on study, only the measurable non-bone marrow parameter was FLC, the difference between involved and uninvolved FLC levels (absolute increase must be >10 mg/dl) Bone marrow plasma cell percentage (absolute % must be 10%)d Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas~• Development of hypercalcemia (corrected serum calcium >11.5 mg/dl) that can be attributed solely to the plasma cell proliferative disorder" (NCT01057225)
Timeframe: From baseline to progression or death up to 3 years

Interventionmonths (Number)
Arm INA

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Progression Free Survival (12 Month)

Progression-free survival time is defined as the time from registration to the earliest date of documentation of disease progression. If a patient dies without a documentation of disease progression the patient will be considered to have had disease progression at the time of their death. If the patient is declared to be a major treatment violation, the patient will be censored on the date the treatment violation was declared to have occurred. In the case of a patient starting treatment and then never returning for any evaluations, the patient will be censored for progression 1 day post-registration. This is reported as the percentage of patients alive and progression free at the 12 month mark. (NCT01057225)
Timeframe: 12 months

Interventionpercentage of participants at 12 months (Number)
All Treated Patients85

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Progession Free Survival (24 Month)

Progression-free survival time is defined as the time from registration to the earliest date of documentation of disease progression. If a patient dies without a documentation of disease progression the patient will be considered to have had disease progression at the time of their death. If the patient is declared to be a major treatment violation, the patient will be censored on the date the treatment violation was declared to have occurred. In the case of a patient starting treatment and then never returning for any evaluations, the patient will be censored for progression 1 day post-registration. This is reported as the percentage of patients alive and progression free at the 24 month mark. (NCT01057225)
Timeframe: 24 months

Interventionpercentage of participants at 24 months (Number)
All Treated Patients76

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Overall Survival (24 Month)

24 Month Overall survival is defined as the proportion of patients to still be alive after 24 months. (NCT01057225)
Timeframe: From baseline to death

Interventionpercentage of patients (Number)
All Treated Patients96

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Overall Survival (12 Month)

12 Month Overall survival is defined as the proportion of patients to still be alive after 12 months. (NCT01057225)
Timeframe: From baseline to death

Interventionpercentage of patients (Number)
All Treated Patients96

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Maximum Tolerated Dose (Phase I)

"To establish the maximum tolerated dose of carfilzomib given in combination with oral cyclophosphamide and thalidomide and dexamethasone.~For this protocol, dose-limiting toxicity (DLT) will be defined as an adverse event attributed (definitely, probably, possibly) in the first or second cycle for patients enrolled to Dose Levels -1 and 0 and in the first cycle only for patients enrolled to Dose Levels 1 and 2.~We are reporting the number of DLTs" (NCT01057225)
Timeframe: From baseline to end of active treatment, up to 12 28-day cycles.

Interventionparticipants (Number)
Phase I: Dose Level -10
Phase I: Dose Level 00
Phase I: Dose Level 10
Phase I: Dose Level 23

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Complete Response (Phase II)

In patients continuing beyond 4 cycles the ability to induce complete response will be evaluated at completion of planned therapy. (NCT01057225)
Timeframe: Following the first 4 courses of treatment

Interventionparticipants (Number)
Dose Level -10
Dose Level 02
Dose Level 13
Dose Level 20

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Percentage of Patients Who Have at Least a Confirmed Very Good Partial Response (Phase II)

"The proportion of patients who have at least a confirmed very good partial response will be calculated by taking the number of patients with a very good partial response or a complete response divided by the total number of patients.~A complete response is defined as:~Negative immunofixation of the serum and urine~If at on study, only the measurable non-bone marrow parameter was FLC, normalization of FLC ratio~< 5% plasma cells in bone marrow~Disappearance of any soft tissue plasmacytomas~A very good partial response is defined as:~Serum and urine M-component detectable by immunofixation but not on electrophoresis or~If at on study, serum measurable, ≥ 90% or greater reduction in serum Mcomponent~Urine M-component <100 mg per 24 hour" (NCT01057225)
Timeframe: Following the first 4 cycles of treatment (28 day cycles)

Interventionpercentage of participants (Number)
Arm I91

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Change From Baseline in the Mean Number of Daily Seizures at 1 Year.

(NCT01061866)
Timeframe: Baseline 3 months and 1 year of treatment

InterventionNumber of Seizures (Mean)
Thalidomide9

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Duration of Response

Measured from end of treatment to progression or death, measured in months. (NCT01125176)
Timeframe: From date of end of treatment to progression or death, whichever occurs first, assessed through study completion up to 100 months.

Interventionmonths (Median)
All Subjects70

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Time to Response

Measured from time of study drug administration to initial response (partial or complete), measured in months. (NCT01125176)
Timeframe: From date of study drug initiation to date of initial response, assessed up to 12 months.

Interventionmonths (Median)
All Subjects10

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Progression Free Survival

Measured from time of study drug administration to progression or death, measured in months. (NCT01125176)
Timeframe: From date of study drug initiation until date of progression or death, whichever occurs first, assessed through study completion up to 100 months.

Interventionmonths (Median)
All Subjects48

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Overall Survival

Measured from time of study drug administration to death, measured in months. (NCT01125176)
Timeframe: From date of study drug initiation to date of death, assessed through study completion up to 105 months.

Interventionmonths (Median)
All Subjects97

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Overall Response Rate as Defined as the Number of Patients Who Experience a Response (Complete or Partial) to Treatment at the Time of Best Response

Response will be evaluated in this study using the International Workshop on CLL (IWCLL) update of the 1996 NCI-Working Group criteria for CLL, which includes assessment of the following: clonal lymphocytes in the peripheral blood by flow cytometry, blood tests for neutrophil count, hemoglobin, and platelet count, CT examination for lymphadenopathy, hepatomegaly, splenomegaly, constitutional symptoms, bone marrow assessment via biopsy/aspirate, and evaluation for disease transformation. (NCT01125176)
Timeframe: From date of study drug initiation until date of best response, assessed up to 6 years.

InterventionParticipants (Count of Participants)
All Subjects12

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Percentage of Participants With a ACR 70 Response at Week 24

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and week 24

Interventionpercentage of participants (Number)
Placebo0.6
Apremilast 20 mg5.4
Apremilast 30 mg10.1

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Percentage of Participants With a Modified PsARC Response at Week 52

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from Baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from Baseline by ≥ 20 mm VAS. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg73.8
Placebo / Apremilast 30 mg71.2
Apremilast 20 mg77.5
Apremilast 30 mg73.6

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from Baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from Baseline by ≥ 20 mm VAS. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo29.8
Apremilast 20 mg38.7
Apremilast 30 mg46.4

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: •78 tender joint count, •76 swollen joint count, •Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; •Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo18.5
Apremilast 20 mg31.0
Apremilast 30 mg42.9

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Percentage of Participants With an ACR 20 Response at Week 24

Percentage of participants with an American College of Rheumatology 20% (ACR20) response at Week 24. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo13.1
Apremilast 20 mg25.6
Apremilast 30 mg35.1

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Percentage of Participants With an ACR 50 Response at Week 24

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo4.2
Apremilast 20 mg14.3
Apremilast 30 mg19.0

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Percentage of Participants With an ACR 50 Response at Week 52

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg25.4
Placebo / Apremilast 30 mg27.9
Apremilast 20 mg24.8
Apremilast 30 mg24.6

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Percentage of Participants With an ACR 70 Response at Week 16

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo1.2
Apremilast 20 mg6.0
Apremilast 30 mg4.2

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Percentage of Participants With an ACR 70 Response at Week 52

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg4.8
Placebo / Apremilast 30 mg14.8
Apremilast 20 mg15.4
Apremilast 30 mg13.8

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Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo19.0
Apremilast 20 mg30.4
Apremilast 30 mg38.1

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo57.4
Apremilast 20 mg66.1
Apremilast 30 mg60.3

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo60.3
Apremilast 20 mg69.5
Apremilast 30 mg69.1

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg65.2
Placebo / Apremilast 30 mg73.1
Apremilast 20 mg85.4
Apremilast 30 mg77.6

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Percentage of Participants With Good or Moderate EULAR Response at Week 24

EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo16.1
Apremilast 20 mg30.4
Apremilast 30 mg42.3

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Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16

A EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo29.8
Apremilast 20 mg46.4
Apremilast 30 mg48.8

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Percentage of Participants With MASES Improvement ≥ 20% at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo49.0
Apremilast 20 mg56.3
Apremilast 30 mg52.6

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Percentage of Participants With MASES Improvement ≥ 20% at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo46.9
Apremilast 20 mg58.3
Apremilast 30 mg60.5

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Percentage of Participants With MASES Improvement ≥ 20% at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 52 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg69.4
Placebo / Apremilast 30 mg55.6
Apremilast 20 mg84.1
Apremilast 30 mg75.3

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Number of Participants With Adverse Events During the Apremilast-Exposure Period

A TEAE is an AE with a start date on or after the date of the first dose of Investigational Product (IP) and no later than 28 days after the last dose of IP. An AE is any noxious, unintended, or untoward medical occurrence, that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly or birth defect, or a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. (NCT01172938)
Timeframe: Baseline to Week 260; median total exposure to Apremilast was 170 weeks

,,
Interventionparticipants (Number)
Treatment Emergent Adverse Events (TEAEs)Drug-related TEAESevere TEAESerious TEAE (SAE)Drug-related SAETEAE leading to drug interruptionTEAE leading to drug withdrawalTEAE leading to death
Apremilast 20 mg (Pre-switch)203963541447271
Apremilast 20 mg/30 mg BID (Post-switch)395161300
Apremilast 30 mg BID1311313049949302

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Number of Participants With Adverse Events During the Placebo-Controlled Period

A Treatment Emergent Adverse Event (TEAE) is an AE with a start date on or after the date of the first dose of Investigational Product (IP). An AE is any noxious, unintended, or untoward medical occurrence, that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly or birth defect, or a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. (NCT01172938)
Timeframe: Week 0 to Week 16 for placebo participants who entered early escape at Week 16 and up to Week 24 for all other participants (placebo participants who remained on placebo through week 24 and participants randomized to the APR 20 mg BID or APR 30 mg BID)

,,
Interventionparticipants (Number)
Treatment Emergent Adverse EventsDrug-related TEAESevere TEAESerious TEAE (SAE)Drug-related Serious AE)TEAE leading to drug interruptionTEAE leading to drug withdrawalTEAE leading to drug death
Apremilast 20 mg1015488010101
Apremilast 30 mg10370119317120
Placebo8132672980

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo39.7
Apremilast 20 mg49.2
Apremilast 30 mg45.6

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg52.2
Placebo / Apremilast 30 mg53.8
Apremilast 20 mg68.8
Apremilast 30 mg63.3

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Percentage of Participants Achieving a MASES Score of Zero at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Placebo15.3
Apremilast 20 mg27.2
Apremilast 30 mg22.8

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Percentage of Participants Achieving a MASES Score of Zero at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo14.3
Apremilast 20 mg31.1
Apremilast 30 mg31.6

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Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52

A EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg82.8
Placebo / Apremilast 30 mg70.0
Apremilast 20 mg75.0
Apremilast 30 mg74.4

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Percentage of Participants With a ACR 20 Response at Week 52

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg53.1
Placebo / Apremilast 30 mg50.0
Apremilast 20 mg63.0
Apremilast 30 mg54.6

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Percentage of Participants With a ACR 50 Response at Week 16

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo6.0
Apremilast 20 mg15.5
Apremilast 30 mg16.1

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.8
Apremilast 20 mg-1.6
Apremilast 30 mg-1.6

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.9
Apremilast 20 mg-1.4
Apremilast 30 mg-1.3

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Change From Baseline in Dactylitis Severity Score at Week 24

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-1.3
Apremilast 20 mg-2.0
Apremilast 30 mg-1.8

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Change From Baseline in Dactylitis Severity Score at Week 16

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.4
Apremilast 20 mg-1.9
Apremilast 30 mg-1.7

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-3.14
Apremilast 20 mg-7.55
Apremilast 30 mg-9.52

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0 to 76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-3.84
Apremilast 20 mg-8.24
Apremilast 30 mg-8.72

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Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 16

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.086
Apremilast 20 mg-0.198
Apremilast 30 mg-0.244

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo1.81
Apremilast 20 mg3.50
Apremilast 30 mg4.23

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Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 24

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.076
Apremilast 20 mg-0.211
Apremilast 30 mg-0.258

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Percentage of Participants Achieving a MASES Score of Zero at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01172938)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg33.3
Placebo / Apremilast 30 mg27.8
Apremilast 20 mg50.7
Apremilast 30 mg38.2

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01172938)
Timeframe: Baseline and week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-2.2
Placebo / Apremilast 30 mg-1.9
Apremilast 20 mg-2.7
Apremilast 30 mg-1.9

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Change From Baseline in Patient's Assessment of Pain at Week 16

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01172938)
Timeframe: Baseline and Week 16

Interventionmm (Least Squares Mean)
Placebo-5.7
Apremilast 20 mg-11.5
Apremilast 30 mg-13.5

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Change From Baseline in Patient's Assessment of Pain at Week 24

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01172938)
Timeframe: Baseline and Week 24

Interventionmm (Least Squares Mean)
Placebo-4.2
Apremilast 20 mg-11.2
Apremilast 30 mg-14.7

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Change From Baseline in SF-36 Physical Function at Week 24

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo1.45
Apremilast 20 mg3.49
Apremilast 30 mg5.01

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Change From Baseline in the CDAI Score at Week 52

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-15.00
Placebo / Apremilast 30 mg-14.03
Apremilast 20 mg-15.41
Apremilast 30 mg-14.54

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Change From Baseline in the Dactylitis Severity Score at Week 52

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-0.8
Placebo / Apremilast 30 mg-2.4
Apremilast 20 mg-2.7
Apremilast 30 mg-1.8

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Change From Baseline in the DAS28 at Week 52

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-1.47
Placebo / Apremilast 30 mg-1.15
Apremilast 20 mg-1.40
Apremilast 30 mg-1.31

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Change From Baseline in the Disease Activity Score (DAS28) at Week 16

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the distal interphalangeal (DIP) joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.26
Apremilast 20 mg-0.73
Apremilast 30 mg-0.79

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Change From Baseline in the Disease Activity Score (DAS28) at Week 24

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.20
Apremilast 20 mg-0.66
Apremilast 30 mg-0.90

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Change From Baseline in the FACIT-Fatigue Scale Score at Week 52

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from Baseline score indicates an improvement." (NCT01172938)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg4.33
Placebo / Apremilast 30 mg4.15
Apremilast 20 mg4.27
Apremilast 30 mg3.67

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from Baseline score indicates an improvement." (NCT01172938)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo1.55
Apremilast 20 mg1.68
Apremilast 30 mg3.88

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from Baseline score indicates an improvement." (NCT01172938)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo1.12
Apremilast 20 mg1.52
Apremilast 30 mg3.33

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Change From Baseline in the Patient Assessment of Pain at Week 52

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01172938)
Timeframe: Baseline and Week 52

Interventionmm (Mean)
Placebo / Apremilast 20 mg-20.2
Placebo / Apremilast 30 mg-21.0
Apremilast 20 mg-17.8
Apremilast 30 mg-20.3

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Change From Baseline in the SF-36 Physical Functioning Domain at Week 52

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg4.46
Placebo / Apremilast 30 mg4.62
Apremilast 20 mg6.98
Apremilast 30 mg5.69

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01172938)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Placebo39.7
Apremilast 20 mg42.4
Apremilast 30 mg38.2

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Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01172938)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-0.27
Placebo / Apremilast 30 mg-0.29
Apremilast 20 mg-0.37
Apremilast 30 mg-0.32

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China Extension: Number of Participants Achieving a Hemoglobin Increase of ≥ 15 g/L Compared to Baseline for ≥ 84 Consecutive Days

A response in the China extension study was defined as an increase in hemoglobin ≥ 15 g/L above baseline value (in the absence of RBC transfusion) for ≥ 84 consecutive days. (NCT01178281)
Timeframe: From the first dose of study drug until treatment discontinuation; median treatment duration was 24.0 weeks.

InterventionParticipants (Count of Participants)
China Extension: Pomalidomide 0.5 mg1

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Duration of RBC-Transfusion Independence

The duration of RBC-transfusion independence is the time from the date at which the first RBC-transfusion independence started to the date of another RBC-transfusion given at least 84 days after the time the transfusion independence started. The duration of the RBC-transfusion independence was analyzed using the Kaplan-Meier method. Data were censored at the end of the treatment phase for participants who had not received another RBC-transfusion after the start of transfusion independence by the end of treatment phase. (NCT01178281)
Timeframe: From first dose of study drug up to 28 days after last dose, as of the data cut-off date of 16 Jan 2013; median treatment duration was 23.6 weeks in the pomalidomide arm and 23.9 weeks in the placebo arm.

Interventionmonths (Median)
Pomalidomide 0.5 mgNA
Placebo5.8

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Overall Survival

The time from randomization to the death or to the latest date when participants are known to be alive. Overall survival was analyzed using Kaplan-Meier method; participants who were alive or lost to follow-up were censored at the latest date they were known to be alive. (NCT01178281)
Timeframe: From first dose of study drug up to end of study; median follow-up time was 19.1 months in the pomalidomide 0.5 mg arm and 17.6 months in the placebo arm.

Interventionmonths (Median)
Pomalidomide 0.5 mg24.2
Placebo26.2

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Percentage of Participants Who Achieved RBC-Transfusion Independence

RBC-transfusion independence was defined as the absence of RBC transfusions for any consecutive 84-day interval. (NCT01178281)
Timeframe: 168 days

Interventionpercentage of participants (Number)
Pomalidomide 0.5 mg17.3
Placebo16.7

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Time to RBC-Transfusion Independence

Time to response was measured from first dose of study drug to the start of the first response. The start date of the response was defined as one day after the last date of an RBC-transfusion for participants who received a RBC-transfusion after the first dose, and as the date of the first dose of study drug for participants who received no RBC-transfusions during the 84 days after the first dose of study drug. (NCT01178281)
Timeframe: 168 days

Interventionweeks (Median)
Pomalidomide 0.5 mg6.9
Placebo2.4

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Change From Baseline in EuroQoL-5D (EQ-5D) Health Index Score

"EQ-5D is a standardized, participant-rated questionnaire to assess health-related quality of life. The EQ-5D includes 2 components: the EQ-5D health state profile (descriptive system) and the EQ-5D visual analog scale (VAS). For the health state profile participants rate their perceived health state today on 5 dimensions: mobility, selfcare, usual activities, pain/discomfort, and anxiety/depression on a Likert-type scale from 1 to 3, where 1 = no problems, 2 = some problems, and 3 = extreme problems. The EQ-5D Health Utility Index (HUI) was generated from the five health state domain scores, and ranges from -0.594 (worst) and 1 (best) imaginable health state, with -0.594 representing an unconscious health state." (NCT01178281)
Timeframe: Baseline and Days 85 and 169

,
Interventionscore on a scale (Mean)
Day 85Day 169
Placebo-0.02980.0766
Pomalidomide 0.5 mg-0.0385-0.0202

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Change From Baseline in EuroQoL-5D (EQ-5D) Visual Analog Scale

EQ-5D is a standardized, participant-rated questionnaire to assess health-related quality of life. The EQ-5D includes 2 components: the EQ-5D health state profile (descriptive system) and the EQ-5D visual analog scale (VAS). On the VAS the participant rates his/her health state on a line from 0 (worst imaginable health) to 100 (best imaginable health). (NCT01178281)
Timeframe: Baseline and Days 85 and 169

,
Interventionunits on a scale (Mean)
Day 85Day 169
Placebo-1.40.3
Pomalidomide 0.5 mg2.02.9

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Change From Baseline in Functional Assessment of Cancer Therapy-Anemia (FACT-An) Total Score

The FACT-An is a 47-item, cancer-specific questionnaire consisting of a core 27-item general questionnaire measuring the four general domains of QoL (physical, social/family, emotional and functional well-being), and an additional 20-item anemia questionnaire (FACT-An Anemia subscale) that measures 13 fatigue-associated items (FACT-F Fatigue subscale) and seven non-fatigue-related items. Each item is scored using a 5-point Likert rating scale (0 = Not at all; 1 = A little bit; 2 = Somewhat; 3 = Quite a bit; and 4 = Very much). FACT-An total score is calculated by adding all the FACT-An subscales together. The total score ranges from 0-188 with higher scores representing better QOL. (NCT01178281)
Timeframe: Baseline and Days 85 and 169

,
Interventionunits on a scale (Mean)
Day 85Day 169
Placebo4.311.9
Pomalidomide 0.5 mg-2.16.2

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Number of Participants With Treatment-emergent Adverse Events (TEAE)

A TEAE is an adverse event (AE) that starts on or after the first dose of study drug. The severity of each AE was graded according to the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE),Version 4.0 and according to the following scale: Grade 1 = Mild (transient or mild discomfort; no limitation in activity; no medical intervention/therapy required); Grade 2 = Moderate (mild to moderate limitation in activity, some assistance may be needed; minimal medical intervention/therapy required); Grade 3 = Severe (marked limitation in activity, assistance usually required; medical intervention/therapy required, hospitalization possible); Grade 4 = Life-threatening (extreme limitation in activity, significant assistance or medical intervention/therapy required, hospitalization or hospice care probable); Grade 5 = Death Drug-related (related) AEs are those suspected by the Investigator as being related to administration of study drug (NCT01178281)
Timeframe: From the first dose of study drug until 28 days after last dose; median treatment duration was 23.7 weeks in the pomalidomide arm, 23.9 weeks in the placebo arm, and 24.0 weeks in the China extension pomalidomide arm.

,,
InterventionParticipants (Count of Participants)
Any adverse event (AE)Adverse event suspected as related to study drugAdverse event leading to dose interruptionDrug-related AE leading to dose interruptionAE leading to discontinuation of study drugRelated AE leading to study drug discontinuationGrade 3/4 adverse eventGrade 3/4 AE related to study drugGrade 3/4 AE leading to study drug discontinuationGrade 3/4 AE leading to dose interruptionGrade 5 adverse eventGrade 5 AE related to study drugSerious adverse event (SAE)SAE related to study drugSAE leading to discontinuation of study drugSAE leading to dose interruption
China Extension: Pomalidomide 0.5 mg12321004001000000
Placebo8132176148441391410329787
Pomalidomide 0.5 mg164904826532110045333617176243122

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Percentage of Participants With an ACR 70 Response at Week 52

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg16.9
Placebo / Apremilast 30 mg14.3
Apremilast 20 mg9.8
Apremilast 30 mg6.8

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Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16

Percentage of participants with an ACR20 response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦C-Reactive Protein. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo18.9
Apremilast 20 mg37.4
Apremilast 30 mg32.1

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo59.1
Apremilast 20 mg62.3
Apremilast 30 mg61.6

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo62.1
Apremilast 20 mg68.8
Apremilast 30 mg68.5

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg95.7
Placebo / Apremilast 30 mg88.9
Apremilast 20 mg80.7
Apremilast 30 mg85.0

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Percentage of Participants With Good or Moderate EULAR Response at Week 24

EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo21.4
Apremilast 20 mg41.7
Apremilast 30 mg33.3

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Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16

A EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo31.4
Apremilast 20 mg53.4
Apremilast 30 mg48.8

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Percentage of Participants With MASES Improvement ≥ 20% at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo52.9
Apremilast 20 mg54.2
Apremilast 30 mg56.4

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Percentage of Participants With MASES Improvement ≥ 20% at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo51.0
Apremilast 20 mg57.0
Apremilast 30 mg57.4

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Percentage of Participants With MASES Improvement ≥ 20% at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 52 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg72.5
Placebo / Apremilast 30 mg79.5
Apremilast 20 mg70.0
Apremilast 30 mg69.2

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Number of Participants With Treatment Emergent Adverse Events During the Placebo-Controlled Phase

"A treatment emergent adverse event (TEAE) is an AE with a start date on or after the date of the first dose of Investigational Product (IP). The severity of each adverse event (AE) and serious AE (SAE) was assessed by the investigator and graded based on a scale from Mild - mild symptoms to Severe AEs (non-serious or serious). A serious adverse event (SAE) is any AE which:~Resulted in death~Was life-threatening~Required inpatient hospitalization or prolongation of existing hospitalization~Resulted in persistent or significant disability/incapacity~Was a congenital anomaly/birth defect~Constituted an important medical event" (NCT01212757)
Timeframe: Week 0 to Week 16 for placebo participants who entered EE at Week 16 and up to Week 24 for all other participants (placebo participants who remained on placebo through week 24 and participants randomized to the APR 20 mg BID or APR 30 mg BID)

,,
InterventionParticipants (Number)
Any TEAEAny Drug-Related TEAEAny Severe TEAEAny Serious TEAE (SAE)Any Drug-Related SAEAny TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to Death
Apremilast 20 mg106533631650
Apremilast 30 mg9657114131120
Placebo72285301130

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Number of Participants With TEAEs During the Apremilast-Exposure Period

"A treatment emergent adverse event (TEAE) is an AE with a start date on or after the date of the first dose of Investigational Product (IP). The severity of each adverse event (AE) and serious AE (SAE) was assessed by the investigator and graded based on a scale from Mild - mild symptoms to Severe AEs (non-serious or serious). A serious adverse event (SAE) is any AE which:~Resulted in death~Was life-threatening~Required inpatient hospitalization or prolongation of existing hospitalization~Resulted in persistent or significant disability/incapacity~Was a congenital anomaly/birth defect~Constituted an important medical event" (NCT01212757)
Timeframe: Week 0 to week 260; overall median duration of exposure to apremilast 20 mg and 30 mg BID was 198 weeks

,,
Interventionparticipants (Number)
Any TEAEAny Drug-related TEAEAny Severe TEAEAny Serious TEAEAny Serious Drug-related TEAEAny TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to Death
Apremilast 20 mg (Pre-switch)2021023541647240
Apremilast 20 mg/30 mg (Post-switch)535251430
Apremilast 30 mg BID2071003741665302

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo0.81
Apremilast 20 mg2.17
Apremilast 30 mg2.91

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 24

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo1.44
Apremilast 20 mg2.97
Apremilast 30 mg3.30

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: - 28 tender joint count (TJC), - 28 swollen joint count (SJC), - Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; - Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-3.30
Apremilast 20 mg-7.75
Apremilast 30 mg-6.81

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-3.21
Apremilast 20 mg-7.71
Apremilast 30 mg-6.35

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Change From Baseline in Dactylitis Severity Score at Week 16

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.1
Apremilast 20 mg-0.8
Apremilast 30 mg-1.3

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Change From Baseline in Dactylitis Severity Score at Week 24

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-1.1
Apremilast 20 mg-0.9
Apremilast 30 mg-1.4

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Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-0.208
Placebo / Apremilast 30 mg-0.310
Apremilast 20 mg-0.192
Apremilast 30 mg-0.330

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Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 16

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.053
Apremilast 20 mg-0.157
Apremilast 30 mg-0.193

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Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 24

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.085
Apremilast 20 mg-0.165
Apremilast 30 mg-0.206

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.0
Apremilast 20 mg-0.9
Apremilast 30 mg-1.4

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.9
Apremilast 20 mg-0.9
Apremilast 30 mg-1.3

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-2.5
Placebo / Apremilast 30 mg-2.5
Apremilast 20 mg-1.7
Apremilast 30 mg-2.1

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Change From Baseline in Patient's Assessment of Pain at Week 16

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01212757)
Timeframe: Baseline and Week 16

Interventionmm (Least Squares Mean)
Placebo-7.0
Apremilast 20 mg-12.5
Apremilast 30 mg-11.9

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Change From Baseline in Patient's Assessment of Pain at Week 24

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01212757)
Timeframe: Baseline and Week 24

Interventionmm (Least Squares Mean)
Placebo-8.0
Apremilast 20 mg-11.5
Apremilast 30 mg-9.7

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Change From Baseline in the CDAI Score at Week 52

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-13.66
Placebo / Apremilast 30 mg-13.13
Apremilast 20 mg-12.03
Apremilast 30 mg-14.38

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Change From Baseline in the Dactylitis Severity Score at Week 52

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-1.9
Placebo / Apremilast 30 mg-2.1
Apremilast 20 mg-1.8
Apremilast 30 mg-1.8

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Change From Baseline in the DAS28 at Week 52

