Page last updated: 2024-10-15

olanzapine

Description

Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4. [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 CID135398745
CHEMBL ID715
CHEBI ID7735
CHEBI ID94534
SCHEMBL ID117695
SCHEMBL ID28763
MeSH IDM0204623

Synonyms (172)

Synonym
AC-665
BIDD:PXR0138
BIDD:GT0332
AKOS005566122
HMS3393H05
AB00639907-06
AB00639907-07
us8802672, olanzapine
bdbm35254
gtpl47
lanzac
zyprexa velotab
alks-7921
c17h20n4s
10h-thieno(2,3-b)(1,5)benzodiazepine, 2-methyl-4-(4-methyl-1-piperazinyl)-
zyprexa intramuscular
zyprexa zydis
ly-170053
zalasta
midax
ly 170053
olansek
2-methyl-4-(4-methyl-1-piperazinyl)-10h-thieno(2,3-b)(1,5)benzodiazepine
olanzapina
olanzapinum
CHEBI:7735 ,
2-methyl-4-(4-methylpiperazin-1-yl)-10h-thieno[2,3-b][1,5]benzodiazepine
zyprexa
2-methyl-4-(4-methyl-1-piperazinyl)-10h-thieno[2,3-b][1,5]benzodiazepine
MLS001424057
C07322
132539-06-1
olanzapine
MLS000759457
smr000466345
DB00334
olanzapin
NCGC00096077-03
NCGC00096077-04
olanzapine (jan/usp/inn)
D00454
NCGC00096077-01
SPECTRUM1505024
zolafren
MLS001195646
MLS001165781
HMS2089M04
HMS2093I04
HMS2051H05
olanzapine mylan
olanzapine teva
olazax disperzi
olanzapine cipla
olanzapine glenmark
olanzapine apotex
olazax
CHEMBL715 ,
ly170053
AKOS000282888
L005958
L000455
2-methyl-4-(4-methylpiperazin-1-yl)-5h-thieno[3,2-c][1,5]benzodiazepine
2-methyl-4-(4-methyl-1-piperazinyl)-5h-thieno[3,2-c][1,5]benzodiazepine
A806453
olanzapine teva
hsdb 8155
zypadhera
olanzapine neopharma
olanzapine [usan:usp:inn:ban]
unii-n7u69t4szr
n7u69t4szr ,
cas-132539-06-1
tox21_111556
dtxcid503388
dtxsid9023388 ,
O0393
nsc_4585
bdbm82479
cas_132539-06-1
HMS2233F24
CCG-100922
BCP9001021
olzapin
5-methyl-8-(4-methylpiperazin-1-yl)-4-thia-2,9-diazatricyclo[8.4.0.0^{3,7}]tetradeca-1(10),3(7),5,8,11,13-hexaene
oferta
HY-14541
CS-1114
FT-0673219
10h-thieno[2,3-b][1,5]benzodiazepine, 2-methyl-4-(4-methyl-1-piperazinyl)-
NCGC00096077-05
olanzapine [usp monograph]
olanzapine [ep monograph]
olanzapine [jan]
olanzapine glenmark europe
olanzapine component of symbyax
olanzapine [inn]
olanzapine [usp-rs]
symbyax component olanzapine
lybalvi component olanzapine
olanzapine [orange book]
olanzapine [who-dd]
olanzapine component of lybalvi
olanzapine [ema epar]
olanzapine [mart.]
olanzapine [usan]
olanzapine [vandf]
olanzapine [mi]
S2493
2-methyl-4-(4-methylpiperazin-1-yl)-10h-benzo[b]thieno[2,3-e][1,4]diazepine
HMS3374L02
2-methyl-4-(4-methyl-1-piperazinyl)-10h-thieno-[2,3-b][1,5]benzodiazepine
SCHEMBL117695
NC00172
SCHEMBL28763
NCGC00096077-06
tox21_111556_1
KS-1090 ,
2-methyl-10-(4-methyl-piperazin-1-yl)-4h-3-thia-4,9-diaza-benzo[f]azulene
2-methyl-4-(4-methyl-1-piperazinyl)-10h-thieno[2,3-b][1,5]benzodiazepine #
AB00639907_09
AB00639907_08
mfcd00866702
SR-01000759343-4
SR-01000759343-6
sr-01000759343
CHEBI:94534
olanzapine, united states pharmacopeia (usp) reference standard
HMS3657I15
olanzapine, pharmaceutical secondary standard; certified reference material
olanzapine for system suitability, european pharmacopoeia (ep) reference standard
olanzapine, >=98% (hplc)
olanzapine, european pharmacopoeia (ep) reference standard
olanzapine 1.0 mg/ml in acetonitrile
olanzapine; 2-methyl-4-(4-methyl-1-piperazinyl)-10h-thieno[2,3-b][1,5]benzodiazepine; ly 170053; lanzac; zyprexa
J-006186
SBI-0206786.P001
HMS3714J03
NCGC00389791-02
olanzapine-d8, 100 mug/ml in acetonitrile, ampule of 1 ml, certified reference material
SW220248-1
BCP04917
HB1786
2-methyl-4-(4-methyl-1-piperazinyl) -10h-thieno[2,3-b][1,5]benzodiazepine
Z1521553472
olanzapine (zyprexa)
(e)-2-methyl-4-(4-methylpiperazin-1-yl)-10h-benzo[b]thieno[2,3-e][1,4]diazepine
Q201872
EN300-119499
5-methyl-8-(4-methylpiperazin-1-yl)-4-thia-2,9-diazatricyclo[8.4.0.0,3,7]tetradeca-1(10),3(7),5,8,11,13-hexaene
NCGC00096077-18
HMS3884J21
AMY7709
HMS3743A09
2-methyl-4-(4-methylpiperazin-1-yl)-10h- thieno[2,3-b][1,5]benzodiazepin
olanzapine (ly-170053)
nsc-754829
nsc-801187
nsc801187
nsc754829
BO164166
olanzapine- bio-x
ps15 - olanzapine
olanzapine (usp-rs)
olanzapine (mart.)
n05ah03
zyprexazydis
olanzapine (ep monograph)
olanzapine (usp monograph)
olanzapine (usan:usp:inn:ban)
2-methyl-4-(4-methyl-1-piperazinyl)-10h-thieno(2,3- b)(1,5)benzodiazepine
zyprexaintramuscular
olanzapine, 1mg/ml in acetonitrile

Research Excerpts

Overview

Olanzapine is a widely adopted atypical antipsychotic medication used to manage schizophrenia. It is a potent antagonist of the M3 acetylcholine muscarinic receptor (M3R), while the downregulated hepatic M3R-AMPKα signalling pathway is involved in metabolic disorders. Its clinical application has been restricted by metabolic-related side effects.