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-1.18
Placebo / Apremilast 30 mg-1.18
Apremilast 20 mg-1.11
Apremilast 30 mg-1.30

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Change From Baseline in the Disease Activity Score (DAS28) at Week 16

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: - 28 tender joint count - 28 swollen joint count, which do not include the distal interphalangeal (DIP) joints, the hip joint, or the joints below the knee; - C-reactive protein (CRP) - Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.27
Apremilast 20 mg-0.74
Apremilast 30 mg-0.67

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Change From Baseline in the Disease Activity Score (DAS28) at Week 24

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.27
Apremilast 20 mg-0.73
Apremilast 30 mg-0.65

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Change From Baseline in the FACIT-Fatigue Scale Score at Week 52

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg1.97
Placebo / Apremilast 30 mg4.95
Apremilast 20 mg2.45
Apremilast 30 mg4.38

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01212757)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo0.63
Apremilast 20 mg0.91
Apremilast 30 mg2.75

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01212757)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo0.52
Apremilast 20 mg0.68
Apremilast 30 mg2.65

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Change From Baseline in the Patient Assessment of Pain at Week 52

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01212757)
Timeframe: Baseline and Week 52

Interventionmm (Mean)
Placebo / Apremilast 20 mg-15.6
Placebo / Apremilast 30 mg-16.0
Apremilast 20 mg-13.5
Apremilast 30 mg-12.9

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Change From Baseline in the SF-36 Physical Functioning Scale Score at Week 52

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg4.13
Placebo / Apremilast 30 mg5.97
Apremilast 20 mg4.05
Apremilast 30 mg4.97

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Placebo40.9
Apremilast 20 mg42.9
Apremilast 30 mg41.1

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212757)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo40.9
Apremilast 20 mg44.2
Apremilast 30 mg46.6

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg78.3
Placebo / Apremilast 30 mg77.8
Apremilast 20 mg57.9
Apremilast 30 mg65.0

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Percentage of Participants Achieving a MASES Score of Zero at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Placebo23.1
Apremilast 20 mg29.0
Apremilast 30 mg20.8

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Percentage of Participants Achieving a MASES Score of Zero at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212757)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo24.0
Apremilast 20 mg29.9
Apremilast 30 mg22.8

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Percentage of Participants Achieving a MASES Score of Zero at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg42.5
Placebo / Apremilast 30 mg41.0
Apremilast 20 mg40.0
Apremilast 30 mg37.2

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Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52

A EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg70.0
Placebo / Apremilast 30 mg64.5
Apremilast 20 mg68.0
Apremilast 30 mg67.5

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Percentage of Participants With a ACR 20 Response at Week 52

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg53.3
Placebo / Apremilast 30 mg47.5
Apremilast 20 mg52.9
Apremilast 30 mg52.6

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Percentage of Participants With a ACR 50 Response at Week 16

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: o Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); o Patient's global assessment of disease activity (measured on a 100 mm VAS); o Physician's global assessment of disease activity (measured on a 100 mm VAS); o Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); o C-Reactive Protein. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo5.0
Apremilast 20 mg14.7
Apremilast 30 mg10.5

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Percentage of Participants With a ACR 70 Response at Week 24

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦C-Reactive Protein. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo3.1
Apremilast 20 mg5.5
Apremilast 30 mg2.5

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Percentage of Participants With a Modified PsARC Response at Week 52

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg78.3
Placebo / Apremilast 30 mg73.3
Apremilast 20 mg72.4
Apremilast 30 mg74.6

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: - 78 tender joint count, - 76 swollen joint count, - Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; - Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo33.3
Apremilast 20 mg47.9
Apremilast 30 mg48.1

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo24.5
Apremilast 20 mg39.9
Apremilast 30 mg32.1

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Percentage of Participants With an ACR 20 Response at Week 24

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦C-Reactive Protein. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo15.7
Apremilast 20 mg31.3
Apremilast 30 mg24.7

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Percentage of Participants With an ACR 50 Response at Week 24

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: o Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); o Patient's global assessment of disease activity (measured on a 100 mm VAS); o Physician's global assessment of disease activity (measured on a 100 mm VAS); o Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); o C-Reactive Protein. (NCT01212757)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo8.8
Apremilast 20 mg14.1
Apremilast 30 mg11.7

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Percentage of Participants With an ACR 50 Response at Week 52

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212757)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg30.5
Placebo / Apremilast 30 mg27.4
Apremilast 20 mg26.7
Apremilast 30 mg18.6

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Percentage of Participants With an ACR 70 Response at Week 16

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: o Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); o Patient's global assessment of disease activity (measured on a 100 mm VAS); o Physician's global assessment of disease activity (measured on a 100 mm VAS); o Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); o C-Reactive Protein. (NCT01212757)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo0.6
Apremilast 20 mg3.7
Apremilast 30 mg1.2

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo60.6
Apremilast 20 mg67.6
Apremilast 30 mg73.8

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Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16

A EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo29.0
Apremilast 20 mg40.2
Apremilast 30 mg51.5

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Percentage of Participants With Good or Moderate EULAR Response at Week 24

EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo20.1
Apremilast 20 mg32.0
Apremilast 30 mg42.5

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg95.5
Placebo / Apremilast 30 mg92.3
Apremilast 20 mg88.5
Apremilast 30 mg91.8

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 24

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo1.03
Apremilast 20 mg2.71
Apremilast 30 mg3.37

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo59.2
Apremilast 20 mg66.2
Apremilast 30 mg71.3

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Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo18.3
Apremilast 20 mg28.4
Apremilast 30 mg40.7

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Percentage of Participants With an ACR 70 Response at Week 52

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg20.8
Placebo / Apremilast 30 mg14.9
Apremilast 20 mg9.2
Apremilast 30 mg10.4

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Percentage of Participants With an ACR 70 Response at Week 16

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo2.4
Apremilast 20 mg4.7
Apremilast 30 mg3.6

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Percentage of Participants With an ACR 50 Response at Week 52

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg28.3
Placebo / Apremilast 30 mg31.8
Apremilast 20 mg25.2
Apremilast 30 mg30.2

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Percentage of Participants With an ACR 50 Response at Week 24

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo7.7
Apremilast 20 mg13.6
Apremilast 30 mg16.2

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Percentage of Participants With an ACR 20 Response at Week 52

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg59.3
Placebo / Apremilast 30 mg58.2
Apremilast 20 mg56.0
Apremilast 30 mg63.0

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Percentage of Participants With an ACR 20 Response at Week 24

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo15.4
Apremilast 20 mg26.6
Apremilast 30 mg31.1

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo23.1
Apremilast 20 mg32.0
Apremilast 30 mg44.3

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo27.2
Apremilast 20 mg37.9
Apremilast 30 mg52.7

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Percentage of Participants With a ACR 50 Response at Week 16

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo8.3
Apremilast 20 mg12.4
Apremilast 30 mg15.0

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Percentage of Participants With a Modified PsARC Response at Week 52

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg81.1
Placebo / Apremilast 30 mg75.8
Apremilast 20 mg71.6
Apremilast 30 mg79.0

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Percentage of Participants With a ACR 70 Response at Week 24

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: ◦ Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); ◦ Patient's global assessment of disease activity (measured on a 100 mm VAS); ◦ Physician's global assessment of disease activity (measured on a 100 mm VAS); ◦ Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); ◦ C-Reactive Protein. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo3.6
Apremilast 20 mg4.1
Apremilast 30 mg5.4

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Number of Participants With Treatment Emergent Adverse Events During the Apremilast Exposure Period

A TEAE is an adverse event (AE) with a start date on or after the date of the first dose of investigational product (IP) and no later than 28 days after the last dose of IP. An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a subject during the course of a study. A serious AE is any AE that results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent or significant disability/incapacity; is a congenital anomaly/birth defect; or constitutes an important medical event. For both AEs and SAEs the investigator assessed the severity of the event according to the grading scale: Mild: asymptomatic or with mild symptoms, Moderate: symptoms causing moderate discomfort or Severe: symptoms causing severe discomfort or pain. (NCT01212770)
Timeframe: Week 0 to Week 260; median duration of exposure to apremilast 20 mg BID was 121.71 weeks and 232.50 weeks for apremilast 30 mg BID

,,
Interventionparticipants (Number)
Any TEAEAny Drug-Related TEAEAny Severe TEAEAny Serious TEAE (SAE)Any Serious Drug-Related TEAEAny TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to death
Apremilast 20 mg (Pre-switch)194982138548300
Apremilast 20/30 mg (Post-switch)6411040401
Apremilast 30 mg2091113054353300

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Number of Participants With Treatment Emergent Adverse Events (TEAEs) During the Placebo-Controlled Phase

A TEAE is an adverse event (AE) with a start date on or after the date of the first dose of investigational product (IP) and no later than 28 days after the last dose of IP. An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a subject during the course of a study. A serious AE is any AE that results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent or significant disability/incapacity; is a congenital anomaly/birth defect; or constitutes an important medical event. For both AEs and SAEs the investigator assessed the severity of the event according to the grading scale: Mild: asymptomatic or with mild symptoms, Moderate: symptoms causing moderate discomfort or Severe: symptoms causing severe discomfort or pain. (NCT01212770)
Timeframe: Week 0 to Week 16 for placebo participants who entered EE at Week 16 and up to Week 24 for all other participants (placebo participants who remained on placebo through week 24 and participants randomized to the APR 20 mg BID or APR 30 mg BID)

,,
Interventionparticipants (Number)
Any TEAEAny Drug-Related TEAEAny Severe TEAEAny Serious TEAE (SAE)Any Serious Drug-Related TEAEAny TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to Death
Apremilast 20 mg1005053020130
Apremilast 30 mg10462106016120
Placebo83338924100

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Percentage of Participants With MASES Improvement ≥ 20% at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 52 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg73.5
Placebo / Apremilast 30 mg75.0
Apremilast 20 mg77.3
Apremilast 30 mg71.3

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Percentage of Participants With MASES Improvement ≥ 20% at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo51.4
Apremilast 20 mg51.5
Apremilast 30 mg54.5

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Percentage of Participants With MASES Improvement ≥ 20% at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo53.2
Apremilast 20 mg48.5
Apremilast 30 mg54.5

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Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52

A EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on the DAS-28 score. A Good Response is defined as an improvement (decrease) in the DAS28 of more than 1.2 compared with Baseline and attainment of a DAS28 score less than or equal to 3.2. A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg64.8
Placebo / Apremilast 30 mg73.1
Apremilast 20 mg69.4
Apremilast 30 mg74.8

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Percentage of Participants Achieving a MASES Score of Zero at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg44.1
Placebo / Apremilast 30 mg43.8
Apremilast 20 mg33.3
Apremilast 30 mg36.8

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Percentage of Participants Achieving a MASES Score of Zero at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo28.4
Apremilast 20 mg20.6
Apremilast 30 mg27.7

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Percentage of Participants Achieving a MASES Score of Zero at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Placebo24.8
Apremilast 20 mg19.6
Apremilast 30 mg20.5

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg68.2
Placebo / Apremilast 30 mg80.8
Apremilast 20 mg75.0
Apremilast 30 mg68.9

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo36.6
Apremilast 20 mg45.1
Apremilast 30 mg46.3

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Week 16

Interventionpercentage of participants (Number)
Placebo35.2
Apremilast 20 mg40.8
Apremilast 30 mg41.3

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Percentage of Participants Achieving a ≥ 75% Improvement in Psoriasis Area and Severity Index Score (PASI75) at Week 52

The percentage of participants with Baseline psoriasis body surface area (BSA) involvement ≥ 3% who achieved 75% or greater improvement from Baseline in Psoriasis Area and Severity Index (PASI) score after 52 weeks. The Psoriasis Area and Severity Index (PASI) score is a combination of the intensity of psoriasis, assessed by erythema (reddening), induration (plaque thickness) and desquamation (scaling) scored on a scale from 0 (none) to 4 (very severe), together with the percentage of the area affected, rated on a scale from 0 (no involvement) to 6 (90% to 100% involvement). PASI scoring is performed at four body areas, the head, arms, trunk, and legs. The total PASI score ranges from 0 to 72. The higher the total score, the more severe the disease. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg33.3
Placebo / Apremilast 30 mg28.6
Apremilast 20 mg28.6
Apremilast 30 mg39.1

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Percentage of Participants Achieving a ≥ 75% Improvement in Psoriasis Area and Severity Index Score (PASI75) at Week 24

The percentage of participants with Baseline psoriasis body surface area (BSA) involvement ≥ 3% who achieved 75% or greater improvement from Baseline in Psoriasis Area and Severity Index (PASI) score after 24 weeks of treatment. The Psoriasis Area and Severity Index (PASI) score is a combination of the intensity of psoriasis, assessed by erythema (reddening), induration (plaque thickness) and desquamation (scaling) scored on a scale from 0 (none) to 4 (very severe), together with the percentage of the area affected, rated on a scale from 0 (no involvement) to 6 (90% to 100% involvement). PASI scoring is performed at four body areas, the head, arms, trunk, and legs. The total PASI score ranges from 0 to 72. The higher the total score, the more severe the disease. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo11.2
Apremilast 20 mg22.2
Apremilast 30 mg25.6

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Percentage of Participants Achieving a ≥ 75% Improvement in Psoriasis Area and Severity Index Score (PASI75) at Week 16

The percentage of participants with Baseline psoriasis body surface area (BSA) involvement ≥ 3% who achieved 75% or greater improvement from Baseline in Psoriasis Area and Severity Index (PASI) score after 16 weeks of treatment. The Psoriasis Area and Severity Index (PASI) score is a combination of the intensity of psoriasis, assessed by erythema (reddening), induration (plaque thickness) and desquamation (scaling) scored on a scale from 0 (none) to 4 (very severe), together with the percentage of the area affected, rated on a scale from 0 (no involvement) to 6 (90% to 100% involvement). PASI scoring is performed at four body areas, the head, arms, trunk, and legs. The total PASI score ranges from 0 to 72. The higher the total score, the more severe the disease. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo7.9
Apremilast 20 mg20.9
Apremilast 30 mg22.2

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Change From Baseline in the SF-36 Physical Functioning Scale Score at Week 52

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg7.76
Placebo / Apremilast 30 mg6.87
Apremilast 20 mg5.68
Apremilast 30 mg5.87

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Change From Baseline in the Patient Assessment of Pain at Week 52

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01212770)
Timeframe: Baseline and Week 52

Interventionmm (Mean)
Placebo / Apremilast 20 mg-19.9
Placebo / Apremilast 30 mg-19.1
Apremilast 20 mg-14.9
Apremilast 30 mg-18.7

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01212770)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo0.83
Apremilast 20 mg2.01
Apremilast 30 mg3.27

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue." (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo1.18
Apremilast 20 mg1.86
Apremilast 30 mg3.72

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Change From Baseline in the FACIT-Fatigue Scale Score at Week 52

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg6.72
Placebo / Apremilast 30 mg5.66
Apremilast 20 mg4.78
Apremilast 30 mg6.20

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Change From Baseline in the Disease Activity Score (DAS28) at Week 24

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.27
Apremilast 20 mg-0.57
Apremilast 30 mg-0.75

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Change From Baseline in the Disease Activity Score (DAS28) at Week 16

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the distal interphalangeal (DIP) joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.28
Apremilast 20 mg-0.54
Apremilast 30 mg-0.74

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Change From Baseline in the DAS28 at Week 52

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: •28 tender joint count •28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; •C-reactive protein (CRP) •Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-1.28
Placebo / Apremilast 30 mg-1.29
Apremilast 20 mg-1.21
Apremilast 30 mg-1.41

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Change From Baseline in the Dactylitis Severity Score at Week 52

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-3.1
Placebo / Apremilast 30 mg-3.8
Apremilast 20 mg-2.9
Apremilast 30 mg-3.6

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Change From Baseline in the CDAI Score at Week 52

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: •28 tender joint count (TJC), •28 swollen joint count (SJC), •Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; •Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-13.54
Placebo / Apremilast 30 mg-12.38
Apremilast 20 mg-12.86
Apremilast 30 mg-14.14

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Change From Baseline in Patient's Assessment of Pain at Week 24

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01212770)
Timeframe: Baseline and week 24

Interventionmm (Least Squares Mean)
Placebo-4.4
Apremilast 20 mg-8.2
Apremilast 30 mg-10.9

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Change From Baseline in Patient's Assessment of Pain at Week 16

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01212770)
Timeframe: Baseline and Week 16

Interventionmm (Least Squares Mean)
Placebo-4.9
Apremilast 20 mg-8.6
Apremilast 30 mg-12.7

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-2.5
Placebo / Apremilast 30 mg-2.2
Apremilast 20 mg-2.2
Apremilast 30 mg-1.9

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Baseline and week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.7
Apremilast 20 mg-1.0
Apremilast 30 mg-1.1

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Archilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.7
Apremilast 20 mg-0.7
Apremilast 30 mg-1.0

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Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 24

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.053
Apremilast 20 mg-0.137
Apremilast 30 mg-0.192

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Change From Baseline in Health Assessment Questionnaire- Disability Index (HAQ-DI) at Week 16

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.065
Apremilast 20 mg-0.131
Apremilast 30 mg-0.192

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Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01212770)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-0.34
Placebo / Apremilast 30 mg-0.34
Apremilast 20 mg-0.33
Apremilast 30 mg-0.35

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Change From Baseline in Dactylitis Severity Score at Week 24

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-1.3
Apremilast 20 mg-1.7
Apremilast 30 mg-2.3

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Change From Baseline in Dactylitis Severity Score at Week 16

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.3
Apremilast 20 mg-1.7
Apremilast 30 mg-2.1

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22. (NCT01212770)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-2.53
Apremilast 20 mg-5.18
Apremilast 30 mg-7.81

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-2.76
Apremilast 20 mg-4.61
Apremilast 30 mg-7.70

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01212770)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo1.14
Apremilast 20 mg2.29
Apremilast 30 mg3.47

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Treatment Free Interval/PFS

The treatment-free interval after treatment with the combination of thalidomide, bortezomib and melphalan (NCT01242267)
Timeframe: PFS was defined as the time from ASCT to disease progression or death from any cause, an average of 9 months

Interventionmonths (Median)
Phase 1/Phase 29.3

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Toxicity Assessment

Assessment of the toxicities resulting from administration of combinations of thalidomide, bortezomib and melphalan (NCT01242267)
Timeframe: Patients will be hospitalized or in the outpatient transplant facility until engraftment and resolution of serious adverse events, a median of 16 (range, 11-24) days

InterventionSerious Adverse Events (Number)
Phase I - Thalidomide Dose Level 600 mg1
Phase I - Thalidomide Dose Level 800 mg0
Phase I - Thalidomide Dose Level 1000 mg0
Phase 23

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Maximum Tolerated Dose of Thalidomide

Maximum tolerated dose of thalidomide used in conjunction with dose-intense melphalan, bortezomib and autologous (syngeneic) HSC support in the salvage therapy of patients who failed a prior treatment with dose-intense melphalan (NCT01242267)
Timeframe: Dose escalation will be based on the assessment of tolerability determined after the last patient of each cohort reaches day +21.

Interventionmg (Number)
Phase 11000
Phase 21000

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Complete Response (CR) and Very Good Partial Response (VgPR) Rate

The complete response (CR) and very good partial response (VgPR) rate in patients undergoing ASCT using thalidomide, bortezomib and melphalan (NCT01242267)
Timeframe: Assessments will be made from Day +28 after transplantation for 3 months and then at 3 month intervals until demonstration of disease progression and initiation of further therapy, an average of 9 months

InterventionParticipants (Count of Participants)
Phase I - Thalidomide Dose Level 600 mg0
Phase I - Thalidomide Dose Level 800 mg3
Phase I - Thalidomide Dose Level 1000 mg1
Phase 213

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Percentage Change From Baseline in the High Sensitivity C-Reactive Protein (CRP) at Week 52

"C-Reactive Protein (CRP) is a substance produced by the liver that increases in the presence of inflammation in the body. An elevated CRP level is identified with blood tests and is considered a non-specific marker for disease." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20mg EE13.34
Placebo/Apremilast 20 mg XO82.14
Apremilast 20 mg104.25
Apremilast 30 mg79.33

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Percentage Change From Baseline in the Tender Joint Count at Week 24

Joint tenderness is the presence of pain in a joint when pressure is applied by the examiner to elicit tenderness. The 68 tender joint count evaluates the following joints: upper-temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, meta-carpophalangeal, proximal interphalangeal and distal interphalangeal; lower: hip, knee, ankle, midtarsal, metatarsophalangeal and proximal interphalangeal. (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo-30.81
Apremilast 20 mg-26.21
Apremilast 30 mg-27.80

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Percentage Change From Baseline in the Tender Joint Count at Week 16

Joint tenderness is the presence of pain in a joint when pressure is applied by the examiner to elicit tenderness. The 68 tender joint count evaluates the following joints: upper-temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, meta-carpophalangeal, proximal interphalangeal and distal interphalangeal; lower: hip, knee, ankle, midtarsal, metatarsophalangeal and proximal interphalangeal. (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo-33.08
Apremilast 20 mg-26.92
Apremilast 30 mg-33.68

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Percentage of Participants Who Achieve an Improvement of at Least 4 Units From Baseline in the Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) at Week 24

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue.~A positive change from baseline score indicates an improvement." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo26.6
Apremilast 20 mg14.6
Apremilast 30 mg26.3

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Percentage Change From Baseline in the Swollen Joint Count at Week 52

Joint swelling is soft tissue swelling that is detectable along the joint margins and is assessed by inspection and direct palpation of the joint, by the examiner. The ACR 66 swollen joint count evaluates the following joints: upper-temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, metacarpophalangeal, proximal interphalangeal and distal interphalangeal; lower: knee, ankle, midtarsal, metatarsophalangeal and proximal interphalangeal. (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20mg EE-59.40
Placebo/Apremilast 20 mg XO-67.73
Apremilast 20 mg-57.31
Apremilast 30 mg-66.74

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Percentage Change From Baseline in the Swollen Joint Count at Week 24

Joint swelling is soft tissue swelling that is detectable along the joint margins and is assessed by inspection and direct palpation of the joint, by the examiner. The ACR 66 swollen joint count evaluates the following joints: upper-temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, metacarpophalangeal, proximal interphalangeal and distal interphalangeal; lower: knee, ankle, midtarsal, metatarsophalangeal and proximal interphalangeal. (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo-34.41
Apremilast 20 mg-32.56
Apremilast 30 mg-41.43

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Percentage Change From Baseline in the Swollen Joint Count at Week 16

Joint swelling is soft tissue swelling that is detectable along the joint margins and is assessed by inspection and direct palpation of the joint, by the examiner. The ACR 66 swollen joint count evaluates the following joints: upper-temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, metacarpophalangeal, proximal interphalangeal and distal interphalangeal; lower: knee, ankle, midtarsal, metatarsophalangeal and proximal interphalangeal. (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo-36.96
Apremilast 20 mg-34.38
Apremilast 30 mg-40.22

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Percentage Change From Baseline in the Subject Global Assessment of Disease Activity at Week 52

"The Subject Global Assessment of Disease Activity was measured asking the participant to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents lowest disease activity, and the right-hand boundary (score = 100 mm) represents highest disease activity. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20 EE14.20
Placebo / Apremilast 20 mg XO33.31
Apremilast 20 mg-5.20
Apremilast 30 mg8.22

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Percentage Change From Baseline in the Subject Global Assessment of Disease Activity at Week 24

"The Subject Global Assessment of Disease Activity was measured asking the participant to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents lowest disease activity, and the right-hand boundary (score = 100 mm) represents highest disease activity. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo15.04
Apremilast 20 mg0.70
Apremilast 30 mg2.54

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Percentage Change From Baseline in the Subject Global Assessment of Disease Activity at Week 16

"The Subject Global Assessment of Disease Activity was measured asking the participant to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents lowest disease activity, and the right-hand boundary (score = 100 mm) represents highest disease activity. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo10.84
Apremilast 20 mg-3.50
Apremilast 30 mg11.19

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Percentage Change From Baseline in the Subject Assessment of Pain at Week 52

"The Subject Assessment of Pain was measured asking the participant to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20mg EE44.63
Placebo/Apremilast 20 mg XO15.78
Apremilast 20 mg-11.69
Apremilast 30 mg-3.73

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Percentage Change From Baseline in the Subject Assessment of Pain at Week 24

"The Subject Assessment of Pain was measured asking the participant to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo28.16
Apremilast 20 mg-6.66
Apremilast 30 mg-9.66

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Percentage Change From Baseline in the Subject Assessment of Pain at Week 16

"The Subject Assessment of Pain was measured asking the participant to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo30.50
Apremilast 20 mg-5.03
Apremilast 30 mg-7.87

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Percentage Change From Baseline in the Physician Global Assessment of Disease Activity at Week 52

"The Physician Global Assessment of Disease Activity was measured asking the physician to assess the subject's current arthritis disease activity by placing a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents lowest disease activity, and the right-hand boundary (score = 100 mm) represents highest disease activity. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20mg EE-41.30
Placebo/Apremilast 20 mg XO-49.10
Apremilast 20 mg-41.19
Apremilast 30 mg-44.85

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Percentage Change From Baseline in the Physician Global Assessment of Disease Activity at Week 24

"The Physician Global Assessment of Disease Activity was measured asking the physician to assess the subject's current arthritis disease activity by placing a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents lowest disease activity, and the right-hand boundary (score = 100 mm) represents highest disease activity. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo-29.98
Apremilast 20 mg-24.13
Apremilast 30 mg-31.78

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Percentage Change From Baseline in the Physician Global Assessment of Disease Activity at Week 16

"The Physician Global Assessment of Disease Activity was measured asking the physician to assess the subject's current arthritis disease activity by placing a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents lowest disease activity, and the right-hand boundary (score = 100 mm) represents highest disease activity. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo-28.82
Apremilast 20 mg-28.22
Apremilast 30 mg-32.66

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Percentage Change From Baseline in the High Sensitivity C-Reactive Protein (CRP) at Week 24

"C-Reactive Protein (CRP) is a substance produced by the liver that increases in the presence of inflammation in the body. An elevated CRP level is identified with blood tests and is considered a non-specific marker for disease." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo39.14
Apremilast 20 mg47.43
Apremilast 30 mg106.22

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Percentage Change From Baseline in the High Sensitivity C-Reactive Protein (CRP) at Week 16

"C-Reactive Protein (CRP) is a substance produced by the liver that increases in the presence of inflammation in the body. An elevated CRP level is identified with blood tests and is considered a non-specific marker for disease." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo41.99
Apremilast 20 mg46.69
Apremilast 30 mg100.04

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Percentage Change From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) Score at Week 24

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo-6.59
Apremilast 20 mg-5.01
Apremilast 30 mg-12.30

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Percentage Change From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) Score at Week 16

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo-9.43
Apremilast 20 mg-3.50
Apremilast 30 mg-10.20

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Percentage Change From Baseline in the Health Assessment Questionnaire - Disability Index (HAQ-DI) Score at Week 52

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20mg EE-13.32
Placebo/Apremilast 20 mg XO-10.53
Apremilast 20 mg-8.20
Apremilast 30 mg-22.46

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Percentage Change From Baseline in Erythrocyte Sedimentation Rate (ESR) at Week 52

"The erythrocyte sedimentation rate (ESR) is a blood test that can reveal inflammatory activity. The subject's blood is placed in a tall, thin tube, red erythrocytes gradually settle to the bottom. Inflammation can cause the cells to clump together. Because these clumps of cells are denser than individual cells, they settle to the bottom more quickly.~The ESR test measures the distance red blood cells fall in a test tube in one hour. The farther the red blood cells have descended, the greater the inflammatory response." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20 EE-6.28
Placebo / Apremilast 20 mg XO17.15
Apremilast 20 mg4.83
Apremilast 30 mg-15.99

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Percentage Change From Baseline in Erythrocyte Sedimentation Rate (ESR) at Week 24

"The erythrocyte sedimentation rate (ESR) is a blood test that can reveal inflammatory activity. The subject's blood is placed in a tall, thin tube, red erythrocytes gradually settle to the bottom. Inflammation can cause the cells to clump together. Because these clumps of cells are denser than individual cells, they settle to the bottom more quickly.~The ESR test measures the distance red blood cells fall in a test tube in one hour. The farther the red blood cells have descended, the greater the inflammatory response." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercent change (Least Squares Mean)
Placebo-0.06
Apremilast 20 mg11.99
Apremilast 30 mg-6.60