ExcerptReference
"Olanzapine is a widely adopted atypical antipsychotic medication used to manage schizophrenia. "( Gluteal muscle damage and rhabdomyolysis after olanzapine poisoning: a case report.
Cui, S; Jian, T; Jian, X; Kan, B; Li, Y; Shi, L; Sun, C; Yu, G, 2021
)
"Olanzapine is a potent antagonist of the M3 acetylcholine muscarinic receptor (M3R), while the downregulated hepatic M3R-AMPKα signalling pathway is involved in metabolic disorders."( Cevimeline co-treatment attenuates olanzapine-induced metabolic disorders via modulating hepatic M3 muscarinic receptor: AMPKα signalling pathway in female rats.
Deng, C; Han, M; Lian, J; Su, Y, 2022
)
"Olanzapine is a commonly used drug in the treatment of schizophrenia, but its clinical application has been restricted by metabolic-related side effects. "( Effect of Co-Treatment of Olanzapine with SEP-363856 in Mice Models of Schizophrenia.
Liang, L; Ma, Y; Ren, X; Xu, J; Xue, Y; Zhang, G; Zhuang, T, 2022
)
"1. Olanzapine is an atypical antipsychotic primarily used to treat schizophrenia and bipolar disorder. "( Metabolism of the antipsychotic drug olanzapine by CYP3A43.
Bureik, M; Liu, S; Machalz, D; Parr, MK; Wolber, G; Wolf, CA; Zhao, J, 2022
)
"Olanzapine is a second-generation antipsychotic with established efficacy in several psychiatric disease states, but its use is limited because of weight gain and metabolic side effects. "( Olanzapine/Samidorphan: A New Combination Treatment for Schizophrenia and Bipolar I Disorder Intended to Reduce Weight Gain.
Corrao, MM; Nelson, LA, 2022
)
"Olanzapine is an effective antipsychotic medication for treatment-resistant schizophrenia (TRS); however, the therapeutic effectiveness of olanzapine has been found to vary in individual patients. "( miR143-3p-Mediated NRG-1-Dependent Mitochondrial Dysfunction Contributes to Olanzapine Resistance in Refractory Schizophrenia.
Chen, D; Chen, L; Cong, Q; Du, H; Fan, L; He, L; Huai, C; Huang, H; Li, M; Liu, C; Liu, Y; Qin, S; Song, C; Sun, J; Wang, C; Wang, G; Wei, M; Xu, Y; Yi, Z; Zeng, R; Zhang, X; Zhang, Y; Zhu, J, 2022
)
"Olanzapine is a thienobenzodiazepine class antipsychotic that strongly antagonises the 5-HT2A serotonin receptor, but acute poisonings are reported rarely. "( Olanzapine poisoning in patients treated at the National Poison Control Centre in Belgrade, Serbia in 2017 and 2018: a brief review of serum concentrations and clinical symptoms.
Antunović, M; Ercegović, GV; Kilibarda, V; Stošić, JJ; Vučinić, S; Vukčević, NP; Đorđević, S, 2022
)
"Olanzapine(OLZ)is a multi-acting receptor-targeted antipsychotic drug approved in Japan in December 2017 for the treatment of anticancer drug-induced nausea and vomiting. "( [Administration Period of Olanzapine as an Antiemetic Drug for Patients on FEC Therapy-A Survey].
Fujii, C; Ishizaka, T; Kamigaki, S; Nishida, S; Ogawa, N; Takeda, T; Tsubaki, M; Tsurushima, K; Yamamura, J; Yanagishita, Y; Yasui, Y, 2022
)
"Olanzapine is an effective antipsychotic drug used in psychiatry to treat psychoses, especially schizophrenia and schizoaffective disorders. "( Olanzapine in oncology palliative care.
Šoukalová, Z, 2022
)
"Olanzapine is an effective antiemetic in cancer patients with tumor-induced nausea and in antiemetic regimens for chemotherapy-induced nausea and vomiting."( Olanzapine in oncology palliative care.
Šoukalová, Z, 2022
)
"Olanzapine is an atypical antipsychotic drug used for mental disorders. "( Population pharmacokinetics and dosing optimization of olanzapine in Chinese paediatric patients: Based on the impact of sex and concomitant valproate on clearance.
Hu, JQ; Huang, SQ; Kong, W; Li, XL; Liu, SJ; Lu, HQ; Lu, HY; Ni, XJ; Shang, DW; Wen, YG; Xiao, T; Yang, HL; Zhang, M; Zhu, XQ, 2022
)
"Olanzapine (OLA) is a common drug used to treat schizophrenia and has recently come under increasing scrutiny as an emerging contaminant. "( The antipsychotic drug olanzapine altered lipid metabolism in the common carp (Cyprinus carpio L.): Insight from the gut microbiota-SCFAs-liver axis.
Chang, X; Feng, J; Meng, X; Shen, Y; Su, X; Wang, X; Yang, G; Yun, L; Zhang, J, 2023
)
"Olanzapine (OZP) is a safe and effective atypical antipsychotic drug used in treating schizophrenia and bipolar disorders. "( Development and evaluation of a drug-in-adhesive transdermal delivery system for delivery of olanzapine.
Banga, AK; Vora, D, 2022
)
"Olanzapine is an atypical antipsychotic and is widely used for prophylaxis of chemotherapy-induced nausea and vomiting in cancer patients. "( Efficacy of Olanzapine for Symptom Relief in Cancer Patients.
Nakagawa, N; Suzuki, M, 2022
)
"Olanzapine (OLA) is an atypical second-generation antipsychotic that exhibits significant pharmacokinetic variability. "( Effects of Age, Sex, and Comedication on the Plasma Concentrations of Olanzapine in Chinese Patients With Schizophrenia Based on Therapeutic Drug Monitoring Data.
Cui, X; Ding, J; Li, Y; Meng, Z; Xing, H; Yang, L; Zhang, S; Zhang, Y,
)
"Olanzapine pamoate is an intramuscular depot injection for the treatment of schizophrenia. "( Case series profile of olanzapine post-injection delirium/sedation syndrome.
Brown, J; Chan, BS; Downes, MA; Harris, K; Isoardi, KZ; Seebaluck, J, 2023
)
"Olanzapine is an antipsychotic agent with species-dependent pharmacokinetic profiles in both humans and animals. "( The Unique Human N10-Glucuronidated Metabolite Formation from Olanzapine in Chimeric NOG-TKm30 Mice with Humanized Livers.
Higuchi, Y; Kato, H; Suemizu, H; Uehara, S; Yamazaki, H; Yoneda, N, 2023
)
"Olanzapine is a commonly used and effective second-generation antipsychotic agent used for the control of paranoia and agitation in schizophrenia and bipolar disorder as well as in the behavioural and psychological symptoms of dementia. "( Delayed-Onset olanzapine-induced rhabdomyolysis.
Lim, JHB; Robinson, B; Savige, J, 2023
)
"Olanzapine (OLZ) is an antipsychotic agent and is a thienobenzodiazepine derivative. "( A review of various analytical methods for the estimation of olanzapine: An antipsychotic drug.
Almalki, WH; Kesharwani, P; S, R; Sheikh, A; Thanikachalam, PV, 2023
)
"Olanzapine is an atypical antipsychotic with antiemetic activity that's recommended in the guidelines for the treatment of chemotherapy induced nausea and vomiting, but outside of oncologic indications there is a lack of research."( Olanzapine for Non-Chemotherapy Related Nausea and Emesis in Patients with a Palliative Care Consult.
Bonar, S; Cook, K; Poole, MFF; Samala, RV; Schneider, HL, 2023
)
"Olanzapine is an antipsychotic drug that is used to prevent nausea and vomiting in palliative care and to treat chemotherapy-induced nausea and vomiting."( Olanzapine as an add-on, pre-operative anti-emetic drug for postoperative nausea or vomiting: a randomised controlled trial.
Grigio, TR; Martins, JVB; Slullitel, A; Sousa, AM; Timmerman, H; Wolff, AP, 2023
)
"Olanzapine (OLZ) is an atypical antipsychotic agent for psychotic disorders. "( Thymoquinone attenuates olanzapine-induced metabolic disorders in rats.
Hosseinzadeh, H; Kaviani, F; Mohsenzadeh, MS; Rameshrad, M; Razavi, BM, 2023
)
"Olanzapine is an atypical antipsychotic drug which is effective in the treatment of schizophrenia. "( Association of smoking cigarettes, age, and sex with serum concentrations of olanzapine in patients with schizophrenia.
Horvat, M; Kadija, M; Lovrić, M; Šagud, M; Ščavničar, A; Živković, M, 2023
)
"Olanzapine is a commonly prescribed atypical antipsychotic agent for treatment of patients with schizophrenia and bipolar disorders. "( CYP1A2 expression rather than genotype is associated with olanzapine concentration in psychiatric patients.
Belič, A; Csukly, G; Fekete, F; Kiss, ÁF; Menus, Á; Minus, A; Monostory, K; Póti, Á; Sirok, D; Tóth, K, 2023
)
"Olanzapine is a frequently used atypical antipsychotic drug known to exert structural brain alterations in animals. "( Olanzapine exposure diminishes perfusion and decreases volume of sensorimotor cortex in rats.
Babinska, Z; Buchtova, M; Drazanova, E; Horska, K; Kotolova, H; Kratka, L; Ruda-Kucerova, J; Skoupy, R; Starcuk, Z; Vaskovicova, N; Vrlikova, L, 2019
)
"Olanzapine is a second-generation antipsychotic (SGA) used frequently in the treatment of schizophrenia and a growing list of off-label conditions. "( Female mice are protected against acute olanzapine-induced hyperglycemia.
Hahn, MK; Medak, KD; Townsend, LK; Wright, DC, 2019
)
"Olanzapine (OLZ) is a second-generation antipsychotic that is used to treat schizophrenia but also causes acute hyperglycemia. "( AMPK β1 activation suppresses antipsychotic-induced hyperglycemia in mice.
Ashworth, KE; Bush, ND; Halm, MK; Kemp, BE; Medak, KD; Shamshoum, H; Townsend, LK; Wright, DC, 2019
)
"Olanzapine is an atypical antipsychotic indicated for the treatment of schizophrenia and, either as monotherapy or as an adjunct to lithium or valproate, for bipolar I disorder. "( Combination of Olanzapine and Samidorphan Has No Clinically Significant Effect on the Pharmacokinetics of Lithium or Valproate.
Graham, C; Sun, L; von Moltke, L; Yagoda, S; Yao, B, 2020
)
"Olanzapine is an atypical antipsychotic antagonist blocking a variety of neurotransmitters in the nausea and vomiting pathophysiology."( Olanzapine as a rescue antiemetic in hematopoietic stem cell transplant.
Greer, D; Kreikemeier, E; Liewer, S; Monson, T, 2020
)
"Olanzapine is a second-generation antipsychotic. "( Generalised tonic-clonic seizures on the subtherapeutic dose of olanzapine.
Chachar, AS; Mansoor, M; Mesiya, MH, 2019
)
"Olanzapine is a thienobenzodiazepine compound. "( A platinum black-modified microelectrode for in situ olanzapine detection in microliter volumes of undiluted serum.
Belmaker, RH; Ben-Yoav, H; Bersudsky, Y; Shukla, RP, 2020
)
"Olanzapine is an antipsychotic drug routinely used for the treatment of schizophrenia. "( Olanzapine-mediated cardiotoxicity is associated with altered energy metabolism in isolated rat hearts.
Arnold, M; Carrel, T; Grman, M; Gulac, P; Longnus, S; Stankovicova, T; Tomasova, L, 2020
)
"Olanzapine is an antipsychotic drug used to treat patients with schizophrenia due to its lower incidence of extrapyramidal symptoms. "( Neuroprotective effects of olanzapine against rotenone-induced toxicity in PC12 cells.
Liang, ZQ; Liu, YL; Shen, X; Song, YZ; Wang, WJ; Wu, JC; Xiong, YJ; Zhao, YF; Zhu, Y; Zuo, WQ, 2020
)
"Olanzapine is an atypical antipsychotic that has affinity for many central nervous system receptors. "( The use of olanzapine as an antiemetic in palliative medicine: a systematic review of the literature.
Da Silva, A; Gamblin, V; Penel, N; Prod'Homme, C; Reich, M; Saudemont, G; Villet, S, 2020
)
"Olanzapine is an atypical antipsychotic drug that has been increasingly used for treatment in schizophrenia. "( Association of the genetic polymorphisms of metabolizing enzymes, transporters, target receptors and their interactions with treatment response to olanzapine in chinese han schizophrenia patients.
Fang, H; Gao, B; Li, J; Shi, J; Song, M; Wang, C; Wang, S; Yan, P, 2020
)
"Olanzapine is a second-generation antipsychotic (SGA) used in the treatment of schizophrenia and a number of off-label conditions. "( GLP1 receptor agonism protects against acute olanzapine-induced hyperglycemia.
Medak, KD; Peppler, WT; Shamshoum, H; Wright, DC, 2020
)
"Olanzapine is a second-generation antipsychotic (AP) drug commonly prescribed for the treatment of schizophrenia. "( N-acetylcysteine prevents olanzapine-induced oxidative stress in mHypoA-59 hypothalamic neurons.
Boz, Z; Hu, M; Huang, XF; Yu, Y, 2020
)
"Olanzapine is an atypical antipsychotic widely used for the treatment of schizophrenia, which often causes serious adverse drug reactions. "( Impact of polymorphisms in transporter and metabolizing enzyme genes on olanzapine pharmacokinetics and safety in healthy volunteers.
Abad-Santos, F; Almenara, S; Koller, D; Martín-Vílchez, S; Mejía-Abril, G; Navares-Gómez, M; Ochoa, D; Román, M; Saiz-Rodríguez, M; Soria-Chacartegui, P; Villapalos-García, G; Zubiaur, P, 2021
)
"IVP olanzapine appears to be a safe route of administration in hospitalized patients, including those receiving multiple doses."( Safety of Intravenous Olanzapine Administration at a Tertiary Academic Medical Center.
Dube, KM; Hunt, NF; Kovacevic, MP; Lupi, KE; McLaughlin, KC, 2021
)
"Olanzapine is an inexpensive and durable agent for the treatment of chemotherapy-induced nausea and vomiting and is also superior to neurokinin-1 receptor antagonists in the control of nausea. "( Low-Dose Olanzapine Plus Granisetron and Dexamethasone for Carboplatin-Induced Nausea and Vomiting in Patients with Thoracic Malignancies: A Prospective Multicenter Phase II Trial.
Arai, T; Fujita, Y; Funaguchi, N; Gomyo, T; Hakamata, J; Hirose, C; Iihara, H; Ikemura, S; Imai, H; Kaito, D; Kawazoe, H; Kotake, M; Minato, K; Ohno, Y; Okura, H; Sakai, C; Shimokawa, M; Suzuki, A, 2021
)
"Olanzapine is a widely used antipsychotic, which increases the weight of SZ patients."( Metabolomics-based understanding of the olanzapine-induced weight gain in female first-episode drug-naïve patients with schizophrenia.
Chen, N; Guan, XN; Guo, YH; Liu, JH; Wang, D; Wang, J; Xiu, MH, 2021
)
"Olanzapine is a common drug used in antipsychotic medication."( What to Do About Missed Doses? A Retrospective Study of Olanzapine in the Elderly.
Hu, J; Huang, S; Li, G; Li, X; Liu, S; Shang, D; Wang, Z; Wen, Y; Xiao, T; Zhu, X, 2021
)
"Olanzapine is an anti-psychotic drug that has been used for preventing and treating Chemotherapy-Induced Nausea and Vomiting (CINV). "( Efficacy and safety of olanzapine for the prevention of chemotherapy-induced nausea and vomiting: A systematic review and meta-analysis.
Nimworapan, M; Permsuwan, U; Yoodee, J, 2017
)
"Olanzapine (OLZ) is a drug that is used in the treatment of schizophrenia and other psychoses, and it belongs to the thienobenzodiazepine class. "( Bionanocomposite systems based on montmorillonite and biopolymers for the controlled release of olanzapine.
Alcântara, ACS; Oliveira, AS; Pergher, SBC, 2017
)
"Olanzapine is a commonly prescribed SGA with a significantly higher MetS risk than that of most antipsychotics."( Metabolic adverse effects of olanzapine on cognitive dysfunction: A possible relationship between BDNF and TNF-alpha.
Cai, J; Chen, M; Fan, W; Fang, X; Mao, Y; Song, L; Tang, W; Yao, P; Zhang, C; Zhang, Y, 2017
)
"Olanzapine is a second-generation antipsychotic increasingly used in emergency medicine for many indications. "( The Use, Safety, and Efficacy of Olanzapine in a Level I Pediatric Trauma Center Emergency Department Over a 10-Year Period.
Blanchard, SR; Cole, JB; Klein, LR; Martel, ML; Nahum, R; Strobel, AM, 2020
)
"Olanzapine is an atypical antipsychotic indicated for the treatment of schizophrenia and known to be effective in the management of delirium. "( Olanzapine induced delirium-a "probable" adverse drug reaction.
MacKintosh, D, 2017
)
"Olanzapine is an orexigenic antipsychotic drug associated with serious metabolic adverse effects in humans. "( Lack of Ovarian Secretions Reverts the Anabolic Action of Olanzapine in Female Rats.
Berge, RK; Fernø, J; González-García, I; López, M; Martins, L; Mellgren, G; Nogueiras, R; Skrede, S; Steen, VM; Tena-Sempere, M, 2017
)
"Olanzapine is a second-generation antipsychotic used in the management of schizophrenia and various off-label conditions. "( Obesity exacerbates the acute metabolic side effects of olanzapine.
Bush, ND; Peppler, WT; Townsend, LK; Wright, DC, 2018
)
"Olanzapine is a widely prescribed antipsychotic drug. "( Exercise Protects Against Olanzapine-Induced Hyperglycemia in Male C57BL/6J Mice.
Bush, N; Castellani, LN; Miotto, PM; Peppler, WT; Wright, DC, 2018
)
"Olanzapine is an atypical antipsychotic, undergoes extensive first pass metabolism, also has poor aqueous solubility and belongs to BCS (Biopharmaceutical Classification System) Class II drug) exhibit low oral bioavailability. "( Enhanced oral bioavailability of an antipsychotic drug through nanostructured lipid carriers.
Anbarasan, A; Arun, R; G, N; Hingarh, PK; Jawahar, N; S, S; Selvaraj, J, 2018
)
"Olanzapine is a marketed antipsychotic agent for treatment of both positive and negative symptoms of schizophrenia. "( Isolation, identification and characterization of two novel process-related impurities in olanzapine.
Cao, L; Chen, L; He, K; Li, J; Liu, B; Wang, Y; Zhang, G; Zhang, W; Zhuang, T, 2018
)
"Olanzapine (OLZ) is an antipsychotic drug used in the treatment of schizophrenia. "( AICAR Prevents Acute Olanzapine-Induced Disturbances in Glucose Homeostasis.
Bush, ND; Townsend, LK; Wright, DC, 2018
)
"Olanzapine is an antipsychotic drug used in psychiatric diseases. "( Successful intravenous lipid emulsion therapy: Olanzapine intoxication.
Akkoc, I; Demirel, A; Kalkan, A; Metin, DD; Sut, R; Yeniocak, S, 2018
)
"Olanzapine is an atypical antipsychotic drug commonly used for the treatment of schizophrenia. "( Development of a population pharmacokinetic model of olanzapine for Chinese health volunteers and patients with schizophrenia.
Dong, F; Ji, S; Li, A; Li, W; Lu, W; Ruan, C; Wang, C; Yan, H; Yue, W; Zhang, D, 2018
)
"Olanzapine is an atypical antipsychotic that has shown efficacy for the treatment of nausea, anxiety, and insomnia. "( Olanzapine with ondansetron and dexamethasone for the prevention of cisplatin-based chemotherapy-induced nausea and vomiting in lung cancer.
Lou, G; Wang, W; Zhang, Y, 2018
)
"Olanzapine is a commonly prescribed antipsychotic available as oral and long-acting injectable (LAI) formulations. "( Age Impacts Olanzapine Exposure Differently During Use of Oral Versus Long-Acting Injectable Formulations: An Observational Study Including 8,288 Patients.
Correll, CU; Hartberg, C; Haslemo, T; Høiseth, G; Molden, E; Refsum, H; Smith, RL; Tveito, M, 2018
)
"Olanzapine (Olz) is an atypical antipsychotic used to treat depression, anxiety and schizophrenia, which can be caused by chronic psychosocial stress. "( Brain Sub/Region-Specific Effects of Olanzapine on c-Fos Expression of Chronically Socially Isolated Rats.
Borgwardt, S; Filipović, D; Gass, P; Inta, D; Lang, UE; Perić, I; Stanisavljević, A, 2019
)
"Olanzapine is an atypical antipsychotic drug most commonly used to manage psychoses and symptoms of irritability and aggressive behavior."( Patient Survival After Acute Voluntary Poisoning With a Huge Dose of Oxcarbazepine and Olanzapine.
Eleftheriotis, G; Galopoulos, D; Kalogera, V; Loupa, C; Malios, I; Marathonitis, G; Meimeti, E, 2018
)
"Olanzapine is an atypical antipsychotic widely used in the treatment of schizophrenia and bipolar disorder."( The IRS/PI3K/Akt signaling pathway mediates olanzapine-induced hepatic insulin resistance in male rats.
Huang, X; Li, Y; Ren, L; Wang, C; Zhou, X, 2019
)
"Olanzapine (OLZ) is a second-generation antipsychotic drug used for treatment of schizophrenia, bipolar disorder, and other neuropsychiatric conditions. "( Lithium is able to minimize olanzapine oxidative-inflammatory induction on macrophage cells.
Aguiar-Ribeiro, EM; Assmann, CE; Azzolin, VF; Barbisan, F; da Cruz Jung, IE; da Cruz, IBM; do Prado-Lima, PAS; Duarte, MMMF; Fernandes, MS; Riffel, RT; Teixeira, CF, 2019
)
"Olanzapine is a second-generation anti-psychotic drug used to prevent neuroinflammation in patients with schizophrenia. "( Chronic olanzapine administration causes metabolic syndrome through inflammatory cytokines in rodent models of insulin resistance.
Chen, Y; Deng, YH; Fang, M; Huo, Y; Li, H; Li, S; Li, W; Liu, S; Lv, Y; Peng, S; Sun, T; Yang, N; Yu, L; Zhang, Z, 2019
)
"Olanzapine is an atypical antipsychotic that is widely used in the treatment of schizophrenia and has shown some degree of efficacy on negative and cognitive symptoms. "( Effects of olanzapine during cognitive and emotional processing in schizophrenia: A review of functional magnetic resonance imaging findings.
Brambilla, P; D'Agostino, A; Del Fabro, L; Delvecchio, G, 2019
)
"Olanzapine (OL) is an atypical antipsychotic drug which suffers from an extensive hepatic metabolism and poor bioavailability. "( Surface modified niosomes of olanzapine for brain targeting via nasal route; preparation, optimization, and
Aboud, HM; Khallaf, RA; Sayed, OM, 2020
)
"Olanzapine is a dopamine D2 receptor antagonist and pramipexole is a mixed dopamine D2 /D3 receptor agonist."( Could pramipexole induce acute mania? A case report.
Bet, PM; Franken, LG; Klumpers, UM, 2013
)
"Olanzapine is an efficacious antipsychotic that can be used in its oral and depot formula (olanzapine pamoate) for the treatment of patients with schizophrenia. "( Drug safety evaluation of olanzapine pamoate.
Kuhnigk, O; Naber, D; Schöttle, D, 2013
)
"Olanzapine is an atypical antipsychotic agent of the thiobenzodiazepine class. "( Olanzapine for the prevention and treatment of chronic nausea and chemotherapy-induced nausea and vomiting.
Navari, RM, 2014
)
"Olanzapine is a first line medication for the treatment of schizophrenia, but it is also one of the atypical antipsychotics carrying the highest risk of weight gain. "( Metformin and berberine prevent olanzapine-induced weight gain in rats.
Davies, GE; Davies, PS; Droke, EA; Ehli, EA; Hu, Y; Nowotny, D; Soundy, TJ; Young, AJ, 2014
)
"Olanzapine is an atypical antipsychotic drug, whose chronic use has been associated with the development of potential adverse effects such as weight gain and cardio-metabolic disorders like hypercholesterolemia and diabetes. "( Nanoencapsulation of olanzapine increases its efficacy in antipsychotic treatment and reduces adverse effects.
Burger, ME; Dimer, FA; Friedrich, RB; Guterres, SS; Ortiz, M; Pase, CS; Pohlmann, AR; Roversi, K, 2014
)
"Olanzapine is a second generation antipsychotic. "( Subchronic olanzapine treatment decreases the expression of pancreatic glucose transporter 2 in rat pancreatic β cells.
Liu, H; Shu, S; Su, D; Wang, G; Wang, M; Yao, L, 2014
)
"Olanzapine is a safe and efficient drug for the prevention of duloxetine-related nausea and vomiting."( Effects of low-dose olanzapine on duloxetine-related nausea and vomiting for the treatment of major depressive disorder.
Chen, M; Han, H; Huang, Z; Wang, J; Zhang, J; Zhang, Y; Zhong, Z, 2014
)
"Olanzapine is an atypical antipsychotic agent, structurally related to clozapine, and extensively used for the treatment of schizophrenia, bipolar disorder-associated mania, and the behavioral symptoms of Alzheimer's disease."( Benzo- and thienobenzo- diazepines: multi-target drugs for CNS disorders.
Botelho, SP; Da Silva, MS; Ishiki, H; Mendonça Júnior, FJ; Scotti, L; Scotti, MT, 2015
)
"Olanzapine is an atypical antipsychotic agent that blocks multiple neuronal receptors involved in the nausea and vomiting pathways. "( A review of olanzapine as an antiemetic in chemotherapy-induced nausea and vomiting and in palliative care patients.
Fatigoni, S; Fonte, C; Roila, F, 2015
)
"Olanzapine (OLZ) is an atypical antipsychotic used in the treatment of schizophrenia and related psychoses. "( In Vitro Characterization of the Human Liver Microsomal Kinetics and Reaction Phenotyping of Olanzapine Metabolism.
Korprasertthaworn, P; McLachlan, AJ; Miners, JO; Polasek, TM; Rowland, A; Sorich, MJ; Tucker, GT, 2015
)
"1. Olanzapine (OLZ) is a widely used atypical antipsychotic agent for the treatment of schizophrenia and other disorders. "( Involvement of oxidative stress and mitochondrial/lysosomal cross-talk in olanzapine cytotoxicity in freshly isolated rat hepatocytes.
Azarmi, Y; Eftekhari, A; Eghbal, MA; Parvizpur, A, 2016
)
"Olanzapine is an atypical antipsychotic drug that inhibits serotonergic, dopaminergic, alpha-1 adrenergic, histaminic, and muscarinic receptors. "( Efficacy and safety of olanzapine for the prophylaxis of chemotherapy-induced nausea and vomiting (CINV) as reported in phase I and II studies: a systematic review.
Chiu, L; Chiu, N; Chow, E; Chow, R; DeAngelis, C; Lam, H; Navari, R; Pasetka, M; Passik, S; Popovic, M, 2016
)
"Olanzapine (OLZ) is an atypical antipsychotic drug that also has mood-stabilizing effects. "( Effects of olanzapine on LPS-induced inflammation in rat primary glia cells.
Azab, AN; Faour-Nmarne, C, 2016
)
"Olanzapine is an atypical antipsychotic with similar pharmacologic properties to droperidol. "( A Large Retrospective Cohort of Patients Receiving Intravenous Olanzapine in the Emergency Department.
Cole, JB; Klein, LR; Martel, ML; Rivard, RL, 2016
)
"Olanzapine is a potent antipsychotic medication that inhibits a wide variety of receptors. "( Efficacy of olanzapine for the prophylaxis and rescue of chemotherapy-induced nausea and vomiting (CINV): a systematic review and meta-analysis.
Chiu, L; Chiu, N; Chow, E; Chow, R; DeAngelis, C; Lam, H; Milakovic, M; Navari, RM; Pasetka, M; Popovic, M; Shumway, NM; Vuong, S, 2016
)
"Olanzapine (OLZ) is a second-generation atypical antipsychotic (AAP) frequently used in acute and maintenance treatment of children and adolescents with psychotic disorders. "( Spontaneous Ejaculations in an Adolescent With Olanzapine Use: Case Report.
Tufan, AE; Yektaş, Ç,
)
"Olanzapine (OLZ) is a typical anti-psychotic drug, which is highly lipophilic in nature, belongs to Biopharmaceutical Classification System (BCS) class II category. "( Enhanced brain targeting efficacy of Olanzapine through solid lipid nanoparticles.
Baskaran, M; Humtsoe, LC; Justin, A; Natarajan, J; Vadivelan, R, 2017
)
"Olanzapine is a widely used atypical antipsychotic with significant weight gain and other metabolic side effects. "( Metabolic Response to Olanzapine in Healthy Chinese Subjects with rs7093146 Polymorphism in Transcription Factor 7-like 2 Gene (TCF7L2): A Prospective Study.
Guo, D; Huang, J; Li, Q; Shu, Y; Yang, H; Ye, Z, 2017
)
"Olanzapine is an excellent alternative for the prophylaxis of CINV. "( Efficacy of olanzapine for the prophylaxis of chemotherapy-induced nausea and vomiting: a meta-analysis.
Cui, Y; Liu, Q; Lu, M; Ma, L; Yang, T; Zhou, Y, 2017
)
"Olanzapine is a second-generation atypical antipsychotic that is increasingly used in preference to older antipsychotic agents. "( Prolonged toxicity after massive olanzapine overdose: two cases with confirmatory laboratory data.
Tse, GH; Waring, WS; Warner, MH, 2008
)
"Olanzapine is an efficacious drug often used as a first-line medication in the treatment for schizophrenia. "( Genetic correlates of olanzapine-induced weight gain in schizophrenia subjects from north India: role of metabolic pathway genes.
Deshpande, SN; Lerer, B; Nimgaonkar, VL; Srivastava, V; Thelma, B, 2008
)
"Olanzapine is a second generation antipsychotic (SGA) with a high level of therapeutic effectiveness in schizophrenia and other psychotic disorders. "( [Olanzapine--high potency antipsychotic drug inducing significant weight gain: a case report].
Britivić, D; Jasović-Gasić, M; Josifović-Kostić, D; Marić, N; Vuković, O,
)
"Olanzapine is a second-generation antipsychotic approved for the treatment of schizophrenia, bipolar mania and associated agitation."( Olanzapine: review of safety 2008.
Citrome, L; Kantrowitz, JT, 2008
)
"Olanzapine is an atypical antipsychotic drug used in the treatment of schizophrenia. "( Potential effect of olanzapine on total antioxidant status and lipid peroxidation in schizophrenic patients.
Ahmed, FA; Al-Chalabi, BM; Thanoon, IA, 2009
)
"Olanzapine is a new antipsychotic therapy registered in Europe for the treatment of schizophrenia since 1996."( [Pattern and evolution of the prescription of olanzapine during one year: Results of the cohort study ECOL].
Chartier, F; Deal, C; Flandre, P; Fourrier-Réglat, A; Gasquet, I; Heurtebize, N; Perrin, E, 2009
)
"Olanzapine is a novel antipsychotic drug known to induce clinically significant weight gain. "( Acute effects of olanzapine on behavioural expression including the behavioural satiety sequence in female rats.
Cooper, GD; Goudie, AJ; Halford, JC, 2010
)
"Olanzapine is a psychotropic agent that belongs to the thienobenzodiazepine class."( A single-dose, randomized, two-way crossover study comparing two olanzapine tablet products in healthy adult male volunteers under fasting conditions.
Elshafeey, AH; Elsherbiny, MA; Fathallah, MM, 2009
)
"Olanzapine is a second-generation antipsychotic that may cause weight gain and metabolic syndrome in some cases. "( The association of olanzapine-induced weight gain with peroxisome proliferator-activated receptor-gamma2 Pro12Ala polymorphism in patients with schizophrenia.
Akin, F; Aydin, N; Barlas, O; Erdal, M; Herken, H; Karadag, F; Sengul, C, 2009
)
"Olanzapine is a safe and efficient drug for prevention of CINV."( Clinical research of Olanzapine for prevention of chemotherapy-induced nausea and vomiting.
Chen, J; Liu, J; Liu, X; Tan, L; Yan, Z; Yang, H; Zhang, D, 2009
)
"Olanzapine is an atypical antipsychotic approved for the treatment of adults and adolescents (aged 13 -17 years) with schizophrenia or bipolar I disorder (manic or mixed episodes)."( Oral olanzapine disposition in adolescents with schizophrenia or bipolar I disorder: a population pharmacokinetic model.
Bergstrom, RF; Hong, Q; Lobo, ED; Quinlan, T; Robertson-Plouch, C, 2010
)
"Olanzapine is an atypical antipsychotic that, in addition to its use in adults, is now indicated for the treatment of schizophrenia, and manic or mixed episodes associated with bipolar I disorder in adolescents aged 13-17 years. "( Olanzapine: in adolescents with schizophrenia or bipolar I disorder.
McCormack, PL, 2010
)
"Olanzapine seems to be a safe and effective treatment for primary DSM-IV trichotillomania."( A randomized, double-blind, placebo-controlled trial of olanzapine in the treatment of trichotillomania.
Bennett, M; Mancini, C; Oakman, J; Patterson, B; Van Ameringen, M, 2010
)
"Olanzapine is an antipsychotic drug that frequently induces weight gain accompanied by increased fat deposition as a side effect. "( Olanzapine affects locomotor activity and meal size in male rats.
Adan, RA; Evers, SS; la Fleur, SE; Luijendijk, MC; van der Zwaal, EM, 2010
)
"Olanzapine is a drug approved for treatment of schizophrenia and mania."( Olanzapine for nausea and vomiting.
Licup, N, 2010
)
"Olanzapine (OLZ) is an atypical antipsychotic drug and is commonly used for the treatment of schizophrenia and bipolar disorder (BD). "( The genotoxic and oxidative damage potential of olanzapine in vitro.
Toğar, B; Türkez, H, 2010
)
"Olanzapine is an atypical antipsychotic with shown efficacy in psychosis treatment."( Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics.
Alberich, S; Barbeito, S; González-Pinto, A; Gutiérrez, A; Haidar, K; Matute, C; Mosquera, F; Ortiz, A; Palomino, A; Vega, P, 2010
)
"Olanzapine is an a-typical antipsychotic drug antagonizing predominantly 5-HT and dopamine, but also histamine, muscarin, and α-adrenergic receptors. "( Olanzapine causes hypothermia, inactivity, a deranged feeding pattern and weight gain in female Wistar rats.
Calcagnoli, F; Evers, SS; Scheurink, AJ; van Dijk, G, 2010
)
"Olanzapine (OLZ) is an atypical antipsychotic whose clinical efficacy is hampered by side effects including weight gain and diabetes. "( Central nervous system delivery of the antipsychotic olanzapine induces hepatic insulin resistance.
Haas, M; Martins, PJ; Obici, S, 2010
)
"Olanzapine is an atypical antipsychotic, and is contraindicated to use with epinephrine, because the a receptor antagonistic action of olanzapine decreases the blood pressure in combination with epinephrine."( [Epidural labor analgesia for a primipara with schizophrenia].
Nakagawa, C; Okada, H; Sato, S; Taniguchi, M; Uchizaki, S, 2010
)
"Olanzapine is a widely used atypical antipsychotic, with well known metabolic side effects such as weight gain, insulin resistance and blood glucose abnormalities. "( Beneficial effect of the insulin sensitizer (HSP inducer) BGP-15 on olanzapine-induced metabolic disorders.
Buday, B; Fleming, A; Korányi, L; Kulcsár, E; Literáti-Nagy, B; Literáti-Nagy, Z; Mandl, J; Péterfai, E; Roth, J; Sümegi, B; Tory, K, 2010
)
"Olanzapine was found to be a dominant cost-effective choice, as it was associated with greater effectiveness at lower total costs relative to aripiprazole."( Cost-effectiveness of olanzapine vs. aripiprazole in the treatment of schizophrenia.
Ascher-Svanum, H; Faries, DE; Kane, JM; Osuntokun, OO; Peng, X; Stauffer, VL; Stensland, MD, 2011
)
"Olanzapine pamoate is an efficacious formulation, particularly for patients with a history of good response to oral olanzapine and doubtful adherence. "( Olanzapine pamoate for the treatment of schizophrenia.
Naber, D, 2011
)
"Olanzapine is an atypical antipsychotic that is useful in schizophrenia and bipolar affective disorder, but its use is associated with troublesome weight gain and metabolic syndrome. "( Metformin for olanzapine-induced weight gain: a systematic review and meta-analysis.
Goyal, N; Jana, AK; Praharaj, SK; Sinha, VK, 2011
)
"Olanzapine is an atypical antipsychotic known to cause considerable weight gain. "( Cannabinoid type 1 receptor gene polymorphisms are not associated with olanzapine-induced weight gain.
Choi, JE; Geum, D; Kang, SG; Kim, L; Koo, SH; Lee, HJ; Park, YM,
)
"Olanzapine is an antipsychotic used in the treatment of schizophrenia, bipolar disorder, and treatment-resistant depression. "( Olanzapine metabolism and the significance of UGT1A448V and UGT2B1067Y variants.
Erickson-Ridout, KK; Lazarus, P; Zhu, J, 2011
)
"Olanzapine is a second-generation atypical antipsychotic agent approved for the treatment of psychotic disorders and mania. "( Olanzapine intoxication-related transient diabetes insipidus.
Alçelik, A; Canan, F; Koçer, E, 2011
)
"Olanzapine is an atypical antipsychotic drug that has been increasingly used in acute treatment of, and therapeutic support for, schizophrenia, bipolar disorder and other psychoses. "( Endocrine and testicular changes induced by olanzapine in adult Wistar rats.
Amorim, MJ; Brito, LT; da Silva Junior, VA; de Amorim Júnior, AA; de Siqueira Bringel, S; de Torres, SM; Morais, RN; Tenorio, BM, 2013
)
"Olanzapine appears to be a superior treatment for hostility in early phases of therapy for first-episode schizophrenia, schizoaffective disorder, and schizophreniform disorder."( Efficacy of antipsychotic drugs against hostility in the European First-Episode Schizophrenia Trial (EUFEST).
Bitter, I; Czobor, P; Derks, EM; Fleischhacker, WW; Kahn, RS; Libiger, J; Volavka, J, 2011
)
"Olanzapine (OZ) is a second-generation or atypical antipsychotic which selectively binds to central dopamine D₂ and serotonin (5-HT(2c)) receptors. "( Development and evaluation of olanzapine-loaded PLGA nanoparticles for nose-to-brain delivery: in vitro and in vivo studies.
Kumar, A; Sawant, KK; Seju, U, 2011
)
"Olanzapine is an atypical antipsychotic with multireceptor affinity and different pharmacological effects, which can result with abnormalities in laboratory investigations."( [Laboratory investigations in acute olanzapine poisonings].
Ciszowski, K; Jawień, W; Sein Anand, J; Wilimowska, J, 2011
)
"Olanzapine is an atypical antipsychotic used for many years in the treatment of schizophrenia and bipolar disorder. "( [Electrocardiographic abnormalities in acute olanzapine poisonings].
Ciszowski, K; Sein Anand, J, 2011
)
"Olanzapine is a second generation antipsychotic of thienobenzodiazepin group, which is used in the treatment of schizophrenia, bipolar disorder, and others, mainly psychiatric. "( [The clinical picture of acute olanzapine poisonings].
Ciszowski, K; Jawień, W; Sein Anand, J; Wilimowska, J, 2011
)
"Olanzapine is an atypical antipsychotic that blocks dopaminergic, serotonergic, adrenergic, histaminergic, and muscarinic receptors."( Olanzapine suppresses the rewarding and discriminative stimulus effects induced by morphine.
Mori, T; Narita, M; Shibasaki, M; Suzuki, T; Torigoe, K; Yoshizawa, K, 2012
)
"Olanzapine is a second-generation antipsychotic, which is also used as a mood stabilizer. "( Olanzapine-induced anaphylactic shock: a case report.
Hansen, A; Prapotnik, M; Roth, C, 2012
)
"Olanzapine is an atypical antipsychotic drug that infrequently has been reported to cause seizures and myoclonus despite a small proconvulsant risk. "( Olanzapine-associated myoclonus.
Haut, SR; Milstein, MJ; Rosen, JB, 2012
)
"Olanzapine is an atypical antipsychotic agent of the thienobenzodiazepine class. "( Olanzapine: palliative medicine update.
Prommer, E, 2013
)
"Olanzapine is a widely used agent for the treatment of schizophrenia.The aim of this study was to evaluate bioequivalence of two 10-mg tablet formulations of olanzapine following single oral dose in adult male volunteers.This was a randomized, single-dose, open-label, crossover bioequivalence study. "( Pharmacokinetics and bioequivalence of 2 tablet formulations of olanzapine in healthy Chinese volunteers: a randomized, open-label, single-dose study.
Chen, Q; Jia, JY; Li, SJ; Liu, GY; Liu, Y; Liu, YM; Lu, C; Qi, YL; Yu, C; Zhang, MQ, 2012
)
"Olanzapine is an atypical antipsychotic drug used for the treatment of schizophrenia."( Effects of fluoxetine, tianeptine and olanzapine on unpredictable chronic mild stress-induced depression-like behavior in mice.
Akar, F; Celikyurt, IK; Erden, F; Gumuslu, E; Kır, HM; Kokturk, S; Mutlu, O; Ulak, G, 2012
)
"Olanzapine is a thienobenzodiazepine that blocks especially the serontonin (5-hydroxytryptamine [5-HT]) 5-HT2A and the dopamine D2 receptors as well as muscarinic (M1), histamine (H1), 5-HT2C, 5-HT3 to 5-HT6, adrenergic (α(l)), and D4 receptors. "( Olanzapine abuse.
Erol, A; Kumsar, NA, 2013
)
"Olanzapine is an atypical antipsychotic for the treatment of schizophrenia, in which memory impairment is a core deficit. "( A randomized controlled trial of olanzapine improving memory deficits in Han Chinese patients with first-episode schizophrenia.
Geng, YG; Li, H; Li, Y; Mu, JL; Su, LY; Wang, CH; Wang, JK; Yang, J, 2013
)
"Olanzapine is a substrate of the cytochrome P450 enzyme (CYP) 1A2. "( Fluvoxamine augmentation of olanzapine in chronic schizophrenia: pharmacokinetic interactions and clinical effects.
Hadjez, J; Härtter, S; Hiemke, C; Jabarin, M; Modai, I; Peled, A; Ritsner, M; Silver, H; Weigmann, H, 2002
)
"Olanzapine is an atypical neuroleptic drug with mood-stabilising properties and few of the side effects commonly associated with conventional neuroleptic treatment. "( A clinical case series of six extremely aggressive youths treated with olanzapine.
Gillberg, C; Rastam, M; Soderstrom, H, 2002
)
"Olanzapine is a widely used, newer antipsychotic agent, which is metabolized by various pathways: hydroxylation and N-demethylation by cytochrome P450, N-oxidation by flavin monooxygenase and direct glucuronidation. "( Glucuronidation of olanzapine by cDNA-expressed human UDP-glucuronosyltransferases and human liver microsomes.
Linnet, K, 2002
)
"Olanzapine was shown to be a suitable treatment for refractory schizophrenia in this series of seriously ill patients. "( Olanzapine for the treatment of chronic refractory schizophrenia: a 12-month follow-up naturalistic study.
Abel, A; Alvarez, V; Blanco, C; Ciudad, A; Cudeiro, F; Ferreiro, MJ; Gómez, Y; López, A; Peña, C; Prieto, R; Rego, C; Rodríguez-Pérez, V, 2002
)
"Olanzapine is an atypical antipsychotic that is reported to be effective without producing the disabling extrapyramidal side effects associated with the older, typical antipsychotic drugs."( Olanzapine for schizophrenia.
Dardennes, RM; Duggan, L; El-Dosoky, A; Fenton, M; Indran, S, 2003
)
"Olanzapine is a novel antipsychotic drug. "( [Analysis of olanzapine in human plasma with reversed-phase high performance liquid chromatography].
Fan, JX; Han, G; Xiao, H; Xie, SP; Yao, H, 2001
)
"Olanzapine is an atypical antipsychotic that has efficacy in adults with psychotic disorders. "( A prospective, open-label trial of olanzapine in adolescents with schizophrenia.
Branicky, LA; Demeter, CA; Findling, RL; McNamara, NK; Schulz, SC; Youngstrom, EA, 2003
)
"Olanzapine is an atypical antipsychotic, which in a number of double-blind, placebo-controlled studies has been found to be more effective than haloperidol for the treatment of positive and negative symptoms of schizophrenia."( High-dose olanzapine for treatment-refractory schizophrenia.
Lerner, V,
)
"Olanzapine is an effective treatment for mania and may be more efficacious than divalproex, though leads to more weight gain. "( Olanzapine alone or in combination for acute mania.
Geddes, JR; Gijsman, HJ; Goodwin, GM; Keck, P; Rendell, JM, 2003
)
"Olanzapine is an atypical antipsychotic effective in the treatment of schizophrenia. "( Investigation of target plasma concentration-effect relationships for olanzapine in schizophrenia.
Ahmad, F; Bulsara, MK; Castle, DJ; Dusci, LJ; Fellows, L; Ilett, KF, 2003
)
"Olanzapine is a safe alternative to haloperidol in delirious critical care patients, and may be of particular interest in patients in whom haloperidol is contraindicated."( Olanzapine vs haloperidol: treating delirium in a critical care setting.
Bergeron, N; Dumont, M; Gottfried, SB; Skrobik, YK, 2004
)
"Olanzapine is an atypical antipsychotic drug that is increasingly used in intentional drug overdoses. "( The clinical picture of olanzapine poisoning with special reference to fluctuating mental status.
Kupferschmidt, H; Meier, PJ; Palenzona, S; Rauber-Luethy, C, 2004
)
"Olanzapine is an atypical antipsychotic with proven therapeutic effect, though it is rarely used in agitated patients. "( Olanzapine in the treatment of agitation in hospitalized patients with schizophrenia and schizoaffective and schizofreniform disorders.
Bidzan, L; Staszewska-Małys, E; Turczyński, J, 2004
)
"Olanzapine is an antipsychotic which, used alone or in combination with benzodiazepines, is effective and well tolerated in treatment of agitation in schizophrenic patients. "( Olanzapine in the treatment of agitation in hospitalized patients with schizophrenia and schizoaffective and schizofreniform disorders.
Bidzan, L; Staszewska-Małys, E; Turczyński, J, 2004
)
"Olanzapine is an antipsychotic medication linked to the development, or exacerbation of, type 2 diabetes mellitus. "( Fatal olanzapine-induced hyperglycemic ketoacidosis.
Avella, J; Hahn, T; Katz, M; Wetli, CV; Wilson, JC, 2004
)
"Olanzapine is an effective drug for the long-term treatment of bipolar disorder but is associated with burdensome weight gain. "( Effects on weight and outcome of long-term olanzapine-topiramate combination treatment in bipolar disorder.
Benabarre, A; Brugue, E; Colom, F; Comes, M; Corbella, B; Goikolea, JM; Martínez-Arán, A; Reinares, M; Sánchez-Moreno, J; Torrent, C; Vieta, E, 2004
)
"Olanzapine is a promising medication for the treatment of stuttering and further research is warranted."( Olanzapine in the treatment of developmental stuttering: a double-blind, placebo-controlled trial.
Brojeni, PH; Franklin, DL; Maguire, GA; Maguire, ME; Nguyen, CT; Riley, GD,
)
"Olanzapine is an atypical antipsychotic drug that has been shown to be neuroprotective in previous in vitro studies."( Post-stress changes in BDNF and Bcl-2 immunoreactivities in hippocampal neurons: effect of chronic administration of olanzapine.
Li, XM; Luo, C; Xu, H, 2004
)
"Olanzapine is an atypical antipsychotic that is approved in the US and Europe for the oral treatment of acute manic episodes in patients with bipolar I disorder, and for maintenance therapy to prevent recurrence in responders. "( Olanzapine: a review of its use in the management of bipolar I disorder.
McCormack, PL; Wiseman, LR, 2004
)
"Olanzapine is an atypical antipsychotic with a low incidence of extrapyramidal-motoric side effects. "( Reversible neutropenia during treatment with olanzapine: three case reports.
Agelink, M; Cordes, J; Klimke, A; Loeffler, S; Streit, M; von Wilmsdorff, M, 2004
)
"Olanzapine is a novel antipsychotic drug with an atypical profile."( Low delta sleep predicted a good clinical response to olanzapine administration in schizophrenic patients.
Brunner, E; Galicia-Polo, L; Herrera-Estrella, M; Rosas, M; Salín-Pascual, RJ,
)
"Olanzapine is an efficacious and widely prescribed atypical antipsychotic agent."( Low-dose fluvoxamine as an adjunct to reduce olanzapine therapeutic dose requirements: a prospective dose-adjusted drug interaction strategy.
Albers, LJ; Aravagiri, M; Endrenyi, L; Marder, SR; Ozdemir, V; Raggi, MA; Reist, C, 2005
)
"Olanzapine is an atypical antipsychotic reported to be effective without producing disabling extrapyramidal adverse effects associated with older, typical antipsychotic drugs."( Olanzapine for schizophrenia.
Dardennes, R; Duggan, L; El-Dosoky, A; Fenton, M; Indran, S; Rathbone, J, 2005
)
"Olanzapine is a safe and effective treatment for patients with acute schizophrenia in the hospital setting, even for patients with prominent positive or agitation symptoms."( Safety, effectiveness, and patterns of use of olanzapine in acute schizophrenia: a multivariate analysis of a large naturalistic study in the hospital setting.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Ciudad, A; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M, 2005
)
"Olanzapine is a widely used atypical antipsychotic drug. "( Olanzapine interactions with nicotine and mecamylamine in rats: effects on memory function.
Beatty, A; Levin, ED; Petro, A,
)
"Olanzapine is an atypical antipsychotic that is approved in the US and Europe for the oral treatment of acute manic episodes in patients with bipolar I disorder and for maintenance therapy to prevent recurrence in responders. "( Spotlight on olanzapine in bipolar I disorder.
McCormack, PL; Wiseman, LR, 2005
)
"Olanzapine is a new atypical antipsychotic drug acting on different receptors. "( [Clinical course of acute poisoning with olanzapine].
Balicka-Slusarczyk, B; Groszek, B; Szczeklik, J; Szpak, D, 2005
)
"Olanzapine (OLZ) is a second-generation antipsychotic agent available in 2 solid oral dosage forms, a standard oral tablet (SOT) and an orally disintegrating tablet (ODT). "( Pharmacokinetics of olanzapine after single-dose oral administration of standard tablet versus normal and sublingual administration of an orally disintegrating tablet in normal volunteers.
DeVane, CL; Donovan, JL; Gefroh, HA; Malcolm, RJ; Markowitz, JS; Wang, JS; Zhu, HJ, 2006
)
"Olanzapine is an atypical antipsychotic agent that can be used as a first-line agent in delusional parasitosis as a safer therapeutic option without a specialized monitoring regimen."( Successful treatment of delusions of parasitosis with olanzapine.
Badreshia, S; Mackley, CL; Meehan, WJ, 2006
)
"Olanzapine is a novel antipsychotic, approved for the acute and maintenance treatment of schizophrenia and bipolar I disorder. "( Olanzapine: a 5-year perspective.
Littrell, KH; Petty, RG; Wolf, NM, 2006
)
"Olanzapine is an atypical antipsychotic drug approved for acute and long-term treatment of bipolar disorder. "( Black hairy tongue associated with olanzapine treatment: a case report.
Annagur, BB; Tamam, L, 2006
)
"Olanzapine is a safely and comprehensively applicable atypical antipsychotic drug, for the treatment of schizophrenia, and of the mild to sever maniac episode. "( [Akathisia in the course of olanzapine treatment].
Csonka, A; Makkos, Z, 2006
)
"Olanzapine is a neuroleptic drug widely prescribed to treat schizophrenia and bipolar disorder. "( Human reward system activation is modulated by a single dose of olanzapine in healthy subjects in an event-related, double-blind, placebo-controlled fMRI study.
Abler, B; Erk, S; Walter, H, 2007
)
"Olanzapine is an atypical antipsychotic that is reported to cause myopathy and raised creatine kinase (CK) levels. "( Olanzapine overdose is associated with acute muscle toxicity.
Bateman, DN; Waring, WS; Wrate, J, 2006
)
"Olanzapine is a second-generation atypical antipsychotic agent approved for the treatment of psychotic disorders and mania. "( A severe case of olanzapine overdose with analytical data.
Ballesteros, MA; Ballesteros, S; de la Torre, CS; Martínez, MA; Rodríguez-Borregán, JC, 2007
)
"Olanzapine is a widely used second generation antipsychotic drug. "( Serum levels of olanzapine in a non-fatal overdose.
Asplund, C; Hägg, S; Lakso, HA; Lennestål, R; Mjörndal, T; Nilsson, M, 2007
)
"Olanzapine is a second-generation atypical antipsychotic drug (AAPD). "( Olanzapine induces SREBP-1-related adipogenesis in 3T3-L1 cells.
Chen, TM; Chen, YH; Yang, LH; Yu, ST, 2007
)
"Olanzapine has proved to be a reliable antipsychotic drug with a greater liability to cause metabolic abnormalities."( Cognition, functioning and quality of life in schizophrenia treatment: results of a one-year randomized controlled trial of olanzapine and quetiapine.
Awad, AG; Fernando, ML; Forrest, C; Parker, G; Senthilal, S; Usmani, Y; Voruganti, LP, 2007
)
"Olanzapine (OLZ) is a widely used antipsychotic substance. "( Large intraindividual variability of olanzapine serum concentrations in adolescent patients.
Bachmann, CJ; Haberhausen, M; Heinzel-Gutenbrunner, M; Remschmidt, H; Theisen, FM, 2008
)
"Olanzapine, which is an 'atypical' antipsychotic, is becoming more widespread in the treatment of AN."( Evaluation of the efficacy and safety of olanzapine as an adjunctive treatment for anorexia nervosa in adolescent females: a randomized, double-blind, placebo-controlled trial.
Buchholz, A; Feder, S; Gaboury, I; Henderson, K; Kourad, K; Ledoux, S; Moher, D; Norris, M; Spettigue, W, 2008
)
"Olanzapine is a second-generation antipsychotic with mood-stabilizing properties and antagonistic activity at several dopamine receptors."( Olanzapine in the treatment of pathological gambling: a negative randomized placebo-controlled trial.
Kaehler, L; Keck, PE; McElroy, SL; Nelson, EB; Welge, JA, 2008
)
"Olanzapine is a potential new "atypical" antipsychotic agent. "( Olanzapine versus placebo and haloperidol: acute phase results of the North American double-blind olanzapine trial.
Beasley, CM; Hamilton, S; Sanger, T; Satterlee, W; Tollefson, G; Tran, P, 1996
)
"Olanzapine (LY170053) is a novel putative atypical antipsychotic that shares many pharmacological and behavioral properties with clozapine."( Antagonism of phencyclidine-induced deficits in prepulse inhibition by the putative atypical antipsychotic olanzapine.
Bakshi, VP; Geyer, MA, 1995
)
"Olanzapine is a potential new "atypical" antipsychotic agent. "( Olanzapine versus placebo: results of a double-blind, fixed-dose olanzapine trial.
Beasley, CM; Hamilton, S; Sanger, T; Satterlee, W; Tollefson, G; Tran, P, 1996
)
"Olanzapine is a new antipsychotic drug with affinity for 5-HT2, D2, D1, and muscarinic receptors. "( A PET study of 5-HT2 and D2 dopamine receptor occupancy induced by olanzapine in healthy subjects.
Farde, L; Halldin, C; Nyberg, S, 1997
)
"Olanzapine is a thienobenzodiazepine derivative which displays efficacy in patients with schizophrenia and related psychoses. "( Olanzapine. A review of its pharmacological properties and therapeutic efficacy in the management of schizophrenia and related psychoses.
Fulton, B; Goa, KL, 1997
)
"Olanzapine (OLZ) is a novel antipsychotic agent with a high affinity for serotonin (5-HT2), dopamine (D1/D2/D4), muscarinic (m1-m5), adrenergic (alpha 1), and histamine (H1) receptors. "( Disposition and metabolism of olanzapine in mice, dogs, and rhesus monkeys.
Bernstein, J; Chiu, A; Franklin, R; Gillespie, T; Hotten, T; Kassahun, K; Mattiuz, E; Murphy, A, 1997
)
"Olanzapine is a new "atypical" antipsychotic agent that belongs chemically to the thienobenzodiazepine class. "( Efficacy of olanzapine: an overview of pivotal clinical trials.
Beasley, CM; Tollefson, GD; Tran, PV, 1997
)
"Olanzapine is a new antipsychotic agent with serotonin/dopamine antagonism action. "( Dosing the antipsychotic medication olanzapine.
Nemeroff, CB, 1997
)
"Olanzapine is a novel antipsychotic agent exhibiting regional mesolimbic dopaminergic selectivity and a broad-based pharmacology encompassing serotonin, dopamine, muscarinic, and adrenergic receptor binding affinities."( Blind, controlled, long-term study of the comparative incidence of treatment-emergent tardive dyskinesia with olanzapine or haloperidol.
Beasley, CM; Potvin, JH; Tamura, RN; Tollefson, GD; Tran, PV, 1997
)
"Olanzapine is a thienobenzodiazepine analog with an in vitro receptor affinity profile similar to that of clozapine. "( Olanzapine: a new antipsychotic agent with efficacy in the management of schizophrenia.
Green, AI; Kando, JC; Patel, JK; Reams, SG; Satterlee, W; Shepski, JC, 1997
)
"Olanzapine is an atypical antipsychotic effective in the treatment of schizophrenic patients. "( Olanzapine plasma concentrations and clinical response in acutely ill schizophrenic patients.
Beasley, C; Perry, PJ; Sanger, T, 1997
)
"Olanzapine is a new antipsychotic drug that has shown efficacy against positive and negative symptoms of schizophrenia, with minimal extrapyramidal side effects."( Olanzapine in treatment-refractory schizophrenia: results of an open-label study. The Spanish Group for the Study of Olanzapine in Treatment-Refractory Schizophrenia.
Alvarez, E; Cuesta, M; García-Bernardo, E; Gómez, JC; Gurpegui, M; Martín, J, 1997
)
"Olanzapine is an "atypical" antipsychotic agent with a high affinity for serotonin 5HT2A/C, 5HT3, 5HT6, and dopamine D1, D2, D3, D4 receptors. "( Olanzapine: interaction study with imipramine.
Callaghan, JT; Cerimele, BJ; Hoyes-Beehler, PJ; Kassahun, KJ; Kondraske, GV; Nyhart, EH, 1997
)
"Olanzapine is a serotonin-dopamine-receptor antagonist indicated for use in the treatment of schizophrenia and other psychotic disorders."( Olanzapine: a serotonin-dopamine-receptor antagonist for antipsychotic therapy.
Bever, KA; Perry, PJ, 1998
)
"Olanzapine is a newly introduced atypical neuroleptic, with a broad receptor profile similar to that of clozapine. "( Olanzapine.
Hale, AS,
)
"Olanzapine is a new atypical antipsychotic recently introduced for the treatment of schizophrenia. "( 5-HT2 and D2 receptor occupancy of olanzapine in schizophrenia: a PET investigation.
DaSilva, J; Houle, S; Jones, C; Kapur, S; Remington, G; Wilson, AA; Zipursky, RB, 1998
)
"Olanzapine is a potent 5-HT2 blocker and shows a higher 5-HT2 than D2 occupancy at all doses. "( 5-HT2 and D2 receptor occupancy of olanzapine in schizophrenia: a PET investigation.
DaSilva, J; Houle, S; Jones, C; Kapur, S; Remington, G; Wilson, AA; Zipursky, RB, 1998
)
"Olanzapine is a recently introduced atypical neuroleptic agent for which little information is available on its use in children. "( Open-label olanzapine treatment in five preadolescent children.
King, BH; Krishnamoorthy, J, 1998
)
"Olanzapine is a newly developed atypical neuroleptic with a marked affinity to the 5-HT2, D2 and D4 dopamine receptors. "( Severe akathisia during olanzapine treatment of acute schizophrenia.
Bachmann, S; Gerdsen, I; Jauss, M; Mundt, C; Pantel, J; Schröder, J, 1998
)
"Olanzapine is a novel atypical antipsychotic drug with few reported extrapyramidal side effects which may be more suitable for controlling hallucinosis in these patients."( Olanzapine in the treatment of hallucinosis in idiopathic Parkinson's disease: a cautionary note.
Ford, KS; Graham, JM; Sagar, HJ; Sussman, JD, 1998
)
"Olanzapine is a relatively new antipsychotic agent which appears to be effective in the treatment of both the positive and negative symptoms of schizophrenia. "( Olanzapine-induced mania.
Brannon, GE; McBride, WA; Reeves, RR, 1998
)
"Olanzapine is a novel antipsychotic, which is effective against both the positive and negative symptoms of schizophrenia and causes fewer extrapyramidal adverse effects than conventional antipsychotics. "( A pharmacokinetic interaction between carbamazepine and olanzapine: observations on possible mechanism.
Bergstrom, RF; Gilfillan, DJ; Lucas, RA, 1998
)
"Olanzapine is a novel antipsychotic agent displaying a unique and pleotrophic pharmacology, which distinguishes it from other existing treatments. "( Review of recent clinical studies with olanzapine.
Kuntz, AJ; Tollefson, GD, 1999
)
"As olanzapine is a drug with a very similar biochemical profile to clozapine, it is important to evaluate whether non-response to olanzapine predicts clozapine non-response."( Treatment-resistant schizophrenic patients respond to clozapine after olanzapine non-response.
Conley, RR; Kelly, DL; Richardson, CM; Tamminga, CA, 1999
)
"Olanzapine is a novel atypical antipsychotic agent with affinity at dopaminergic, serotonergic, muscarinic, adrenergic and histaminergic binding sites."( Olanzapine acute administration in schizophrenic patients increases delta sleep and sleep efficiency.
Galicia-Polo, L; Herrera-Estrella, M; Laurrabaquio, MR; Salin-Pascual, RJ, 1999
)
"Olanzapine is a new atypical antipsychotic agent that belongs to the same chemical class as clozapine. "( In vivo effects of olanzapine on striatal dopamine D(2)/D(3) receptor binding in schizophrenic patients: an iodine-123 iodobenzamide single-photon emission tomography study.
Dresel, S; Hahn, K; Mager, T; Meisenzahl, E; Möller, HJ; Rossmüller, B; Tatsch, K, 1999
)
"Olanzapine is a new antipsychotic drug, pharmacodynamically similar to clozapine, but putatively devoid of haematological iatrogenicity. "( Olanzapine-induced neutropenia after clozapine-induced neutropenia.
Benedetti, F; Cavallaro, R; Smeraldi, E, 1999
)
"Olanzapine is a tricyclic neuroleptic agent that due to structural similarities was expected to be a safe alternative to clozapine, which has a 0.5-2% risk of agranulocytosis. "( Two cases of olanzapine-induced reversible neutropenia.
Grohmann, R; Pedrosa, F; Rüther, E; Schwerdtner, I; Steinwachs, A, 1999
)
"Olanzapine is an effective antipsychotic medication in older adults with schizophrenia, and is associated with significant improvement in extrapyramidal side effects."( Olanzapine therapy in elderly patients with schizophrenia.
Brescan, D; Perez, D; Ramirez, LF; Sajatovic, M, 1998
)
"Olanzapine is an atypical antipsychotic agent which is at least as effective as the conventional agent haloperidol and the atypical agent risperidone. "( Olanzapine. A pharmacoeconomic review of its use in schizophrenia.
Foster, RH; Goa, KL, 1999
)
"Olanzapine is a cost-effective alternative to conventional agents for the treatment of moderately to severely ill patients with longstanding schizophrenia."( Olanzapine. A pharmacoeconomic review of its use in schizophrenia.
Foster, RH; Goa, KL, 1999
)
"Olanzapine proved to be an adequate treatment choice for NIA patients."( Measuring neuroleptic-induced akathisia by three-channel actometry.
Holi, M; Lauerma, H; Markkula, J; Rimon, R; Tuisku, K, 1999
)
"Olanzapine is an atypical antipsychotic medication that was approved for use in the United States in 1996. "( Olanzapine overdose in an 18-month-old child.
Butera, AS; Catalano, G; Catalano, MC; Cooper, DS, 1999
)
"Olanzapine is an atypical antipsychotic that is reported to be effective without producing the disabling extrapyramidal side effects associated with the older, typical antipsychotic drugs."( Olanzapine for schizophrenia.
Dardennes, RM; Duggan, L; El-Dosoky, A; Fenton, M; Indran, S, 2000
)
"Olanzapine is a novel antipsychotic effective in reducing positive and negative symptoms of schizophrenia and with a safe side-effect profile. "( Efficacy and tolerability of olanzapine in elderly patients with psychotic disorders: a prospective study.
Brenner, R; Concepcion, NM; Florita, CD; Kaur, A; Madhusoodanan, S; Menon, G; Nunez, G; Reddy, H; Suresh, P, 2000
)
"Olanzapine is an atypical antipsychotic drug which shows a high antagonistic affinity to the D1, D2 and D4 and the 5-HT2A and 5-HT2c receptors. "( Effective open-label treatment of tourette's disorder with olanzapine.
Aschauer, HN; De Zwaan, M; Kasper, S; Resinger, E; Schindler, SD; Stamenkovic, M; Willinger, U, 2000
)
"Olanzapine is an atypical antipsychotic with potent antimuscarinic properties in vitro (K(i) = 2-25 nM). "( In vivo olanzapine occupancy of muscarinic acetylcholine receptors in patients with schizophrenia.
Egan, MF; Jones, DW; Knable, MB; Lafargue, T; Pickar, D; Raedler, TJ; Urbina, RA; Weinberger, DR, 2000
)
"Olanzapine is an antipsychotic drug that has been on the market since 1996. "( Overdose and death with olanzapine: two case reports.
Cawthon, B; Gerber, JE, 2000
)
"Olanzapine is a relatively new atypical anti-psychotic agent first introduced in November of 1996 under the trade name of zyprexa."( Neuroleptic malignant syndrome associated with olanzapine therapy: a case report.
Privette, T; Stanfield, SC, 2000
)
"Olanzapine is an atypical antipsychotic that is effective in the treatment of schizophrenia. "( Olanzapine plasma concentrations and clinical response: acute phase results of the North American Olanzapine Trial.
Beasley, C; Lund, BC; Perry, PJ; Sanger, T, 2001
)
"Olanzapine is an atypical antipsychotic agent whose side effects include sedation, weight gain, and increased creatinine kinase and transaminase levels."( A case report of olanzapine-induced hypersensitivity syndrome.
Bergman, R; Eilam, O; Hayek, T; Raz, A; Yungerman, T, 2001
)
"Olanzapine is a potentially useful antipsychotic drug, with significant short-term effects on behavioral changes, mainly in patients with severe psychiatric symptoms at the onset. "( Short-term effects of olanzapine in Huntington disease.
Brusa, L; Cannella, M; Porcellini, A; Ruggieri, S; Simonelli, M; Squitieri, F, 2001
)
"Olanzapine is a serotonin-dopamine receptor antagonist primarily used in the treatment of psychotic illnesses. "( Olanzapine: an atypical antipsychotic for schizophrenia.
Lund, BC; Perry, PJ, 2000
)
"Olanzapine may prove to be a useful adjunctive therapy in some self-induced dermatoses including acne excorieé."( Olanzapine may be an effective adjunctive therapy in the management of acne excoriée: a case report.
Gupta, AK; Gupta, MA,
)
"1. Olanzapine is a novel atypical antipsychotic with affinity for a number of neurotransmitter receptors including dopamine D1, D2, D4, serotonin 5HT2A, 5HT2C, histamine H1, a1-adrenergic, and muscarinic receptors. "( Dopamine receptor responsivity in schizophrenic patients in a drug-free state and after treatment with olanzapine.
Hatzimanolis, J; Lykouras, L; Markianos, M; Oulis, P, 2001
)
"Olanzapine (Zyprexa) is an atypical neuroleptic used in adult and pediatric patients for the management of schizophrenia. "( Diabetic ketoacidosis associated with olanzapine in an adolescent patient.
Scott, SM; Selva, KA, 2001
)
"Olanzapine is a favorable drug with a potential treatment of delirium, psychotic depression, mood disorders and nausea with a single drug in advanced cancer patients. "( Olanzapine: another psychotropic?
Davis, MP; Dickerson, ED,
)
"Olanzapine is a commonly used atypical antipsychotic medication for which therapeutic drug monitoring has been proposed as clinically useful. "( A high-performance liquid chromatography assay with ultraviolet detection for olanzapine in human plasma and urine.
Boulton, DW; DeVane, CL; Markowitz, JS, 2001
)
"Olanzapine is a relatively new antipsychotic drug used in the United States for the treatment of schizophrenia. "( Tissue distribution of olanzapine in a postmortem case.
Felo, JA; Jenkins, AJ; Merrick, TC, 2001
)
"Olanzapine appears to be a good abortive agent for cluster headache. "( Olanzapine as an abortive agent for cluster headache.
Rozen, TD, 2001
)
"Olanzapine is an atypical antipsychotic that is becoming more widely used in children and adolescents. "( Hyperglycemia and hypertriglyceridemia secondary to olanzapine.
Domon, SE; Webber, JC, 2001
)
"Olanzapine is an effective and safe antipsychotic drug. "( [Olanzapine: pharmacology, pharmacokinetics and therapeutic drug monitoring].
Baumann, P; Grasmäder, K; Hiemke, C; Rao, ML, 2001
)
"Olanzapine is an atypical antipsychotic drug with a more favourable safety profile than typical antipsychotics with a hitherto unknown topographic quantitative electroencephalogram (QEEG) profile."( Multilead quantitative electroencephalogram profile and cognitive evoked potentials (P300) in healthy subjects after a single dose of olanzapine.
Czekalla, J; Dierks, T; Frölich, L; Holstein, W; Hubl, D; Kleinlogel, H; Maurer, K; Weinandi, T, 2001
)
"Olanzapine is an 'atypical' antipsychotic indicated for the treatment of schizophrenia. "( The pharmacovigilance of olanzapine: results of a post-marketing surveillance study on 8858 patients in England.
Biswasl, PN; Freemantle, S; Pearcel, GL; Shakir, SA; Wilton, LV, 2001
)
"Olanzapine appears to be a safe and effective agent in the treatment of women with criteria-defined BPD, significantly affecting all 4 core areas of borderline psychopathology (i.e., affect, cognition, impulsivity, and interpersonal relationships)."( Olanzapine treatment of female borderline personality disorder patients: a double-blind, placebo-controlled pilot study.
Frankenburg, FR; Zanarini, MC, 2001
)
"Olanzapine is an atypical antipsychotic medication indicated for the treatment of schizophrenia and other manifestations of psychotic illness. "( Hypotension and bradycardia in a healthy volunteer following a single 5 mg dose of olanzapine.
Boulton, DW; DeVane, CL; Liston, HL; Markowitz, JS; Risch, SC, 2002
)
"Olanzapine appears to be a clinically efficacious and safe drug for the treatment of the symptoms of delirium in the hospitalized medically ill."( An open trial of olanzapine for the treatment of delirium in hospitalized cancer patients.
Breitbart, W; Gibson, C; Tremblay, A,
)