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Percentage Change From Baseline in Erythrocyte Sedimentation Rate (ESR) at Week 16

"The erythrocyte sedimentation rate (ESR) is a blood test that can reveal inflammatory activity. The subject's blood is placed in a tall, thin tube, red erythrocytes gradually settle to the bottom. Inflammation can cause the cells to clump together. Because these clumps of cells are denser than individual cells, they settle to the bottom more quickly.~The ESR test measures the distance red blood cells fall in a test tube in one hour. The farther the red blood cells have descended, the greater the inflammatory response." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent change (Least Squares Mean)
Placebo6.81
Apremilast 20 mg13.98
Apremilast 30 mg-9.39

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Change From Baseline in the Medical Outcome Study Short Form 36-item (SF-36) Physical Functioning Domain at Week 52

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01285310)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo/Apremilast 20mg EE2.11
Placebo/Apremilast 20 mg XO3.50
Apremilast 20 mg2.56
Apremilast 30 mg5.23

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Change From Baseline in the Medical Outcome Study Short Form 36-item (SF-36) Physical Functioning Domain at Week 24

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01285310)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo1.78
Apremilast 20 mg1.66
Apremilast 30 mg3.76

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Change From Baseline in the Medical Outcome Study Short Form 36-item (SF-36) Physical Functioning Domain at Week 16

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). The concepts measured by the SF-36 are not specific to any age, disease, or treatment group, allowing comparison of relative burden of different diseases and the relative benefit of different treatments. Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from baseline score indicates an improvement. (NCT01285310)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Mean)
Placebo1.48
Apremilast 20 mg1.64
Apremilast 30 mg3.33

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24

"The FACIT-Fatigue scale was a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue.~A positive change from baseline score indicates an improvement." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo1.7
Apremilast 20 mg0.5
Apremilast 30 mg3.4

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16

"The FACIT-Fatigue scale was a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue.~A positive change from baseline score indicates an improvement." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo2.7
Apremilast 20 mg1.5
Apremilast 30 mg2.6

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Change From Baseline in the FACIT-Fatigue Scale Score at Week 52

"The FACIT-Fatigue scale was a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue.~A positive change from baseline score indicates an improvement." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo/Apremilast 20mg EE3.50
Placebo/Apremilast 20 mg XO3.18
Apremilast 20 mg2.87
Apremilast 30 mg3.47

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Change From Baseline in the Disease Activity Score 28 (DAS 28) Using CRP at Week 52

"The DAS28 measures the severity of disease at a specific time and is derived from the following variables:~28 tender joint count (TJC28)~28 swollen joint count (SJC28), which do not include the distal interphalangeal (DIP) joints, the hip joint, or the joints below the knee;~C-reactive protein (CRP)~Subject's global assessment of disease activity (SGA).~DAS28 values range from 2.0 to 10.0 while higher values mean a higher disease activity.~A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo/Apremilast 20mg EE-1.18
Placebo/Apremilast 20 mg XO-1.68
Apremilast 20 mg-1.10
Apremilast 30 mg-1.38

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Change From Baseline in the Clinical Disease Activity Index (CDAI) at Week 52

"The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the:~28 tender joint count (TJC),~28 swollen joint count (SJC),~Subject's Global Assessment of Disease Activity measured on a 100 mm visual analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest;~Physician's Global Assessment of Disease Activity -measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest.~The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI:~Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22" (NCT01285310)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo/Apremilast 20mg EE-16.22
Placebo/Apremilast 20 mg XO-20.70
Apremilast 20 mg-14.77
Apremilast 30 mg-17.68

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Change From Baseline in the Clinical Disease Activity Index (CDAI) at Week 24

"The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the:~28 tender joint count (TJC),~28 swollen joint count (SJC),~Subject's Global Assessment of Disease Activity measured on a 100 mm visual analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest;~Physician's Global Assessment of Disease Activity -measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest.~The CDAI score ranges from 0-76 where lower scores indicate less disease activity.The following thresholds of disease activity have been defined for the CDAI:~Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22" (NCT01285310)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-10.40
Apremilast 20 mg-9.46
Apremilast 30 mg-11.63

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Change From Baseline in the Clinical Disease Activity Index (CDAI) at Week 16

"The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the:~28 tender joint count (TJC),~28 swollen joint count (SJC),~Subject's Global Assessment of Disease Activity measured on a 100 mm visual analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest;~Physician's Global Assessment of Disease Activity -measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest.~The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI:~Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22" (NCT01285310)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Mean)
Placebo-11.52
Apremilast 20 mg-9.49
Apremilast 30 mg-11.38

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Percentage Change From Baseline in the Tender Joint Count at Week 52

Joint tenderness is the presence of pain in a joint when pressure is applied by the examiner to elicit tenderness. The 68 tender joint count evaluates the following joints: upper-temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, meta-carpophalangeal, proximal interphalangeal and distal interphalangeal; lower: hip, knee, ankle, midtarsal, metatarsophalangeal and proximal interphalangeal. (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercent change (Mean)
Placebo/Apremilast 20mg EE-55.47
Placebo/Apremilast 20 mg XO-62.70
Apremilast 20 mg-43.88
Apremilast 30 mg-54.03

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Change From Baseline in Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 16

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Mean)
Placebo-0.106
Apremilast 20 mg-0.114
Apremilast 30 mg-0.209

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Percentage of Participants Who Achieve an Improvement of ≥ 0.22 Units From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 24

The Health Assessment Questionnaire - Disability Index (HAQ-DI) is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo20.3
Apremilast 20 mg25.6
Apremilast 30 mg32.9

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Percentage of Participants With an American College of Rheumatology 50% Improvement (ACR 50) Response at Week 52

"Percentage of participants with an American College of Rheumatology 50% Improvement (ACR 50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met:~≥ 50% improvement in 68 tender joint count;~≥ 50% improvement in 66 swollen joint count; and~≥ 50% improvement in at least 3 of the 5 following parameters:~Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index [(HAQ-DI)]); C-Reactive Protein." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE3.4
Placebo/Apremilast 20 mg XO11.9
Apremilast 20 mg4.9
Apremilast 30 mg5.3

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Percentage of Participants Who Achieve Low Disease Activity or Remission Based on the Clinical Disease Activity Index (CDAI) ≤ 10 at Week 24

"The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the:~28 tender joint count (TJC),~28 swollen joint count (SJC),~Subject's Global Assessment of Disease Activity measured on a 100 mm visual analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest;~Physician's Global Assessment of Disease Activity -measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest.~The CDAI score ranges from 0-76 where lower scores indicate less disease activity.The following thresholds of disease activity have been defined for the CDAI:~Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22" (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo16.5
Apremilast 20 mg12.2
Apremilast 30 mg21.1

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Percentage of Participants With an American College of Rheumatology 50% Improvement (ACR 50) Response at Week 24

"Percentage of participants with an American College of Rheumatology 50% Improvement (ACR 50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met:~≥ 50% improvement in 68 tender joint count;~≥ 50% improvement in 66 swollen joint count; and~≥ 50% improvement in at least 3 of the 5 following parameters:~Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index [(HAQ-DI)]); C-Reactive Protein." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo6.3
Apremilast 20 mg4.9
Apremilast 30 mg15.8

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Percentage of Participants With an American College of Rheumatology 50% Improvement (ACR 50) Response at Week 16

"Percentage of participants with an American College of Rheumatology 50% Improvement (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met:~≥ 50% improvement in 68 tender joint count;~≥ 50% improvement in 66 swollen joint count; and~≥ 50% improvement in at least 3 of the 5 following parameters:~Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index [(HAQ-DI)]); C-Reactive Protein." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo11.4
Apremilast 20 mg4.9
Apremilast 30 mg9.2

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Percentage of Participants With an American College of Rheumatology 20% Improvement (ACR 20) Response at Week 52

"Percentage of participants with an American College of Rheumatology 20% Improvement (ACR 20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met:~≥ 20% improvement in 68 tender joint count;~≥ 20% improvement in 66 swollen joint count; and~≥ 20% improvement in at least 3 of the 5 following parameters: Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index ([HAQ-DI]); C-Reactive Protein." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE47.8
Placebo/Apremilast 20 mg XO51.3
Apremilast 20 mg30.9
Apremilast 30 mg38.2

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Percentage of Participants With an American College of Rheumatology 20% Improvement (ACR 20) Response at Week 24

"Percentage of participants with an American College of Rheumatology 20% Improvement (ACR 20) response. A participant was a responder if the following 3 criteria for improvement from baseline were met:~≥ 20% improvement in 68 tender joint count;~≥ 20% improvement in 66 swollen joint count; and~≥ 20% improvement in at least 3 of the 5 following parameters: Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index ([HAQ-DI]); C-Reactive Protein" (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo24.1
Apremilast 20 mg19.5
Apremilast 30 mg27.6

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Percentage of Participants With an American College of Rheumatology 20% Improvement (ACR 20) Response at Week 16

"Percentage of participants with an American College of Rheumatology 20% Improvement (ACR 20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met:~≥ 20% improvement in 68 tender joint count;~≥ 20% improvement in 66 swollen joint count; and~≥ 20% improvement in at least 3 of the 5 following parameters: Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index ([HAQ-DI]); C-Reactive Protein." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo35.4
Apremilast 20 mg28
Apremilast 30 mg34.2

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Percentage of Participants Who Achieve the European League Against Rheumatism (EULAR) Response Criteria Using CRP at Week 52

"The EULAR response criteria classify each subject as a good, moderate or non-responder to treatment based on the degree of improvement from baseline and the level of disease activity at the endpoint. EULAR response is derived using the individual subject's DAS28 as the measure of severity of disease.~Good or moderate response is defined as follows: Good response: DAS28 at the time point ≤ 3.2 and improvement from baseline > 1.2 Moderate response: DAS28 at the time point > 3.2 and improvement from baseline > 1.2, or DAS28 at the time point ≤ 5.1 and improvement from baseline > 0.6 and ≤ 1.2" (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE69.6
Placebo/Apremilast 20 mg XO82.1
Apremilast 20 mg63.0
Apremilast 30 mg65.5

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Percentage of Participants Who Achieve the European League Against Rheumatism (EULAR) Response Criteria Using CRP at Week 24

"EULAR response criteria classify each participant as a good, moderate or non-responder to treatment based on the degree of improvement from baseline and the level of disease activity at the endpoint. EULAR response is derived using the individual subject's DAS28 as the measure of severity of disease.~Good or moderate response is defined as follows: Good response: DAS28 at the time point ≤ 3.2 and improvement from baseline > 1.2 Moderate response: DAS28 at the time point > 3.2 and improvement from baseline > 1.2, or DAS28 at the time point ≤ 5.1 and improvement from baseline > 0.6 and ≤ 1.2" (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo40.5
Apremilast 20 mg29.3
Apremilast 30 mg35.5

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Percentage of Participants Who Achieve the European League Against Rheumatism (EULAR) Response Criteria Using CRP at Week 16

"EULAR response criteria classify each participant as a good, moderate or non-responder to treatment based on the degree of improvement from baseline and the level of disease activity at the endpoint. EULAR response is derived using the individual subject's DAS28 as the measure of severity of disease.~Good or moderate response is defined as follows: Good response: DAS28 at the time point ≤ 3.2 and improvement from baseline > 1.2 Moderate response: DAS28 at the time point > 3.2 and improvement from baseline > 1.2, or DAS28 at the time point ≤ 5.1 and improvement from baseline > 0.6 and ≤ 1.2" (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo46.8
Apremilast 20 mg41.5
Apremilast 30 mg44.7

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Percentage of Participants Who Achieve an Improvement of ≥ 0.22 Units From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 52

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE58.3
Placebo/Apremilast 20 mg XO43.6
Apremilast 20 mg40.0
Apremilast 30 mg58.2

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Percentage of Participants Who Achieve an Improvement of at Least 4 Units From Baseline in the Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-Fatigue) at Week 52

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE41.7
Placebo/Apremilast 20 mg XO61.5
Apremilast 20 mg45.5
Apremilast 30 mg40.0

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Percentage of Participants Who Achieve an Improvement of at Least 4 Units From Baseline in the Functional Assessment of Chronic Illness Therapy -Fatigue (FACIT-Fatigue) at Week 16

"The FACIT-Fatigue scale was a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue.~A positive change from baseline score indicates an improvement." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo39.2
Apremilast 20 mg35.4
Apremilast 30 mg42.1

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Percentage of Participants Who Achieve Low Disease Activity or Remission Based on the Clinical Disease Activity Index (CDAI) ≤ 10 at Week 52

"The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the:~28 tender joint count (TJC),~28 swollen joint count (SJC),~Subject's Global Assessment of Disease Activity measured on a 100 mm visual analog scale (VAS),, where 0 mm = lowest disease activity and 100 mm = highest;~Physician's Global Assessment of Disease Activity -measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest.~The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI:~Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22" (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE16.7
Placebo/Apremilast 20 mg XO41.0
Apremilast 20 mg25.0
Apremilast 30 mg27.3

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Percentage of Participants Who Achieve Low Disease Activity or Remission Based on the Clinical Disease Activity Index (CDAI) ≤ 10 at Week 16

"The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the:~28 tender joint count (TJC),~28 swollen joint count (SJC),~Subject's Global Assessment of Disease Activity measured on a 100 mm visual analog scale (VAS), where 0 mm = lowest disease activity and 100 mm = highest;~Physician's Global Assessment of Disease Activity -measured on a 100 mm VAS, where 0 mm = lowest disease activity and 100 mm = highest.~The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI:~Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22" (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo17.7
Apremilast 20 mg12.2
Apremilast 30 mg10.5

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Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo/Apremilast 20mg EE-0.219
Placebo/Apremilast 20 mg XO-0.192
Apremilast 20 mg-0.155
Apremilast 30 mg-0.277

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Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 24

The Health Assessment Questionnaire - Disability Index (HAQ-DI) is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Mean)
Placebo-0.069
Apremilast 20 mg-0.080
Apremilast 30 mg-0.227

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Change From Baseline in Disease Activity Score 28 (DAS28) Using CRP at Week 24

"The DAS28 measures the severity of disease at a specific time and is derived from the following variables:~28 tender joint count~28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee;~C-reactive protein (CRP)~Subject's Global Assessment of Disease Activity.~DAS28 values range from 2.0 to 10.0 while higher values mean a higher disease activity.~A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.82
Apremilast 20 mg-0.78
Apremilast 30 mg-0.91

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Change From Baseline in Disease Activity Score 28 (DAS28) (Using C-Reactive Protein) (CRP) at Week 16

"The DAS28 measures the severity of disease at a specific time and is derived from the following variables:~28 tender joint count (TJC28)~28 swollen joint count (SJC28), which do not include the distal interphalangeal (DIP) joints, the hip joint, or the joints below the knee;~C-reactive protein (CRP)~Subject's global assessment of disease activity (SGA )~DAS28 values range from 2.0 to 10.0 while higher values mean a higher disease activity.~A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission." (NCT01285310)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.90
Apremilast 20 mg-0.73
Apremilast 30 mg-0.90

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Percentage of Participants With an American College of Rheumatology 70% Improvement (ACR 70) Response at Week 52

"Percentage of participants with an American College of Rheumatology 70% Improvement (ACR 70) response. A participant was a responder if the following 3 criteria for improvement from baseline were met:~≥ 70% improvement in 68 tender joint count;~≥ 70% improvement in 66 swollen joint count; and~≥ 70% improvement in at least 3 of the 5 following parameters: Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index ([HAQ-DI]); C-Reactive Protein" (NCT01285310)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo/Apremilast 20mg EE0.0
Placebo/Apremilast 20 mg XO5.0
Apremilast 20 mg7.1
Apremilast 30 mg5.5

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Percentage of Participants With an American College of Rheumatology 70% Improvement (ACR 70) Response at Week 24

"Percentage of participants with an American College of Rheumatology 70% Improvement (ACR 70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met:~≥ 70% improvement in 68 tender joint count;~≥ 70% improvement in 66 swollen joint count; and~≥ 70% improvement in at least 3 of the 5 following parameters:~Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index [(HAQ-DI)]); C-Reactive Protein." (NCT01285310)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo3.8
Apremilast 20 mg2.4
Apremilast 30 mg5.3

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Percentage of Participants Who Achieve an Improvement of ≥ 0.22 Units From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 16

The Health Assessment Questionnaire - Disability Index (HAQ-DI) was a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative mean changes from Baseline in the overall score indicate improvement in functional ability. (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo39.2
Apremilast 20 mg35.4
Apremilast 30 mg52.6

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Percentage of Participants With an American College of Rheumatology 70% Improvement (ACR 70) Response at Week 16

"Percentage of participants with an American College of Rheumatology 70% Improvement (ACR70) response. A participant was a responder if the following 3 criteria for improvement from baseline were met:~≥ 70% improvement in 68 tender joint count;~≥ 70% improvement in 66 swollen joint count; and~≥ 70% improvement in at least 3 of the 5 following parameters: Subject's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Subject's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Subject's self-assessment of physical function (Health Assessment Questionnaire - Disability Index ([HAQ-DI]); C-Reactive Protein" (NCT01285310)
Timeframe: Baseline and Week 16

Interventionpercent of participants (Number)
Placebo2.5
Apremilast 20 mg1.2
Apremilast 30 mg0.0

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8; Low Disease Activity: > 2.8 and ≤ 10; Moderate Disease Activity: > 10 and ≤ 22; High Disease Activity: > 22. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-2.23
Apremilast 20 mg-7.30
Apremilast 30 mg-7.36

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 16

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: • 28 tender joint count (TJC), • 28 swollen joint count (SJC), • Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; • Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22 (NCT01307423)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.98
Apremilast 20 mg-6.89
Apremilast 30 mg-7.63

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 24

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). SF-36 domain scores were first calculated to range from 0 to100 and then transformed to norm-based scores (the norm-based scores in the US general population have an average of 50 and a standard deviation of 10). Norm-based scores were used in analyses, with higher scores indicating a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from baseline score indicates an improvement. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo0.16
Apremilast 20 mg2.13
Apremilast 30 mg3.88

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Change From Baseline in 36-item Short Form Health Survey (SF-36) Physical Functioning Domain at Week 16

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). SF-36 domain scores were first calculated to range from 0 to100 and then transformed to norm-based scores (the norm-based scores in the US general population have an average of 50 and a standard deviation of 10). Norm-based scores were used in analyses, with higher scores indicating a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from baseline score indicates an improvement. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo0.01
Apremilast 20 mg2.39
Apremilast 30 mg3.19

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Percentage of Participants With a ACR 50 Response at Week 24

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo6.3
Apremilast 20 mg16.0
Apremilast 30 mg12.5

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Percentage of Participants With a ACR 50 Response at Week 16

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 50% improvement in 78 tender joint count; • ≥ 50% improvement in 76 swollen joint count; and • ≥ 50% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. (NCT01307423)
Timeframe: Baseline and Week 16

InterventionPercentage of participants (Number)
Placebo4.5
Apremilast 20 mg11.4
Apremilast 30 mg11.4

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Percentage of Participants With a ACR 20 Response at Week 52

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: ≥ 20% improvement in 78 tender joint count; ≥ 20% improvement in 76 swollen joint count; and ≥ 20% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg59.7
Placebo / Apremilast 30 mg56.7
Apremilast 20 mg53.4
Apremilast 30 mg58.7

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Percentage of Participants With ≥ 20% Improvement in Maastricht Ankylosing Spondylitis Entheses Score at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo46.1
Apremilast 20 mg48.7
Apremilast 30 mg63.1

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Percentage of Participants Achieving Good or Moderate EULAR Response at Week 52

The EULAR response criteria classify each subject as a good, moderate or non-responder to treatment based on the degree of improvement from baseline and the level of disease activity at the endpoint. EULAR response is derived using the individual subject's DAS28 as the measure of severity of disease. A Good response is defined as follows: Good response: DAS28 at the time point ≤ 3.2 and improvement from baseline > 1.2 A Moderate Response is defined as either: an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. Two-sided 95% confidence interval is based on the Clopper-Pearson method (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg64.5
Placebo / Apremilast 30 mg73.5
Apremilast 20 mg75.4
Apremilast 30 mg79.0

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Percentage of Participants Achieving a MASES Score of Zero at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo22.6
Apremilast 20 mg29.1
Apremilast 30 mg37.8

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Percentage of Participants Achieving a Dactylitis Score of Zero at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo35.6
Apremilast 20 mg46.1
Apremilast 30 mg40.5

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Change From Baseline in the SF-36v2 Physical Functioning Scale Score at Week 52

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) is a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores were used in analyses, calibrated so that 50 is the average score and the standard deviation equals 10. Higher scores indicate a higher level of functioning. The physical functioning domain assesses limitations in physical activities because of health problems. A positive change from Baseline score indicates an improvement. (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg7.76
Placebo / Apremilast 30 mg6.87
Apremilast 20 mg5.68
Apremilast 30 mg5.87

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Change From Baseline in the Participants Assessment of Pain Using the Visual Analog Scale at Week 52

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01307423)
Timeframe: Baseline and Week 52

Interventionmm (Mean)
Placebo/Apremilast 20 mg-13.1
Placebo / Apremilast 30 mg-18.9
Apremilast 20 mg-15.6
Apremilast 30 mg-14.2

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 24

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo0.25
Apremilast 20 mg1.37
Apremilast 30 mg2.58

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) Score at Week 16

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01307423)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo0.07
Apremilast 20 mg1.19
Apremilast 30 mg2.62

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Change From Baseline in the FACIT-Fatigue Scale Score at Week 52

"The FACIT-Fatigue scale is a 13-item self-administered questionnaire that assesses both the physical and functional consequences of fatigue. Each question is answered on a 5-point scale, where 0 means not at all, and 4 means very much. The FACIT-Fatigue scale score ranges from 0 to 52, with higher scores denoting lower levels of fatigue. A positive change from baseline score indicates an improvement." (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg6.03
Placebo / Apremilast 30 mg4.27
Apremilast 20 mg2.39
Apremilast 30 mg5.89

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Percentage of Participants With an ACR 50 Response at Week 52

Percentage of participants with an American College of Rheumatology 50% (ACR50) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: ≥ 50% improvement in 78 tender joint count; ≥ 50% improvement in 76 swollen joint count; and ≥ 50% improvement in at least 3 of the 5 following parameters: o Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg30.6
Placebo / Apremilast 30 mg25.4
Apremilast 20 mg27.1
Apremilast 30 mg31.9

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Change From Baseline in the Disease Activity Score (DAS28) After 16 Weeks of Treatment

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.15
Apremilast 20 mg-0.61
Apremilast 30 mg-0.68

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Change From Baseline in the DAS28 at Week 52

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-1.08
Placebo / Apremilast 30 mg-1.28
Apremilast 20 mg-1.37
Apremilast 30 mg-1.39

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Change From Baseline in the Dactylitis Severity Score at Week 52

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-2.2
Placebo / Apremilast 30 mg-2.9
Apremilast 20 mg-2.2
Apremilast 30 mg-2.9

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Change From Baseline in the CDAI Score at Week 52

The Clinical Disease Activity Index (CDAI) is a composite index that is calculated as the sum of the: 28 tender joint count (TJC), 28 swollen joint count (SJC), Patient's Global Assessment of Disease Activity measured on a 10 cm visual analog scale (VAS), where 0 cm = lowest disease activity and 10 cm = highest; Physician's Global Assessment of Disease Activity -measured on a 10 cm VAS, where 0 cm = lowest disease activity and 10 cm = highest. The CDAI score ranges from 0-76 where lower scores indicate less disease activity. The following thresholds of disease activity have been defined for the CDAI: Remission: ≤ 2.8 Low Disease Activity: > 2.8 and ≤ 10 Moderate Disease Activity: > 10 and ≤ 22 High Disease Activity: > 22. (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-11.0
Placebo / Apremilast 30 mg-14.67
Apremilast 20 mg-14.32
Apremilast 30 mg-13.98

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Change From Baseline in Patient's Assessment of Pain at Week 16

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01307423)
Timeframe: Baseline and Week 16

Interventionmm (Least Squares Mean)
Placebo-2.6
Apremilast 20 mg-7.7
Apremilast 30 mg-10.5

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Change From Baseline in Participants Assessment of Pain at Week 24

"The participant was asked to place a vertical line on a 100-mm visual analog scale on which the left-hand boundary (score = 0 mm) represents no pain, and the right-hand boundary (score = 100 mm) represents pain as severe as can be imagined. The distance from the mark to the left-hand boundary was recorded in millimeters." (NCT01307423)
Timeframe: Baseline and Week 24

Interventionmm (Least Squares Mean)
Placebo-3.8
Apremilast 20 mg-9.4
Apremilast 30 mg-9.6

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 52

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-1.7
Placebo/Apremilast 30 mg-1.8
Apremilast 20 mg-1.5
Apremilast 30 mg-1.8

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 24

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.6
Apremilast 20 mg-0.9
Apremilast 30 mg-1.5

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Change From Baseline in Maastricht Ankylosing Spondylitis Entheses Score (MASES) at Week 16

The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-0.5
Apremilast 20 mg-0.5
Apremilast 30 mg-1.5

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Change From Baseline in Health Assessment Questionnaire- Disability Index [HAQ-DI]) at Week 24

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative changes from Baseline in the overall score indicate improvement in functional ability. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo0.012
Apremilast 20 mg-0.156
Apremilast 30 mg-0.207

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Number of Participants With Treatment Emergent Adverse Events During the Placebo Controlled Phase

A TEAE is an adverse event (AE) with a start date on or after the date of the first dose of investigational product (IP) and no later than 28 days after the last dose of IP. An AE is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a subject during the course of a study. A serious AE is any AE that results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent or significant disability/incapacity; is a congenital anomaly/birth defect; or constitutes an important medical event. For both AEs and SAEs the investigator assessed the severity of the event according to the grading scale: Mild: asymptomatic or with mild symptoms, Moderate: symptoms causing moderate discomfort or Severe: symptoms causing severe discomfort or pain. (NCT01307423)
Timeframe: Week 0 to Week 16 for placebo participants who entered EE at Week 16 and up to Week 24 for all other participants (placebo participants who remained on placebo through week 24 and participants randomized to the APR 20 mg BID or APR 30 mg BID)

,,
InterventionParticipants (Count of Participants)
Any TEAEAny Drug-Related TEAEAny Severe TEAEAny Serious TEAE (SAE)Drug-Related (SAE)Any TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to Death
Apremilast 20mg87404301140
Apremilast 30mg9958211960
Placebo7325650840

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Number of Participants With Treatment Emergent Adverse Events During the Apremilast Exposure Period

A TEAE is an adverse event (AE) with a start date on or after the date of the first dose of investigational product (IP) and no later than 28 days after the last dose of IP. An AE is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a subject during the course of a study. A serious AE is any AE that results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent or significant disability/incapacity; is a congenital anomaly/birth defect; or constitutes an important medical event. For both AEs and SAEs the investigator assessed the severity of the event according to the grading scale: Mild: asymptomatic or with mild symptoms, Moderate: symptoms causing moderate discomfort or Severe: symptoms causing severe discomfort or pain. (NCT01307423)
Timeframe: Week 0 to Week 260; median duration of exposure to apremilast 20 mg BID was 168.93 weeks and 229.36 weeks for apremilast 30 mg BID

,,
InterventionParticipants (Count of Participants)
Any TEAEAny Drug-Related TEAEAny Severe TEAEAny Serious TEAE (SAE)Drug-Related (SAE)Any TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WirhdrawalAny TEAE Leading to Death
Apremilast 20 mg (Pre-Switch)188892435641220
Apremilast 20/30 mg (Post-Switch)6016351520
Apremilast 30 mg2041132336636260

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Percentage of Participants With Pre-existing Enthesopathy Whose MASES Improves From Baseline to 0 at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 24 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval was based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

Interventionpercentage of participants (Number)
Placebo / Apremilast 20 mg39.0
Placebo / Apremilast 30 mg61.9
Apremilast 20 mg39.6
Apremilast 30 mg45.9

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Percentage of Participants With Pre-existing Enthesopathy Whose Maastricht Ankylosing Spondylitis Entheses Score Improves to 0 at Week 16