Effects

Olanzapine has a high affinity for the 5HT(2A) receptor, which is up to 5 times greater than the dopamine receptor. Olanzapine pamoate has a higher cost of treatment than the oral form and requires administration in a hospital setting.

Olanzapine has been found to have antiemetic properties due to its ability to inhibit multiple serotonergic, dopaminergic, alpha-1 adrenergic and histamine receptors. Olanzapine use has been reported during pregnancy and breastfeeding, but there are no controlled clinical trials assessing the safety of olanZapine exposure to infants and fetuses.

ExcerptReference
"Olanzapine has a related chemical structure and comparable receptor-binding profile as clozapine, which demonstrated superior efficacy in combination studies, but has a more unfavorable side-effect profile compared to olanzapine."( A randomized double-blind controlled trial to assess the benefits of amisulpride and olanzapine combination treatment versus each monotherapy in acutely ill schizophrenia patients (COMBINE): methods and design.
Baumgärtner, J; Brockhaus-Dumke, A; Cordes, J; Correll, CU; Engelke, C; Englisch, S; Feyerabend, S; Gaebel, W; Gouzoulis-Mayfrank, E; Gründer, G; Hasan, A; Heres, S; Jäger, M; Kluge, M; Kolbe, H; Lange, C; Langguth, B; Leucht, S; Makiol, C; Meisenzahl-Lechner, E; Neff, A; Poeppl, T; Reske, D; Riesbeck, M; Schmidt-Kraepelin, C; Verde, PE; Wobrock, T; Zink, M, 2020
)
"Olanzapine pamoate has a higher cost of treatment than the oral form and requires administration in a hospital setting (unlike other long-acting antipsychotics), and the cost-effectiveness of this treatment may be questioned. "( [Cost-effectiveness study of olanzapine pamoate: Mirror-image analysis after one year].
Burgot, G; Drapier, D; Langrée, B; Marie, N; Potaufeu, J, 2019
)
"Olanzapine has a profile similar to that of clozapine and shares its seizure-inducing potential."( Olanzapine-induced clinical seizure: a case report.
Anjith, D; Behere, RV; Gangadhar, BN; Rao, NP; Venkatasubramanian, G,
)
"Olanzapine has a high affinity for the 5HT(2A) receptor, which is up to 5 times greater than the dopamine receptor, resulting in less propensity to the development of extrapyramidal side effects."( Olanzapine: palliative medicine update.
Prommer, E, 2013
)
"Olanzapine has a higher propensity to cause derangement of some parameters of lipid profile than risperidone. "( Comparison of fasting blood sugar and serum lipid profile changes after treatment with atypical antipsychotics olanzapine and risperidone.
Bhutani, G; Gupta, R; Kaushal, J, 2012
)
"Olanzapine has a beneficial effect on neurocognitive function in patients with a first episode of psychosis. "( Comparative effect of atypical and conventional antipsychotic drugs on neurocognition in first-episode psychosis: a randomized, double-blind trial of olanzapine versus low doses of haloperidol.
Christensen, BK; Gur, RC; Hamer, RM; Keefe, RS; Lewine, RR; Lieberman, JA; Sanger, TM; Seidman, LJ; Sharma, T; Sitskoorn, MM; Tohen, M; Tollefson, GD; Yurgelun-Todd, DA, 2004
)
"Olanzapine has a U.S. "( Variables associated with high olanzapine dosing in a state hospital.
Botts, S; de Leon, J; Littrell, R, 2004
)
"Olanzapine has a more benign adverse effect profile than typical antipsychotic agents and eliminates the need for electrocardiographic monitoring."( Successful treatment of delusions of parasitosis with olanzapine.
Badreshia, S; Mackley, CL; Meehan, WJ, 2006
)
"Olanzapine has a receptor profile that is similar to that of clozapine: it is relatively nonselective at dopamine receptor subtypes and it shows selectivity for mesolimbic and mesocortical over striatal dopamine tracts (electrophysiology; Fos)."( In vitro and in vivo biochemistry of olanzapine: a novel, atypical antipsychotic drug.
Bymaster, FP; Calligaro, DO; DeLapp, NW; Moore, NA; Nelson, DL; Rasmussen, K; Wong, DT, 1997
)
"Olanzapine has a favorable acute and tardive extrapyramidal symptom profile relative to haloperidol and caused substantially less elevation of serum prolactin."( Dosing the antipsychotic medication olanzapine.
Nemeroff, CB, 1997
)
"Olanzapine has a receptor affinity profile similar to that of clozapine."( Olanzapine in the treatment of adolescent acute mania: a report of seven cases.
Foster, KD; Keck, PE; McElroy, SL; Sorter, MT; Soutullo, CA, 1999
)
"Olanzapine has a multireceptorial binding profile including a greater affinity for serotonin 5-HT(2A) than for dopamine D(2) receptors."( Olanzapine: a review of its use in the treatment of bipolar I disorder.
Bhana, N; Perry, CM, 2001
)
"Olanzapine has been reported to be an effective antiemetic in patients receiving carboplatin-based chemotherapy. "( Effects of adding a neurokinin-1 receptor antagonist to 5 mg olanzapine, a 5-hydroxytryptamine-3 receptor antagonist, and dexamethasone for preventing carboplatin-induced nausea and vomiting: a propensity score-matched analysis.
Abe, M; Fujita, Y; Hayasaki, Y; Hirose, C; Iihara, H; Imai, H; Inui, N; Karayama, M; Kawazoe, H; Morishige, KI; Nakamura, K; Ohno, Y; Suda, T; Suzuki, A; Tanaka, K; Uozumi, R; Yamamoto, S, 2022
)
"As olanzapine has shown poor bioavailability and permeability in the brain, the sustained release of olanzapine from the designed carriers could enhance pharmacokinetic effectiveness."( Sustained delivery of olanzapine from sunflower oil-based polyol-urethane nanoparticles synthesised through a cyclic carbonate ring-opening reaction.
Babanejad, N; Dorkoosh, F; Farhadian, A; Mozafari, M; Nabid, MR; Saeb, MR; Zarrintaj, P, 2019
)
"Olanzapine has been used for the treatment of schizophrenia and other mental disorders. "( The dosage-dependent effects of cevimeline in preventing olanzapine-induced metabolic side-effects in female rats.
Deng, C; Lian, J, 2020
)
"Olanzapine has been found to have antiemetic properties due to its ability to inhibit multiple serotonergic, dopaminergic, alpha-1 adrenergic and histamine receptors. "( Secondary and cumulative meta-analysis of olanzapine for antiemetic prophylaxis for chemotherapy-induced nausea and vomiting: do we still need to study its effectiveness?
Chiu, L; Chow, R; DeAngelis, C; Lock, M; Simone, CB, 2021
)
"Olanzapine use has been reported during pregnancy and breastfeeding, but there are no controlled clinical trials assessing the safety of olanzapine exposure to infants and fetuses. "( Olanzapine in pregnancy and breastfeeding: a review of data from global safety surveillance.
Brunner, E; Dey, DK; Falk, DM; Jones, M; Shatapathy, CC, 2013
)
"Olanzapine has been investigated as an alternative to antidepressants and a mood stabilizer for acute bipolar depression."( Efficacy of olanzapine monotherapy for treatment of bipolar I depression: a randomized, double-blind, placebo controlled study.
Du, H; Huang, DS; Liang, GM; Tong, JH; Wang, M; Zhu, G, 2014
)
"Olanzapine has shown efficacy for CINV prophylaxis and the treatment of breakthrough CINV."( Reviewing current and emerging antiemetics for chemotherapy-induced nausea and vomiting prophylaxis.
Natale, JJ, 2015
)
"Olanzapine has been reported to induce priapism in several adult cases with schizophrenia and/or mood disorders but very rarely reported in children."( Olanzapine-induced Priapism in a Child with Asperger's Syndrome.
Bozkurt, H; Şahin, S, 2017
)
"Olanzapine treatment has been associated with clinically meaningful weight increases, hypertriglyceridemia, insulin resistance, and diabetes mellitus. "( Aripiprazole added to overweight and obese olanzapine-treated schizophrenia patients.
Borba, CP; Boxill, R; Cather, C; Copeland, PM; Evins, AE; Fan, X; Freudenreich, O; Goff, DC; Henderson, DC; Sharma, B, 2009
)
"Olanzapine has been recently tried to relieve anxiety and hyperactivity in adolescents with eating disorders (EDs). "( No unexpected adverse events and biochemical side effects of olanzapine as adjunct treatment in adolescent girls with eating disorders.
Rosling, A; Swenne, I, 2011
)
"Olanzapine has been demonstrated to have opioid-sparing properties."( Olanzapine: palliative medicine update.
Prommer, E, 2013
)
"Olanzapine has been shown to be a safe and effective agent for the prevention of chemotherapy-induced nausea and vomiting (CINV). "( The use of olanzapine versus metoclopramide for the treatment of breakthrough chemotherapy-induced nausea and vomiting in patients receiving highly emetogenic chemotherapy.
Gray, SE; Nagy, CK; Navari, RM, 2013
)
"Olanzapine and clozapine have been associated with the greatest weight gain of the newer antipsychotics."( Clinical issues associated with maintenance treatment of patients with schizophrenia.
Guthrie, SK, 2002
)
"Olanzapine has been shown to be better tolerated in comparison with conventional antipsychotics in a large unselected sample of acutely psychotic schizophrenic in-patients. "( Safety of olanzapine versus conventional antipsychotics in the treatment of patients with acute schizophrenia. A naturalistic study.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M; Sacristán, JA, 2003
)
"Olanzapine, which has been used anecdotally for chronic nausea in advanced cancer patients, might be a useful treatment for the prevention of delayed emesis in chemotherapy patients."( A retrospective chart review of the use of olanzapine for the prevention of delayed emesis in cancer patients.
Beaver, M; Brown, J; Comparet, J; Dickerson, P; Gray, D; Kirsh, KL; Passik, SD; Theobald, DE; Trowbridge, R, 2003
)
"Olanzapine has been found to be effective and tolerable, also under naturalistic acute treatment conditions."( Objective and subjective efficacy as well as tolerability of olanzapine in the acute treatment of 120 patients with schizophrenia spectrum disorders.
Holzbach, R; Krausz, M; Lambert, M; Moritz, S; Naber, D; Postel, N, 2003
)
"Olanzapine has been considered to be similar to clozapine, but olanzapine intoxication appeared to have a relatively benign clinical course as compared with clozapine intoxication."( [Intoxications with atypical antipsychotic drugs--data of the Acute Intoxication Unit in Wrocław].
Antończyk, A; Kochman, K; Magdalan, J; Porebska, B; Przewłocki, M; Wasyko-Smolarek, M, 2004
)
"Olanzapine has been proven effective in some chronic pain conditions."( Atypical antipsychotics in the treatment of fibromyalgia: a case series with olanzapine.
Calandre, EP; Dominguez, I; García-Leiva, JM; Hidalgo, J; Rico-Villademoros, F, 2005
)
"Olanzapine has been hypothesized to have superior efficacy in patients with treatment-resistant schizophrenia. "( Olanzapine treatment of residual positive and negative symptoms.
Ball, MP; Buchanan, RW; Carpenter, WT; Gold, JM; Kirkpatrick, B; McMahon, RP; Weiner, E, 2005
)
"Olanzapine has been successfully used in the treatment of delirium."( Can olanzapine cause delirium in the elderly?
Lim, CJ; Tampi, RR; Trevino, C, 2006
)
"Olanzapine therapy has been associated with such adverse effects as sedation, hyperlipidemia, weight gain, and insulin resistance, all of which were infrequent in our patients."( Successful treatment of delusions of parasitosis with olanzapine.
Badreshia, S; Mackley, CL; Meehan, WJ, 2006
)
"Olanzapine, however, has been increasingly used in higher doses as clinicians attempt to find a more tolerable therapy for those refractory to conventional agents."( Plasma concentrations of high-dose olanzapine in a double-blind crossover study.
Conley, RR; Kelly, DL; Richardson, CM; Yu, Y, 2006
)
"Olanzapine has been shown to cause or have a contributory role in the development of hyperglycemia and diabetes mellitus. "( Olanzapine-induced hyperglycemic ketoacidosis and corresponding acetone concentrations post-mortem: a forensic interpretation.
House, CJ, 2007
)
"Olanzapine has been one of the first atypical antipsychotics available for intramuscular administration."( [New formulations of olanzapine in the treatment of acute agitation].
Bartkó, G, 2006
)
"Olanzapine has been reported as a risk factor for acute pancreatitis."( Fatal hyponatremia and other metabolic disturbances associated with psychotropic drug polypharmacy.
Alfirevic, Z; Degoricija, V; Vucicevic, Z; Vukicevic-Badouin, D, 2007
)
"Olanzapine has been used for over a decade for treatment of schizophrenia and bipolar disorder. "( Abuse of olanzapine by substance abusers.
Reeves, RR, 2007
)
"Olanzapine has been reported as less likely to cause EPS and may improve some negative signs."( The relationship between negative symptoms of schizophrenia and extrapyramidal side effects with haloperidol and olanzapine.
Allan, ER; Alpert, M; Connolly, B; Crichton, J; Sison, CE, 1998
)
"Olanzapine has been associated with slight increases in hepatic transaminases."( Olanzapine: a serotonin-dopamine-receptor antagonist for antipsychotic therapy.
Bever, KA; Perry, PJ, 1998
)
"Olanzapine has been associated with insulin resistance and new-onset diabetes mellitus. "( Olanzapine-associated severe hyperglycemia, ketonuria, and acidosis: case report and review of literature.
Doraiswamy, PM; McLendon, BM; Seaburg, HL, 2001
)
"Olanzapine has been shown to be superior to placebo for the treatment of mania. "( The impact of response to previous mood stabilizer therapy on response to olanzapine versus placebo for acute mania.
Baker, RW; Goldberg, JF; Milton, DR; Schuh, LM; Stauffer, VL; Tohen, M, 2002
)
"Olanzapine has been shown to be very effective in these situations and its use is suggested as first-choice therapy."( Ecstasy-induced psychotic disorder: six-month follow-up study.
Calle, R; Gutiérrez-Fraile, M; Iraurgi, I; Jiménez-Lerma, JM; Landabaso, MA; Sanz, J, 2002
)

Actions

Olanzapine can lower seizure threshold and induce epileptiform discharges. Olanzapine caused an increase in average meal size accompanied by reduced meal frequency, without clearly affecting food preference.

ExcerptReference
"An olanzapine-induced increase was observed in plasma triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels in patients with schizophrenia (all P < 0.05)."( Effects of olanzapine treatment on lipid profiles in patients with schizophrenia: a systematic review and meta-analysis.
Dai, W; Ding, C; Huang, X; Li, R; Su, X; Xiao, J; Xing, Z; Zhang, Y; Zhu, W, 2020
)
"Olanzapine caused an 80% increase of slow wave sleep whereas clozapine caused a 6% decrease."( Olanzapine and clozapine differently affect sleep in patients with schizophrenia: results from a double-blind, polysomnographic study and review of the literature.
Dalal, M; Dittmann, RW; Himmerich, H; Hinze-Selch, D; Kluge, M; Kraus, T; Pollmächer, T; Rummel-Kluge, C; Schacht, A; Schuld, A; Wehmeier, PM, 2014
)
"Olanzapine can lower seizure threshold and induce epileptiform discharges."( Olanzapine-induced clinical seizure: a case report.
Anjith, D; Behere, RV; Gangadhar, BN; Rao, NP; Venkatasubramanian, G,
)
"Olanzapine caused an increase in average meal size accompanied by reduced meal frequency, without clearly affecting food preference."( Olanzapine affects locomotor activity and meal size in male rats.
Adan, RA; Evers, SS; la Fleur, SE; Luijendijk, MC; van der Zwaal, EM, 2010
)
"Olanzapine produced more increase in glucose than amisulpride, aripiprazole, quetiapine, risperidone and ziprasidone; no difference was found with clozapine."( Head-to-head comparisons of metabolic side effects of second generation antipsychotics in the treatment of schizophrenia: a systematic review and meta-analysis.
Davis, JM; Hunger, H; Kissling, W; Komossa, K; Leucht, S; Lobos, CA; Rummel-Kluge, C; Schmid, F; Schwarz, S, 2010
)
"Olanzapine can cause NMS, mainly in susceptible or predisposed patients."( Olanzapine-associated neuroleptic malignant syndrome.
Christodoulou, NG; Havaki-Kontaxaki, BJ; Kontaxakis, VP; Paplos, KG, 2002
)
"Olanzapine caused an increase in apoptosis at the same c"( Predicting drug-induced agranulocytosis: characterizing neutrophil-generated metabolites of a model compound, DMP 406, and assessing the relevance of an in vitro apoptosis assay for identifying drugs that may cause agranulocytosis.
Iverson, S; Uetrecht, JP; Zahid, N, 2002
)
"Olanzapine did cause more weight gain than its comparators but current data are not statistically significant (3-12 months, n=535, WMD 2.2kg CI -0.6-5)."( Olanzapine for schizophrenia.
Dardennes, RM; Duggan, L; El-Dosoky, A; Fenton, M; Indran, S, 2003
)
"Olanzapine had a lower incidence of extrapyramidal symptoms and better subjective acceptance of medication."( Safety, effectiveness, and quality of life of olanzapine in first-episode schizophrenia: a naturalistic study.
Ciudad, A; Gascón, J; Gómez, JC; Montes, JM, 2003
)
"Olanzapine did not increase progesterone or corticosterone levels."( Effects of olanzapine infusions to the ventral tegmental area on lordosis and midbrain 3alpha,5alpha-THP concentrations in rats.
Frye, C; Seliga, A, 2003
)
"Olanzapine can cause considerable rapid weight gain.This review highlights the need for large, independent, well designed, conducted and reported pragmatic randomised studies."( Risperidone versus olanzapine for schizophrenia.
Hosalli, P; Jayaram, MB, 2005
)
"The olanzapine-induced increase in Stat3 activity could underlie the increase in RGS7 protein expression in vivo as previously demonstrated in cultured cells."( Chronic olanzapine activates the Stat3 signal transduction pathway and alters expression of components of the 5-HT2A receptor signaling system in rat frontal cortex.
Battaglia, G; D'Souza, DN; Damjanoska, KJ; Garcia, F; Muma, NA; Singh, RK; Van de Kar, LD; Vercillo, MS; Zemaitaitis, B; Zhang, Y, 2007
)
"Olanzapine has lower alpha(1)-adrenergic and dopaminergic blockade properties, thus changing risperidone to olanzapine may be an alternative modality in risperidone-induced enuresis when antipsychotic treatment is crucial."( Risperidone-induced enuresis in two children with autistic disorder.
Hergüner, S; Mukaddes, NM, 2007
)
"Olanzapine had lower affinity for alpha 2-adrenergic receptors and relatively low affinity for 5HT1 subtypes, GABAA, beta-adrenergic receptors, and benzodiazepine binding sites."( Radioreceptor binding profile of the atypical antipsychotic olanzapine.
Bymaster, FP; Calligaro, DO; Falcone, JF; Marsh, RD; Moore, NA; Seeman, P; Tye, NC; Wong, DT, 1996
)
"Olanzapine does not inhibit CYP isozymes."( Olanzapine. Pharmacokinetic and pharmacodynamic profile.
Beasley, CM; Bergstrom, RF; Callaghan, JT; Ptak, LR, 1999
)
"Olanzapine was tried because it has caused weight gain in other patient groups."( Case reports of olanzapine treatment of anorexia nervosa.
Gray, N; Kaye, WH; La Via, MC, 2000
)
"Olanzapine did cause more weight gain than its comparators but current data are not statistically significant (3-12 months, n=535, WMD 2.2kg CI -0.6-5)."( Olanzapine for schizophrenia.
Dardennes, RM; Duggan, L; El-Dosoky, A; Fenton, M; Indran, S, 2000
)
"Olanzapine induced a lower striatal D2 occupancy than haloperidol."( Double-blind olanzapine vs. haloperidol D2 dopamine receptor blockade in schizophrenic patients: a baseline-endpoint.
Bernardo, M; Catafau, AM; Font, M; Gómez, JC; Gutiérrez, F; Lomeña, F; López-Carrero, C; Parellada, E; Pavía, J; Salamero, M, 2001
)

Treatment

Olanzapine treatment has been associated with clinically meaningful weight increases, hypertriglyceridemia, insulin resistance, and diabetes mellitus. Olanzapine-treated adolescents were likely to experience greater increases in bodyweight, sedation, blood lipids, serum prolactin and liver t.