Percentage of participants with pre-existing enthesopathy whose MASES improves to 0 after 16 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo19.1
Apremilast 20 mg21.4
Apremilast 30 mg36.9

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Percentage of Participants With Pre-existing Dactylitis Whose Dactylitis Severity Score Improves to 0 at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo33.3
Apremilast 20 mg42.7
Apremilast 30mg40.5

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Percentage of Participants With Pre-existing Dactylitis Whose Dactylitis Severity Score Improves From Baseline to 0 at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improves to zero after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit and ranges from 0 to 20. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg75.0
Placebo / Apremilast 30 mg78.9
Apremilast 20 mg68.6
Apremilast 30 mg68.8

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Percentage of Participants With Pre-existing Dactylitis Whose Dactylitis Severity Score Improves From Baseline by ≥ 1 at Week 52

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 52 weeks. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg93.8
Placebo / Apremilast 30 mg94.7
Apremilast 20 mg87.1
Apremilast 30 mg85.9

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Percentage of Participants With MASES Improvement ≥ 20% at Week 52

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 52 weeks. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg70.7
Placebo / Apremilast 30 mg81.0
Apremilast 20 mg65.9
Apremilast 30 mg69.4

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Percentage of Participants With MASES Improvement ≥ 20% at Week 24

Percentage of participants with pre-existing enthesopathy whose MASES improved by ≥ 20% from Baseline after 24 weeks of treatment. The Maastricht Ankylosing Spondylitis Enthesitis Score quantitates inflammation of the entheses (enthesitis) by assessing pain at the following entheses (sites where tendons or ligaments insert into the bone): 1st costochondral joints left/right; 7th costochondral joints left/right; posterior superior iliac spine left/right; anterior superior iliac spine left/right; iliac crest left/right; 5th lumbar spinous process; and the proximal insertion of the Achilles tendon left/right. The MASES, ranging from 0 to 13, is the number of painful entheses out of 13 entheses. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo48.7
Apremilast 20 mg54.7
Apremilast 30 mg66.7

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Percentage of Participants With Good or Moderate European League Against Rheumatism (EULAR) Response at Week 16

The EULAR response criteria classify each subject as a good, moderate or non-responder to treatment based on the degree of improvement from baseline and the level of disease activity at the endpoint. EULAR response is derived using the individual subject's DAS28 as the measure of severity of disease. Good or moderate response is defined as follows: Good response: DAS28 at the time point ≤ 3.2 and improvement from baseline > 1.2 Moderate response: DAS28 at the time point > 3.2 and improvement from baseline > 1.2, or DAS28 at the time point ≤ 5.1 and improvement from baseline > 0.6 and ≤ 1.2 (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo25.0
Apremilast 20 mg41.1
Apremilast 30 mg44.3

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Percentage of Participants With Good or Moderate EULAR Response at Week 24

The EULAR response reflects an improvement in disease activity and an attainment of a lower degree of disease activity based on th DAS-28. Good or moderate response is defined as follows: Good response: DAS28 at the time point ≤ 3.2 and improvement from baseline > 1.2 Moderate response: DAS28 at the time point > 3.2 and improvement from baseline > 1.2, or DAS28 at the time point ≤ 5.1 and improvement from baseline > 0.6 and ≤ 1.2 A Moderate Response is defined as either: • an improvement (decrease) in the DAS28 of greater than 0.6 and less than or equal to 1.2 and attainment of a DAS28 score of less than or equal to 5.1 or, • an improvement (decrease) in the DAS28 of more than 1.2 and attainment of a DAS28 score of greater than 3.2. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo17.0
Apremilast 20 mg34.9
Apremilast 30 mg28.4

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 24

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 24 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo57.8
Apremilast 20 mg69.7
Apremilast 30 mg63.1

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Percentage of Participants With Dactylitis Improvement ≥ 1 Point at Week 16

Percentage of participants with pre-existing dactylitis whose dactylitis severity score improved by ≥ 1 after 16 weeks of treatment. Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet was rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo60.0
Apremilast 20 mg66.3
Apremilast 30 mg61.9

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Percentage of Participants With an American College of Rheumatology 20% (ACR20) Response at Week 16

A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: -Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); -Patient's global assessment of disease activity (measured on a 100 mm VAS); -Physician's global assessment of disease activity (measured on a 100 mm VAS); -Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); -C-Reactive Protein. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo15.9
Apremilast 20mg28.0
Apremilast 30mg30.7

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Percentage of Participants With an ACR 70 Response at Week 52

A participant was a responder if the following 3 criteria for improvement from Baseline were met: ≥ 70% improvement in 78 tender joint count; ≥ 70% improvement in 76 swollen joint count; and ≥ 70% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg8.2
Placebo / Apremilast 30 mg10.3
Apremilast 20 mg13.7
Apremilast 30 mg18.1

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Percentage of Participants With an ACR 20 Response at Week 24

Percentage of participants with an American College of Rheumatology 20% (ACR20) response. A participant was a responder if the following 3 criteria for improvement from baseline were met: • ≥ 20% improvement in 78 tender joint count; • ≥ 20% improvement in 76 swollen joint count; and • ≥ 20% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo13.1
Apremilast 20 mg29.1
Apremilast 30 mg24.4

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 24

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0=lowest disease activity and 100=highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0=lowest disease activity and 100=highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo17.0
Apremilast 20 mg36.6
Apremilast 30 mg35.2

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Percentage of Participants With a Modified Psoriatic Arthritis Response Criteria (PsARC) Response at Week 16

Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0=lowest disease activity and 100=highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0=lowest disease activity and 100=highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo24.4
Apremilast 20 mg38.9
Apremilast 30 mg45.5

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Percentage of Participants With a Modified PsARC Response at Week 52

Measure Description: Modified PsARC response is defined as improvement in at least 2 of the 4 measures, at least one of which must be tender joint count or swollen joint count, and no worsening in any of the 4 measures: • 78 tender joint count, • 76 swollen joint count, • Patient global assessment of disease activity, measured on a 100 mm visual Analog scale (VAS), where 0=lowest disease activity and 100=highest; • Physician global assessment of disease activity, measured on a 100 mm VAS, where 0=lowest disease activity and 100=highest. Improvement or worsening in joint counts is defined as decrease or increase, respectively, from baseline by ≥ 30%, and improvement or worsening in global assessments is defined as decrease or increase, respectively, from baseline by ≥ 20 mm VAS. Two-sided 95% confidence interval is based on the Clopper-Pearson method. (NCT01307423)
Timeframe: Baseline and Week 52

InterventionPercentage of Participants (Number)
Placebo / Apremilast 20 mg73.8
Placebo / Apremilast 30 mg79.1
Apremilast 20 mg75.6
Apremilast 30 mg75.9

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Percentage of Participants With a ACR 70 Response at Week 24

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionpercentage of participants (Number)
Placebo4.0
Apremilast 20 mg4.0
Apremilast 30mg4.5

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Percentage of Participants With a ACR 70 Response at Week 16

Percentage of participants with an American College of Rheumatology 70% (ACR70) response. A participant was a responder if the following 3 criteria for improvement from Baseline were met: • ≥ 70% improvement in 78 tender joint count; • ≥ 70% improvement in 76 swollen joint count; and • ≥ 70% improvement in at least 3 of the 5 following parameters: Patient's assessment of pain (measured on a 100 mm visual analog scale [VAS]); Patient's global assessment of disease activity (measured on a 100 mm VAS); Physician's global assessment of disease activity (measured on a 100 mm VAS); Patient's self-assessment of physical function (Health Assessment Questionnaire - Disability Index (HAQ-DI)); C-Reactive Protein. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionpercentage of participants (Number)
Placebo1.1
Apremilast 20 mg4.0
Apremilast 30 mg4.0

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Change From Baseline in Health Assessment Questionnaire- Disability Index [HAQ-DI]) at Week 16

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative changes from baseline in the overall score indicate improvement in functional ability. (NCT01307423)
Timeframe: Baseline and Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo0.012
Apremilast 20 mg-0.156
Apremilast 30mg-0.205

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Change From Baseline in Health Assessment Questionnaire - Disability Index (HAQ-DI) at Week 52

The Health Assessment Questionnaire - Disability Index is a patient-reported questionnaire consisting of 20 questions referring to eight domains: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and usual activities. Participants assessed their ability to do each task over the past week using the following response categories: without any difficulty (0); with some difficulty (1); with much difficulty (2); and unable to do (3). Scores on each task are summed and averaged to provide an overall score ranging from 0 to 3, where zero represents no disability and three very severe, high-dependency disability. Negative changes from Baseline in the overall score indicate improvement in functional ability. (NCT01307423)
Timeframe: Baseline and Week 52

Interventionunits on a scale (Mean)
Placebo / Apremilast 20 mg-0.21
Placebo / Apremilast 30 mg-0.25
Apremilast 20 mg-0.32
Apremilast 30 mg-0.39

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Change From Baseline in Disease Activity Score (DAS 28) at Week 24

The DAS28 measures the severity of disease at a specific time and is derived from the following variables: • 28 tender joint count • 28 swollen joint count, which do not include the DIP joints, the hip joint, or the joints below the knee; • C-reactive protein (CRP) • Patient's global assessment of disease activity. DAS28(CRP) scores range from 0 to approximately 10, with the upper bound dependent on the highest possible level of CRP. A DAS28 score higher than 5.1 indicates high disease activity, a DAS28 score less than 3.2 indicates low disease activity, and a DAS28 score less than 2.6 indicates clinical remission. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-0.22
Apremilast 20 mg-0.69
Apremilast 30 mg-0.68

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Change From Baseline in Dactylitis Severity Score at Week 24

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01307423)
Timeframe: Baseline and Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo-1.0
Apremilast 20 mg-2.0
Apremilast 30 mg-1.7

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Change From Baseline in Dactylitis Severity Score at Week 16

Dactylitis is characterized by swelling of the entire finger or toe. Each digit on the hands and feet will be rated as zero for no dactylitis or 1 for dactylitis present. The dactylitis severity score is the sum of the individual scores for each digit. The dactylitis severity score, ranging from 0 to 20, is the number of digits on the hands and feet with dactylitis present. (NCT01307423)
Timeframe: Baseline to Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.0
Apremilast 20 mg-1.9
Apremilast 30 mg-1.7

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Overall Survival (OS)

OS was defined as the time between randomization and death. Death of a participant regardless of the cause was considered as an event. (NCT01539083)
Timeframe: Up to 5 years

Interventionmonths (Median)
Thalidomide + Prednisolone [TP Consolidation]NA
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]NA

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Disease-free Survival (DFS)

DFS, defined as the duration from the start of CR to the time of relapse from CR. DFS applied only to participants in CR. CR as per IMWG criteria is negative immunofixation on serum and urine and disappearance of soft tissue plasmacytomas and <5 percent plasma cells in bone marrow. Relapse from CR: reappearance of serum or urine M-protein by immunofixation or electrophoresis; development of >= 5 percent plasma cells in the bone marrow; appearance of any other sign of progression (ie, new plasmacytoma, lytic bone lesion, or hypercalcaemia). (NCT01539083)
Timeframe: Up to 5 years

Interventionmonths (Median)
Thalidomide + Prednisolone [TP Consolidation]18.53
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]13.37

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Consolidation Phase: Percentage of Participants With Complete Response (CR) and Very Good Partial Response (VGPR) at Month 12

CR as per IMWG criteria is defined as negative immunofixation on the serum and urine and disappearance of soft tissue plasmacytomas and less than (<) 5 percent plasma cells in bone marrow. VGPR as per IMWG criteria is defined as serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90 percent or greater reduction in serum M-protein plus urine M-protein level <100 milligram (mg) per 24 hours. (NCT01539083)
Timeframe: Month 12

Interventionpercentage of participants (Number)
Thalidomide + Prednisolone [TP Consolidation]81.3
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]92.9

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Consolidation Phase: Change From Baseline in FACT/GOG-NTX Total Score at the End of the Consolidation Phase

Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-NTX) consists of 10 items and evaluates symptoms and concerns associated specifically with chemotherapy-induced neuropathy. 1 FACT/GOG-NTX total score has a range of 0 to 108 with a higher score indicating better quality of life. (NCT01539083)
Timeframe: Baseline, Month 12

Interventionunits on a scale (Mean)
Thalidomide + Prednisolone [TP Consolidation]2.9
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]1.0

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Consolidation Phase: Percentage of Participants With Stringent Complete Response (sCR) at Months 3, 6, 9 and 12

sCR as per IMWG criteria is CR plus normal free light chain (FLC) ratio and absence of clonal cells in bone marrow. CR is negative immunofixation on serum and urine and disappearance of soft tissue plasmacytomas and <5 percent plasma cells in bone marrow. (NCT01539083)
Timeframe: Months 3, 6, 9 and 12

,
Interventionpercentage of participants (Number)
Month 3Month 6Month 9Month 12
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]23.528.630.628.6
Thalidomide + Prednisolone [TP Consolidation]20.827.126.026.0

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Consolidation Phase: Percentage of Participants With Complete Response (CR) at Months 3, 6, 9 and 12

CR as per IMWG criteria is negative immunofixation on serum and urine and disappearance of soft tissue plasmacytomas and <5 percent plasma cells in bone marrow. (NCT01539083)
Timeframe: Months 3, 6, 9 and 12

,
Interventionpercentage of participants (Number)
Month 3Month 6Month 9Month 12
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]36.744.952.053.1
Thalidomide + Prednisolone [TP Consolidation]36.544.849.051.0

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Consolidation Phase: Change From Baseline in AQOL-6D Scores at the End of the Consolidation Phase

The assessment of quality of life-6D (AQoL-6D) is a multi-attribute health-related quality of life instrument (QoL). It comprises dimension scores for independent living, relationships, mental health, coping, pain, senses, and utility score for AQol-6D. Each scale ranges between 1 (best QoL) and -0.04 (worst possible QoL). (NCT01539083)
Timeframe: Baseline, Month 12

,
Interventionunits on a scale (Mean)
Independent LivingRelationshipsMental HealthCopingPainSensesAQoL-6D Utility score
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]0.140.050.180.050.200.000.11
Thalidomide + Prednisolone [TP Consolidation]0.150.060.180.080.200.030.11

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Progression Free Survival (PFS)

PFS, calculated as the time between randomization to disease progression or death (regardless of cause), whichever occurred first. Progressive disease as per IMWG criteria: increase of >= 25 percent from lowest response level in Serum M-component and/or (the absolute increase must be >=0.5 gram per deciliter [g/dL]) Urine M-component and/or (the absolute increase must be >=200 mg/24 hour. Only in participants without measurable serum and urine M-protein levels: the difference between involved and uninvolved free light chain levels. The absolute increase must be >10 mg/dL. Bone marrow plasma cell percentage: the absolute percent must be >=10 percent. Definite development of new bone lesions or soft tissue plasmacytomas or definite increase in the size of existing bone lesions or soft tissue plasmacytomas. Development of hypercalcemia (corrected serum calcium >11.5 mg/dL or 2.65 millimole per liter (mmol/L) that can be attributed solely to the plasma cell proliferative disorder. (NCT01539083)
Timeframe: Baseline until progressive disease (up to 5 years)

Interventionmonths (Median)
Thalidomide + Prednisolone [TP Consolidation]22.05
Bortezomib + Thalidomide + Prednisolone [VTP Consolidation]22.51

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Event-Free Survival (EFS)

To determine whether, in comparison to Total Therapy II, the median Event-Free Survival (EFS) can be increased from 4.8 years to 7.2 years, which represents an increase in median EFS of approximately 50%, based on an intent-to-treat analysis. (NCT01548573)
Timeframe: 8 years

Intervention ()
Tandem Autologous Stem Cell Transplant0

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Identification of Drug Resistant Genes

To determine whether repeated bone marrow samples analyzed for gene expression profiling (GEP) can identify genes related to drug resistance in myeloma. The drug resistant genes or the gene products might then be targeted specifically to eradicate myeloma cells surviving tandem transplantation. (NCT01548573)
Timeframe: 5 years

Intervention ()
Tandem Transplant in MM <12 Mos of Prior Treatment0

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Number of Grade 3 Non-hematologic and Grade 4 Hematologic Serious Adverse Events Associated With the Addition of Bortezomib, Thalidomide, and Dexamethasone Into Autologous Transplant Regimens.

To determine whether bortezomib, thalidomide and dexamethasone with transplant 1 and velcade/gemcitabine with transplant 2 can be safely incorporated into well-tested pre-transplant regimens of high-dose melphalan and carmustine/melphalan in doses equivalent to the BEAM(BCNU, etoposide, arabinoside, melphalan)regimen. Treatment-related toxicities will be compared to those reported in the literature using similar intensive approaches. (NCT01548573)
Timeframe: 2 years

Intervention ()
Tandem Transplant in MM <12 Mos of Prior Treatment0

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Overall Survival

To determine the median overall survival based on an intent-to-treat analysis, which should exceed 10 years, based on the projected 10-year survival of Total Therapy III, keeping in mind that participants are included in this protocol with up to 12 months of prior therapy. (NCT01548573)
Timeframe: 10 years

Intervention ()
Tandem Transplant in MM <12 Mos of Prior Treatment0

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Number of Participants With Treatment Emergent Adverse Events During the Apremilast Exposure Period

A TEAE was an adverse event (AE) with a start date on or after the date of the first dose of IP and no later than 28 days after the last dose of IP for participants who discontinued early. A serious AE = results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect; or constitutes an important medical event. The severity of AEs was assessed based on the following scale: Mild = asymptomatic or mild symptoms, clinical or diagnostic observations only; Moderate = symptoms cause moderate discomfort; Severe = symptoms causing severe pain discomfort. (NCT01583374)
Timeframe: Week 0 to week 260; overall mean duration of exposure to apremilast 20 mg and 30 mg BID was 160.96 weeks

,,
InterventionParticipants (Count of Participants)
Any Treatment Emergent Adverse EventAny Severe TEAEAny Serious TEAEAny TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to Death
Apremilast 20 mg11451222180
Apremilast 20/30 mg47881141
Apremilast 30 mg239234151341

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Percentage of Participants Who Achieved an Assessment of SpondyloArthritis International Society 20 (ASAS 20) Response at Week 16

"ASAS 20 was defined as achieving an improvement from baseline of ≥ 20% and ≥ 1 unit in at least 3 of 4 ASAS domains on a scale of 0 to 10 units and no worsening from baseline of ≥ 20% and ≥ 1 unit in the remaining ASAS domain on a scale of 0 to 10 units. The 4 ASAS domains are:~Patient Global Assessment of Disease (0 - 10 unit Numerical Rating Scale [NRS]); participant marks a box with an X on a 0 - 10 unit NRS; the left-hand box of 0 = not active and the right-hand box = very active~Total Back Pain (0 to 10 unit NRS); participant marks a box with an X on a 0 - 10 unit NRS; the left-hand box of 0 = no pain and the right-hand box = most severe pain~Function (Bath AS Functional Index [BASFI] NRS 0 - 10 unit); participant provides a self-administered survey of 10 questions assessing for degree of mobility and functional ability~Inflammation domain is determined by the mean of 2 Bath AS Disease Activity Index NRS Questions #5 and #6 for morning stiffness) (0 - 10 unit)" (NCT01583374)
Timeframe: Baseline and Week 16

InterventionPercentage of Participants (Number)
Placebo36.6
Apremilast 20 mg35.0
Apremilast 30 mg32.5

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Number of Participants With Treatment Emergent Adverse Events (TEAEs) During the Placebo Controlled Phase

A TEAE was an adverse event (AE) with a start date on or after the date of the first dose of IP and no later than 28 days after the last dose of IP for participants who discontinued early. A serious AE = results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect; or constitutes an important medical event. The severity of AEs was assessed based on the following scale: Mild = asymptomatic or mild symptoms, clinical or diagnostic observations only; Moderate = symptoms cause moderate discomfort; Severe = symptoms causing severe pain discomfort. (NCT01583374)
Timeframe: From Week 0 to Week 24; the median duration of exposure was 23.57 weeks for the placebo arm, 23.71 weeks for the apremilast 20 mg arm and 24.00 weeks for the apremilast 30 mg arm.

,,
InterventionParticipants (Count of Participants)
Any Treatment Emergent Adverse EventAny Drug-related TEAEAny Severe TEAEAny Serious TEAEAny Serious Drug-related TEAEAny TEAE Leading to Drug InterruptionAny TEAE Leading to Drug WithdrawalAny TEAE Leading to Death
Apremilast 20 mg914423013110
Apremilast 30 mg885156314130
Placebo83240101470

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Change From Baseline in the Radiographic Score Using the Modified Stoke Ankylosing Spondylitis Spine Score (m-SASSS) at Week 104 and Week 260

"The Modified Stoke Ankylosing Spondylitis Spine Score is a scoring method used to determine the amount or degree of ankylosing spondylitis disease that is in the spine based on x-ray radiographs of the spine. The m-SASSS scores 0-3.~0 = No abnormality, 1 = Erosion, Sclerosis or Squaring, 2 = Syndesmophyte, 3 = Total bony Bridging at each Site. An increase in the m-SASSS indicated a worsening of AS disease." (NCT01583374)
Timeframe: Baseline to Week 104 and 260

,,,,
InterventionUnits on a Scale (Mean)
Week 104Week 260
Apremilast 20 mg0.993.14
Apremilast 20 mg/ Apremilast 30 mg0.822.21
Apremilast 20 mg/Apremilast 20 mg1.123.83
Apremilast 30 mg0.651.79
Placebo/Apremilast 30 mg0.981.92

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Percentage of Participants Who Achieved an Assessment of SpondyloArthritis International Society 20 (ASAS) Response at Week 24

"ASAS 20 was defined as achieving an improvement from baseline of ≥ 20% and ≥ 1 unit in at least 3 of 4 ASAS domains on a scale of 0 to 10 units and no worsening from baseline of ≥ 20% and ≥ 1 unit in the remaining ASAS domain on a scale of 0 to 10 units. The 4 ASAS domains are:~Patient Global Assessment of Disease (0 - 10 unit Numerical Rating Scale [NRS]); participant marks a box with an X on a 0 - 10 unit NRS; the left-hand box of 0 = not active and the right-hand box = very active~Total Back Pain (0 to 10 unit NRS); participant marks a box with an X on a 0 - 10 unit NRS; the left-hand box of 0 = no pain and the right-hand box = most severe pain~Function (Bath AS Functional Index [BASFI] NRS 0 - 10 unit); participant provides a self-administered survey of 10 questions assessing for degree of mobility and functional ability~Inflammation domain is determined by the mean of 2 Bath AS Disease Activity Index NRS Questions #5 and #6 for morning stiffness) (0 - 10 unit)" (NCT01583374)
Timeframe: Baseline and Week 24

InterventionPercentage of Participants (Number)
Placebo31.7
Apremilast 20 mg36.2
Apremilast 30 mg33.7

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Change From Baseline in Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) at Week 24

The BASDAI is a composite score based on a participant self-administered survey of six questions measured using a 0 to 10 unit numerical rating scale (NRS) that assessed the participants' five major symptoms of AS: 1) fatigue; 2) spinal pain; 3) peripheral joint pain/swelling; 4) areas of localized tenderness; 5a) morning stiffness severity upon wakening; 5b) morning stiffness duration upon wakening. The participant was asked to mark the box with an X on a 0 to 10 unit NRS for each of the 6 questions. To give each of the five symptoms equal weighting, the mean of the two scores relating to morning stiffness was taken. The resulting 0 to 50 score was divided by 5 to give a final 0 to 10 BASDAI score. A BASDAI score of 4 or greater was considered to be indicative of active AS disease. (NCT01583374)
Timeframe: Baseline and Week 24

InterventionUnits on a Scale (Least Squares Mean)
Placebo-1.21
Apremilast 20 mg-1.30
Apremilast 30 mg-1.18

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Change From Baseline in Bath Ankylosing Spondylitis Functional Index (BASFI) at Week 24

The BASFI is a composite score based on a self-administered survey of 10 questions using a 0 to 10 unit numerical rating scale (NRS) that assesses the degree of mobility and functional ability. The survey consists of 8 questions regarding function in AS and the last 2 reflect the ability to manage everyday life. The patient marks a box with an X on a 0 to 10 unit NRS for 10 questions; the left-hand box of 0 = easy; the right-hand box = impossible. The resulting 0 to 100 score is divided by 10 to give a final 0 to 10 BASFI score. The overall score is the mean of the 10 items and ranges from 0 to 10. A higher score correlates to reduced functional ability. (NCT01583374)
Timeframe: Baseline and Week 24

InterventionUnits on a Scale (Least Squares Mean)
Placebo-0.94
Apremilast 20 mg-1.11
Apremilast 30 mg-0.99

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Change From Baseline in Bath Ankylosing Spondylitis Metrology Index-Linear (BASMI-Linear) at Week 24

The BASMI-Linear was designed to assess axial status (ie, cervical, dorsal and lumbar spine, hips, and pelvic soft tissue) and to define clinically significant changes in spinal movement. Five dimensions of movement (lateral lumbar flexion, tragus to wall, forward lumbar flexion, maximal intermalleolar distance, and cervical rotation) were measured and normalized on 0 to 10 unit NRS. The average of these scores was the total BASMI score, ranging from 0-10 with higher values indicating more severe limitation in spinal mobility. (NCT01583374)
Timeframe: Baseline and Week 24

InterventionUnits on a Scale (Least Squares Mean)
Placebo-0.19
Apremilast 20 mg-0.16
Apremilast 30 mg-0.13

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Change From Baseline in the Ankylosing Spondylitis Quality of Life (ASQoL) Summary Score at Week 24

The ASQoL is a validated disease specific patient reported outcomes instrument to assess the impact of ankylosing spondylitis on the quality of life of individuals with emphasis on the ability of the person to fulfill his or her needs. It consisted of 18 items requesting a yes (score=1) or no (score=0) response to questions related to the impact of pain on sleep, mood, motivation, ability to cope, activities of daily living, independence, relationships, and social life. The summary score ranges 0-18 with higher scores indicating worse quality of life. (NCT01583374)
Timeframe: Baseline and Week 24

InterventionUnits on a Scale (Least Squares Mean)
Placebo-1.77
Apremilast 20 mg-1.50
Apremilast 30 mg-1.52

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Change From Baseline in the Physical Component Summary Score (PCS) of Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) at Week 24

The Medical Outcome Study Short Form 36-Item Health Survey, Version 2 (SF-36) was a self-administered instrument that measures the impact of disease on overall quality of life and consists of 36 questions in eight domains (physical function, pain, general and mental health, vitality, social function, physical and emotional health). Norm-based scores (based on US general population with mean of 50 and standard deviation of 10) were used in analyses. Higher scores indicate a higher level of functioning. The PCS encompasses physical functioning, role-physical, and bodily pain, as well as general health and vitality. A positive change from baseline score indicates an improvement (NCT01583374)
Timeframe: Baseline and Week 24

InterventionUnits on a Scale (Least Squares Mean)
Placebo3.50
Apremilast 20 mg3.46
Apremilast 30 mg3.79

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Percentage of All Participants Who Received Treatment Without Cyclophosphamide and Had Grade 3 or Higher Nonhematologic Adverse Events (AEs)

AE=any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. SAE=a medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency/abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. Treatment-related=having certain, probable, possible, or unknown relationship to study drug. Grade (Gr) 1=Mild, Gr 2=Moderate, Gr 3=Severe, Gr 4=Life-threatening or disabling, Gr 5=Death. (NCT01632150)
Timeframe: From the first dose of study drug until the earlier of discontinuation from E-Td or the time when cyclophosphamide was initiated

InterventionPercentage of participants (Number)
Thalidomide + Elotuzumab + Dexamethasone55.0

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Percentage of Participants Who Received Treatment Including Cyclophosphamide and Had Grade 3 or Higher Nonhematologic Adverse Events (AEs)

AE=any new unfavorable symptom, sign, or disease or worsening of a preexisting condition that may not have a causal relationship with treatment. SAE=a medical event that at any dose results in death, persistent or significant disability/incapacity, or drug dependency/abuse; is life-threatening, an important medical event, or a congenital anomaly/birth defect; or requires or prolongs hospitalization. Treatment-related=having certain, probable, possible, or unknown relationship to study drug. Grade (Gr) 1=Mild, Gr 2=Moderate, Gr 3=Severe, Gr 4=Life-threatening or disabling, Gr 5=Death. (NCT01632150)
Timeframe: From the first dose of study drug until the last dose of treatment, including cyclophosphamide treatment