ExcerptReference
"In olanzapine-treated mice, the expression of Hmgcs2, a negative regulator of apoptosis, was significantly down-regulated in the dorsal raphe nucleus, where the expressions of Pla2g4e, Slc6a4 and Gnai1 involved in serotonergic synapse were significantly upregulated."( [Bioinformatic analysis of differentially expressed proteins in the dorsal raphe nucleus of rats after continuous treatment with olanzapine].
Huang, P; Li, H; Liu, Q; Tang, Y; Wang, Y; Zhu, J, 2022
)
"Olanzapine is the treatment most frequently prescribed and studied with 7 randomized double-blind controlled trials."( Efficacy and tolerance of second-generation antipsychotics in anorexia nervosa: A systematic scoping review.
Blanchet, C; Carretier, E; Guessoum, SB; Ludot, M; Moro, MR; Thorey, S, 2023
)
"Olanzapine treatment caused a mild 26% increase in LPO levels, but the effect was non-significant."( Increased levels of lipid and protein oxidation in rat prefrontal cortex after treatment by lithium, valproic acid, and olanzapine.
Arslan, MA; Bilgici, B; Gümrükçüoğlu, Tİ; Karaustaoğlu, A; Tunçel, ÖK, 2023
)
"Olanzapine treatment showed better continuation rates at 26 and 52 after hospital discharge than aripiprazole, whereas maintenance with the two antipsychotics did not differ significantly at 104 weeks, due reduced tolerability of long-term olanzapine treatment."( Comparison between olanzapine and aripiprazole treatment for 104 weeks after hospital discharge in schizophrenia spectrum disorders: a multicenter retrospective cohort study in a real-world setting.
Harada, T; Hosokawa, T; Kishi, Y; Miyaji, C; Nomura, A; Okahisa, Y; Sakamoto, S; Takaki, M; Takao, S; Takeda, T; Washida, K; Yada, Y; Yamada, N; Yoshimura, Y, 2023
)
"Olanzapine treatment also led to a significant increase in mu opioid receptor availability in the arcuate nucleus, which contains both satiety and hunger controlling neurons."( Changes in hypothalamic mu-opioid receptor expression following acute olanzapine treatment in female rats: Implications for feeding behavior.
Krogsbaek, M; Landau, AM; Larsen, NY; Nyengaard, JR; Sanchez, C, 2023
)
"olanzapine. Patients treated with olanzapine had higher IRI, FBG, and FINS levels than did patients treated with aripiprazole, ziprasidone, or risperidone, with significant differences (aripiprazole vs."( Insulin resistance induced by olanzapine and other second-generation antipsychotics in Chinese patients with schizophrenia: a comparative review and meta-analysis.
Deng, Y; Lei, J; Li, W; Wu, S; Yu, L, 2019
)
"Olanzapine treatment was associated with the highest change in weight, with higher doses resulting in more weight gain."( Effects of long-term antipsychotics treatment on body weight: A population-based cohort study.
Bazo-Alvarez, JC; Carpenter, JR; Hayes, JF; Morris, TP; Petersen, I, 2020
)
"Olanzapine treatment was associated with the highest increase in weight. "( Effects of long-term antipsychotics treatment on body weight: A population-based cohort study.
Bazo-Alvarez, JC; Carpenter, JR; Hayes, JF; Morris, TP; Petersen, I, 2020
)
"Olanzapine-treated rats had decreased medial entorhinal cortical thickness compared to vehicle-treated rats."( Decreased medial entorhinal cortical thickness in olanzapine exposed female rats is not ameliorated by exercise.
Barr, AM; Beasley, CL; Boyda, HN; Hercher, C; Honer, WG; Ker, AH; Lang, DJ; Procyshyn, RM; Woodward, ML, 2020
)
"Olanzapine treatment significantly increased the feed intake, weight gain, adiposity index, while reduced body temperature and locomotor activity which were reversed by berberine treatment."( Berberine attenuated olanzapine-induced metabolic alterations in mice: Targeting transient receptor potential vanilloid type 1 and 3 channels.
Bansal, Y; Bishnoi, M; Kondepudi, KK; Kuhad, A; Medhi, B; Singh, DP; Singh, R; Sodhi, RK, 2020
)
"Olanzapine-treated rats demonstrated significantly elevated body weight gain, food intake, feeding efficiency, total white fat mass, liver mass, and plasma triglyceride levels, which could be partly reversed by the co-treatment with cevimeline in a dosage-dependent manner."( The dosage-dependent effects of cevimeline in preventing olanzapine-induced metabolic side-effects in female rats.
Deng, C; Lian, J, 2020
)
"Olanzapine treatment resulted in similar improvements (PANSS and CGI-S LS mean ± SE of -5.3 ± 1.84 [P = .004] and -0.44 ± 0.12 [P < .001], respectively)."( Efficacy and Safety of a Combination of Olanzapine and Samidorphan in Adult Patients With an Acute Exacerbation of Schizophrenia: Outcomes From the Randomized, Phase 3 ENLIGHTEN-1 Study.
DiPetrillo, L; Jiang, Y; Kunovac, J; McDonnell, D; Potkin, SG; Silverman, BL; Simmons, A, 2020
)
"Olanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O + S co-treatment significantly reversed body weight gain but without significant effects on food intake. "( Brown adipose tissue activity is modulated in olanzapine-treated young rats by simvastatin.
Deng, C; Feng, X; Hu, CH; Liu, L; Liu, X; Zeng, Y, 2020
)
"Olanzapine treatment also altered the mRNA expression of hypothalamic appetite-regulating and nutrient-sensing factors, inflammatory genes and TRPV1/TRPV3, which were reversed with ruthenium red and capsazepine treatment."( Role of TRPV1/TRPV3 channels in olanzapine-induced metabolic alteration: Possible involvement in hypothalamic energy-sensing, appetite regulation, inflammation and mesolimbic pathway.
Bansal, Y; Bishnoi, M; Khare, P; Kondepudi, KK; Kuhad, A; Medhi, B; Singh, R; Sodhi, RK, 2020
)
"The olanzapine alone-treated group had the highest bile acid level, followed by the olanzapine with Tat-3L4F (1 μmol kg-1) group, olanzapine with Tat-3L4F (10 μmol kg-1) group, and vehicle group."( A Novel Synthetic Interfering Peptide Tat-3L4F Attenuates Olanzapine-Induced Weight Gain Through Disrupting Crosstalk Between Serotonin Receptor 2C and Protein Phosphatase and Tensin Homolog in Rats.
Chen, Y; Fang, X; Wang, D; Wang, Y; Yu, L; Zhang, C, 2020
)
"Olanzapine treatment increased the body weight, blood glucose and triglyceride levels, and the number of adipocytes in the liver. "( Coadministration of metformin prevents olanzapine-induced metabolic dysfunction and regulates the gut-liver axis in rats.
Huang, HX; Liu, ZQ; Luo, C; Mao, XY; Wang, X; Zhou, HH, 2021
)
"Olanzapine treated mHypoA-59 cells were then assessed for mitophagy markers and oxidative stress; including quantification of lysosomes, autophagosomes, LC3B-II, p62, superoxide anion (O"( N-acetylcysteine prevents olanzapine-induced oxidative stress in mHypoA-59 hypothalamic neurons.
Boz, Z; Hu, M; Huang, XF; Yu, Y, 2020
)
"Olanzapine treatments for 1, 8 and 36 days significantly activated the inflammatory IKKβ/NFκB signaling, and increased the expression of TNF-α, IL-6, IL-1β and immune-related proteins such as iNOS, TLR4 and CD14. "( Olanzapine Induces Inflammation and Immune Response via Activating ER Stress in the Rat Prefrontal Cortex.
Deng, C; He, M; Huang, XF; Li, WT; Qian, K; Sun, TL; Zhang, BH, 2021
)
"Olanzapine treatment caused a preferential shift toward carbohydrate oxidation (or reduced fat oxidation), elevated blood triglycerides and a reduction in locomotor activity."( Prevention of the adverse effects of olanzapine on lipid metabolism with the antiepileptic zonisamide.
Cowley, MA; Oldfield, BJ; Stefanidis, A; Watt, MJ, 2017
)
"62 olanzapine- or clozapine-treated patients with illness duration of at least four years were selected from an international multicenter study on the characterization of negative symptoms. "( Inverse association between negative symptoms and body mass index in chronic schizophrenia.
Bernardo, M; Bobes, J; Fernandez-Egea, E; Garcia-Alvarez, L; Garcia-Portilla, MP; Garcia-Rizo, C; Mané, A; Mezquida, G; Savulich, G; Toll, A, 2018
)
"Olanzapine treatment increased serum glucagon and lead to rapid increases in blood glucose concentrations in WT mice. "( Glucagon receptor knockout mice are protected against acute olanzapine-induced hyperglycemia.
Castellani, LN; Charron, MJ; Peppler, WT; Sutton, CD; Whitfield, J; Wright, DC, 2017
)
"Olanzapine treatment reduced RER in the dark and light phases (most consistently in the 4-hours post-treatment), while ICV insulin reduced average RER predominantly in the dark phase, but also at the end of the light cycle."( Effects of acute olanzapine exposure on central insulin-mediated regulation of whole body fuel selection and feeding.
Abela, AR; Ahasan, Z; Benarroch, L; Castellani, LN; Giacca, A; Hahn, MK; Kowalchuk, C; Remington, GJ; Teo, C; Wilkin, J; Wilson, V, 2018
)
"Olanzapine treatment (mean [standard deviation] duration = 12.3 [7.6] weeks) was associated with a significant decrease in blood ghrelin levels with a medium effect size (SMD = -0.48, 95% CI -0.88 to -0.08, p = 0.018)."( Meta-analysis of ghrelin alterations in schizophrenia: Effects of olanzapine.
Goetz, RL; Miller, BJ, 2019
)
"Olanzapine treatment significantly increased fasting plasma insulin concentration, the index of the homeostasis model assessment of insulin resistance (HOMA-IR), and hepatic triglyceride and fatty droplet accumulation in rats. "( The IRS/PI3K/Akt signaling pathway mediates olanzapine-induced hepatic insulin resistance in male rats.
Huang, X; Li, Y; Ren, L; Wang, C; Zhou, X, 2019
)
"Olanzapine (100 uM) treatment caused a significant increase in IL-6 while aripiprazole (20 uM) significantly decreased IL-10."( Antipsychotics differentially regulate insulin, energy sensing, and inflammation pathways in hypothalamic rat neurons.
Belsham, DD; Hahn, MK; Kanagasundaram, P; Kowalchuk, C, 2019
)
"Olanzapine treatment for 8 days in rats was associated with activated PERK-eIF2α signaling and IKKβ-NFκB signaling in the hypothalamus, accompanied by increased food intake and weight gain."( Olanzapine-induced endoplasmic reticulum stress and inflammation in the hypothalamus were inhibited by an ER stress inhibitor 4-phenylbutyrate.
Chen, J; Gao, G; He, M; Hu, J; Huang, XF; Li, J; Li, W; Sun, T; Zhou, T, 2019
)
"Olanzapine (6 mg/kg) treatment significantly altered glucose and lipid homeostasis which was further accompanied by elevated levels of proinflammatory cytokines, ghrelin and leptin."( Modeling of antipsychotic-induced metabolic alterations in mice: An experimental approach precluding psychosis as a predisposing factor.
Bansal, Y; Kuhad, A; Medhi, B; Saroj, P; Singh, R; Sodhi, RK, 2019
)
"Olanzapine treatment was associated with significant weight gain."( Combination use of atomoxetine hydrochloride and olanzapine in the treatment of attention-deficit/hyperactivity disorder with comorbid disruptive behavior disorder in children and adolescents 10-18 years of age.
Holzer, B; Lehman, R; Lopes, V, 2013
)
"Olanzapine-treated rats showed greater central adiposity."( Routine exercise ameliorates the metabolic side-effects of treatment with the atypical antipsychotic drug olanzapine in rats.
Barr, AM; Boyda, HN; Choy, HH; Honer, WG; Lant, N; Li, L; Pang, CC; Procyshyn, RM; Ramos-Miguel, A; Töpfer, E; Wong, R, 2014
)
"Olanzapine treatment significantly decreased glucose effectiveness (P = 0.041) and raised fasting glucose over 4.25 hours (P = 0.03) as compared to placebo."( Acute effects of single-dose olanzapine on metabolic, endocrine, and inflammatory markers in healthy controls.
Arenovich, T; Chintoh, A; Clarke, L; Cohn, T; Fletcher, P; Giacca, A; Gomes, S; Hahn, MK; McIntyre, RS; Powell, V; Remington, GJ; Teo, C; Wolever, TM, 2013
)
"Olanzapine treatment for six weeks effectively decreased the breakdown of myelin and oligodendrocytes loss of cuprizone-fed mice."( Olanzapine ameliorates neuropathological changes and increases IGF-1 expression in frontal cortex of C57BL/6 mice exposed to cuprizone.
Adilijiang, A; Hartle, K; Huang, Q; Kong, J; Li, XM; Tan, Q; Wang, J; Wang, L; Xu, H; Zhang, D; Zhang, H; Zhang, Y; Zhang, Z, 2014
)
"Olanzapine-treated rats had higher body weight (227.4 ± 8.9 vs. "( Subchronic olanzapine treatment decreases the expression of pancreatic glucose transporter 2 in rat pancreatic β cells.
Liu, H; Shu, S; Su, D; Wang, G; Wang, M; Yao, L, 2014
)
"Olanzapine augmentation treatment generally did not improve SWS but did improve sleep continuity and depression. "( Sleep architecture and cognitive changes in olanzapine-treated patients with depression: a double blind randomized placebo controlled trial.
du Toit, R; Hawken, ER; Jokic, R; Lazowski, LK; Milev, R; Townsend, B, 2014
)
"The olanzapine-only treatment significantly increased the D₂R binding in the Cg, NAc, and CPu, while the betahistine-only treatment reduced D₂R binding."( Chronic betahistine co-treatment reverses olanzapine's effects on dopamine D₂ but not 5-HT2A/2C bindings in rat brains.
Deng, C; Huang, XF; Lian, J; Pai, N, 2015
)
"Olanzapine treatment also enhanced activation of autophagy with increased expression of LC3-II, expression of protein p62, a substrate of autophagy, being decreased."( Autophagy involvement in olanzapine-mediated cytotoxic effects in human glioma cells.
Chen, XH; Liang, ZQ; Liu, RS; Wang, YX; Xu, SQ, 2014
)
"Olanzapine is used for treatment of psychiatric conditions but causes substantial weight gain. "( Olanzapine for cachexia in patients with advanced cancer: an exploratory study of effects on weight and metabolic cytokines.
Abdelrahim, M; Dalal, S; Falchook, GS; Fu, S; Hess, K; Hong, DS; Ilustre, A; Janku, F; Kurzrock, R; Naing, A; Ouyang, F; Wheler, J, 2015
)
"Olanzapine treatment suppressed NF-κB activation and iNOS expression and caused modulation of GSH-dependent defense systems but failed to reverse CSIS-induced increase in hepatic proinflammatory cytokines."( Olanzapine modulation of hepatic oxidative stress and inflammation in socially isolated rats.
Filipović, D; Gass, P; Todorović, N; Tomanović, N, 2016
)
"Olanzapine co-treatment prevented these PCP-induced effects in normal neurons but not in neurons from NRG1-knockout mice."( Olanzapine Prevents the PCP-induced Reduction in the Neurite Outgrowth of Prefrontal Cortical Neurons via NRG1.
Huang, XF; Yu, Y; Zhang, Q, 2016
)
"Olanzapine treatment and antipsychotic exposure time were the main modifiable risk factors for T2DM development in antipsychotic-exposed youth."( Type 2 Diabetes Mellitus in Youth Exposed to Antipsychotics: A Systematic Review and Meta-analysis.
Arango, C; Carbon, M; Correll, CU; De Hert, M; Galling, B; Gerhard, T; Guo, JJ; Kahl, KG; Lane, HY; Liao, CH; Martin, A; Nielsen, J; Nielsen, RE; Olfson, M; Roldán, A; Stubbs, B; Sung, FC; Vancampfort, D, 2016
)
"Olanzapine (OLZ) treatment is associated with a high risk of weight gain, and may cause abnormalities in glycolipid metabolism. "( Effect of Serum Leptin on Weight Gain Induced by Olanzapine in Female Patients with Schizophrenia.
Fukui, N; Ono, S; Saito, M; Sawamura, K; Someya, T; Sugai, T; Suzuki, Y; Tsuneyama, N; Watanabe, J, 2016
)
"Olanzapine treatment did not lead to changes in serum levels of ghrelin, FGF-21 and pro-inflammatory markers IL-1a, IL-6 and TNF-α at any time-point of the study."( Olanzapine-depot administration induces time-dependent changes in adipose tissue endocrine function in rats.
Babinska, Z; Demlova, R; Horska, K; Karpisek, M; Kotolova, H; Opatrilova, R; Ruda-Kucerova, J; Suchy, P, 2016
)
"Olanzapine-treated patients were also most likely to achieve response of negative symptoms and improvement in social functioning, and to stay on the initial medication longer."( Real-world Effectiveness of Antipsychotics for the Treatment of Negative Symptoms in Patients with Schizophrenia with Predominantly Negative Symptoms.
Haro, JM; Moneta, MV; Montgomery, W; Novick, D; Treuer, T, 2017
)
"Olanzapine treatment was started with a daily dosage of 15 mg."( Olanzapine treatment during breast feeding: a case report.
Bartels, M; Gaertner, HJ; Lutz, UC; Orlikowsky, T; Wiatr, G, 2008
)
"Olanzapine pretreatment induced hyperglycemia and markedly decreased plasma insulin and C-peptide in response to the glucose challenge."( Insulin resistance and decreased glucose-stimulated insulin secretion after acute olanzapine administration.
Chintoh, AF; Cohn, TA; Fletcher, PJ; Giacca, A; Lam, C; Lam, L; Mann, SW; Nobrega, JN; Remington, G, 2008
)
"Olanzapine treatment seems to have very little additional impact in regard to the QT variability."( Influence of olanzapine on QT variability and complexity measures of heart rate in patients with schizophrenia.
Bär, KJ; Berger, S; Koschke, M; Schulz, S; Tancer, M; Voss, A; Yeragani, VK, 2008
)
"Olanzapine-treated patients were also more likely to respond, and did so more rapidly than patients on other monotherapies (p < .001)."( Long-term antipsychotic monotherapy for schizophrenia: disease burden and comparative outcomes for patients treated with olanzapine, quetiapine, risperidone, or haloperidol monotherapy in a pan-continental observational study.
Anders, M; Dossenbach, M; Irimia, V; Kotler, M; Logozar-Perkovic, D; Lowry, AJ; Pecenak, J; Peciukaitiene, D; Smulevich, AB; Szulc, A; Treuer, T; West, TM, 2008
)
"Olanzapine-treated patients had significantly greater increases in weight and in glucose, cholesterol, triglyceride, uric acid, and prolactin levels than divalproex-treated patients."( Olanzapine versus divalproex versus placebo in the treatment of mild to moderate mania: a randomized, 12-week, double-blind study.
Aaronson, ST; Amsterdam, JD; Banov, M; Bardenstein, L; Bowden, C; Goodwin, GM; Grecu-Gabos, I; Kryzhanovskaya, L; Oliff, HS; Prelipceanu, D; Shekhar, A; Sun, B; Tochilov, V; Tohen, M; Vieta, E, 2008
)
"Olanzapine-treated patients also experienced longer time to depressive symptomatic relapse (85 versus 22 days, p=0.001) and manic symptomatic relapse (too few relapses to calculate versus 42 days, p<0.001) than did placebo-treated patients."( Maintenance of response following stabilization of mixed index episodes with olanzapine monotherapy in a randomized, double-blind, placebo-controlled study of bipolar 1 disorder.
Bowden, CL; Calabrese, JR; Sachs, GS; Sutton, VK; Tohen, M, 2009
)
"More olanzapine-treated versus placebo-treated patients completed the trial (68.1% versus 42.9%, p =.020). "( Olanzapine versus placebo in adolescents with schizophrenia: a 6-week, randomized, double-blind, placebo-controlled trial.
Bauer, T; Carlson, J; Dittmann, R; Frazier, J; Kryzhanovskaya, L; McDougle, C; Robertson-Plouch, C; Schulz, SC; Tohen, M; Wang, W; Xu, W, 2009
)
"Olanzapine-treated adolescents with schizophrenia experienced significant symptom improvement. "( Olanzapine versus placebo in adolescents with schizophrenia: a 6-week, randomized, double-blind, placebo-controlled trial.
Bauer, T; Carlson, J; Dittmann, R; Frazier, J; Kryzhanovskaya, L; McDougle, C; Robertson-Plouch, C; Schulz, SC; Tohen, M; Wang, W; Xu, W, 2009
)
"Olanzapine-treated patients with HTR2C haplotype C (-759C, -697C, and 23Ser) had higher BMI (P = 0.029) and C peptide levels (P = 0.029) compared with patients with haplotype B (-759T, -697C, and 23Cys)."( Association between HTR2C and HTR2A polymorphisms and metabolic abnormalities in patients treated with olanzapine or clozapine.
Dahl, ML; Gunes, A; Melkersson, KI; Scordo, MG, 2009
)
"Olanzapine treatment is associated with greater effects on adiposity and lipids than aripiprazole in both white and black/Hispanic subjects, suggesting that antipsychotic choice and intensive monitoring are important in minimizing metabolic risk, especially in nonwhite patients."( The moderating impact of ethnicity on metabolic outcomes during treatment with olanzapine and aripiprazole in patients with schizophrenia.
Baker, RA; Kim, E; Meyer, JM; Rosenblatt, LC; Whitehead, R, 2009
)
"Olanzapine treatment for 2 months significantly increased serum TAS levels (37.8%) and reduced serum MDA levels (22.2%) in comparison to respective pretreatment values."( Potential effect of olanzapine on total antioxidant status and lipid peroxidation in schizophrenic patients.
Ahmed, FA; Al-Chalabi, BM; Thanoon, IA, 2009
)
"Ten olanzapine-treated subjects and 11 clozapine-treated subjects were enrolled in the study. "( Ziprasidone as an adjuvant for clozapine- or olanzapine-associated medical morbidity in chronic schizophrenia.
Borba, CP; Boxill, R; Cather, C; Copeland, PM; Evins, AE; Fan, X; Forstbauer, SI; Freudenreich, O; Goff, DC; Henderson, DC; Miley, K; Sharma, B, 2009
)
"Olanzapine treatment for 7 days significantly increased the levels of the regulator of G protein signaling (RGS7) protein, RGS7 mRNA levels, and activation of JAK2 in rat frontal cortex."( Activation of the JAK-STAT pathway by olanzapine is necessary for desensitization of serotonin2A receptor-stimulated phospholipase C signaling in rat frontal cortex but not serotonin2A receptor-stimulated hormone release.
Battaglia, G; Carrasco, GA; Garcia, F; Jia, C; Muma, NA; Singh, RK, 2010
)
"Olanzapine-treated patients had significantly longer time to efficacy-related discontinuation (p < .001) and a significantly lower efficacy-related discontinuation rate (olanzapine, 8.9% vs."( A 28-week, randomized, double-blind study of olanzapine versus aripiprazole in the treatment of schizophrenia.
Breier, A; Kane, JM; Kryzhanovskaya, LA; Osuntokun, O; Stauffer, VL; Watson, SB; Xu, W, 2009
)
"Olanzapine-treated patients had significantly greater improvement in symptom efficacy at 28 weeks as well as significantly greater mean increases in weight and glucose and significantly greater worsening on lipids parameters."( A 28-week, randomized, double-blind study of olanzapine versus aripiprazole in the treatment of schizophrenia.
Breier, A; Kane, JM; Kryzhanovskaya, LA; Osuntokun, O; Stauffer, VL; Watson, SB; Xu, W, 2009
)
"Olanzapine treatment resulted in a consistent and statistically significant advantage in maintenance of response compared to treatment with risperidone, quetiapine and ziprasidone; but not compared to treatment with aripiprazole."( Maintenance of response with atypical antipsychotics in the treatment of schizophrenia: a post-hoc analysis of 5 double-blind, randomized clinical trials.
Ascher-Svanum, H; Ball, T; Conley, R; Liu, L; Stauffer, V, 2009
)
"Olanzapine-treated subjects had the highest insulin concentrations and the lowest SHBG, adiponectin, and cortisol concentrations."( Hormonal markers of metabolic dysregulation in patients with severe mental disorders after olanzapine treatment under real-life conditions.
Andreassen, OA; Birkeland, KI; Birkenaes, AB; Friis, S; Opjordsmoen, S, 2009
)
"Olanzapine treatment has been associated with clinically meaningful weight increases, hypertriglyceridemia, insulin resistance, and diabetes mellitus. "( Aripiprazole added to overweight and obese olanzapine-treated schizophrenia patients.
Borba, CP; Boxill, R; Cather, C; Copeland, PM; Evins, AE; Fan, X; Freudenreich, O; Goff, DC; Henderson, DC; Sharma, B, 2009
)
"On olanzapine treatment, adjusted mean prolactin levels at the 3rd and 6th months of treatment were significantly higher than at the 1st month; at the 12th month it was lower than at the 1st month, but the difference was not significant."( Short- and long-term effects on prolactin of risperidone and olanzapine treatments in children and adolescents.
D'Arrigo, C; de Leon, J; Diaz, FJ; Gagliano, A; Germanò, E; Migliardi, G; Siracusano, R; Spina, E, 2009
)
"Olanzapine-treated patients showed a significantly greater increase than risperidone-treated patients in a fasting measure of insulin resistance (P = .041), and olanzapine patients showed greater decreases in insulin sensitivity during OGTT (P = .023) compared to risperidone-treated patients."( Effects of olanzapine and risperidone on glucose metabolism and insulin sensitivity in chronic schizophrenic patients with long-term antipsychotic treatment: a randomized 5-month study.
Cornwell, J; Davis, JM; Hu, Q; Kelly, E; Khan, A; Lindenmayer, JP; Smith, RC; Vaidhyanathaswamy, S; Viviano, TF, 2009
)
"Olanzapine treatment suppressed body weight gain and decreased food intake in WT mice, but also reduced fat body mass and locomotor activity, whereas D2R(-/-) mice did not show these changes."( Effects of atypical antipsychotic drugs on body weight and food intake in dopamine D2 receptor knockout mice.
Baik, JH; Choi, SY; Noh, JS; Yoon, S, 2010
)