InterventionPercentage of participants (Number)
Thalidomide + Elotuzumab + Dexamethasone + Cyclophosphamide62.5

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Percentage of All Participants Who Received Treatment Including Cyclophosphamide and Had 1 Dose Reduction or Discontinued Due to an Adverse Event

Elotuzumab dose reduction was not permitted. Thalidomide dose reduction, delay, interruptions, or discontinuation was permitted in the event of toxicity. Dexamethasone dose reduction was also permitted in the event of toxicity and in the setting of infusion reactions;dose delays were allowed as clinically indicated at the discretion of the investigator. Cyclophosphamide dose reduction, delay, interruption, or discontinuation was permitted in the event of toxicity. (NCT01632150)
Timeframe: From the first dose of study drug until the last dose of treatment, including cyclophosphamide treatment

InterventionPercentage of participants (Number)
Thalidomide + Elotuzumab + Dexamethasone + Cyclophosphamide65.0

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Percentage of All Participants Who Received Treatment Without Cyclophosphamide and Had 1 Dose Reduction or Discontinued Due to an Adverse Event

Elotuzumab dose reduction was not permitted. Thalidomide dose reduction, delay, interruptions, or discontinuation was permitted in the event of toxicity. Dexamethasone dose reduction was also permitted in the event of toxicity and in the setting of infusion reactions;dose delays were allowed as clinically indicated at the discretion of the investigator. (NCT01632150)
Timeframe: From the first dose of study drug until the earlier of discontinuation from E-Td or the time when cyclophosphamide was initiated

InterventionPercentage of participants (Number)
Thalidomide + Elotuzumab + Dexamethasone57.5

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Number of Hospitalizations

A hospitalization was defined as at least one overnight stay in an intensive care unit and/or non-intensive care unit. If a single hospitalization included both an intensive care unit stay and a non-intensive care unit stay, the hospitalization was counted only once (as an intensive care unit stay). The mean number of hospitalizations is reported in this outcome measure. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionhospitalizations (Mean)
Arm A: Ixazomib + Dexamethasone1.8
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide1.4

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2-Year Vital Organ (Heart or Kidney) Deterioration and Mortality Rate

Cardiac (Heart) deterioration was defined as the need for hospitalization for heart failure. Kidney deterioration was defined as progression to end-stage renal disease (ESRD) with the need for maintenance dialysis or renal transplantation. Vital organ deterioration was evaluated by an adjudication committee. Percentages were rounded off to the nearest decimal. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: Up to 2 years

Interventionpercentage of participants (Number)
Arm A: Ixazomib + Dexamethasone47
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide54

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Percentage of Participants With Overall Hematologic Response

Overall hematologic response was defined as the percentage of participants with complete response (CR), very good partial response (VGPR) and partial response (PR) based on central laboratory results and the 2010 International Society of Amyloidosis (ISA) Consensus Criteria as assessed by an adjudication committee. CR: Complete disappearance of M-protein from serum and urine on immunofixation, and normalization of free light chain (FLC) ratio. VGPR: differential free light chain (difference between involved and uninvolved FLC levels; dFLC) < 40 mg/L. PR: ≥50% reduction in dFLC. Percentages were rounded off to the nearest decimal. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionpercentage of participants (Number)
Arm A: Ixazomib + Dexamethasone53
Arm B: Dexamethasone + Melphalan58
Arm B: Dexamethasone + Cyclophosphamide30
Arm B: Dexamethasone + Thalidomide50
Arm B: Dexamethasone + Lenalidomide51

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Percentage of Participants With Complete Hematologic Response

Complete hematologic response was defined as the percentage of participants with CR based on central laboratory results and the 2010 ISA Consensus Criteria as assessed by the investigator. CR: Complete disappearance of M-protein from serum and urine on immunofixation, and normalization of FLC ratio. Percentages were rounded off to the nearest decimal. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionpercentage of participants (Number)
Arm A: Ixazomib + Dexamethasone30
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide17

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Percentage of Participants With Best Vital Organ (Cardiac and/or Kidney) Response

Vital organ (heart and kidney) response rate was defined as the percentage of participants who achieved vital organ response according to central laboratory results and ISA criteria as evaluated by an adjudication committee. A vital organ response was defined as response of 1 or 2 of the involved vital organs with no change from Baseline in the rest of involved vital organs. Percentages were rounded off to the nearest decimal. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionpercentage of participants (Number)
Arm A: Ixazomib + Dexamethasone19
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide12

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Overall Survival

Overall survival was defined as the time from the date of randomization to the date of death. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone69.55
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide43.17

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EuroQol 5-Dimension 3-Level (EQ-5D-3L) Visual Analogue Scale Score

The EQ visual analogue scale (VAS) records the participant's self-rated health on a 20 centimeter vertical VAS that ranges from 0 (worst imaginable health state) to 100 (best imaginable health state). Baseline is defined as the value collected at the time closest to, but prior to, the start of study drug administration. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: At Week 28 of the OS follow-up

Interventionscore on a scale (Mean)
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide23.0

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Duration of Hematologic Response

Duration of hematologic response (DOR) was defined as the time from the date of first documentation of a hematologic response to the date of first documented hematologic disease progression as determined by the investigator. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From time of first documented response to disease progression (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + DexamethasoneNA
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide21.19

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Change From Baseline in SF-36 Physical Component Summary Score at Week 28 of the PFS Follow-up

SF-36 Version 2 is a multipurpose, participant completed, short-form health survey with 36 questions that consists of an 8-scale profile of functional health and well-being scores as well as psychometrically-based physical and mental health summary measures. Physical component summary (PCS) is mostly contributed by physical function (PF), role physical (RP), bodily pain (BP), and general health (GH). Mental component summary (MCS) is mostly contributed by mental health (MH), role emotional (RE), social function (SF), and vitality (VT). Each component on the SF-36 item health survey is scored from 0 (best) to 100 (worst). Total score ranges from 0-100, where higher scores are associated with less disability and better quality of life. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: Baseline, Week 28 of the PFS Follow-up

Interventionscore on a scale (Mean)
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide10.3

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Change From Baseline in Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-Ntx) Score at Week 28 of the PFS Follow-up

The FACT/GOG-Ntx is a participant completed questionnaire that comprises 11 individual items evaluating symptoms of neurotoxicity on a 5-point scale where: 0=not at all (best) to 4=very much for a total possible score of 0 to 44. Symptom scores are inverted so that higher scores of FACT/GOG-Ntx indicate higher quality of life or functioning. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: Baseline, Week 28 of the PFS Follow-up

Interventionscore on a scale (Mean)
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide0.0

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Change From Baseline in Amyloidosis Symptom Scale Total Score at Week 28 of the PFS Follow-up

The amyloidosis symptom scale questionnaire is a participant completed questionnaire that evaluates symptom severity of 3 symptoms: Swelling, Shortness of Breath and Dizziness, each rated on an 11-point scale where: 0=no symptoms to 10=very severe symptoms. Higher scores indicate worsening of symptoms. Total Score is the sum of all responses from the amyloidosis symptom scale ranging from 0 to 30. Higher scores represent higher levels of symptomatology or problems and a negative change from baseline indicates improvement. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: Baseline, Week 28 of the PFS Follow-up

Interventionscore on a scale (Mean)
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide-16.0

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Change From Baseline in 36-item Short Form General Health Survey (SF-36) Mental Component Summary Score at Week 28 of the PFS Follow-up

SF-36 Version 2 is a multipurpose, participant completed, short-form health survey with 36 questions that consists of an 8-scale profile of functional health and well-being scores as well as psychometrically-based physical and mental health summary measures. Physical component summary (PCS) is mostly contributed by physical function (PF), role physical (RP), bodily pain (BP), and general health (GH). Mental component summary (MCS) is mostly contributed by mental health (MH), role emotional (RE), social function (SF), and vitality (VT). Each component on the SF-36 item health survey is scored from 0 (best) to 100 (worst). Total score ranges from 0-100, where higher scores are associated with less disability and better quality of life. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: Baseline, Week 28 of the PFS Follow-up

Interventionscore on a scale (Mean)
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide2.0

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Hematologic Disease Progression Free Survival

Hematologic disease PFS was defined as the time from the date of randomization to the date of first documentation of hematologic PD according to central laboratory results and ISA criteria as evaluated by an adjudication committee, or death due to any cause, whichever occurred first. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone29.50
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide27.73

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Plasma Concentration of Ixazomib

As prespecified in the protocol, data for this outcome measure was planned to be collected for ixazomib arm group only. (NCT01659658)
Timeframe: Cycle 1, Day 1: 1, 4 hours postdose, Day 14: 144 hours postdose; Cycle 2, Day 1: predose, Day 14: 144 hours postdose; Cycles 3 to 10, Day 1: predose (cycle length=28 days)

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
Cycle 1 Day 1: 1 Hour Post-doseCycle 1 Day 14: 4 Hours Post-doseCycle 1 Day 14: 144 Hours Post-doseCycle 2 Day 1: Pre-doseCycle 2 Day 14: 144 Hours Post-doseCycle 3 Day 1: Pre-doseCycle 4 Day 1 Pre-doseCycle 5 Day 1 Pre-doseCycle 6 Day 1: Pre-doseCycle 7 Day 1: Pre-doseCycle 8 Day 1: Pre-doseCycle 9 Day 1: Pre-doseCycle 10 Day 1: Pre-dose
Arm A: Ixazomib + Dexamethasone16.51810.6523.8752.0004.7262.1872.2762.2642.2352.2992.0382.1432.232

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Progression Free Survival (PFS)

PFS was defined as the time from the date of randomization to the date of first documentation of hematologic disease progression, or organ (cardiac or renal) progression, or death due to any cause, whichever occurred first according to central laboratory results and ISA criteria as evaluated by the investigator. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone11.86
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide7.62

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Number of Participants in Each Category of the EuroQol 5-Dimensional (EQ-5D) Questionnaire Score

The European Quality of Life (EuroQOL) 5-Dimensional (EQ-5D) is a patient completed questionnaire consisting of 2 pages: the EQ-5D descriptive system and the EQ visual analogue scale (EQ VAS). The descriptive system comprises 5 dimensions (mobility, self-care, usual activities, pain/discomfort, anxiety/depression). Each dimension has 3 possible choices: no problems to extreme problems. Higher scores=worsening of the quality of life. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: At Week 28 of the OS follow-up

,
InterventionParticipants (Count of Participants)
Mobility: No Problems in Walking AboutMobility: Some Problem in Walking AboutMobility: Confined to BedSelf-Care: No Problems With Self- CareSelf-Care: Some Problems Washing or DressingSelf-Care: Unable to Wash or DressUsual Activities: No Problems With Performing Usual ActivitiesUsual Activities: Some Problem With Performing Usual ActivitiesUsual Activities: Unable to Performing Usual ActivitiesPain/Discomfort: No Pain or DiscomfortPain/Discomfort: Moderate Pain or DiscomfortPain/Discomfort: Extreme Pain or DiscomfortAnxiety/Depression: Not Anxious or DepressedAnxiety/Depression: Moderately Anxious or DepressedAnxiety/Depression: Extremely Anxious or Depressed
Arm A: Ixazomib + Dexamethasone000000000000000
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide010010010010001

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Vital Organ Progression Free Survival

Vital organ PFS is defined as the time from the date of randomization to the date of first documentation of progression of vital organ (heart or kidney) according to central laboratory results and ISA criteria as evaluated by an adjudication committee, or death due to any cause, whichever occurs first. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone15.77
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide11.01

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Time to Vital Organ (Heart or Kidney) Deterioration and Mortality Rate

Time to vital organ deterioration or death was assessed by the investigator and defined as the time from randomization to vital organ (heart or kidney) deterioration or death, whichever occurs first. Cardiac deterioration is defined as the need for hospitalization for heart failure. Kidney deterioration is defined as progression to ESRD with the need for maintenance dialysis or renal transplantation. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From randomization to time of vital organ deterioration or death (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone38.67
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide26.09

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Time To Treatment Failure (TTF)

TTF was defined as the time from randomization to the date of first documented treatment failure. Treatment failure was defined as: 1) death due to any cause; 2) hematologic progression or major organ progression according to central laboratory results and ISA criteria as evaluated by the investigator; 3) clinically morbid organ disease requiring additional therapy; or 4) withdrawn for any reason. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until discontinuation of study drug due to disease progression or unacceptable toxicity, or death whichever occurs first (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone10.32
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide5.32

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Time To Subsequent Anticancer Treatment

Time to subsequent anticancer therapy was defined as the time from randomization to the first date of subsequent anticancer therapy. Participants without subsequent anticancer therapy were censored at the date of death or last known to be alive. As prespecified in the protocol, data was planned to be collected and analyzed in a combined way for non-ixazomib arm groups in this outcome measure. (NCT01659658)
Timeframe: From first dose of study drug until subsequent anticancer treatment (up to 115 months)

Interventionmonths (Median)
Arm A: Ixazomib + Dexamethasone26.48
Arm B: Dexamethasone + Melphalan/Cyclophosphamide/Thalidomide/Lenalidomide12.45

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Number of Participants With Serious Adverse Events (SAEs)

A SAE was defined as any untoward medical occurrence that at any dose resulted in death, was life-threatening, required inpatient hospitalization or prolongation of an existing hospitalization, resulted in persistent or significant disability or incapacity, was a congenital anomaly/birth defect or medically important event. (NCT01659658)
Timeframe: From first dose of study drug through 30 days after administration of the last dose of study drug (up to 115 months)

InterventionParticipants (Count of Participants)
Arm A: Ixazomib + Dexamethasone44
Arm B: Dexamethasone + Melphalan11
Arm B: Dexamethasone + Cyclophosphamide2
Arm B: Dexamethasone + Thalidomide0
Arm B: Dexamethasone + Lenalidomide17

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Duration of Response by Independent Response Adjudication Committee (IRAC)

"Duration of myeloma response is defined as the duration from the time when the IMWG response criteria are first met for sCR or CR or VGPR or PR until the first date the response criteria are met for PD or until the subject died from any cause, whichever occurs first.~Complete Response: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and ≤ 5% plasma cells in bone marrow~SCR: CR+ Normal FLC ratio and Absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine Mprotein level < 100 mg per 24 hours~PR: ≥ 50% reduction of serum M-Protein and reduction in 24-hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hours~Progressive Disease: Please refer to Primary outcome measure for definition~SD: Not meeting criteria for CR, VGPR, PR, or progressive disease" (NCT01734928)
Timeframe: From randomization to progressive disease or death during the IRAC assessment period, up to approximately 42 months

InterventionMonths (Median)
Treatment 1: POM+BTZ+LD-DEX13.70
Treatment 2: BTZ+LD-DEX10.94

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Number of Participants With Grade 3-4 Treatment Emergent Adverse Events (TEAE)

Treatment-emergent adverse events (TEAEs) are defined as any AE occurring or worsening on or after the first dose date of the study treatment and within 28 days after the last dose date. (NCT01734928)
Timeframe: From first dose to 28 days after the last dose (up to approximately 44 months

InterventionParticipants (Count of Participants)
Treatment 1: POM+BTZ+LD-DEX259
Treatment 2: BTZ+LD-DEX194

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Number of Participants With Grade 5 Treatment Emergent Adverse Events (TEAE)

Treatment-emergent adverse events (TEAEs) are defined as any AE occurring or worsening on or after the first dose date of the study treatment and within 28 days after the last dose date. (NCT01734928)
Timeframe: From first dose to 28 days after the last dose (up to approximately 44 months

InterventionParticipants (Count of Participants)
Treatment 1: POM+BTZ+LD-DEX29
Treatment 2: BTZ+LD-DEX12

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Overall Survival (OS)

Overall survival (OS) is calculated as the time from randomization to death from any cause. (NCT01734928)
Timeframe: From randomization to date of death, up to approximately 65 months

InterventionMonths (Median)
Treatment 1: POM+BTZ+LD-DEX35.58
Treatment 2: BTZ+LD-DEX31.61

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Progression Free Survival by Independent Response Adjudication Committee (IRAC)

"Progression free survival (PFS) will be calculated as the time between the randomization and progressive disease (PD) or death.~Progressive Disease is defined as an Increase of ≥ 25% from nadir in:~Serum M-component and/or (the absolute increase must be ≥ 0.5 g/dL)g~Urine M-component and/or (the absolute increase must be ≥ 200 mg/24 hours)~In patients without measurable serum and urine M-protein levels the difference between involved and uninvolved FLC levels, the absolute increase must be > 100 mg/dL.~Bone marrow plasma cell percentage, the absolute % must be ≥ 10%h~Definite development of new bone lesions or soft tissue plasmacytomas increase in the size of existing bone lesions or soft tissue plasmacytomas. -Development of hypercalcemia (corrected serum calcium > 11.5 mg/dL or 2.65 mmol/L) that can be attributed solely to the plasma cell proliferative disorder." (NCT01734928)
Timeframe: From randomization to progressive disease or death during the IRAC assessment period, up to approximately 42 months

InterventionMonths (Median)
Treatment 1: POM+BTZ+LD-DEX11.20
Treatment 2: BTZ+LD-DEX7.10

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Overall Response Rate by Independent Response Adjudication Committee (IRAC)

"The ORR together with the relative proportions in each response category (ie, stringent CR [sCR], CR, very good PR [VGPR], PR, SD, and PD) by treatment using the IMWG criteria will be examined.~Complete Response: Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and ≤ 5% plasma cells in bone marrow~SCR: CR+ Normal FLC ratio and Absence of clonal cells in bone marrow by immunohistochemistry or immunofluorescence~VGPR: Serum and urine M-protein detectable by immunofixation but not on electrophoresis or 90% or greater reduction in serum M-protein plus urine Mprotein level < 100 mg per 24 hours~PR: ≥ 50% reduction of serum M-Protein and reduction in 24-hour urinary M-protein by ≥ 90% or to < 200 mg per 24 hours~Progressive Disease: Please refer to Primary outcome measure for definition~SD: Not meeting criteria for CR, VGPR, PR, or progressive disease" (NCT01734928)
Timeframe: From randomization to progressive disease or death during the IRAC assessment period, up to approximately 42 months

,
InterventionParticipants (Count of Participants)
Stringent complete responseComplete ReponseVery Good Partial ResponsePartial ResponseStable DiseaseProgressive DiseaseNot Evaluable
Treatment 1: POM+BTZ+LD-DEX9351048332117
Treatment 2: BTZ+LD-DEX2940881061617

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Number of Patients Who Demonstrate a Response (Complete, Partial, Minor) to Treatment

"Response criteria for subjects with WM is based upon the Consensus Panel Recommendations from the Third International Workshop on Waldenstrom Macroglobulinemia.~Overall response rate (CR + PR + MR) measured at time of best response." (NCT01779167)
Timeframe: Approximately 24 months

Interventionparticipants (Number)
All Patients0

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Percentage of Participants Able to Complete Full Course Therapy

Percentage of participants able to complete the full course of therapy. (NCT01849783)
Timeframe: Up to 6 years

InterventionParticipants (Count of Participants)
Autologous Stem Cell Transplant24

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Median Progression Free Survival (mPFS)

PFS is defined as the time from the start of DPACE to the date of first documentation of disease progression as assessed by the International Myeloma Working Group response criteria or death due to any cause. Progression is defined using the International Myeloma Working Group response criteria, an increase of greater than or equal to 25% from the lower response value. (NCT01849783)
Timeframe: From the start of DPACE for all participants who have had at least one day of protocol treatment. Up to 6 years.

Interventionmonths (Median)
Autologous Stem Cell Transplant76.4

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Mean Change in Quality-Of-Life Indicators Post-Transplant

Measured using the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ-C30) and Multiple Myeloma module (QLQ-MY20). The EORTC QLQ-C30 includes functional scales (physical, role, emotional, cognitive, and social) and global health status. The EORTC QLQ-MY20 includes disease symptoms and treatment side effects scales. Scores are averaged and transformed to 0-100 scale. For functional and global health status, a positive change from baseline (pre-DPACE) indicates improvement whereas for the symptom scales a negative change from baseline (pre-DPACE) indicates improvement. (NCT01849783)
Timeframe: Pre-DPACE, Pre-maintenance, every 6 months for up to 2 years during maintenance. Up to 6 years.

Interventionscore on a scale (Mean)
Change in Physical Functioning at Pre-MaintenanceChange in Physical Functioning at Maintenance Cycle 6Change in Physical Functioning at Maintenance Cycle 12Change in Physical Functioning at Maintenance Cycle 18Change in Physical Functioning at Maintenance Cycle 24Change in Role Functioning at Pre-MaintenanceChange in Role Functioning at Maintenance Cycle 6Change in Role Functioning at Maintenance Cycle 12Change in Role Functioning at Maintenance Cycle 18Change in Role Functioning at Maintenance Cycle 24Change in Emotional Functioning at Pre-MaintenanceChange in Emotional Functioning at Maintenance Cycle 6Change in Emotional Functioning at Maintenance Cycle 12Change in Emotional Functioning at Maintenance Cycle 18Change in Emotional Functioning at Maintenance Cycle 24Change in Cognitive Functioning at Pre-MaintenanceChange in Cognitive Functioning at Maintenance Cycle 6Change in Cognitive Functioning at Maintenance Cycle 12Change in Cognitive Functioning at Maintenance Cycle 18Change in Cognitive Functioning at Maintenance Cycle 24Change in Social Functioning at Pre-MaintenanceChange in Social Functioning at Maintenance Cycle 6Change in Social Functioning at Maintenance Cycle 12Change in Social Functioning at Maintenance Cycle 18Change in Social Functioning at Maintenance Cycle 24Change in Global Health Status at Pre-MaintenanceChange in Global Health Status at Maintenance Cycle 6Change in Global Health Status at Maintenance Cycle 12Change in Global Health Status at Maintenance Cycle 18Change in Global Health Status at Maintenance Cycle 24Change in Distress Symptoms at Pre-MaintenanceChange in Distress Symptoms at Maintenance Cycle 6Change in Distress Symptoms at Maintenance Cycle 12Change in Distress Symptoms at Maintenance Cycle 18Change in Distress Symptoms at Maintenance Cycle 24Change in Side Effects of Treatment at Pre-MaintenanceChange in Side Effects of Treatment at Maintenance Cycle 6Change in Side Effects of Treatment at Maintenance Cycle 12Change in Side Effects of Treatment at Maintenance Cycle 18Change in Side Effects of Treatment at Maintenance Cycle 24
Autologous Stem Cell Transplant1.3-0.61.15.44.67.48.74.47.06.08.75.51.45.88.30.4-4.6-5.1-6.0-3.6-1.02.7-4.90.8-1.55.40.2-3.1-0.13.46.25.95.73.85.3-3.3-0.7-5.1-2.4-2.7

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Number of Participants With Response

Primary endpoint is response rate (RR) measured by the proportion of patients receiving the combination, whose disease stabilizes, or returns to at least its previous response level prior to progression, assessed at 3-months after starting the combination.1.Stringent Complete Remission (sCR): Follows criteria for CR, plus:Normal FLC ratio, Absence of clonal cells in the BM; Complete Remission (CR) All of the following criteria are met:Negative SIFE and UIFE:Disappearance of any soft tissue plasmacytomas:< 5% plasma cells in the BM. 2.Very Good Partial Response (VGPR):One or more of the following must be present:Serum and urine M-protein detectable by immunofixation but not on electrophoresis:≥ 90% reduction in serum M-protein and urine M-protein level < 100 mg/24 hours.Partial Response (PR) Both of the following must be present:≥ 50% reduction in SPEP:Reduction in 24-hour UPEP by ≥ 90% or to < 200 mg/24 hours.3.Stable Disease (SD)Does not meet the criteria for CR, VGPR, PR, or PD.4.Pr (NCT01927718)
Timeframe: 3 months

InterventionParticipants (Count of Participants)
Thalidomide + Lenalidomide2

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Percent Change From Baseline in the Psoriasis Affected Body Surface Area (BSA) at Week 16

"BSA is a measurement of involved skin. The overall BSA affected by psoriasis is estimated based on the palm area of the subject's hand (entire palmar surface or handprint including the fingers), which equates to approximately 1% of total body surface area." (NCT01988103)
Timeframe: Baseline to Week 16

Interventionpercent change (Least Squares Mean)
Placebo7.5
Apremilast 20mg-21.6
Apremilast 30mg-30.5

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Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at Week 16

"Dermatology Life Quality Index (DLQI) was developed as a practical questionnaire for use in a dermatology clinical setting to assess limitations related to the impact of skin disease. The instrument contains 10 items dealing with the participants skin. With the exception of Item Number 7, the participant responds on a four-point scale, ranging from Very Much (score 3) to Not at All or Not relevant (score 0). Item Number 7 is a multi-part item, the first part of which ascertains whether the participant's skin prevented them from working or studying (Yes or No, scores 3 or 0 respectively), and if No, then the participant is asked how much of a problem the skin has been at work or study over the past week, with response alternatives being A lot, A little, or Not at all (scores 2, 1, or 0 respectively). The DLQI total score has a possible range from 0 to 30, with 30 corresponding to the worst quality of life, and 0 corresponding to the best." (NCT01988103)
Timeframe: Baseline to Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo1.3
Apremilast 20mg-0.5
Apremilast 30mg-2.2

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Change From Baseline in Pruritus Visual Analogue Scale 100-mm (VAS) at Week 16

The pruritus visual analog scale (VAS) was used to measure the amount of itching and discomfort a participant experiences. Participant's assessment of pruritus (Itch) asked: On average, how much itch have you had because of your condition in the past week? Higher scores correspond to more severe symptom or disease. The participant places a vertical line on a 100-mm VAS on which the left-hand boundary represents no itch at all and the right-hand boundary represents the worst itch imaginable. The distance from the vertical line to the left-hand boundary is recorded. VAS scores range from 0 to 100 mm, where higher scores correspond to worse pruritis (itch). (NCT01988103)
Timeframe: Baseline to Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo7.1
Apremilast 20mg-7.5
Apremilast 30mg-17.7

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Change From Baseline in Mental Component Summary (MCS) Score of the Medical Outcome Study Short Form 36-item (SF-36) Health Survey Version 2.0 at Week 16

SF-36 is a 36-item general health status instrument often used in clinical trials and health services research. It consists of 8 scales: physical function (PF), role limitations-physical (RP), vitality (VT), general health perceptions (GH), bodily pain (BP), social function (SF), role limitations-emotional (RE), and mental health (MH). Scale scores range from 0 to 100, with higher scores indicating better quality of life (better functioning) (NCT01988103)
Timeframe: Baseline to Week 16

Interventionunits on a scale (Least Squares Mean)
Placebo-1.59
Apremilast 20mg-0.71
Apremilast 30mg0.27

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Number of Participants With Adverse Events (AE) in the Placebo Controlled Phase

An AE was any noxious, unintended, or untoward medical occurrence, that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly or birth defect, or a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. An AE is a treatment emergent AE if the AE start date is on or after the date of the first dose of study drug and no later than 28 days after the last dose. (NCT01988103)
Timeframe: Baseline to Week 16

,,
Interventionparticipants (Number)
≥ At least 1 TEAE≥ 1 Drug-related TEAE≥ At least 1 Severe TEAE≥ 1 Serious TEAEAny Serious Drug-related TEAE≥ 1 TEAE leading to Drug Interruption≥ 1 TEAE Leading to Drug Withdrawal≥ 1 TEAE Leading to Death
Apremilast 20mg49184422100
Apremilast 30mg4425000060
Placebo358100240

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Number of Participants With Adverse Events (AE) in the During the Apremilast-exposure Period

An AE was any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a preexisting condition) was considered an AE. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly or birth defect, or a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. An AE is a treatment emergent AE if the AE start date is on or after the date of the first dose of study drug and no later than 28 days after the last dose. (NCT01988103)
Timeframe: From the first dose of apremilast (either Week 0 or Week 16 for participants originally randomized to placebo who were re-randomized at Week 16) until 28 days after the last dose of apremilast.

,
Interventionparticipants (Number)
≥ At Least 1 TEAE≥ 1 Drug-related TEAR≥ At Least 1 Severe TEAE≥ 1 Serious TEAEAny Serious Drug-related TEAE≥ 1 TEAE leading to Drug Interruption≥ 1 TEAE Leading to Drug Withdrawal≥ 1 TEAE Leading to Death
Apremilast 20mg9434121156191
Apremilast 30mg89372202100

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Percentage of Participants Who Achieved a Static Physician's Global Assessment (sPGA) Score of Clear (0) or Almost Clear (1) With at Least 2 Point Reduction From Baseline to Week 16

The sPGA is a measure of psoriasis disease severity at the time of evaluation by the Investigator. It does not compare assessments across visits or rely on investigator recall or prior disease. The sPGA is a 6-point scale ranging from 0 (clear, except for residual discoloration) to 5 (severe; majority of plaques have severe thickness, erythema, and scaling). The investigator examines all of the lesions on the participant and assigns a score ranging from 0 to 5 for thickness, erythema and degree of scaling. Scores for thickness, erythema and scaling are then summed and the mean of these 3 scores equals the overall sPGA score. (NCT01988103)
Timeframe: Baseline to Week 16

Interventionpercentage of participants (Number)
Placebo8.8
Apremilast 20mg23.9
Apremilast 30mg29.6

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Percentage of Participants Who Achieved a 75% Improvement (Response) From Baseline in the Psoriasis Area and Severity Index (PASI-75) at Week 16

PASI-75 response is the percentage of participants who achieved at least a 75% reduction (improvement) from baseline in PASI score at Week 16. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The PASI score was set to missing if any severity score or degree of involvement was missing. (NCT01988103)
Timeframe: Baseline to Week 16

Interventionpercentage of participants (Number)
Placebo7.1
Apremilast 20mg23.5
Apremilast 30mg28.2

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Percentage of Participants Who Achieved a 50% Improvement From Baseline (Response) Reduction in the PASI-50 at Week 16

PASI-50 response is the percentage of participants who achieved at least a 50% reduction (improvement) from baseline in PASI score at Week 16. The improvement in PASI score was used as a measure of efficacy. The PASI was a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness and scaling) and degree of skin surface area involvement on defined anatomical regions. PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). The PASI score was set to missing if any severity score or degree of involvement is missing. (NCT01988103)
Timeframe: Baseline to Week 16

Interventionpercentage of participants (Number)
Placebo21.4
Apremilast 20mg41.2
Apremilast 30mg50.6

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Percent Change From Baseline in the Psoriasis Area and Severity Index (PASI) Score

The PASI is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. The PASI is a validated instrument that has become standard in clinical trials for psoriasis. The PASI scores range from 0 to 72, with higher scores reflecting a greater disease severity. (NCT01988103)
Timeframe: Baseline to Week 16

Interventionpercent change (Least Squares Mean)
Placebo-3.7
Apremilast 20mg-33.1
Apremilast 30mg-43.1

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Percentage Change From Baseline in the Eczema Area and Severity Index (EASI) Score at Week 12.

EASI is a validated composite scoring system integrating the proportion of the body region (area) involved and the intensity of key signs of atopic dermatitis (AD). A representative lesion is selected for each of the four body regions for assessing the intensity of each of the four signs (erythema, induration /papulation, excoriation, and lichenification). Symptoms (eg, pruritus) and secondary signs (eg, xerosis, scaling) are excluded from the assessment. The total EASI score ranges from 0 to 72. A higher score indicated worse disease status, and a negative change from baseline indicated improvement. (NCT02087943)
Timeframe: Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Placebo-10.98
Apremilast 30 mg-25.99
Apremilast 40 mg-31.57

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Percentage of Participants Who Achieved a Score of 0 (Cleared) or 1 (Almost Cleared) and at Least a 2-point Reduction From Baseline in a Static Physician's Global Assessment of Acute Signs (sPGA-A) at Week 12.

"The sPGA-A is intended to assess the global severities (ie, a visual average integrating all areas of AD) of key acute clinical signs of AD, including erythema, induration/papulation, oozing/crusting (lichenification excluded) based on a 5-point scale of cleared (0), almost cleared (1), mild (2), moderate (3) and severe (4)." (NCT02087943)
Timeframe: Baseline to Week 12

Interventionpercentage of participants (Number)
Placebo6.3
Apremilast 30 mg3.4
Apremilast 40 mg14.3

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Percentage of Participants Who Achieved at Least a 50% Reduction From Baseline in the EASI Score (EASI 50) at Week 12

The EASI 50 reduction (defined as ≥ 50% reduction from baseline in EASI score) was selected to serve as the key responder endpoint. A ≥ 50% improvement is clinically meaningful for this population. (NCT02087943)
Timeframe: Baseline to Week 12

Interventionpercentage of participants (Number)
Placebo32.8
Apremilast 30 mg31.0
Apremilast 40 mg42.9

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The Percentage Change From Baseline in the Average Weekly Pruritus Numerical Rating Scale (NRS) Score at Week 4

"The participant completed a daily diary recording the average intensity of pruritus they experienced during the preceding 24 hrs. The intensity of pruritus was assessed using a validated 11-point NRS, ranging from 0 (no pruritus) to 10 (the worst pruritus imaginable). It should be noted that this NRS is distinct from the pruritus, Visual Analogue Scale (VAS) in the Modified SCORAD Index with respect to recall period (three days for the VAS). The weekly NRS score was calculated as the average of the NRS scores over 7 days within the specified week. A higher score indicated worse disease status, and a negative change from baseline indicated improvement." (NCT02087943)
Timeframe: Baseline to Week 4

Interventionpercent change (Least Squares Mean)
Placebo-4.83
Apremilast 30 mg-10.00
Apremilast 40 mg-9.00

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Number of Participants With Treatment Emergent Adverse Events (TEAEs) During the Placebo Controlled Period

A TEAE is an adverse event with a start date on or after the date of the first dose of IP and no later than 28 days after the last dose of IP for participants who discontinued early. An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a pre existing condition) should be considered an AE. A serious AE is any which results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect; constitutes an important medical event. (NCT02087943)
Timeframe: Baseline to Week 12

,,
Interventionparticipants (Number)
TEAEDrug-related TEAESevere TEAESerious TEAE (SAE)Drug-related SAETEAE Leading to Drug InterruptionTEAE Leading to Drug WithdrawalDeath
Apremilast 30 mg3626010020
Apremilast 40 mg4427121460
Placebo308000310

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Number of Participants With TEAEs During the Apremilast Exposure Period

A TEAE is an adverse event with a start date on or after the date of the first dose of investigational product (IP) and no later than 28 days after the last dose of IP. An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology. Any worsening (ie, any clinically significant adverse change in the frequency or intensity of a pre existing condition) should be considered an AE. A serious AE is any which results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect; constitutes an important medical event. (NCT02087943)
Timeframe: Baseline to Week 24; median duration of apremilast 30 mg was 23.3 weeks and 22.4 weeks for apremilast 40 mg

,
Interventionparticipants (Number)
TEAEDrug-related TEAESevere TEAESerious TEAE (SAE)Drug-related SAETEAE Leading to Drug InterruptionTEAE Leading to Drug WithdrawalDeath
Apremilast 30 mg4929120030
Apremilast 40 mg6138132890

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The Remission Rate for Participants With High-risk Myeloma

Toward improving the clinical outcomes of research subjects with high-risk MM (HR-MM) in the context of the immediately preceding TT5 trial 2008-02 and TT3 trials 2003-33 and 2006-66, TT5B will attempt to accelerate and sustain, at 2 years from starting therapy, the proportion of subjects in complete remission (AS-CR-2) by reducing host-imposed toxicity and thus facilitating timely completion of highly synergistic 8-drug combination therapy, including the next generation proteasome inhibitor, Carfilzomib (CFZ). This will result in avoiding MM re-growth that, we postulate, ensued in TT3 during recovery phases from severe de-conditioning. Furthermore, we speculate that the incidence of positive minimal residual disease (MRD) will be reduced with the addition of one cycle of consolidation therapy. (NCT02128230)
Timeframe: from baseline to either death or study completion for each subject (up to approximately 48 months)

InterventionParticipants (Number)
Total Therapy 5B0

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Group 2: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 2: Apremilast Immediate Release6669.26
Group 2: Apremilast Modified Release 45700.66
Group 2: Apremilast Modified Release 54843.46
Group 2: Apremilast Modified Release 65259.40

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Group 2: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 2: Apremilast Immediate Release6635.78
Group 2: Apremilast Modified Release 45634.92
Group 2: Apremilast Modified Release 54780.60
Group 2: Apremilast Modified Release 65177.46

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Group 2: Half-life of Apremilast in Terminal Phase (T1/2)

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Geometric Mean)
Group 2: Apremilast Immediate Release8.16
Group 2: Apremilast Modified Release 48.98
Group 2: Apremilast Modified Release 58.43
Group 2: Apremilast Modified Release 68.75

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Group 2: Observed Maximum Plasma Concentration (Cmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng/mL (Geometric Mean)
Group 2: Apremilast Immediate Release405.38
Group 2: Apremilast Modified Release 4368.45
Group 2: Apremilast Modified Release 5298.96
Group 2: Apremilast Modified Release 6325.20

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Group 2: Relative Bioavailability of Apremilast Test Formulations Relative to Reference

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞[test]) / (AUC0-∞[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 2: Apremilast Modified Release 485.48
Group 2: Apremilast Modified Release 572.62
Group 2: Apremilast Modified Release 678.86

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Group 2: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞/Dose[test]) / (AUC0-∞/Dose[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 2: Apremilast Modified Release 454.71
Group 2: Apremilast Modified Release 546.48
Group 2: Apremilast Modified Release 650.47

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Group 2: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Median)
Group 2: Apremilast Immediate Release2.00
Group 2: Apremilast Modified Release 44.00
Group 2: Apremilast Modified Release 53.00
Group 2: Apremilast Modified Release 64.00

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Group 3: Apparent Total Plasma Clearance (CL/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

InterventionL/h (Geometric Mean)
Group 3: Apremilast Immediate Release10.87
Group 3: Apremilast Modified Release 817.87
Group 3: Apremilast Modified Release 918.35

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Group 3: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 3: Apremilast Immediate Release5518.28
Group 3: Apremilast Modified Release 84477.63
Group 3: Apremilast Modified Release 94359.49

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Group 3: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 3: Apremilast Immediate Release5493.38
Group 3: Apremilast Modified Release 84427.56
Group 3: Apremilast Modified Release 94310.62

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Group 3: Half-life of Apremilast in Terminal Phase (T1/2)

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Geometric Mean)
Group 3: Apremilast Immediate Release6.45
Group 3: Apremilast Modified Release 86.58
Group 3: Apremilast Modified Release 97.05

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Group 3: Observed Maximum Plasma Concentration (Cmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng/mL (Geometric Mean)
Group 3: Apremilast Immediate Release378.59
Group 3: Apremilast Modified Release 8344.61
Group 3: Apremilast Modified Release 9334.51

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Group 3: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞/Dose[test]) / (AUC0-∞/Dose[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 3: Apremilast Modified Release 845.64
Group 3: Apremilast Modified Release 944.44

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Group 3: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Median)
Group 3: Apremilast Immediate Release3.00
Group 3: Apremilast Modified Release 84.00
Group 3: Apremilast Modified Release 94.00

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Group 4: Apparent Total Plasma Clearance (CL/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

InterventionL/h (Geometric Mean)
Group 4: Apremilast Immediate Release8.57
Group 4: Apremilast Modified Release 1113.92
Group 4: Apremilast Modified Release 1213.62
Group 4: Apremilast Modified Release 1316.83
Group 4: Apremilast Modified Release 1414.88

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Group 4: Apparent Total Volume of Distribution (Vz/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionliters (Geometric Mean)
Group 4: Apremilast Immediate Release77.30
Group 4: Apremilast Modified Release 11148.66
Group 4: Apremilast Modified Release 12147.59
Group 4: Apremilast Modified Release 13172.16
Group 4: Apremilast Modified Release 14153.18

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Group 4: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 4: Apremilast Immediate Release7000.35
Group 4: Apremilast Modified Release 115747.12
Group 4: Apremilast Modified Release 125875.19
Group 4: Apremilast Modified Release 134753.79
Group 4: Apremilast Modified Release 145374.83

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Group 4: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 4: Apremilast Immediate Release6976.02
Group 4: Apremilast Modified Release 115701.21
Group 4: Apremilast Modified Release 125811.24
Group 4: Apremilast Modified Release 134700.70
Group 4: Apremilast Modified Release 145324.80

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Group 4: Half-life of Apremilast in Terminal Phase (T1/2)

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Geometric Mean)
Group 4: Apremilast Immediate Release6.25
Group 4: Apremilast Modified Release 117.40
Group 4: Apremilast Modified Release 127.51
Group 4: Apremilast Modified Release 137.09
Group 4: Apremilast Modified Release 147.13

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Group 4: Observed Maximum Plasma Concentration (Cmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng/mL (Geometric Mean)
Group 4: Apremilast Immediate Release438.90
Group 4: Apremilast Modified Release 11480.59
Group 4: Apremilast Modified Release 12481.10
Group 4: Apremilast Modified Release 13316.43
Group 4: Apremilast Modified Release 14450.23

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Group 4: Relative Bioavailability of Apremilast Test Formulations Relative to Reference

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞[test]) / (AUC0-∞[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 4: Apremilast Modified Release 1182.10
Group 4: Apremilast Modified Release 1283.31
Group 4: Apremilast Modified Release 1368.71
Group 4: Apremilast Modified Release 1477.68

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Group 4: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞/Dose[test]) / (AUC0-∞/Dose[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 4: Apremilast Modified Release 1146.18
Group 4: Apremilast Modified Release 1246.86
Group 4: Apremilast Modified Release 1338.65
Group 4: Apremilast Modified Release 1443.70

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Group 4: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Median)
Group 4: Apremilast Immediate Release3.00
Group 4: Apremilast Modified Release 114.00
Group 4: Apremilast Modified Release 124.00
Group 4: Apremilast Modified Release 134.01
Group 4: Apremilast Modified Release 143.52

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Group 1: Number of Participants With Treatment-emergent Adverse Events

"An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology.~A treatment-emergent AE (TEAE) was defined as any AE that occurred after dosing of the study drug.~A serious adverse event (SAE) is any AE occurring at any dose that:~Resulted in death;~Was life-threatening;~Required inpatient hospitalization or prolongation of existing hospitalization;~Resulted in persistent or significant disability/incapacity;~Was a congenital anomaly/birth defect;~Constituted an important medical event." (NCT02236988)
Timeframe: Adverse events were collected for 7 to 10 days after each treatment.

,,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAEs related to study drugSerious adverse eventsSerious adverse events related to study drugDiscontinuations due to adverse eventsDeaths
Group 1: Apremilast Immediate Release540000
Group 1: Apremilast Modified Release 1410000
Group 1: Apremilast Modified Release 2220000
Group 1: Apremilast Modified Release 3110000

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Group 2: Number of Participants With Treatment-emergent Adverse Events

"An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology.~A treatment-emergent AE (TEAE) was defined as any AE that occurred after dosing of the study drug.~A serious adverse event (SAE) is any AE occurring at any dose that:~Resulted in death;~Was life-threatening;~Required inpatient hospitalization or prolongation of existing hospitalization;~Resulted in persistent or significant disability/incapacity;~Was a congenital anomaly/birth defect;~Constituted an important medical event." (NCT02236988)
Timeframe: Adverse events were collected for 7 to 10 days after each treatment.

,,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAEs related to study drugSerious adverse eventsSerious adverse events related to study drugDiscontinuations due to adverse eventsDeaths
Group 2: Apremilast Immediate Release440000
Group 2: Apremilast Modified Release 4420000
Group 2: Apremilast Modified Release 5650000
Group 2: Apremilast Modified Release 6540000

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Group 3: Number of Participants With Treatment-emergent Adverse Events

"An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology.~A treatment-emergent AE (TEAE) was defined as any AE that occurred after dosing of the study drug.~A serious adverse event (SAE) is any AE occurring at any dose that:~Resulted in death;~Was life-threatening;~Required inpatient hospitalization or prolongation of existing hospitalization;~Resulted in persistent or significant disability/incapacity;~Was a congenital anomaly/birth defect;~Constituted an important medical event." (NCT02236988)
Timeframe: Adverse events were collected for 7 to 10 days after each treatment.

,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAEs related to study drugSerious adverse eventsSerious adverse events related to study drugDiscontinuations due to adverse eventsDeaths
Group 3: Apremilast Immediate Release510000
Group 3: Apremilast Modified Release 8300000
Group 3: Apremilast Modified Release 9320000

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Group 4: Number of Participants With Treatment-emergent Adverse Events

"An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology.~A treatment-emergent AE (TEAE) was defined as any AE that occurred after dosing of the study drug.~A serious adverse event (SAE) is any AE occurring at any dose that:~Resulted in death;~Was life-threatening;~Required inpatient hospitalization or prolongation of existing hospitalization;~Resulted in persistent or significant disability/incapacity;~Was a congenital anomaly/birth defect;~Constituted an important medical event." (NCT02236988)
Timeframe: Adverse events were collected for 7 to 10 days after each treatment.

,,,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAE related to study drugSerious adverse eventsSerious adverse events related to study drugDiscontinuation due to adverse eventsDeaths
Group 4: Apremilast Immediate Release1390000
Group 4: Apremilast Modified Release 11770000
Group 4: Apremilast Modified Release 12760000
Group 4: Apremilast Modified Release 13760000
Group 4: Apremilast Modified Release 14970000

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Group 3: Relative Bioavailability of Apremilast Test Formulations Relative to Reference

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞[test]) / (AUC0-∞[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 3: Apremilast Modified Release 881.14
Group 3: Apremilast Modified Release 979.00

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Group 1: Apparent Total Plasma Clearance (CL/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

InterventionL/h (Geometric Mean)
Group 1: Apremilast Immediate Release8.63
Group 1: Apremilast Modified Release 117.32
Group 1: Apremilast Modified Release 215.12
Group 1: Apremilast Modified Release 314.57

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Group 1: Apparent Total Volume of Distribution (Vz/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionliters (Geometric Mean)
Group 1: Apremilast Immediate Release88.65
Group 1: Apremilast Modified Release 1185.65
Group 1: Apremilast Modified Release 2149.97
Group 1: Apremilast Modified Release 3153.23

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Group 1: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 1: Apremilast Immediate Release6955.76
Group 1: Apremilast Modified Release 14330.66
Group 1: Apremilast Modified Release 24961.51
Group 1: Apremilast Modified Release 35147.83

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Group 1: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Group 1: Apremilast Immediate Release6918.49
Group 1: Apremilast Modified Release 14277.83
Group 1: Apremilast Modified Release 24925.69
Group 1: Apremilast Modified Release 35103.07

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Group 1: Half-life of Apremilast in Terminal Phase (T1/2)

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Geometric Mean)
Group 1: Apremilast Immediate Release7.12
Group 1: Apremilast Modified Release 17.43
Group 1: Apremilast Modified Release 26.88
Group 1: Apremilast Modified Release 37.29

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Group 1: Observed Maximum Plasma Concentration (Cmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionng/mL (Geometric Mean)
Group 1: Apremilast Immediate Release409.96
Group 1: Apremilast Modified Release 1267.85
Group 1: Apremilast Modified Release 2329.78
Group 1: Apremilast Modified Release 3345.11

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Group 1: Relative Bioavailability of Apremilast Test Formulations Relative to Reference

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞[test]) / (AUC0-∞[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 1: Apremilast Modified Release 162.26
Group 1: Apremilast Modified Release 271.33
Group 1: Apremilast Modified Release 374.01

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Group 1: Relative Bioavailability of Apremilast Test Formulations Relative to Reference Corrected by Dose

"Relative bioavailability of each test formulation compared to the reference formulation corrected by dose, calculated as:~(AUC0-∞/Dose[test]) / (AUC0-∞/Dose[reference]) * 100%." (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionpercent availability (Geometric Mean)
Group 1: Apremilast Modified Release 139.85
Group 1: Apremilast Modified Release 245.65
Group 1: Apremilast Modified Release 347.37

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Group 1: Time to Observed Maximum Plasma Concentration (Tmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionhours (Median)
Group 1: Apremilast Immediate Release3.00
Group 1: Apremilast Modified Release 14.00
Group 1: Apremilast Modified Release 24.00
Group 1: Apremilast Modified Release 34.00

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Group 2: Apparent Total Plasma Clearance (CL/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

InterventionL/h (Geometric Mean)
Group 2: Apremilast Immediate Release9.00
Group 2: Apremilast Modified Release 413.16
Group 2: Apremilast Modified Release 515.48
Group 2: Apremilast Modified Release 614.26

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Group 2: Apparent Total Volume of Distribution (Vz/F) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02236988)
Timeframe: IR reference formulation: predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the first dose; MR formulations: predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, and 72 hours postdose.

Interventionliters (Geometric Mean)
Group 2: Apremilast Immediate Release105.88
Group 2: Apremilast Modified Release 4170.51
Group 2: Apremilast Modified Release 5188.24
Group 2: Apremilast Modified Release 6180.10
Group 3: Apremilast Immediate Release101.23
Group 3: Apremilast Modified Release 8169.71
Group 3: Apremilast Modified Release 9186.69

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Overall Survival

(NCT02424851)
Timeframe: 1 month post end of treatment and 1 year post randomisation

InterventionParticipants (Count of Participants)
Arm A (BBD)9
Arm B (BTD)13

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Renal Response After Two Cycles of Trial Treatment

(NCT02424851)
Timeframe: End of 2nd treatment cycle, week 6

,
InterventionParticipants (Count of Participants)
Partial responseMinor responseNo repsonse
Arm A (BBD)294
Arm B (BTD)076

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Quality of Life Measured by the EQ-5D-3L Questionnaire at Baseline and 1 Month Follow up

"The EQ-5D-3L descriptive system comprises the following five dimensions: mobility, self-care, usual activities, pain/discomfort and anxiety/depression. Each dimension is scored on a scale of 1 to 3: 1 (no problems), 2 (some problems), and 3 (extreme problems). Higher score equates to a worse outcome.~As stated in the official EQ-5D user guide, patient responses to the 5 questions were converted into a single index value as per Dolan P (1997). Modeling valuations for EuroQol health states. Med Care 35(11):1095-108. These index values, with country specific value sets, facilitate the calculation of quality-adjusted life years (QALYs) that are used to inform economic evaluations of health care interventions. In the UK, the values range from -0.594 to +1." (NCT02424851)
Timeframe: Baseline and 1 month follow up

,
InterventionUnits on a scale (Mean)
Baseline1 month FU
Arm A (BBD)0.720.69
Arm B (BTD)0.690.80

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Haematological and Non-haematological Toxicity in Both Treatment Arms

(NCT02424851)
Timeframe: End of weeks 3, 6, 9, 12 (after receiving 4 cycles of therapy), 30 days after final treatment and 12 months after randomisation

,
InterventionEvents (Number)
Serious adverse eventsAdverse events
Arm A (BBD)23
Arm B (BTD)06

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Number of Participants With >50% Reduction From Baseline in Serum Free Light Chain

(NCT02424851)
Timeframe: End of week 6 (after receiving two cycles of therapy)

InterventionParticipants (Count of Participants)
Arm A (BBD)13
Arm B (BTD)3

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Percentage of Participants Who Achieved at Least a 75% Improvement (Response) in the Psoriasis Area and Severity Index (PASI)-75 From Baseline at Week 16

The PASI score is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage of participants (Number)
Placebo8.2
Apremilast21.6

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Percentage of Participants With Scalp Psoriasis Who Achieved a Clear (0) or Minimal (1) on Scalp Physician's Global Assessment (ScPGA) Scale at Week 16.

The ScPGA assessed scalp involvement, if present at baseline. The 6-point ScPGA scale includes three dimensions (Plaque Thickening, Scaling, and Erythema) and a global assessment. Scores range from 0 (clear), 1 (minimal), 2 (mild), 3 (moderate), 4 (severe), to 5 (very severe). Analysis of ScPGA was restricted to the participants with scalp involvement at baseline. (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage of participants (Number)
Placebo38.2
Apremilast50.0

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Mean Change From Baseline in Pruritus Visual Analog Scale (VAS)

The Pruritus VAS assessment was conducted at the baseline visit and each post-baseline visit. The participant was asked to place a vertical stroke on a 100 mm VAS on which the left-hand boundary (0) represents no itch, and the right-hand boundary (100) represents itch as severe as can be imagined. The distance from the mark to the left-hand boundary will be recorded. The Pruritus VAS score ranges from 0 to 100. Higher scores correspond to more severe symptom. (NCT02425826)
Timeframe: Baseline to Weeks 1 and 16 (end of phase)

,
Interventionunits on a scale (Mean)
Week 1Week 16
Apremilast-13.9-19.2
Placebo-9.6-10.2

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Number of Participants Who Experienced Treatment-emergent Adverse Events (TEAEs) During the Apremilast-Exposure Phase

Treatment-Emergent Adverse Events (TEAEs) are defined as any AEs that begin or worsen on or after the start of study drug through 28 days after the last dose of study drug or study treatment discontinuation date, whichever was later. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly/birth defect, or is a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. (NCT02425826)
Timeframe: Date of first dose of apremilast during the placebo controlled phase or date of first dose of apremilast after week 16; overall maximum duration of exposure was 61.5 weeks during apremilast-exposure phase

Interventionparticipants (Number)
≥ At Least 1 TEAE≥ 1 Drug-related TEAE≥ At Least 1 Severe TEAE≥ At Least 1 Serious TEAE≥ 1 Serious Drug-related TEAE≥ 1 TEAE leading to drug withdrawal≥ 1 TEAE Leading to drug interruptionAny TEAE leading to death
Apremilast14298510114270

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Percentage of Participants With Scalp Psoriasis Who Were Initially Randomized to Apremilast and Maintained the Scalp Physician's Global Assessment (ScPGA) Response From Week 16 to Week 52.