"Olanzapine-treated adolescents were likely to experience greater increases in bodyweight, sedation, blood lipids, serum prolactin and liver transaminase levels than olanzapine-treated adults."( Olanzapine: in adolescents with schizophrenia or bipolar I disorder.
McCormack, PL, 2010
)
"Olanzapine-treated patients gained significantly more baseline-to-endpoint weight versus risperidone- (3.3 kg [N = 713; median exposure [ME, days] = 68] versus 1.8 kg [N = 697; ME = 65], p < 0.001), ziprasidone-(2.8 kg [N = 463; ME = 168] versus -1.3 kg [N = 443; ME = 89], p < 0.001), and aripiprazole-treated patients (3.7 kg [N = 273; ME = 104] versus 0.5 kg [N = 275; ME = 187], p < 0.001)."( Metabolic parameters in patients treated with olanzapine or other atypical antipsychotics.
Acharya, N; Carlson, JL; Corya, SA; Kryzhanovskaya, LA; Millen, B; Osuntokun, O; Robertson-Plouch, C; Xu, WI, 2011
)
"Olanzapine treatment (10-100 microM) increased basal BDNF gene promoter activity in a dose-dependent manner and increased protein levels at high dose, and inhibitors of protein kinase A (PKA), H-89 (10 microM), phosphatidylinositol 3-kinase (PI3K), wortmannin (0.01 microM), PKC (protein kinase C), GF109203 (10 microM), calcium/calmodulin kinase II (CaMKII), and KN-93 (20 microM) partially attenuated the stimulatory effect of olanzapine on BDNF promoter activity. "( Effects of olanzapine on brain-derived neurotrophic factor gene promoter activity in SH-SY5Y neuroblastoma cells.
Cho, HY; Kim, YH; Lee, JG; Park, SW; Seo, MK, 2010
)
"Olanzapine-treated patients should receive regular weight monitoring."( Weight changes over time in adults treated with the oral or depot formulations of olanzapine: a pooled analysis of 86 clinical trials.
Beasley, CM; Campbell, GM; Millen, BA, 2011
)
"Olanzapine treatment did not result in an alteration of 24h food intake, but diurnal patterns of feeding behavior and body temperature were dramatically changed."( Olanzapine causes hypothermia, inactivity, a deranged feeding pattern and weight gain in female Wistar rats.
Calcagnoli, F; Evers, SS; Scheurink, AJ; van Dijk, G, 2010
)
"Olanzapine treatment was associated with statistically significantly greater total utility scores relative to aripiprazole (0.78 vs. "( Cost-effectiveness of olanzapine vs. aripiprazole in the treatment of schizophrenia.
Ascher-Svanum, H; Faries, DE; Kane, JM; Osuntokun, OO; Peng, X; Stauffer, VL; Stensland, MD, 2011
)
"Olanzapine-treated patients showed significantly greater improvements than all other groups at week 24 on all 5 PANSS factors (P = .028 for negative; P < .001 for all others) and on 3 QLS items."( Factors associated with adherence to treatment with olanzapine and other atypical antipsychotic medications in patients with schizophrenia.
Feldman, PD; Liu-Seifert, H; Osuntokun, OO, 2012
)
"Olanzapine-treated patients experienced significantly greater improvements in these specific symptoms than patients treated with the other atypical antipsychotics examined."( Factors associated with adherence to treatment with olanzapine and other atypical antipsychotic medications in patients with schizophrenia.
Feldman, PD; Liu-Seifert, H; Osuntokun, OO, 2012
)
"Olanzapine treated rats fed a chow diet grew more slowly than vehicle controls but olanzapine treated animals fed a high fat/sugar diet grew faster than control animals on the same diet."( Olanzapine effects on body composition, food preference, glucose metabolism and insulin sensitivity in the rat.
Shepherd, PR; Smith, GC; Vickers, MH, 2011
)
"Olanzapine treatment decreased the ratio index in the NOR test, whereas sertindole and clozapine had no effect in naive mice."( Effects of olanzapine, sertindole and clozapine on MK-801 induced visual memory deficits in mice.
Akar, FY; Celikyurt, IK; Erden, F; Mutlu, O; Tanyeri, P; Ulak, G, 2011
)
"Olanzapine treatment in rats promoted endocrinological changes and lesions in the testis, leading to a disturbance in spermatogenesis."( Endocrine and testicular changes induced by olanzapine in adult Wistar rats.
Amorim, MJ; Brito, LT; da Silva Junior, VA; de Amorim Júnior, AA; de Siqueira Bringel, S; de Torres, SM; Morais, RN; Tenorio, BM, 2013
)
"Olanzapine treatment resulted in increased levels of a disialylated biantennary glycan and reduced levels of a number of disialylated bi- and triantennary glycans on whole serum glycoproteins."( Antipsychotic treatment of acute paranoid schizophrenia patients with olanzapine results in altered glycosylation of serum glycoproteins.
Bahn, S; Bones, J; Doherty, M; Guest, PC; Leweke, FM; Manning, G; McManus, C; Rahmoune, H; Rothermundt, M; Rudd, PM; Saldova, R; Telford, JE, 2012
)
"Olanzapine treatment led to a significant decrease in the average intensity score of nausea from 2.4±0.7 to 0.2±0.4 (P<0.001)."( Olanzapine for the relief of nausea in patients with advanced cancer and incomplete bowel obstruction.
Kaneishi, K; Kawabata, M; Morita, T, 2012
)
"For olanzapine-treated patients, risk factors included smoking status, previous episode history, amount of time patients had a 21-Item Hamilton Depression Rating Scale (HDRS-21) score ≤ 8 at pre-randomization, and HDRS-21 score at randomization."( Variables as mediators or moderators in predicting relapse to any type of mood episode in a bipolar maintenance study.
Jen, KY; Leboyer, M; Tohen, M; Wang, WV, 2012
)
"Olanzapine treatment is associated with tolerability issues such as metabolic adverse effects (e.g."( Comparing tolerability of olanzapine in schizophrenia and affective disorders: a meta-analysis.
Brunelle, S; Moteshafi, H; Stip, E; Zhornitsky, S, 2012
)
"For olanzapine treated animals, weight gain was significantly greater in the minipump sample compared to both s.c."( Chronic olanzapine administration in rats: effect of route of administration on weight, food intake and body composition.
Chintoh, A; Fletcher, P; Giacca, A; Hahn, M; Mann, S; Nobrega, J; Remington, G, 2013
)
"The olanzapine-treated patients showed a significantly lower maximal DFEN-evoked PRL response and a significantly lower group x time overall PRL release compared with the untreated patient group."( D-fenfluramine-evoked serotonergic responses in olanzapine-treated schizophrenic patients.
Curtis, VA; Jones, H; Lucey, JV; Pilowsky, LS; Wright, P, 2002
)
"Olanzapine treated subjects achieved statistically significantly greater rates of clinical response, euthymia and remission than those assigned to placebo, 55% versus 29.5%, 50% versus 27%, and 18% versus 7%, respectively."( Rates of response, euthymia and remission in two placebo-controlled olanzapine trials for bipolar mania.
Baker, RW; Chengappa, KN; Gershon, S; Kupfer, DJ; Shao, L; Tohen, M; Yatham, LN, 2003
)
"The olanzapine treatment of schizophrenia was characterised by significant antipsychotic efficacy including both positive and negative symptoms. "( [Effect of olanzapine treatment on cognitive functions in patients with schizophrenia].
Lis, J; Radziwiłłowicz, P; Radziwiłłowicz, W,
)
"Olanzapine-treated patients showed a significantly greater reduction in Positive and Negative Syndrome Scale (PANSS) total, Brief Psychiatric Rating Scale (BPRS) total, and PANSS General Psychopathology scores at endpoint compared to the risperidone-treated patients."( Olanzapine vs risperidone in the management of schizophrenia: a randomized double-blind trial in Australia and New Zealand.
Andersen, S; Catts, S; Crawford, AM; Fraser, A; Grainger, D; Gureje, O; Hustig, H; Keks, N; Lambert, T; McGrath, J; Miles, W; Tran, P, 2003
)
"Olanzapine-treated patients also showed significantly improved AWAD scores."( Safety, effectiveness, and quality of life of olanzapine in first-episode schizophrenia: a naturalistic study.
Ciudad, A; Gascón, J; Gómez, JC; Montes, JM, 2003
)
"Olanzapine-treated patients experienced a lower rate of treatment-emergent parkinsonism and akathisia but had significantly more weight gain, compared with the haloperidol-treated patients."( Comparative efficacy and safety of atypical and conventional antipsychotic drugs in first-episode psychosis: a randomized, double-blind trial of olanzapine versus haloperidol.
Green, AI; Gur, RE; Hamer, RM; Kahn, R; Lieberman, JA; McEvoy, J; Perkins, D; Sharma, T; Tohen, M; Tollefson, G; Wei, H; Zipursky, R, 2003
)
"Olanzapine-treated patients experienced significantly greater reductions in Simpson-Angus Scale scores than did haloperidol- (p <.001), risperidone- (p <.001), or clozapine-treated (p =.032) patients."( An integrated analysis of acute treatment-emergent extrapyramidal syndrome in patients with schizophrenia during olanzapine clinical trials: comparisons with placebo, haloperidol, risperidone, or clozapine.
Beasley, CM; Berg, PH; Carlson, CD; Cavazzoni, PA; Kane, JM; Wei, H, 2003
)
"The olanzapine-treated patients showed significant improvement in both the positive and negative symptoms of schizophrenia by the end of the study."( Olanzapine in Chinese treatment-resistant patients with schizophrenia: an open-label, prospective trial.
Chang, CC; Chen, PS; Chiu, NY; Lee, IH; Lee, JR; Yang, YK, 2003
)
"Olanzapine may be a treatment option for patients who fail to respond to treatment with other antipsychotics. "( Switching treatment-resistant patients with schizophrenia or schizoaffective disorder to olanzapine: a one-year open-label study with five-year follow-up.
Karagianis, JL; LeDrew, KK; Walker, DJ, 2003
)
"olanzapine treatment, compared with a general worsening during i.m."( Intramuscular olanzapine and intramuscular haloperidol in acute schizophrenia: antipsychotic efficacy and extrapyramidal safety during the first 24 hours of treatment.
Alaka, K; Battaglia, J; Birkett, M; Bitter, I; Breier, A; Chouinard, G; Ferchland-Howe, I; Jones, B; Lindborg, SR; Meehan, K; Morris, PL; Pickard, A; Roth, J; Taylor, CC; Wright, P, 2003
)
"Olanzapine-treated patients had significantly higher plasma triglyceride concentrations (2.01 +/-1.05 vs."( Development of an atherogenic metabolic risk factor profile associated with the use of atypical antipsychotics.
Alméras, N; Bouchard, RH; Cadrin, C; Demers, MF; Després, JP; Mottard, JP; Roy, MA; Villeneuve, J, 2004
)
"Olanzapine treatment led to rapid phosphorylation of kinases from all three pathways in PC12 cells."( Olanzapine produces trophic effects in vitro and stimulates phosphorylation of Akt/PKB, ERK1/2, and the mitogen-activated protein kinase p38.
Bradley, RJ; Dwyer, DS; Lu, XH, 2004
)
"Olanzapine treatment is associated with substantial weight gain. "( The effect of famotidine addition on olanzapine-induced weight gain in first-episode schizophrenia patients: a double-blind placebo-controlled pilot study.
Fuchs, C; Gil-Ad, I; Maayan, R; Poyurovsky, M; Tal, V; Weizman, A, 2004
)
"Olanzapine treatment was more beneficial for patients; comparing to other antipsychotic treatment less extrapyramidal symptoms and sexual dysfunctions were observed."( [Prospective observational study of outpatients with schizophrenia in Poland: preliminary 6 month efficacy and tolerability results].
Araszkiewicz, A; Debowska, G; Kolesaric, A; Lis, J; Meder, J; Sierosławska, K; Treuer, T,
)
"Olanzapine-treated patients should be monitored with glucose, lipid, pancreatic function and liver function tests, and the olanzapine should be discontinued if the results of these tests worsen."( Olanzapine-induced pancreatitis: a case report.
Carlsson, H; Nielsen, EW; Waage, C, 2004
)
"Olanzapine-treated patients experienced modest but significant improvement in PANSS-Cognitive score (olanzapine: -4.25 n = 124; placebo: -1.69 n = 120, p < 01), regardless of age, gender, mania subtype (pure, mixed), course (rapid or non-rapid cycling), or the presence or absence of psychotic features. "( Improvement of Positive and Negative Syndrome Scale cognitive score associated with olanzapine treatment of acute mania.
Huang, LX; Namjoshi, MA; Schuh, LM; Shi, L; Tohen, M; Trzepacz, PT, 2004
)
"Olanzapine or fluoxetine treatment also increased the number of proliferating cells in the prelimbic cortex."( Chronic olanzapine or fluoxetine administration increases cell proliferation in hippocampus and prefrontal cortex of adult rat.
Duman, RS; Fujioka, T; Kodama, M, 2004
)
"Olanzapine treatment was either initiated or patients were switched from other antipsychotics to olanzapine. "( [Subjective and objective evaluation of olanzapine treatment in schizophrenia].
Jarema, M; Murawiec, S; Tafliński, T,
)
"Olanzapine treatment of patients suffering from schizophrenia proved to be efficacious in both objective and subjective evaluation."( [Subjective and objective evaluation of olanzapine treatment in schizophrenia].
Jarema, M; Murawiec, S; Tafliński, T,
)
"Olanzapine-treated patients had a significant reduction in extrapyramidal symptoms and subjective measures of stiffness and dry mouth, but the increases in systolic blood pressure and weight in olanzapine-treated patients were significantly greater than they were in haloperidol-treated patients."( Olanzapine treatment of residual positive and negative symptoms.
Ball, MP; Buchanan, RW; Carpenter, WT; Gold, JM; Kirkpatrick, B; McMahon, RP; Weiner, E, 2005
)
"Olanzapine-treated patients exhibited significant weight increases, whereas ziprasidone-treated patients exhibited weight loss."( Comparison of the metabolic effects observed in patients treated with ziprasidone versus olanzapine.
Brown, RR; Estoup, MW, 2005
)
"Olanzapine treatment reduced development of ABA in rats by reducing running wheel activity, starvation-induced hypothermia and activation of the hypothalamus-pituitary-adrenal axis. "( Olanzapine reduces physical activity in rats exposed to activity-based anorexia: possible implications for treatment of anorexia nervosa?
Adan, RA; Hillebrand, JJ; Kas, MJ; van Elburg, AA; van Engeland, H, 2005
)
"Olanzapine treatment reduced wheel running and thereby diminished development of ABA in rats. "( Olanzapine reduces physical activity in rats exposed to activity-based anorexia: possible implications for treatment of anorexia nervosa?
Adan, RA; Hillebrand, JJ; Kas, MJ; van Elburg, AA; van Engeland, H, 2005
)
"Olanzapine-treated patients were more likely to report reduced social and family interaction, as well as reduced sexual behavior and less participation in active recreational and pastime activities."( Patients' opinions of olanzapine and risperidone following long-term treatment: results from a cross-sectional survey.
McGrath, BM; Tempier, RP, 2005
)
"Olanzapine treatment resulted in significantly greater psychopathology improvement and higher response and completion rates than ziprasidone treatment, while ziprasidone was superior for weight change and lipid profile."( Olanzapine versus ziprasidone: results of a 28-week double-blind study in patients with schizophrenia.
Berg, PH; Breier, A; Cavazzoni, P; Gattaz, WF; Kane, JM; Naber, D; Roychowdhury, SM; Thakore, JH; Walker, DJ, 2005
)
"Olanzapine treatment was associated with increased rates of slow (70.4% vs."( Electroencephalogram slowing, sleepiness and treatment response in patients with schizophrenia during olanzapine treatment.
Jernajczyk, W; Szafranski, T; Waliniowska, E; Wichniak, A; Wierzbicka, A, 2006
)
"Olanzapine-treated, non-rapid cyclers experienced greater mania improvement than rapid cyclers."( Rapid versus non-rapid cycling as a predictor of response to olanzapine and divalproex sodium for bipolar mania and maintenance of remission: post hoc analyses of 47-week data.
Baker, RW; Brown, E; Schuh, LM; Suppes, T; Tohen, M, 2005
)
"The olanzapine-treated group also had lower, but not statistically significant, PANSS General Psychopathology Subscale scores and fewer positive urine toxicology screens compared with those in the haloperidol group."( The efficacy of olanzapine for decreasing cue-elicited craving in individuals with schizophrenia and cocaine dependence: a preliminary report.
Kaune, M; Losonczy, MF; Smelson, DA; Steinberg, ML; Williams, J; Ziedonis, D, 2006
)
"Olanzapine-treated patients experienced significantly lower eosinophil counts and higher elevations in low-density lipoproteins and standing blood pressure than non-switched patients."( Improvement in hyperprolactinemia and reproductive comorbidities in patients with schizophrenia switched from conventional antipsychotics or risperidone to olanzapine.
Ahl, J; Kinon, BJ; Liu-Seifert, H; Maguire, GA, 2006
)
"Olanzapine-treated patients experienced significantly (P < 0.05) greater increases in triglycerides, HgbA1c, and weight."( A 24-week randomized study of olanzapine versus ziprasidone in the treatment of schizophrenia or schizoaffective disorder in patients with prominent depressive symptoms.
Adams, DH; Ascher-Svanum, H; Edwards, SB; Kinon, BJ; Lipkovich, I; Siris, SG, 2006
)
"Olanzapine treatment was found to have significantly better effects than typical agents on negative and depressive symptom scores, and significantly greater improvements than risperidone on negative and cognitive symptoms."( Treatment with olanzapine, risperidone or typical antipsychotic drugs in Asian patients with schizophrenia.
Dyachkova, Y; Habil, H; Lee, C; Lee, P; Wu, KH, 2006
)
"Olanzapine treatment reduced nocturnal plasma melatonin by 55% (p<0.001), which was restored to control levels by olanzapine+melatonin."( Olanzapine-induced weight gain and increased visceral adiposity is blocked by melatonin replacement therapy in rats.
Burke, BL; Crites, NJ; Raskind, MA; Rasmussen, DD; Tapp, AM, 2007
)
"Olanzapine-treated patients had significantly higher mean fasting triglyceride levels (2.3 +/- 1.8 mmol/L) than risperidone- (1.7 +/- 0.9 mmol/L, P = 0.022), but not typical antipsychotic-treated patients (1.8 +/- 1 mmol/L)."( Cross-sectional comparison of fasting lipids in normoglycemic patients with schizophrenia during chronic treatment with olanzapine, risperidone, or typical antipsychotics.
Cavazzoni, P; Hardy, TA; Kryzhanovskaya, L; Marquez, E; Taylor, CC, 2006
)
"Olanzapine-treated patients showed significantly greater improvement on positive symptoms and on several measures of functioning including Global Assessment of Functioning Scale, Quality of Life Instrumental Role domain, and level of effort in psychosocial or occupational rehabilitation programs."( Randomized, double-blind 6-month comparison of olanzapine and quetiapine in patients with schizophrenia or schizoaffective disorder with prominent negative symptoms and poor functioning.
Ascher-Svanum, H; Gulliver, AH; Kinon, BJ; Kollack-Walker, S; Liu-Seifert, H; Noordsy, DL, 2006
)
"Olanzapine-treated patients reported more extrapyramidal symptoms (EPS)-related adverse events (18%) than aripiprazole-treated patients (10%)."( Effectiveness of long-term aripiprazole therapy in patients with acutely relapsing or chronic, stable schizophrenia: a 52-week, open-label comparison with olanzapine.
Chrzanowski, WK; Marcus, RN; McQuade, RD; Nyilas, M; Torbeyns, A, 2006
)
"Olanzapine-treated patients had significantly more weight gain compared with the haloperidol and risperidone groups (p < .001)."( A practical clinical trial comparing haloperidol, risperidone, and olanzapine for the acute treatment of first-episode nonaffective psychosis.
Crespo-Facorro, B; Llorca, J; Luis Vázquez-Barquero, J; Martínez-García, O; Pérez-Iglesias, R; Ramirez-Bonilla, M, 2006
)
"Olanzapine-treated patients had greater HAM-D-21 (p = .040) and CGI-BP (p = .026) score improvement across the study."( Olanzapine versus risperidone in the treatment of manic or mixed States in bipolar I disorder: a randomized, double-blind trial.
Baker, RW; Brown, EB; Jamal, HH; Perlis, RH; Schuh, LM; Tohen, M; Zarate, CA, 2006
)
"Olanzapine/reboxetine-treated patients showed a significantly lower increase in body weight (mean = 3.31 kg, SD = 2.73) than their olanzapine/placebo-treated counterparts (mean = 4.91 kg, SD = 2.45)."( Attenuating effect of reboxetine on appetite and weight gain in olanzapine-treated schizophrenia patients: a double-blind placebo-controlled study.
Faragian, S; Fuchs, C; Gil-Ad, I; Levi, A; Maayan, R; Pashinian, A; Poyurovsky, M, 2007
)
"The olanzapine-treated group showed statistically significant improvements: PANSS-EC (F=122.9; df=2.4; p=0.000), ACES (F=68.2; df=2.8; p=0.000)."( Olanzapine orally-disintegrating tablet in severe psychotic agitation: a naturalistic study.
Alvarez, E; Martín, JL; Pascual, JC; Pérez, V; Puigdemont, D; Safont, G,
)
"Olanzapine-treated patients experienced more weight gain than the haloperidol-treated group (F = 7.044, df = 1,33; p ( A randomized controlled trial of olanzapine versus haloperidol in the treatment of primary negative symptoms and neurocognitive deficits in schizophrenia.
Abad, MT; Iskander, A; Khan, A; Lindenmayer, JP; Parker, B, 2007
)
"Olanzapine treatment for 24 h increased the levels of 5-HT(2A) receptors in both cytosol (234 +/- 34% of control level) and membrane fractions (206 +/- 14% of control levels) and RGS7 proteins in both cytosol (193 +/- 32% of control levels) and membrane fractions (160 +/- 18% of control levels) as measured on Western blots."( Olanzapine increases RGS7 protein expression via stimulation of the Janus tyrosine kinase-signal transducer and activator of transcription signaling cascade.
Muma, NA; Shi, J; Singh, RK; Zemaitaitis, BW, 2007
)
"One olanzapine-treated patient was diagnosed with diabetes."( Metabolic control in patients with schizophrenia treated with amisulpride or olanzapine.
De Hert, M; Mortimer, A; Peuskens, J, 2007
)
"Olanzapine-treated SZ patients carrying the ancestral homozygote genotype showed a higher BMI for rs7973796 (P = 0.016 with the LSMeans t-test) than the variant homozygotes."( Possible association of the pro-melanin-concentrating hormone gene with a greater body mass index as a side effect of the antipsychotic olanzapine.
Bouchard, RH; Bureau, A; Chagnon, YC; Gendron, D; Maziade, M; Mérette, C; Roy, MA, 2007
)
"Olanzapine treatment resulted in no significant change in right or left hippocampal volume. "( A longitudinal study on the effects of typical versus atypical antipsychotic drugs on hippocampal volume in schizophrenia.
Barr, AM; Honer, WG; Khorram, B; Kopala, LC; Lang, DJ; Panenka, WJ; Smith, GN; Vandorpe, RA, 2007
)
"Olanzapine-treated patients showed significantly greater baseline-to-end point mean improvements in the primary efficacy measure, Brief Psychiatric Rating Scale total, compared with chlorpromazine-treated patients (least-squares means: olanzapine, -21.1; chlorpromazine, -10.4; P < 0.001)."( Olanzapine versus chlorpromazine in the treatment of schizophrenia: a pooled analysis of four 6-week, randomized, open-label studies in the Middle East and North Africa.
Dominguez, S; Dossenbach, M; Huang, X; Kryzhanovskaya, L; Saylan, M; Treuer, T, 2007
)
"With olanzapine treatment, RGS4 protein levels increase in the membrane-fraction and decrease in the cytosolic fraction by similar amounts suggesting a redistribution of RGS4 protein within neurons."( Chronic olanzapine activates the Stat3 signal transduction pathway and alters expression of components of the 5-HT2A receptor signaling system in rat frontal cortex.
Battaglia, G; D'Souza, DN; Damjanoska, KJ; Garcia, F; Muma, NA; Singh, RK; Van de Kar, LD; Vercillo, MS; Zemaitaitis, B; Zhang, Y, 2007
)
"All olanzapine-treated groups demonstrated significant increases in food intake (P<0.001)."( Ziprasidone and aripiprazole attenuate olanzapine-induced hyperphagia in rats.
Neill, JC; Reynolds, GP; Snigdha, S; Thumbi, C, 2008
)
"Olanzapine pretreatment significantly attenuated thioperamide-induced hypophagia."( Comparative effects of olanzapine and ziprasidone on hypophagia induced by enhanced histamine neurotransmission in the rat.
Clifton, PG; Davoodi, N; Kalinichev, M, 2008
)
"Olanzapine treatment resulted in improvements in positive and general psychiatric symptoms, as well as quality of life. "( Clinical and pharmacoeconomic evaluation of switch to olanzapine in veterans with schizophrenia or schizoaffective disorder.
Ambrose, SM; Cates, ME; Davis, LL; Johnson, JD; Kashner, TM; Lowe, JS; Thomas, BL; Ward, LC; Williford, RB, 2008
)
"Olanzapine treatment for agitation and psychosis related to Alzheimer's disease is cost effective when compared with no treatment. "( A markov model of the cost effectiveness of olanzapine treatment for agitation and psychosis in Alzheimer's disease.