The ScPGA will assess scalp involvement, if present at baseline. The 6-point ScPGA scale includes three dimensions (Plaque Thickening, Scaling, and Erythema) and a global assessment with scores range from 0 (clear), 1 (minimal), 2 (mild), 3 (moderate), 4 (severe), to 5 (very severe). Analysis of ScPGA is restricted to the participants with scalp involvement at baseline. (NCT02425826)
Timeframe: Week 16 to Week 52

Interventionpercentage of participants (Number)
Responder status at Week 16Responder status maintained at Week 52
Apremilast50.080.4

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Treatment Satisfaction Questionnaire for Medication (TSQM) Version II at Week 16

The TSQM version II is an 11-question self-administered instrument to understand a participation's satisfaction with the current therapy. The TSQM scale comprises four domains, on which participants evaluate their medication (i.e., effectiveness, side effects, convenience and global satisfaction. TSQM scores range from 0 to 100 for each domain; a higher score mean indicates higher satisfaction with treatment. (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

,
Interventionunits on a scale (Mean)
TSQM-EffectivenessTSQM-Side EffectsTSQM-ConvenienceTSQM-Global Satisfaction
Apremilast57.2578.5066.9363.24
Placebo38.8175.0065.6848.74

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Percentage of Participants Who Achieved a sPGA Score of Clear (0) or Almost Clear (1) at Week 16 From Baseline

The sPGA is an assessment by the investigator of the overall disease severity at the time of evaluation. Erythema (E), induration (I), and desquamation (D) are scored on a 6-point scale, ranging from 0 (clear) to 5 (very severe), with an overall sPGA calculated as (E + I + D)/3. Scores for each assessment are averaged and rounded to the nearest whole number to result in the final sPGA score. (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage of participants (Number)
Placebo9.6
Apremilast30.4

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Percentage of Participants Who Achieved a Clear (0) or Very Mild (1) on Patient Global Assessment (PtGA) Scale at Week 16 From Baseline

The PtGA response rate is defined as the percentage of participants achieving 0 (clear) or 1 (very mild) on the PtGA scale at Week 16. The PtGA is the assessment by the participant of the overall disease severity at the time of evaluation. The PtGA is a 5-point scale ranging from 0 (clear) to 4 (severe). (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage of participants (Number)
Placebo20.5
Apremilast33.8

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Mean Percentage Change From Baseline in the Product of BSA (%) x sPGA at Week 52

"BSA is a measurement of involved skin. The overall BSA affected by psoriasis is estimated based on the palm area of the participant's hand (entire palmar surface or handprint including the fingers), which equates to approximately 1% of total body surface area. The sPGA is a 6-point scale ranging from 0 (clear), 1 (almost clear), 2 (mild), 3 (moderate), to 4 (severe), 5 (very severe) incorporating a separate assessment of the severity of the three primary signs of the plaques of all involved areas: erythema, scaling and plaque elevation with an overall sPGA calculated as (E + I + D)/3. Scores for each assessment are rounded to the nearest whole number to result in the final score." (NCT02425826)
Timeframe: Baseline to Week 52

Interventionpercentage change (Mean)
Placebo-Apremilast-42.23
Apremilast-55.45

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Mean Percentage Change From Baseline in the Product of BSA (%) and the sPGA Which is Considered as the Total Psoriasis Severity Index at Week 16

"BSA is a measurement of involved skin. The overall BSA affected by psoriasis is estimated based on the palm area of the participant's hand (entire palmar surface or handprint including the fingers), which equates to approximately 1% of total body surface area. The sPGA is a 6-point scale ranging from 0 (clear), 1 (almost clear), 2 (mild), 3 (moderate), to 4 (severe), 5 (very severe) incorporating a separate assessment of the severity of the three primary signs of the plaques of all involved areas: erythema, scaling and plaque elevation with an overall sPGA calculated as (E + I + D)/3. Scores for each assessment are rounded to the nearest whole number to result in the final score. The range of BSA*sPGA mean percentage change from baseline to week 16 (end of phase) were -100 to 344.4 and -100 to 100 for the placebo and apremilast groups respectively. Higher scores represented worse outcomes." (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage change (Mean)
Placebo-10.17
Apremilast-48.07

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Mean Percentage Change From Baseline in Psoriasis Area Severity Index Score (PASI) at Week 16

The PASI score is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage change (Mean)
Placebo-3.87
Apremilast-40.72

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Mean Change From Baseline in the Dermatology Life Quality Index (DLQI) Total Score at Week 16

"DLQI is a simple, compact, and practical questionnaire for use in a dermatology clinical setting to assess limitations related to the impact of skin disease. The instrument contains ten items dealing with the participant's skin. With the exception of Item Number 7, the participant responds on a four-point scale, ranging from Very Much (score 3) to Not at All or Not relevant (score 0). Item Number 7 is a multi-part item, the first part of which ascertains whether the participant's skin prevented them from working or studying (Yes or No, scores 3 or 0 respectively), and if No, then the participant is asked how much of a problem the skin has been at work or study over the past week, with response alternatives being A lot, A little, or Not at all (scores 2, 1, or 0 respectively). The DLQI total score is derived by summing all item scores, which has a possible range of 0 to 30, with 30 corresponding to the worst quality of life, and 0 corresponding to the best." (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionunits on a scale (Mean)
Placebo-2.4
Apremilast-4.8

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Treatment Satisfaction Questionnaire for Medication (TSQM) Version II at Week 52

The TSQM version II is an 11-question self-administered instrument to understand a participants satisfaction on the current therapy. The TSQM scale comprises four domains, on which participants evaluate their medication (i.e., effectiveness, side effects, convenience and global satisfaction. TSQM scores range from 0 to 100 for each domain; a higher score indicates higher satisfaction with treatment. (NCT02425826)
Timeframe: Baseline to week 52

,
Interventionunits on a scale (Mean)
TSQM-EffectivenessTSQM-Side EffectsTSQM-ConvenienceTSQM-Global Satisfaction
Apremilast54.1375.4571.7659.92
Placebo-Apremilast57.6877.2972.7459.24

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Number of Participants Who Experienced Treatment-Emergent Adverse Events (TEAEs) During the Placebo Controlled Phase

Treatment-Emergent Adverse Events (TEAEs) are defined as any AEs that begin or worsen on or after the start of study drug through 28 days after the last dose of study drug or study treatment discontinuation date, whichever was later. A serious AE (SAE) is any untoward adverse event that is fatal, life-threatening, results in persistent or significant disability or incapacity, requires or prolongs existing in-patient hospitalization, is a congenital anomaly/birth defect, or is a condition that may jeopardize the patient or may require intervention to prevent one of the outcomes listed above. (NCT02425826)
Timeframe: From first dose of study drug to Week 16; maximum duration of exposure was 20.1 weeks during placebo controlled phase

,
Interventionparticipants (Number)
≥ At Least 1 TEAE≥ 1 Drug-related TEAE≥ At Least 1 Severe TEAE≥ At Least 1 Serious TEAE≥ 1 Serious Drug-related TEAE≥ 1 TEAE leading to drug withdrawal≥ 1 TEAE Leading to drug interruptionAny TEAE leading to death
Apremilast9271330590
Placebo3521100330

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Percentage of Participants Who Achieved at Least a 50% Improvement (Response) in the Psoriasis Area and Severity Index (PASI)-50 From Baseline at Week 16.

The PASI score is a measure of psoriatic disease severity taking into account qualitative lesion characteristics (erythema, thickness, and scaling) and degree of skin surface area involvement on defined anatomical regions. Erythema, thickness, and scaling are scored on a scale of 0 (none) to 4 (very severe) on 4 anatomic regions of the body: head, trunk, upper limbs, and lower limbs. Degree of involvement on each of the 4 anatomic regions is scored on a scale of 0 (no involvement) to 6 (90% to 100% involvement). PASI scores range from 0 to 72, with higher scores reflecting greater disease severity. (NCT02425826)
Timeframe: Baseline to Week 16 (end of phase)

Interventionpercentage of participants (Number)
Placebo24.7
Apremilast53.4

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Number of Participants With Dose-Limiting Toxicities as Assessed by Reported Data

Dose-Limiting Toxicities (Dose escalation phase), between the time of receiving the first registered dose of carfilzomib in cycle 1 and day 1 cycle 2, in order to establish the Maximum Tolerated Dose (MTD) of carfilzomib in combination with thalidomide and dexamethasone, will be assessed based on reported data. The number of reported dose limiting toxicities will be reported. (NCT02545907)
Timeframe: After 1 cycle of treatment; to be completed within 1 year.

InterventionParticipants (Count of Participants)
Dose Level 00
Dose Level 11

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Number of Patients Experiencing Dose Delays Based on Reported Data.

The number of patients experiencing dose delays will be assessed based on reported data. (NCT02545907)
Timeframe: Within 6 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population2
Dose Level 1- Safety Population1

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Compliance Profile of KTD Based on Reported Chemotherapy Compliance Data.

The compliant profile of participants to KTD will be assessed by determining the number of missed doses from recorded data. Participants will be regarded as compliant if participants have missed no more than 14 days of thalidomide, 2 days of dexamethasone, and 1 dose of carfilzomib per cycle. Compliance will be reported in terms of the number of participants who were compliant. (NCT02545907)
Timeframe: Within 6 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population1
Dose Level 1- Safety Population5

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Number of Patients Progression-free at 6 Months Based on Reported Data.

"The number of patients who are progression-free at 6 months will be assessed based on reported data. Patients who are progression-free will have not had an haematological relapse or organ progression.~Haematological relapse is defined as:~From CR: Increase in the aberrant serum free light chain concentration to outside the normal range and by a factor of ≥2 from that at the time of CR or re-appearance of the original paraprotein~From PR or VGPR: Increase in the aberrant free light chain concentration by a factor of ≥2 from that at the time of PR (≥50% change in ratio away from normal in patients with renal failure) or doubling of the serum paraprotein level (if starting >5g/L) or doubling and increase of serum paraprotein to >5g/L (if starting <5g/L)~Organ progression is defined, by organ, as:~Heart: Interventricular septal thickness increased by >2 mm compared with baseline or 20% decline in ejection fraction~Kidney: 50% increase (at least 1 g/day) in 24-hr urinary" (NCT02545907)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population3
Dose Level 1- Safety Population7

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Number of Patients Withdrawing From Treatment Based on Reported Data.

The number of patients withdrawing from treatment will be assessed based on reported data. (NCT02545907)
Timeframe: Within 6 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population0
Dose Level 1- Safety Population0

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Clonal Response Rate Within 3 Months, at 3 Months, Within 6 Months and at 6 Months as Determined by Paraprotein and Free Light Chain Assessment.

"Participant clonal response rate within 3 months, at 3 months, within 6 months and at 6 months will be assessed. The percentage of participants who achieve at least a partial response will be reported.~Clonal response is defined as:~CR: Negative immunofixation of serum and urine (serum alone in anuric patients) AND normal FLC concentration and kappa/lambda FLC ratio (FLC ratio alone in renal failure) AND ≤5% plasma cells in bone marrow without clonality by immunohistochemistry or immunofluorescencea~VGPR: >90% reduction in serum paraprotein or abnormal component of FLC or dFLC over the starting value or dFLC <40mg/L~PR: ≥50% decrease in aberrant FLC concentration or dFLC (or ≥50% decrease in dFLC if renal failure) or serum paraprotein but not fulfilling criteria for CR or VGPR~MR: >25% but <50% decrease in aberrant FLC or dFLC or paraprotein~NR: Not meeting FLC criteria for CR, PR or MR" (NCT02545907)
Timeframe: Within 3 months, at 3 months, within 6 months and at 6 months

,
InterventionParticipants (Count of Participants)
Within 3 cyclesAt the end of cycle 3Within 6 cyclesAt the end of cycle 6
Dose Level 0- Safety Population1122
Dose Level 1- Safety Population5555

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Time to Amyloidotic Organ Response Based on Reported Data.

The time to amyloidotic organ response (as outlined above) will be assessed based on reported data. The number of months this takes will be reported. (NCT02545907)
Timeframe: Within 6 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population0
Dose Level 1- Safety Population0

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Time to Maximum Response Based on Reported Data.

The time to maximum response to treatment will be assessed by determining the time required for each participant to achieve maximum response (defined above), and will be presented on Kaplan-Meier curves. The number of months taken to achieve this maximum response will be reported. Time to maximum response was analysed overall only, and not by arm due the small sample size. (NCT02545907)
Timeframe: Within 6 months

Interventionmonths (Median)
Safety Population5.3

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Number of Deaths at 6 Months Based on Reported Data.

The number of deaths at 6 months will be assessed and reported based on reported data. (NCT02545907)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population0
Dose Level 1- Safety Population0

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Number of Participants Experiencing Grade 3 or 4 Toxicity as Assessed by CTCAE v4.0.

The percentage of patients treated who experience any grade 3 or 4 toxicity as assessed by CTCAE v4.0 throughout all treatment cycles will be assessed based on reported data. (NCT02545907)
Timeframe: Between informed consent provided and 30 days post last trial treatment administration, up to 7 months

InterventionParticipants (Count of Participants)
Dose Level 0- Safety Population2
Dose Level 1- Safety Population3

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Area Under the Concentration-time Curve From Time Zero to the Last Measured Time Point (AUC0-t) for Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. AUC from time zero to the last measured time point was calculated by the linear trapezoidal method. (NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionng*h/mL (Geometric Mean)
Treatment A: Apremilast 30 mg Tablet - Fasted3130
Treatment B: Apremilast 30 mg Oral Suspension - Fasted2740
Treatment C: Apremilast 30 mg Oral Suspension - Fed3160

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Lag Time (Tlag) of Apremilast

Lag time is the delay between the time of administration and start of absorption. (NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionhours (Median)
Treatment A: Apremilast 30 mg Tablet - Fasted0.00
Treatment B: Apremilast 30 mg Oral Suspension - Fasted0.00
Treatment C: Apremilast 30 mg Oral Suspension - Fed0.00

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Maximum Observed Plasma Concentration (Cmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionng/mL (Geometric Mean)
Treatment A: Apremilast 30 mg Tablet - Fasted323
Treatment B: Apremilast 30 mg Oral Suspension - Fasted274
Treatment C: Apremilast 30 mg Oral Suspension - Fed215

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Relative Bioavailability (F) of Apremilast Oral Suspension Formulation

Relative bioavailability of the oral suspension formulation compared to the tablet formulation, calculated as (AUC0-∞/Dose[oral suspension]) / (AUC0-∞/Dose[tablet]) * 100%. (NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionpercent availability (Geometric Mean)
Treatment B: Apremilast 30 mg Oral Suspension - Fasted87.6
Treatment C: Apremilast 30 mg Oral Suspension - Fed101

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Number of Participants With Treatment-emergent Adverse Events

"An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the participant's health, including laboratory test values, regardless of etiology.~A treatment-emergent AE (TEAE) was defined as any AE that occurred after dosing of the study drug.~A serious adverse event (SAE) is any AE occurring at any dose that:~Resulted in death;~Was life-threatening;~Required inpatient hospitalization or prolongation of existing hospitalization;~Resulted in persistent or significant disability/incapacity;~Was a congenital anomaly/birth defect;~Constituted an important medical event." (NCT02641353)
Timeframe: From first dose of study drug in treatment period 1 to 8 days after the last dose; up to 18 days.

,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAEs related to study drugSerious adverse eventsTEAEs leading to discontinuationTEAEs leading to death
Treatment A: Apremilast 30 mg Tablet - Fasted84000
Treatment B: Apremilast 30 mg Oral Suspension - Fasted107000
Treatment C: Apremilast 30 mg Oral Suspension - Fed64000

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Area Under the Concentration-time Curve From Time Zero to Infinity (AUC0-∞) for Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. AUC from time zero to infinity was calculated as (AUC0-t + Ct/λz), where Ct is the last quantifiable concentration, and λz is the apparent terminal rate constant. (NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionng*h/mL (Geometric Mean)
Treatment A: Apremilast 30 mg Tablet - Fasted3160
Treatment B: Apremilast 30 mg Oral Suspension - Fasted2760
Treatment C: Apremilast 30 mg Oral Suspension - Fed3190

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Time to Maximum Observed Plasma Concentration (Tmax) of Apremilast

Concentrations of apremilast in plasma were measured using a validated liquid chromatography tandem mass spectrometry assay. (NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionhours (Median)
Treatment A: Apremilast 30 mg Tablet - Fasted2.00
Treatment B: Apremilast 30 mg Oral Suspension - Fasted2.00
Treatment C: Apremilast 30 mg Oral Suspension - Fed5.00

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Terminal Elimination Half-life (T1/2) of Apremilast

(NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

Interventionhours (Geometric Mean)
Treatment A: Apremilast 30 mg Tablet - Fasted7.89
Treatment B: Apremilast 30 mg Oral Suspension - Fasted8.51
Treatment C: Apremilast 30 mg Oral Suspension - Fed7.54

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Apparent Clearance of Apremilast From Plasma After Extravascular Administration (CL/F)

(NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

InterventionL/h (Geometric Mean)
Treatment A: Apremilast 30 mg Tablet - Fasted9.51
Treatment B: Apremilast 30 mg Oral Suspension - Fasted10.9
Treatment C: Apremilast 30 mg Oral Suspension - Fed9.42

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Apparent Volume of Distribution of Apremilast During the Terminal Phase (Vz/F)

(NCT02641353)
Timeframe: Predose and at 0.5, 1, 1.5, 2, 3, 5, 8, 12, 24, 36, 48, 60 and 72 hours after dosing on day 1 of each treatment period.

InterventionL (Geometric Mean)
Treatment A: Apremilast 30 mg Tablet - Fasted108
Treatment B: Apremilast 30 mg Oral Suspension - Fasted133
Treatment C: Apremilast 30 mg Oral Suspension - Fed102

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Part 2: Peak Maximum Plasma Concentration (Cmax) of Apremilast

(NCT02777554)
Timeframe: Apremilast IR: Predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the morning dose. Apremilast XL: Predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, 60, and 72 hours postdose.

Interventionng/mL (Geometric Mean)
Part 2: Apremilast 30 mg IR BID (Fasted)379
Part 2: Apremilast 75 mg XL (Fasted)402
Part 2: Apremilast 75 mg XL (Standard Meal)436
Part 2: Apremilast 75 mg XL (High Fat Meal)496

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Part 2: Area Under the Plasma Concentration-time Curve From Time Zero to the Last Observable Concentration (AUC0-t) of Apremilast

(NCT02777554)
Timeframe: Apremilast IR: Predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the morning dose. Apremilast XL: Predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, 60, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Part 2: Apremilast 30 mg IR BID (Fasted)7030
Part 2: Apremilast 75 mg XL (Fasted)6650
Part 2: Apremilast 75 mg XL (Standard Meal)7580
Part 2: Apremilast 75 mg XL (High Fat Meal)7400

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Part 2: Area Under the Plasma Concentration-time Curve From Time Zero Extrapolated to Infinity (AUC0-∞) of Apremilast

(NCT02777554)
Timeframe: Apremilast IR: Predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, 24, 36, 48, 60, and 72 hours after the morning dose. Apremilast XL: Predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, 24, 30, 36, 48, 60, and 72 hours postdose.

Interventionng*h/mL (Geometric Mean)
Part 2: Apremilast 30 mg IR BID (Fasted)7100
Part 2: Apremilast 75 mg XL (Fasted)6680
Part 2: Apremilast 75 mg XL (Standard Meal)7600
Part 2: Apremilast 75 mg XL (High Fat Meal)7450

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Part 1: Peak Maximum Plasma Concentration (Cmax) of Apremilast

(NCT02777554)
Timeframe: Apremilast IR: Day 7 predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, and 24 hours after the morning dose. Apremilast XL: Day 7 predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, and 24 hours after the morning dose.

Interventionng/mL (Geometric Mean)
Part 1: Apremilast 30 mg IR BID451
Part 1: Apremilast 75 mg XL QD459

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Part 1: Area Under the Concentration-time Curve From Time Zero to 24 Hours Postdose (AUC0-24) of Apremilast

(NCT02777554)
Timeframe: Apremilast IR: Day 7 predose and at 0.5, 1, 2, 3, 5, 8, 12, 12.5, 13, 14, 15, 17, 20, and 24 hours after the morning dose. Apremilast XL: Day 7 predose and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 14, 16, 20, and 24 hours after the morning dose.

Interventionng*hr/mL (Geometric Mean)
Part 1: Apremilast 30 mg IR BID6370
Part 1: Apremilast 75 mg XL QD6090

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Number of Participants With Treatment-emergent Adverse Events

"An adverse event (AE) is any noxious, unintended, or untoward medical occurrence that may appear or worsen in a participant during the course of a study. It may be a new intercurrent illness, a worsening concomitant illness, an injury, or any concomitant impairment of the subject's health, including laboratory test values, regardless of etiology.~A serious AE is any AE occurring at any dose that:~Resulted in death;~Was life-threatening;~Required inpatient hospitalization or prolongation of existing hospitalization;~Resulted in persistent or significant disability/incapacity;~Was a congenital anomaly/birth defect;~Constituted an important medical event. The Investigator determined the relationship between the administration of study drug and the occurrence of each AE as Not Suspected or Suspected as defined in the Protocol." (NCT02777554)
Timeframe: Part 1: Up to 7 days after last dose in each treatment period (14 days); Part 2: Up to 7 days after each dose.

,,,,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAE related to study drugSerious adverse eventsSerious adverse events related to study drugTEAE leading to discontinuationTEAE related to study drug leading to discontinuationDeaths
Part 1: Apremilast 30 mg IR BID504500330
Part 1: Apremilast 75 mg XL QD474100550
Part 2: Apremilast 30 mg IR BID (Fasted)2200110
Part 2: Apremilast 75 mg XL (Fasted)4300000
Part 2: Apremilast 75 mg XL (High Fat Meal)2200000
Part 2: Apremilast 75 mg XL (Standard Meal)3200000

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Overall Survival

Overall survival, defined as the time to patients' death, is measured. (NCT03043105)
Timeframe: From date of randomization until the date of death from any cause, assessed up to 36 months.

Interventionmonths (Mean)
TCP Treatment Group32.16

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Progression-free Survival

Progression-free survival (PFS) is defined as the time to death or treatment failure. Treatment failure is defined as: sustained increase in grade ≥2 disease-related symptoms persisting ≥12 weeks; new disease-related grade ≥3 symptoms; sustained >1 point increase in ECOG-PS persisting for ≥12 weeks; radiological progression; or initiation of another treatment for MCD. (NCT03043105)
Timeframe: From date of randomization until the date of first documented progression or date of death from any cause, whichever came first, assessed up to 36 months

Interventionmonths (Mean)
TCP Treatment Group23.32

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Change in SF-36 Score

SF-36 score is a self-administered scoring system which reflects a patient's general health status. SF-36 contains 8 dimensions, including physical functioning, role physical, role emotional, vitality, mental health, social functioning, bodily pain, and general health. Each dimension ranges from 0 to 100. Higher scores mean better outcome. SF-36 score at baseline was compared with SF-36 score at 24 weeks. (NCT03043105)
Timeframe: From baseline to 24 weeks after treatment.

Interventionscore on a scale (Mean)
physical functioningrole physicalrole emotionalvitalitymental healthsocial functioningbodily paingeneral health
TCP Treatment Group15.126.719.611.18.513.615.89.1

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Number of Patients With Durable Tumor and Symptomatic Response

Durable tumor and symptomatic response is complete response (CR) + partial response (PR). CR: complete disappearance of all measurable and evaluable disease (eg, pleural effusion) and resolution of baseline symptoms attributed to multicentric Castleman's disease, sustained for at least 18 weeks. PR: >=50 percent decrease in sum of the product of the diameters of indicator lesion(s), with at least stable disease in all other evaluable disease in the absence of treatment failure sustained for at least 6 months. (NCT03043105)
Timeframe: From baseline to the time point when a patient achieves treatment response for 24 weeks.

InterventionParticipants (Count of Participants)
TCP Treatment Group12

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Serum Levels of Thalidomide

Serum levels of thalidomide by liquid chromatography and tandem mass spectrometry (HPLC-MS/MS) (NCT03122431)
Timeframe: 12 months

Interventionng/mL (Mean)
SLE/Cutaneous Lupus With Thalidomide415.1

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Serum Levels of Hydroxycloroquine

Serum levels of hydroxycloroquine by LCMS (NCT03122431)
Timeframe: 12 months

Interventionng/mL (Mean)
Inactive SLE With Standard Dose of HCQ991.6
Inactive SLE With Reduced Dose of HCQ569.0

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs)

Treatment-emergent adverse events were defined as any adverse events (AE) occurring from the first dose of pomalidomide until 28 days after the last dose. The severity of each AE was graded according to the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE), Version 4.03 and according to the following scale: Grade 1: Mild (transient or mild discomfort; no limitation in activity or medical intervention required); Grade 2: Moderate (mild to moderate limitation in activity, assistance may be needed; minimal medical intervention required); Grade 3: Severe (marked limitation in activity, assistance and medical intervention required, hospitalization possible); Grade 4: Life-threatening (extreme limitation in activity, significant assistance or medical intervention required, hospitalization or hospice care probable); Grade 5: Death. Drug-related AEs are those suspected by the Investigator as being related to administration of study drug. (NCT03257631)
Timeframe: From first dose of pomalidomide until 28 days after the last dose; median treatment duration was 84 days in the DIPG group, 112.0 days in the ependymoma group, 40.5 days in the high-grade glioma group and 57.0 days in the medulloblastoma group.

,,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAE related to study drugSerious TEAESerious TEAE related to study drugGrade 3/4 TEAEGrade 3/4 TEAE related to study drugTEAE leading to deathTEAE leading to dose reductionTEAE leading to dose interruptionTEAE leading to study drug discontinuation
Diffuse Intrinsic Pontine Glioma11581835142
Ependymoma8740621031
High-grade Glioma211413614103252
Medulloblastoma9840641020

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Percentage of Participants With an Objective Response or Long-term Stable Disease

Objective response and long-term stable disease rate was defined as the percentage of participants who achieved either an objective response, defined as a complete response (CR) or partial response (PR) in the first 6 cycles of treatment (or within 3 cycles for DIPG), or long-term stable disease (SD) defined as SD maintained for ≥ 6 cycles (≥ 3 cycles for DIPG), measured from first dose date. Disease assessments were based on magnetic resonance imaging (MRI) assessed by an independent central review. CR: Disappearance of all lesions and no new lesions. PR: A reduction of ≥ 50% in the size of measurable lesions compared to baseline, and/or persistence of non-target lesions with no progression or decrease in size. SD: A decrease of < 50% or an increase of < 25% in the size of measurable lesions and no evidence of new lesions, response does not meet the criteria for CR, PR, or progressive disease, and/or the persistence of non-target lesions with no progression or decrease in size. (NCT03257631)
Timeframe: 6 months (first 6 cycles) or 3 months (first 3 cycles) for participants in the DIPG group

Interventionpercentage of participants (Number)
Diffuse Intrinsic Pontine Glioma0
Ependymoma11.1
High-grade Glioma10.5
Medulloblastoma0

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Kaplan-Meier Estimate of Duration of Response

Duration of response is defined as the time from the date of the first objective response (complete response or partial response) to disease progression, for participants with a response. Participants who did not have disease progression or had not died were censored at the time of their last disease assessment or at the time of start of new anticancer therapy, whichever occurred first. Progressive disease (PD): ≥ 25% increase in the size of the measurable lesions taking as a reference the smallest disease measurement recorded since the start of protocol therapy (nadir), or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions, or if spine MRI and/or lumbar cerebrospinal fluid (CSF) cytology were previously negative and became positive. (NCT03257631)
Timeframe: From the first dose of pomalidomide to the data cut-off date of 15 March 2019; median overall time on follow-up was 4.86 months (3.78, 5.65, 4.04, and 8.38 months in each group respectively).

Interventionweeks (Median)
High-grade GliomaNA

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Percentage of Participants With Long-term Stable Disease

Long-term stable disease (SD) rate was defined as the percentage of participants who achieved SD maintained for ≥ 6 cycles (or > 3 cycles for DIPG), measured from the date of first dose of treatment. Disease assessments were based on MRI and assessed by an independent central review. SD: A decrease of < 50% or an increase of < 25% in the size of measurable lesions and no evidence of new lesions, response does not meet the criteria for CR, PR, or progressive disease, and/or the persistence of non-target lesions with no progression or decrease in size. (NCT03257631)
Timeframe: 6 months (first 6 cycles) or 3 months (first 3 cycles) for participants in the DIPG group

Interventionpercentage of participants (Number)
Diffuse Intrinsic Pontine Glioma0
Ependymoma11.1
High-grade Glioma5.3
Medulloblastoma0

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Kalan-Meier Estimate of Overall Survival

Overall survival was defined as the time from the date of the first dose to the date of death (any cause). Participants who were alive were censored at the last known time that the participant was alive. (NCT03257631)
Timeframe: From the first dose of pomalidomide to the data cut-off date of 15 March 2019; median overall time on follow-up was 4.86 months (3.78, 5.65, 4.04, and 8.38 months in each group respectively).

Interventionmonths (Median)
Diffuse Intrinsic Pontine Glioma3.78
Ependymoma12.02
High-grade Glioma5.06
Medulloblastoma11.60

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Kaplan-Meier Estimate of Progression-Free Survival (PFS)

Progression-free survival was defined as the time from the date of first dose of pomalidomide until the date progressive disease (PD) was first observed or until the date of death due to any cause, whichever occurred first. Participants who did not have PD or had not died at the time of analysis were censored at the time of their last disease assessment or at the start of new anticancer therapy, whichever occurred first. Progressive Disease (PD): ≥ 25% increase in the size of the measurable lesions taking as a reference the smallest disease measurement recorded since the start of protocol therapy (nadir), or the appearance of one or more new lesions and/or unequivocal progression of existing non-target lesions, or if spine MRI and/or lumbar CSF cytology were previously negative and became positive. (NCT03257631)
Timeframe: From the first dose of pomalidomide to the data cut-off date of 15 March 2019; median overall time on follow-up was 4.86 months (3.78, 5.65, 4.04, and 8.38 months in each group respectively).

Interventionweeks (Median)
Diffuse Intrinsic Pontine Glioma11.29
Ependymoma8.43
High-grade Glioma7.86
Medulloblastoma8.43

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Percentage of Participants Who Achieved an Objective Response

Objective response rate was defined as the percentage of participants who achieved a complete response (CR) or partial response (PR) within the first 6 cycles of treatment (or within 3 cycles for participants in the DIPG group). Disease assessments were based on MRI and assessed by an independent central review. CR: Disappearance of all lesions and no new lesions. PR: A reduction of ≥ 50% in the size of measurable lesions compared to baseline, and/or the persistence of non-target lesions with no progression or decrease in size. (NCT03257631)
Timeframe: 6 months (first 6 cycles) or 3 months (first 3 cycles) for participants in the DIPG group

Interventionpercentage of participants (Number)
Diffuse Intrinsic Pontine Glioma0
Ependymoma0
High-grade Glioma5.3
Medulloblastoma0

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Minimum Response (MR)

Minimum response (MR) or better with elotuzumab and lenalidomide for each study arm. The Consensus on Uniform Reporting of Response will be used to evaluate response. Myeloma participants enrolled in this clinical study will be assessed for disease response after every cycle. (NCT03411031)
Timeframe: Up to 60 days post last study treatment

InterventionParticipants (Count of Participants)
A: Elotuzumab + Lenalidomide at 25 mg2
B: Elotuzumab + Lenalidomide at 10 mg3

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Overall Response

Overall response with elotuzumab and lenalidomide for each study arm. Overall Response is defined as best Overall Response, as Complete Response or Partial Response. Response will be assessed per the uniform response criteria of the International Myeloma Working Group(IMWG). Myeloma participants enrolled in this clinical study will be assessed for disease response after every cycle. Complete Response= Negative immunofixation on the serum and urine and disappearance of any soft tissue plasmacytomas and <5% plasma cells in bone marrow aspirates; Partial Response= ≥50% reduction of serum M-protein plus reduction in 24 h urinary M-protein by ≥90% or to <200 mg per 24 h; (NCT03411031)
Timeframe: Up to 60 days post last study treatment

InterventionParticipants (Count of Participants)
A: Elotuzumab + Lenalidomide at 25 mg1
B: Elotuzumab + Lenalidomide at 10 mg2

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Percentage of Participants With Progression Free Survival (PFS)

Progression free survival (PFS) is defined as the time of randomization to date of death from any cause, date of relapse/progression, or the last follow-up date, whichever comes first. The Kaplan-Meier method will be used to estimate PFS for each Study Arm. The method of Brookmeyer and Crowley will be used to construct 95% confidence interval. (NCT03411031)
Timeframe: An average of 8 months

Interventionpercentage of participants (Number)
A: Elotuzumab + Lenalidomide at 25 mg11.1
B: Elotuzumab + Lenalidomide at 10 mg22.2

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Lanadelumab Sub-protocol: Percentage of Participants Who Died Before or on Day 29

All-cause mortality is death due to any cause. Participants with an unknown alive/death status on Day 29 were considered alive for this analysis, with the exception of patients with a score of 7 who were discharged to hospice care before or on Day 29. (NCT04590586)
Timeframe: Day 1 to Day 29

Interventionpercentage of participants (Number)
Lanadelumab + Standard of Care32.0
Lanadelumab Placebo Control30.0

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Apremilast Sub-protocol: Percentage of Participants Who Died Before or on Day 29

All-cause mortality is death due to any cause. Participants with an unknown alive/death status on Day 29 were considered alive for this analysis, with the exception of patients with a score of 7 who were discharged to hospice care before or on Day 29. (NCT04590586)
Timeframe: Day 1 to Day 29

Interventionpercentage of participants (Number)
Apremilast + Standard of Care17.5
Apremilast Placebo Control17.4

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Lanadelumab Sub-protocol: Percentage of Participants With a ≥ 2-point Improvement From Baseline or Fit for Discharge on the Clinical Severity Status 8-Point Ordinal Scale at Day 29

"Fit for discharge is defined as achieving a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale. Participants with an ordinal scale score of 7 must not have been discharged to hospice care to be considered as fit for discharge. Participants with a missing clinical severity score at Day 29 were considered as not having met the event at Day 29.~The clinical severity status 8-point ordinal scale scores are:~Death~Hospitalized, on invasive mechanical ventilation or extracorporeal membrane oxygenation (ECMO)~Hospitalized, on noninvasive ventilation or high-flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care (COVID-19 related or otherwise)~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Baseline (Day 1) and Day 29

Interventionpercentage of participants (Number)
Lanadelumab + Standard of Care72.0
Lanadelumab Placebo Control63.3

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Lanadelumab Sub-protocol: Time to Confirmed Clinical Recovery Without Rehospitalization Through Day 29

"Confirmed clinical recovery means the participant is fit for discharge from hospital, defined by achieving a score of 6 (hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care), 7 (not hospitalized, limitation on activities and/or requiring home oxygen), or 8 (not hospitalized, no limitations on activities) on the clinical severity status 8-point ordinal scale, without being re-hospitalized prior to Day 29.~The Kaplan-Meier estimate of the time to confirmed clinical recovery through Day 29, without re-hospitalization through Day 29, was calculated from Study Day 1 to the earliest date on which the participant had a score of 6, 7, or 8 up to Day 29. Participants who never reached a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale before or on Day 29 were censored at Day 29. Participants who discontinued from the study before or on Day 29 were censored at time of discontinuation from study." (NCT04590586)
Timeframe: Day 1 (the day of the first dose of study drug for randomized participants who received at least one dose of study drug or the day of randomization for randomized participants who did not receive any study drug) to Day 29

Interventiondays (Median)
Lanadelumab + Standard of Care10.0
Lanadelumab Placebo Control15.5

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Zilucoplan Sub-protocol: Percentage of Participants Who Achieved Sustained Clinical Recovery

"Sustained clinical recovery is defined as being fit for discharge (achieving a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale) by Day 29, without re-hospitalization by Day 60. Participants with a score of 7 discharged to hospice care were not considered fit for discharge. Participants who died or discontinued from study or with a missing clinical recovery status at Day 60 were not considered having sustained clinical recovery.~Clinical severity status 8-point ordinal scale:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Day 60

Interventionpercentage of participants (Number)
Zilucoplan + Standard of Care55.0
Zilucoplan Placebo Control64.0

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Zilucoplan Sub-protocol: Percentage of Participants Who Died Before or on Day 29

All-cause mortality is death due to any cause. Participants with an unknown alive/death status on Day 29 were considered alive for this analysis, with the exception of patients with a score of 7 who were discharged to hospice care before or on Day 29. (NCT04590586)
Timeframe: Day 1 to Day 29

Interventionpercentage of participants (Number)
Zilucoplan + Standard of Care18.0
Zilucoplan Placebo Control24.0

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Zilucoplan Sub-protocol: Time to Confirmed Clinical Recovery Without Rehospitalization Through Day 29

"Confirmed clinical recovery means the participant is fit for discharge from hospital, defined by achieving a score of 6 (hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care), 7 (not hospitalized, limitation on activities and/or requiring home oxygen), or 8 (not hospitalized, no limitations on activities) on the clinical severity status 8-point ordinal scale, without being re-hospitalized prior to Day 29.~The Kaplan-Meier estimate of the time to confirmed clinical recovery through Day 29, without re-hospitalization through Day 29, was calculated from Study Day 1 to the earliest date on which the participant had a score of 6, 7, or 8 up to Day 29. Participants who never reached a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale before or on Day 29 were censored at Day 29. Participants who discontinued from the study before or on Day 29 were censored at time of discontinuation from study." (NCT04590586)
Timeframe: Day 1 (the day of the first dose of study drug for randomized participants who received at least one dose of study drug or the day of randomization for randomized participants who did not receive any study drug) to Day 29

Interventiondays (Median)
Zilucoplan + Standard of Care14.0
Zilucoplan Placebo Control15.0

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Zilucoplan Sub-protocol: Percentage of Participants With a ≥ 2-point Improvement From Baseline or Fit for Discharge on the Clinical Severity Status 8-Point Ordinal Scale at Day 29

"Fit for discharge is defined as achieving a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale. Participants with an ordinal scale score of 7 must not have been discharged to hospice care to be considered as fit for discharge. Participants with a missing clinical severity score at Day 29 were considered as not having met the event at Day 29.~The clinical severity status 8-point ordinal scale scores are:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high-flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care (COVID-19 related or otherwise)~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Baseline (Day 1) and Day 29

Interventionpercentage of participants (Number)
Zilucoplan + Standard of Care66.0
Zilucoplan Placebo Control69.3

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Apremilast Sub-protocol: Clinical Severity Status 8-Point Ordinal Scale Score at Days 8, 15, and 29

"The clinical severity status 8-point ordinal scale scores are:~Death~Hospitalized, on invasive mechanical ventilation or extracorporeal membrane oxygenation (ECMO)~Hospitalized, on noninvasive ventilation or high flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care (COVID-19 related or otherwise)~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities~Participants with a score of 7 who were discharged to hospice care are counted with participants with a score of 1 (death) for this endpoint." (NCT04590586)
Timeframe: Day 8, Day 15, and Day 29

InterventionParticipants (Count of Participants)
Day 872273936Day 872273930Day 1572273936Day 1572273930Day 2972273930Day 2972273936
5 (Hospitalized, not requiring supplemental oxygen6 (Hospitalized, not requiring supplemental oxygen7 (Not hospitalized, limitation on activities and/8 (Not hospitalized, no limitations on activities)Missing1 (Death or discharged to hospice care)2 (Hospitalized on invasive mechanical ventilation3 (Hospitalized on noninvasive ventilation or high4 (Hospitalized, requiring supplemental oxygen)
Apremilast + Standard of Care11
Apremilast + Standard of Care22
Apremilast Placebo Control20
Apremilast + Standard of Care25
Apremilast + Standard of Care26
Apremilast Placebo Control26
Apremilast + Standard of Care31
Apremilast Placebo Control40
Apremilast + Standard of Care36
Apremilast Placebo Control33
Apremilast + Standard of Care38
Apremilast Placebo Control34
Apremilast + Standard of Care5
Apremilast Placebo Control24
Apremilast + Standard of Care16
Apremilast Placebo Control13
Apremilast + Standard of Care9
Apremilast Placebo Control9
Apremilast Placebo Control8
Apremilast + Standard of Care10
Apremilast Placebo Control5
Apremilast + Standard of Care46
Apremilast Placebo Control48
Apremilast + Standard of Care78
Apremilast Placebo Control79
Apremilast Placebo Control2
Apremilast Placebo Control31
Apremilast Placebo Control6
Apremilast Placebo Control3
Apremilast + Standard of Care6
Apremilast Placebo Control1
Apremilast + Standard of Care0
Apremilast + Standard of Care34
Apremilast + Standard of Care110
Apremilast Placebo Control104
Apremilast + Standard of Care4

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Lanadelumab Sub-protocol: Clinical Severity Status 8-Point Ordinal Scale Score at Days 8, 15, and 29

"The clinical severity status 8-point ordinal scale scores are:~Death~Hospitalized, on invasive mechanical ventilation or extracorporeal membrane oxygenation (ECMO)~Hospitalized, on noninvasive ventilation or high flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care (COVID-19 related or otherwise)~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities~Participants with a score of 7 who were discharged to hospice care are counted with participants with a score of 1 (death) for this endpoint." (NCT04590586)
Timeframe: Day 8, Day 15, and Day 29

InterventionParticipants (Count of Participants)
Day 872273928Day 872273927Day 1572273928Day 1572273927Day 2972273927Day 2972273928
1 (Death or discharged to hospice care)2 (Hospitalized on invasive mechanical ventilation3 (Hospitalized on noninvasive ventilation or high4 (Hospitalized, requiring supplemental oxygen)5 (Hospitalized, not requiring supplemental oxygen6 (Hospitalized, not requiring supplemental oxygen7 (Not hospitalized, limitation on activities and/Missing8 (Not hospitalized, no limitations on activities)
Lanadelumab + Standard of Care4
Lanadelumab + Standard of Care3
Lanadelumab Placebo Control4
Lanadelumab Placebo Control6
Lanadelumab + Standard of Care1
Lanadelumab + Standard of Care2
Lanadelumab + Standard of Care8
Lanadelumab Placebo Control7
Lanadelumab Placebo Control1
Lanadelumab Placebo Control3
Lanadelumab Placebo Control13
Lanadelumab + Standard of Care7
Lanadelumab Placebo Control9
Lanadelumab Placebo Control2
Lanadelumab Placebo Control0
Lanadelumab + Standard of Care0
Lanadelumab + Standard of Care5
Lanadelumab + Standard of Care12

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Apremilast Sub-protocol: Percentage of Participants Who Achieved Oxygen-Free Recovery at Day 29

Oxygen-free recovery at Day 29 is defined as being alive, discharged, and not receiving supplemental oxygen at Day 29. Participants who reached a score of 7 on the ordinal scale for clinical severity who were discharged to hospice care before or on Day 29 were considered as not discharged at Day 29. Participants with a missing oxygen-free recovery status at Day 29 were considered as not having an oxygen-free recovery. (NCT04590586)
Timeframe: Day 29

Interventionpercentage of participants (Number)
Apremilast + Standard of Care59.8
Apremilast Placebo Control63.7

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Apremilast Sub-protocol: Percentage of Participants Who Achieved Sustained Clinical Recovery

"Sustained clinical recovery is defined as being fit for discharge (achieving a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale) by Day 29, without re-hospitalization by Day 60. Participants with a score of 7 discharged to hospice care were not considered fit for discharge. Participants who died or discontinued from study or with a missing clinical recovery status at Day 60 were not considered having sustained clinical recovery.~Clinical severity status 8-point ordinal scale:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Day 60

Interventionpercentage of participants (Number)
Apremilast + Standard of Care66.0
Apremilast Placebo Control66.3

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Apremilast Sub-protocol: Percentage of Participants With a ≥ 2-point Improvement From Baseline or Fit for Discharge on the Clinical Severity Status 8-Point Ordinal Scale at Day 29

"Fit for discharge is defined as achieving a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale. Participants with an ordinal scale score of 7 must not have been discharged to hospice care to be considered as fit for discharge. Participants with a missing clinical severity score at Day 29 were considered as not having met the event at Day 29.~The clinical severity status 8-point ordinal scale scores are:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high-flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care (COVID-19 related or otherwise)~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Baseline (Day 1) and Day 29

Interventionpercentage of participants (Number)
Apremilast + Standard of Care74.7
Apremilast Placebo Control77.9

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Apremilast Sub-protocol: Time to Confirmed Clinical Recovery Without Rehospitalization Through Day 29

"Confirmed clinical recovery means the participant is fit for discharge from hospital, defined by achieving a score of 6 (hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care), 7 (not hospitalized, limitation on activities and/or requiring home oxygen), or 8 (not hospitalized, no limitations on activities) on the clinical severity status 8-point ordinal scale, without being re-hospitalized prior to Day 29.~The Kaplan-Meier estimate of the time to confirmed clinical recovery through Day 29, without re-hospitalization through Day 29, was calculated from Study Day 1 to the earliest date on which the participant had a score of 6, 7, or 8 up to Day 29. Participants who never reached a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale before or on Day 29 were censored at Day 29. Participants who discontinued from the study before or on Day 29 were censored at time of discontinuation from study." (NCT04590586)
Timeframe: Day 1 (the day of the first dose of study drug for randomized participants who received at least one dose of study drug or the day of randomization for randomized participants who did not receive any study drug) to Day 29

Interventiondays (Median)
Apremilast + Standard of Care14.0
Apremilast Placebo Control14.0

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Zilucoplan Sub-protocol: Percentage of Participants Who Achieved Oxygen-Free Recovery at Day 29

Oxygen-free recovery at Day 29 is defined as being alive, discharged, and not receiving supplemental oxygen at Day 29. Participants who reached a score of 7 on the ordinal scale for clinical severity who were discharged to hospice care before or on Day 29 were considered as not discharged at Day 29. Participants with a missing oxygen-free recovery status at Day 29 were considered as not having an oxygen-free recovery. (NCT04590586)
Timeframe: Day 29

Interventionpercentage of participants (Number)
Zilucoplan + Standard of Care54.0
Zilucoplan Placebo Control60.0

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Zilucoplan Sub-protocol: Percentage of Participants Who Achieved Clinical Recovery by Days 8, 15, and 29

"Clinical recovery is defined as being fit for discharge, i.e., the achievement of a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale. Participants with a score of 7 discharged to hospice care were not considered fit for discharge. Participants who discontinued the study on or before Days 8, 15, or 29 or with a missing clinical recovery status were considered as not having clinical recovery at each respective time point.~Clinical severity status 8-point ordinal scale:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high-flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Day 8, Day 15, and Day 29

,
Interventionpercentage of participants (Number)
Day 8Day 15Day 29
Zilucoplan + Standard of Care33.053.060.0
Zilucoplan Placebo Control30.753.366.7

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Zilucoplan Sub-protocol: Number of Participants With Treatment-emergent Adverse Events

"An adverse event is any untoward medical occurrence in a participant, temporally associated with the use of study treatment, whether or not considered related to study treatment. A TEAE is an AE that occurs after the first dose of study drug. A serious AE is any AE that resulted in death, was life-threatening, required inpatient hospitalization or prolongation of hospitalization, resulted in persistent disability/incapacity, a congenital anomaly/birth defect, or an important medical event that may jeopardize the patient or require intervention to prevent an outcome listed above.~The Investigator assessed the intensity of each AE according to the CTCAE grades:~Grade 1 Mild; asymptomatic or mild symptoms;~Grade 2 Moderate; minimal, local or noninvasive intervention indicated;~Grade 3 Severe or medically significant, not immediately life-threatening;~Grade 4 Life-threatening; urgent intervention indicated;~Grade 5 Death due to AE." (NCT04590586)
Timeframe: From first dose of study drug to end of study (Day 60)

,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAE with a CTCAE grade ≥ 3Serious TEAETEAE leading to dose modificationTEAE leading to discontinuation of study drug
Zilucoplan Placebo + Standard of Care43201
Zilucoplan Placebo Control47292955
Zilucoplan+ Standard of Care65343107

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Lanadelumab Sub-protocol: Percentage of Participants Who Achieved Clinical Recovery by Days 8, 15, and 29

"Clinical recovery is defined as being fit for discharge, i.e., the achievement of a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale. Participants with a score of 7 discharged to hospice care were not considered fit for discharge. Participants who discontinued the study on or before Days 8, 15, or 29 or with a missing clinical recovery status were considered as not having clinical recovery at each respective time point.~Clinical severity status 8-point ordinal scale:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high-flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Day 8, Day 15, and Day 29

,
Interventionpercentage of participants (Number)
Day 8Day 15Day 29
Lanadelumab + Standard of Care44.056.060.0
Lanadelumab Placebo Control36.756.763.3

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Lanadelumab Sub-protocol: Number of Participants With Treatment-emergent Adverse Events (TEAEs)

"An adverse event (AE) is any untoward medical occurrence in a participant, temporally associated with the use of study treatment, whether or not considered related to study treatment. A TEAE is an AE that occurs after the first dose of study drug. A Serious AE is any AE that resulted in death, was life-threatening, required inpatient hospitalization or prolongation of hospitalization, resulted in persistent disability/incapacity, a congenital anomaly/birth defect, or an important medical event that may jeopardize the patient or require intervention to prevent an outcome listed above.~The Investigator assessed the intensity of each AE according to the Common Terminology Criteria for Adverse Events (CTCAE):~Grade 1 Mild; asymptomatic or mild symptoms;~Grade 2 Moderate; minimal, local or noninvasive intervention indicated;~Grade 3 Severe or medically significant, not immediately life-threatening;~Grade 4 Life-threatening; urgent intervention indicated;~Grade 5 Death due to AE." (NCT04590586)
Timeframe: From first dose of study drug to end of study (Day 60)

,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAE with a CTCAE grade ≥ 3Serious TEAETEAE leading to dose modificationTEAE leading to discontinuation of study drug
Lanadelumab + Standard of Care17111121
Lanadelumab Placebo + Standard of Care11100
Lanadelumab Placebo Control22181835

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Apremilast Sub-protocol: Percentage of Participants Who Achieved Clinical Recovery at Days 8, 15, and 29

"Clinical recovery is defined as being fit for discharge, i.e., the achievement of a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale. Participants with a score of 7 discharged to hospice care were not considered fit for discharge. Participants who discontinued the study on or before Days 8, 15, or 29 or with a missing clinical recovery status were considered as not having clinical recovery at each respective time point.~Clinical severity status 8-point ordinal scale:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high-flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Day 8, Day 15, and Day 29

,
Interventionpercentage of participants (Number)
Day 8Day 15Day 29
Apremilast + Standard of Care36.657.766.0
Apremilast Placebo Control35.860.072.1

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Apremilast Sub-protocol: Number of Participants With Treatment-emergent Adverse Events (TEAEs)

"An adverse event (AE) is any untoward medical occurrence in a participant, temporally associated with the use of study treatment, whether or not considered related to study treatment. A TEAE is an AE that occurs after the first dose of study drug. A serious AE is any AE that resulted in death, was life-threatening, required inpatient hospitalization or prolongation of hospitalization, resulted in persistent disability/incapacity, a congenital anomaly/birth defect, or an important medical event that may jeopardize the patient or require intervention to prevent an outcome listed above.~The Investigator assessed the intensity of each AE according to the CTCAE grades:~Grade 1 Mild; asymptomatic or mild symptoms;~Grade 2 Moderate; minimal, local or noninvasive intervention indicated;~Grade 3 Severe or medically significant, not immediately life-threatening;~Grade 4 Life-threatening; urgent intervention indicated;~Grade 5 Death due to AE." (NCT04590586)
Timeframe: From first dose of study drug to end of study (Day 60)

,,
InterventionParticipants (Count of Participants)
Any treatment-emergent adverse event (TEAE)TEAE with a CTCAE grade ≥ 3Serious TEAETEAE leading to dose modificationTEAE leading to discontinuation of study drug
Apremilast + Standard of Care1024851169
Apremilast Placebo + Standard of Care1005455611
Apremilast Placebo Control1035757612

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Zilucoplan Sub-protocol: Clinical Severity Status 8-Point Ordinal Scale Score at Days 8, 15, and 29

"The clinical severity status 8-point ordinal scale scores are:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care (COVID-19 related or otherwise)~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities~Participants with a score of 7 who were discharged to hospice care are counted with participants with a score of 1 (death) for this endpoint." (NCT04590586)
Timeframe: Day 8, Day 15, and Day 29

InterventionParticipants (Count of Participants)
Day 872273932Day 872273931Day 1572273932Day 1572273931Day 2972273931Day 2972273932
1 (Death or discharged to hospice care)2 (Hospitalized on invasive mechanical ventilation3 (Hospitalized on noninvasive ventilation or high4 (Hospitalized, requiring supplemental oxygen)5 (Hospitalized, not requiring supplemental oxygen6 (Hospitalized, not requiring supplemental oxygen7 (Not hospitalized, limitation on activities and/8 (Not hospitalized, no limitations on activities)Missing
Zilucoplan Placebo Control5
Zilucoplan + Standard of Care24
Zilucoplan Placebo Control14
Zilucoplan + Standard of Care12
Zilucoplan Placebo Control8
Zilucoplan Placebo Control10
Zilucoplan Placebo Control1
Zilucoplan + Standard of Care22
Zilucoplan Placebo Control9
Zilucoplan + Standard of Care11
Zilucoplan Placebo Control12
Zilucoplan + Standard of Care8
Zilucoplan + Standard of Care16
Zilucoplan Placebo Control7
Zilucoplan + Standard of Care3
Zilucoplan Placebo Control3
Zilucoplan + Standard of Care10
Zilucoplan Placebo Control6
Zilucoplan + Standard of Care2
Zilucoplan + Standard of Care0
Zilucoplan + Standard of Care25
Zilucoplan + Standard of Care31
Zilucoplan Placebo Control26
Zilucoplan + Standard of Care5
Zilucoplan + Standard of Care14
Zilucoplan Placebo Control18
Zilucoplan + Standard of Care1
Zilucoplan Placebo Control0
Zilucoplan + Standard of Care20
Zilucoplan + Standard of Care44
Zilucoplan Placebo Control35
Zilucoplan Placebo Control2

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Lanadelumab Sub-protocol: Percentage of Participants Who Achieved Oxygen-Free Recovery at Day 29

Oxygen-free recovery at Day 29 is defined as being alive, discharged, and not receiving supplemental oxygen at Day 29. Participants who reached a score of 7 on the ordinal scale for clinical severity who were discharged to hospice care before or on Day 29 were considered as not discharged at Day 29. Participants with a missing oxygen-free recovery status at Day 29 were considered as not having an oxygen-free recovery. (NCT04590586)
Timeframe: Day 29

Interventionpercentage of participants (Number)
Lanadelumab + Standard of Care52.0
Lanadelumab Placebo Control56.7

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Lanadelumab Sub-protocol: Percentage of Participants Who Achieved Sustained Clinical Recovery

"Sustained clinical recovery is defined as being fit for discharge (achieving a score of 6, 7, or 8 on the clinical severity status 8-point ordinal scale) by Day 29, without re-hospitalization by Day 60. Participants with a score of 7 discharged to hospice care were not considered fit for discharge. Participants who died or discontinued from study or with a missing clinical recovery status at Day 60 were not considered having sustained clinical recovery.~Clinical severity status 8-point ordinal scale:~Death~Hospitalized, on invasive mechanical ventilation or ECMO~Hospitalized, on noninvasive ventilation or high flow oxygen devices~Hospitalized, requiring supplemental oxygen~Hospitalized, not requiring supplemental oxygen, requiring ongoing medical care~Hospitalized, not requiring supplemental oxygen, no longer requires ongoing medical care~Not hospitalized, limitation on activities and/or requiring home oxygen~Not hospitalized, no limitations on activities" (NCT04590586)
Timeframe: Day 60

Interventionpercentage of participants (Number)
Lanadelumab + Standard of Care40.0
Lanadelumab Placebo Control56.7

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Area Under the Concentration-time Curve of Apremilast in Plasma Over the Time Interval From 0 to the Last Quantifiable Data Point (AUC0-tz)

The area under the concentration-time curve of apremilast in plasma over the time interval from 0 to the last quantifiable data point (AUC0-tz) is reported. (NCT04811573)
Timeframe: 1 hour (h) before and 30 minutes (min), 1h, 1h30min, 2h, 2h30min, 3h, 3h30min, 4h, 5h, 6h, 8h, 11h, 15h, 24h, 36h, 48h after study drug administration.

Interventionhour * nanogram / milliliter (h*ng/mL) (Geometric Mean)
EU-Otezla Fasted (A; Tfasted)2390
US-Otezla Fasted (B; R1fasted)2430
EU-Otezla Fed (C; Tfed)2580
US-Otezla Fed (D; R1fed)2580
Japan-Otezla Fasted (E; R2fasted)2350

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Area Under the Concentration-time Curve of Apremilast in Plasma Over the Time Interval From 0 Extrapolated to Infinity (AUC0-∞)

The area under the concentration-time curve of apremilast in plasma over the time interval from 0 extrapolated to infinity (AUC0-∞) is reported. (NCT04811573)
Timeframe: 1 hour (h) before and 30 minutes (min), 1h, 1h30min, 2h, 2h30min, 3h, 3h30min, 4h, 5h, 6h, 8h, 11h, 15h, 24h, 36h, 48h after study drug administration.

Interventionhour * nanogram / milliliter (h*ng/mL) (Geometric Mean)
EU-Otezla Fasted (A; Tfasted)2420
US-Otezla Fasted (B; R1fasted)2460
EU-Otezla Fed (C; Tfed)2600
US-Otezla Fed (D; R1fed)2600
Japan-Otezla Fasted (E; R2fasted)2370

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Maximum Measured Concentration of Apremilast in Plasma (Cmax)

The maximum measured concentration of apremilast in plasma (Cmax) is reported. (NCT04811573)
Timeframe: 1 hour (h) before and 30 minutes (min), 1h, 1h30min, 2h, 2h30min, 3h, 3h30min, 4h, 5h, 6h, 8h, 11h, 15h, 24h, 36h, 48h after study drug administration.

Interventionnanogram / milliliter (ng/mL) (Geometric Mean)
EU-Otezla Fasted (A; Tfasted)298
US-Otezla Fasted (B; R1fasted)301
EU-Otezla Fed (C; Tfed)303
US-Otezla Fed (D; R1fed)271
Japan-Otezla Fasted (E; R2fasted)299

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