Kirbach, S; Mintzer, J; Nietert, PJ; Simpson, K, 2008
)
"Olanzapine treated patients had similar levels of striatal D2 binding in vivo (1.41 +/- 0.06) as those treated with clozapine (1.49 +/- 0.04)."( Dopamine D2 receptor occupancy in vivo by the novel atypical antipsychotic olanzapine--a 123I IBZM single photon emission tomography (SPET) study.
Busatto, GF; Costa, DC; Ell, PJ; Kerwin, RW; Nohria, V; Pilowsky, LS; Sharma, T; Sigmundsson, T; Taylor, M, 1996
)
"The olanzapine-treated patients had fewer motor and cardiovascular side effects than the chlorpromazine-treated patients."( Olanzapine compared with chlorpromazine in treatment-resistant schizophrenia.
Bartko, JJ; Conley, RR; Gounaris, C; Hegerty, J; Lingle, J; Love, R; Peszke, M; Richardson, C; Tamminga, CA; Zaremba, S, 1998
)
"Olanzapine-treated patients had fewer side effects than chlorpromazine-treated patients."( Olanzapine compared with chlorpromazine in treatment-resistant schizophrenia.
Bartko, JJ; Conley, RR; Gounaris, C; Hegerty, J; Lingle, J; Love, R; Peszke, M; Richardson, C; Tamminga, CA; Zaremba, S, 1998
)
"Olanzapine-treated subjects experienced less relapse (P = 0.034). "( Oral olanzapine versus oral haloperidol in the maintenance treatment of schizophrenia and related psychoses.
Beasley, CM; Dellva, MA; Tollefson, GD; Tran, PV; Wentley, AL, 1998
)
"Olanzapine-treated patients further showed statistically significant improvements in the Simpson-Angus scale and Barnes Akathisia Scale scores, while haloperidol-treated patients showed a worsening on both measures."( Olanzapine versus haloperidol treatment in first-episode psychosis.
Beasley, C; Grundy, S; Lieberman, JA; Sanger, TM; Tohen, M; Tollefson, GD, 1999
)
"Olanzapine-treated patients achieved a statistically significant greater improvement than haloperidol treated patients on overall measures of efficacy, including clinical response. "( Olanzapine versus haloperidol in the treatment of schizoaffective disorder. Acute and long-term therapy.
Beasley, CM; Berg, PH; Lu, Y; Sanger, TM; Tollefson, GD; Tran, PV, 1999
)
"Olanzapine-treated patients improved in 5 of 8 domains to a significantly greater degree than did haloperidol patients."( Reliability, validity, and application of the medical outcomes study 36-item short-form health survey (SF-36) in schizophrenic patients treated with olanzapine versus haloperidol.
Croghan, TW; Heilman, DK; Johnstone, BM; Obenchain, RL; Tunis, SL, 1999
)
"Olanzapine treated subjects showed reduced day 4 deficit (compared with day 1), with no significant difference from placebo beyond 6 h post dose."( A comparison of the effects of olanzapine, haloperidol and placebo on cognitive and psychomotor functions in healthy elderly volunteers.
Beuzen, JN; Taylor, N; Wesnes, K; Wood, A, 1999
)
"Olanzapine treatment was initiated at 5 mg daily and was increased based on clinical judgement up to a maximum of 40 mg daily."( Olanzapine for patients with treatment-resistant schizophrenia: a naturalistic case-series outcome study.
Bird, DC; Dursun, SM; Flinn, J; Gardner, DM, 1999
)
"Olanzapine treatment in the acute phase led to significantly lower inpatient ($US5125 vs $US5795, p = 0.038) and outpatient ($US663 vs $US692, p = 0.001) costs, resulting in a significant overall reduction in mean total medical costs of $US388 (p = 0.033)."( Clinical and economic outcomes of olanzapine compared with haloperidol for schizophrenia. Results from a randomised clinical trial.
Edgell, ET; Genduso, LA; Hamilton, SH; Revicki, DA; Tollefson, G, 1999
)
"Olanzapine-treated patients (205 +/- 142 days) experienced significantly (p < 0.001) longer evaluation periods than haloperidol-treated patients (132 +/- 129 days)."( [Economic comparison of olanzapine versus haloperidol in treatment of schizophrenia in France].
Allicar, MP; Gregor, KJ; Le Pen, C; Lilliu, H; Olivier, V,
)
"Olanzapine treatment was associated with significantly better clinical outcomes and per diem total direct medical cost than haloperidol treatment. "( [Economic comparison of olanzapine versus haloperidol in treatment of schizophrenia in France].
Allicar, MP; Gregor, KJ; Le Pen, C; Lilliu, H; Olivier, V,
)
"Olanzapine-treated patients had serum anticholinergic levels that were less than one fifth those of the clozapine-treated patients."( Anticholinergic differences among patients receiving standard clinical doses of olanzapine or clozapine.
Brar, JS; Chengappa, KN; Kirshner, MA; Levine, J; Parepally, H; Pollock, BG; Zoretich, RA, 2000
)
"Olanzapine treatment was started, in dose 10 mg a day."( [A case of mania following olanzapine administration].
Borysewicz, K; Borysewicz, W,
)
"Olanzapine-treated patients demonstrated a statistically significant greater mean (+/- SD) improvement in Y-MRS total score than placebo-treated patients (-14.8 +/- 12.5 and -8.1 +/- 12.7, respectively; P<.001), which was evident at the first postbaseline observation 1 week after randomization and was maintained throughout the study (last observation carried forward). "( Efficacy of olanzapine in acute bipolar mania: a double-blind, placebo-controlled study. The Olanzipine HGGW Study Group.
Banov, MC; Breier, A; Francis, J; Grundy, SL; Jacobs, TG; Janicak, PG; McElroy, SL; Risser, R; Sanger, T; Tohen, M; Tollefson, GD; Toma, V; Zhang, F, 2000
)
"Olanzapine-treated patients experienced superior improvements compared to haloperidol-treated patients on all efficacy measures assessed in both phases."( Functional outcomes in schizophrenia: a comparison of olanzapine and haloperidol in a European sample.
Breier, A; Edgell, ET; Hamilton, SH; Revicki, DA, 2000
)
"Olanzapine treatment was associated with weight gain and elevated levels of insulin, leptin, and blood lipids as well as insulin resistance, with 3 patients diagnosed to have diabetes mellitus. "( Elevated levels of insulin, leptin, and blood lipids in olanzapine-treated patients with schizophrenia or related psychoses.
Brismar, KE; Hulting, AL; Melkersson, KI, 2000
)
"Olanzapine-treated patients were more likely to maintain response compared with risperidone-treated patients (p = 0.048)."( Olanzapine versus risperidone. A prospective comparison of clinical and economic outcomes in schizophrenia.
Andersen, SW; Breier, A; Dulisse, B; Edgell, ET; Johnstone, BM; Revicki, D, 2000
)
"In olanzapine-treated patients, improvement in BPRS agitation and positive symptom scores was significantly greater at weeks 4, 5, and 6 (agitation scores, p < or = .01; positive symptom scores, p < .05) (OC)."( Effective resolution with olanzapine of acute presentation of behavioral agitation and positive psychotic symptoms in schizophrenia.
Hill, AL; Kinon, BJ; Milton, DR; Roychowdhury, SM, 2001
)
"Olanzapine-treated patients exhibited statistically significantly greater improvements from baseline (last observation carried forward) on all efficacy measurements. "( Superior efficacy of olanzapine over haloperidol: analysis of patients with schizophrenia from a multicenter international trial.
Crawford, AM; Gomez, JC, 2001
)
"Olanzapine treatment for patients with delirium was effective and safe."( An open pilot trial of olanzapine for delirium in the Korean population.
Bahk, WM; Chae, JH; Jun, T; Kim, KS; Pae, CU, 2001
)
"Olanzapine treatment was associated with significant improvement in mean YMRS score (-19.0 +/- 9.2, p < 0.001)."( A prospective open-label treatment trial of olanzapine monotherapy in children and adolescents with bipolar disorder.
Biederman, J; Feldman, PD; Frazier, JA; Garfield, SB; Gonzalez-Heydrich, J; Jacobs, TG; Kim, GS; Nowlin, ZM; Rater, MA; Risser, RC; Sohma, M; Tarazi, RA; Tohen, M; Toma, V, 2001
)
"Olanzapine-treated patients had significantly higher DAI-10 scores and significantly better treatment compliance compared to both risperidone- and haloperidol-treated patients."( Subjective response to antipsychotic treatment and compliance in schizophrenia. A naturalistic study comparing olanzapine, risperidone and haloperidol (EFESO Study).
Edgell, E; García-Cabeza, I; Gómez, JC; González de Chavez, M; Sacristán, JA, 2001
)
"Olanzapine-treated subjects used less as needed (PRN) antipsychotic medication compared to pre-olanzapine treatment period."( The use of concomitant medications in psychiatric inpatients treated with either olanzapine or other antipsychotic agents: a naturalistic study at a state psychiatric hospital.
Atzert, R; Baird, JW; Brar, JS; Chakravorty, S; Chalasani, L; Chengappa, KN; Delaney, JA; Levine, J; Parepally, H; Patel, AM, 2002
)
"The olanzapine treatment group had significantly greater mean improvement of mania ratings and a significantly greater proportion of patients achieving protocol-defined remission, compared with the divalproex treatment group. "( Olanzapine versus divalproex in the treatment of acute mania.
Altshuler, LL; Baker, RW; Breier, A; Gilmore, JA; Ketter, TA; Milton, DR; Risser, R; Suppes, T; Tohen, M; Tollefson, GA; Zarate, CA, 2002
)
"Treatment with olanzapine (6 mg/kg, intraperitoneally) or fenofibrate (100 mg/kg, orally) have been started 5 weeks after isolation, then behavioral tests, hippocampal content of neurotransmitters, and brain-derived neurotrophic factor (BDNF) were assessed."( Fenofibrate ameliorates olanzapine's side effects without altering its central effect: emphasis on FGF-21-adiponectin axis.
Ali, AA; El-Bakly, WM; El-Demerdash, E; El-Kilany, SS; Galal, A, 2021
)
"Treatment with olanzapine/quetiapine occurred in 18,317 of the cohort."( Associations between off-label low-dose olanzapine or quetiapine and cardiometabolic mortality.
Abri, P; Andell, P; Berge, J; Movahed, P; Ragazan, DC, 2022
)
"Treatment with olanzapine depot is associated with a rare but potentially adverse reaction, namely post-injection delirium/sedation syndrome (PDSS), characterized by delirium and/or sedation. "(
Alaoui-Ismaili, Z; Baandrup, L; Barzanji, AF; Mohammad, M, 2023
)
"For treatment, olanzapine appears to be nearly universally effective at low doses, but randomized trial evidence is lacking."( Prevention of Steroid-Induced Neuropsychiatric Complications With Neuroleptic Drugs: A Review.
Akid, I; Bienvenu, OJ; Nanavati, J; Nesbit, S; Smith, TJ, 2022
)
"Cotreatment with olanzapine blocked the anorexigenic effect of peripheral, but not central estradiol."( Lack of Ovarian Secretions Reverts the Anabolic Action of Olanzapine in Female Rats.
Berge, RK; Fernø, J; González-García, I; López, M; Martins, L; Mellgren, G; Nogueiras, R; Skrede, S; Steen, VM; Tena-Sempere, M, 2017
)
"Treatment with olanzapine (0.5 mg/kg) for the duration of 14 days produced a significant increase in food intake and body weight as compared to control."( A role of neuropeptide CART in hyperphagia and weight gain induced by olanzapine treatment in rats.
Kokare, DM; Nakhate, KT; Subhedar, NK, 2018
)
"Treatment with olanzapine plus samidorphan resulted in a statistically significant lower weight gain (37% lower weight gain compared with olanzapine plus placebo)."( Mitigation of Olanzapine-Induced Weight Gain With Samidorphan, an Opioid Antagonist: A Randomized Double-Blind Phase 2 Study in Patients With Schizophrenia.
Correll, CU; DiPetrillo, L; Ehrich, EW; Jiang, Y; Martin, WF; Pathak, S; Silverman, BL; Weiden, PJ, 2019
)
"Pretreatment with olanzapine blocked MK-801-induced disruption of PPI."( Atypical antipsychotic olanzapine reversed deficit on prepulse inhibition of the acoustic startle reflex produced by microinjection of dizocilpine (MK-801) into the inferior colliculus in rats.
Carvalheira, R; Labbate, G; Longo, BM; Medeiros, P; Melo-Thomas, L; Silva, RC; Zangrando, J, 2013
)
"Treatment with olanzapine, risperidone and clozapine is often associated with weight gain."( Atypical antipsychotics for psychosis in adolescents.
Datta, SS; Furtado, VA; Kumar, A; Russell, PS; Wright, SD, 2013
)
"Treatment with olanzapine caused a significant decrease in hippocampal volume in sedentary rats."( Effects of chronic exercise and treatment with the antipsychotic drug olanzapine on hippocampal volume in adult female rats.
Barr, AM; Beasley, CL; Boyda, HN; Hercher, C; Honer, WG; Procyshyn, RM; Töpfer, E; Wong, C; Wu, CH, 2013
)
"Treatment with olanzapine relieved her psychotic symptoms but caused severe dystonias, daily myoclonic jerks, and tremors."( Topiramate improves psychiatric symptoms in a patient with Lewy body dementia.
Ochoa, JG, 2014
)
"Treatment with olanzapine had only a modest effect in altering the trajectory of weight loss."( Olanzapine for cachexia in patients with advanced cancer: an exploratory study of effects on weight and metabolic cytokines.
Abdelrahim, M; Dalal, S; Falchook, GS; Fu, S; Hess, K; Hong, DS; Ilustre, A; Janku, F; Kurzrock, R; Naing, A; Ouyang, F; Wheler, J, 2015
)
"Treatment with olanzapine OST and ODT similarly increased the 12h mean PRL concentrations and the secreted PRL mass."( Olanzapine shifts the temporal relationship between the daily acrophase of serum prolactin and cortisol concentrations rhythm in healthy men.
Frolich, M; Pijl, H; Roelfsema, F; Vidarsdottir, S, 2009
)
"Treatment with olanzapine/sertraline was associated with higher remission rates during the trial than olanzapine/placebo (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.12-1.47; P < .001); 41.9% of subjects who underwent combination therapy were in remission at their last assessment compared with 23.9% of subjects treated with monotherapy (chi(2)(1) = 9.53, P = .002). "( A double-blind randomized controlled trial of olanzapine plus sertraline vs olanzapine plus placebo for psychotic depression: the study of pharmacotherapy of psychotic depression (STOP-PD).
Flint, AJ; Heo, M; Leon, AC; Meyers, BS; Mulsant, BH; Papademetriou, E; Peasley-Miklus, C; Rothschild, AJ; Whyte, EM, 2009
)
"Treatment with olanzapine (atypical antipsychotic drug) is frequently associated with various metabolic anomalies, including obesity, dyslipidemia, and diabetes mellitus. "( Short-term treatment with olanzapine does not modulate gut hormone secretion: olanzapine disintegrating versus standard tablets.
Holst, JJ; Pijl, H; Rehfeld, JF; Roelfsema, F; Streefland, T; Vidarsdottir, S, 2010
)
"Treatment with olanzapine was associated with increases in DMN connectivity with ventromedial prefrontal cortex, but not in posterior regions of DMN."( Treatment with olanzapine is associated with modulation of the default mode network in patients with Schizophrenia.
Bertolino, A; Blasi, G; Caforio, G; Di Giorgio, A; Fazio, L; Gelao, B; Lo Bianco, L; Nardini, M; Papazacharias, A; Popolizio, T; Romano, R; Sambataro, F; Taurisano, P, 2010
)
"Treatment with olanzapine is associated with obesity, diabetes mellitus, and dyslipidemia. "( Orally disintegrating and oral standard olanzapine tablets similarly elevate the homeostasis model assessment of insulin resistance index and plasma triglyceride levels in 12 healthy men: a randomized crossover study.
Frölich, M; Pijl, H; Roelfsema, F; Vidarsdottir, S; Vlug, P, 2010
)
"Treatment with olanzapine ODT and OST equally elevated the homeostasis model assessment of insulin resistance (HOMA-IR) (P = .005). "( Orally disintegrating and oral standard olanzapine tablets similarly elevate the homeostasis model assessment of insulin resistance index and plasma triglyceride levels in 12 healthy men: a randomized crossover study.
Frölich, M; Pijl, H; Roelfsema, F; Vidarsdottir, S; Vlug, P, 2010
)
"Treatment with olanzapine was continued for 10 weeks, with weekly tests of metabolic indices."( Intermittent treatment with olanzapine causes sensitization of the metabolic side-effects in rats.
Barr, AM; Boyda, HN; Honer, WG; Pang, CC; Procyshyn, RM; Tse, L; Wong, D, 2012
)
"Only treatment with olanzapine 5-10 mg/d was associated with significantly greater mean change from baseline to endpoint in ZAN-BPD total score relative to placebo (-8.5 vs -6.8, respectively; P = .010; effect size = 0.29; 95% CI, 0.06-0.52)."( A dose comparison of olanzapine for the treatment of borderline personality disorder: a 12-week randomized, double-blind, placebo-controlled study.
Corya, S; Deberdt, W; Detke, HC; Kryzhanovskaya, L; Lin, D; Schulz, SC; Tanaka, Y; Zanarini, MC; Zhao, F, 2011
)
"Treatment with olanzapine had a greater effect on multiple domains of psychosocial functioning compared with placebo, suggesting that in addition to improving manic symptoms, pharmacologic interventions may lessen some of psychosocial deficits experienced by adolescents with bipolar disorder."( Health-related quality of life as measured by the child health questionnaire in adolescents with bipolar disorder treated with olanzapine.
Bitter, SM; Case, M; Chang, K; DelBello, MP; Findling, RL; Ganocy, SJ; Olsen, BT; Tohen, M, 2012
)
"Rats treated with olanzapine exhibited significant body weight gain and increased food intake."( Reducing olanzapine-induced weight gain side effect by using betahistine: a study in the rat model.
Deng, C; Huang, XF; Lian, J; Pai, N, 2012
)
"Treatment with olanzapine, 5HT-2 and D1/ D2 antagonist, significantly improved the clinical picture as Boyd et al. "( Stuttering treated with olanzapine: a case report.
Mozos-Ansorena, A; Pérez-García, M; Pérez-Pérez, J; Portela-Traba, B; Tabernero-Lado, A,
)
"The treatment with olanzapine enabled most of the youngsters to continue school."( [Olanzapine in the first episode of schizophrenia in young adults].
Dabkowska, M,
)
"Treatment with olanzapine and risperidone were identified as risk factors of weight gain versus haloperidol."( Weight gain in patients with schizophrenia treated with risperidone, olanzapine, quetiapine or haloperidol: results of the EIRE study.
Bobes, J; Fernández, I; Garcia-Garcia, M; García-Portilla, MP; Hernández, G; Rejas, J; Rico-Villademoros, F, 2003
)
"Treatment with olanzapine was associated with a better response over risperidone on the psychological domain of the World Health Organisation-Quality Of Life [Brief] (WHO-QOL-BREF) scale ( p = 0.02)."( The impact upon extra-pyramidal side effects, clinical symptoms and quality of life of a switch from conventional to atypical antipsychotics (risperidone or olanzapine) in elderly patients with schizophrenia.
Ames, D; Chiu, E; Hall, K; Harrigan, S; Hassett, A; Macfarlane, S; Mastwyk, M; O'Connor, DW; Opie, J; Ritchie, CW, 2003
)
"Treatment with olanzapine was also associated with a statistically significant improvement in verbal fluency."( Randomized, controlled, double-blind, multicenter comparison of the cognitive effects of ziprasidone versus olanzapine in acutely ill inpatients with schizophrenia or schizoaffective disorder.
Harvey, PD; Romano, S; Siu, CO, 2004
)
"Treatment with olanzapine was started anew or switched from a conventional antipsychotic drug."( Weight gain during long-term treatment with olanzapine: a case series.
Haberfellner, EM; Rittmannsberger, H, 2004
)
"Treatment with olanzapine was associated with significantly greater weight gain than treatment with risperidone in Chinese schizophrenia patients in Hong Kong. "( Atypical antipsychotics and weight gain in Chinese patients: a comparison of olanzapine and risperidone.
Lee, E; Leung, CM; Wong, E, 2004
)
"The treatment with olanzapine caused significant improvement of schizophrenia positive, negative and affective symptoms. "( [Subjective and objective evaluation of olanzapine treatment in schizophrenia].
Jarema, M; Murawiec, S; Tafliński, T,
)
"On treatment with olanzapine, valproic acid, and perazine there was only moderate improvement."( Acute psychosis with a mediastinal carcinoma metastasis.
Connemann, BJ; Freudenmann, RW; Kassubek, J; Schönfeldt-Lecuona, C; Tumani, H, 2005
)
"Rats treated with olanzapine and clozapine presented a decrease in motor activity level at the same time."( Influence of chronic treatment with olanzapine, clozapine and scopolamine on performance of a learned 8-arm radial maze task in rats.
Gibert-Rahola, J; Micó, JA; Ortega-Alvaro, A, 2006
)
"Treatment with olanzapine may impact a patient's weight; thus, long-term weight gain and potential predictors (e.g., age and gender) and correlates (e.g., cholesterol and glucose levels) of weight gain were investigated in OFC-treated patients with MDD."( Long-term weight gain in patients treated with open-label olanzapine in combination with fluoxetine for major depressive disorder.
Andersen, SW; Clemow, DB; Corya, SA, 2005
)
"Treatment with olanzapine (20 mg) resulted not only in a fast reduction of tic severity and frequency, but also in a reduction of obsessive-compulsive behaviours."( Olanzapine in Gilles de la Tourette syndrome: beyond tics.
Audenaert, K; De Saedeleer, S; Naudts, KH; Van den Eynde, F; van Heeringen, C, 2005
)
"Treatment with olanzapine appears to be more cost-effective than that with the other atypical antipsychotics in Thai schizophrenic patients."( Cost analysis of the treatment of schizophrenia in Thailand: a simulation model comparing olanzapine, risperidone, quetiapine, ziprasidone and haloperidol.
Birinyi-Strachan, L; Davey, P; Kongsakon, R; Leelahanaj, T; Price, N, 2005
)
"Treatment with olanzapine resulted in a greater numerical improvement than risperidone in all SFS domains and reached statistical significance in such categories as social engagement or withdrawal (p = 0.01), independence (performance) (p = 0.0098), independence (competence) (p = 0.04), recreational activities (p = 0.0391), and occupation/employment (p = 0.0024) in which the greatest difference between the olanzapine and risperidone groups was found (0.86 vs."( Improvement in social functioning in outpatients with schizophrenia with prominent negative symptoms treated with olanzapine or risperidone in a 1 year randomized, open-label trial.
Alvarez, E; Bousoño, M; Ciudad, A; Gómez, JC; Olivares, JM, 2006
)
"Treatment with olanzapine was also associated with a higher frequency of remission compared with other antipsychotic agents."( Remission and relapse in the outpatient care of schizophrenia: three-year results from the Schizophrenia Outpatient Health Outcomes study.
Alonso, J; Haro, JM; Lépine, JP; Novick, D; Ratcliffe, M; Suarez, D, 2006
)
"Treatment with olanzapine moderately decreased, while treatment with fluphenazine significantly increased plasma cortisol levels and muscle rigidity."( The effects of olanzapine and fluphenazine on plasma cortisol, prolactin and muscle rigidity in schizophrenic patients: a double blind study.
Jakovljevic, M; Ljubicic, D; Marcinko, D; Mihaljevic-Peles, A; Muck-Seler, D; Mustapic, M; Pivac, N; Relja, M, 2007
)
"Treatment with olanzapine for 8 weeks improved both positive and negative symptoms of schizophrenia."( Effects of olanzapine on plasma levels of catecholamine metabolites, cytokines, and brain-derived neurotrophic factor in schizophrenic patients.
Hori, H; Ida, Y; Ikenouchi, A; Mitoma, M; Nakamura, J; Yamada, Y; Yoshimura, R, 2007
)
"Treatment with olanzapine increased the neuronal differentiation suppressed by the exposure to thapsigargin (10 nM)."( Olanzapine potentiates neuronal survival and neural stem cell differentiation: regulation of endoplasmic reticulum stress response proteins.
Hashimoto, E; Kurosawa, S; Saito, S; Saito, T; Toki, S; Ukai, W, 2007
)
"Treatment with olanzapine was associated with greater decreases in Y-BOCS total score than treatment with risperidone in total group (N = 122: -2.2 vs -0.3, z = -2.651, P < 0.01), in patients with baseline Y-BOCS total score greater than 0 (n = 58: -5.1 vs -0.4, z = -2.717, P < 0.01), and in patients with baseline Y-BOCS total score greater than 10 (n = 29: -7.1 vs -0.6, z = -2.138, P = 0.032)."( Obsessive-compulsive symptoms in a randomized, double-blind study with olanzapine or risperidone in young patients with early psychosis.
de Haan, L; Laan, W; Linszen, D; van Beveren, N; van den Brink, W; van Nimwegen, L, 2008
)
"Treatment with olanzapine was more effective in terms of QALYs gained than all of the other antipsychotic treatments."( Cost-utility analysis of treatment with olanzapine compared with other antipsychotic treatments in patients with schizophrenia in the pan-European SOHO study.
Brown, J; Haro, JM; Hong, J; Knapp, M; Kontodimas, S; Novick, D; Ratcliffe, M; Tzivelekis, S; Windmeijer, F, 2008
)
"Pre-treatment with olanzapine (3.0, 4.5 mg/kg, but not 1.5 mg/kg) significantly attenuated conditioned place preference produced by cocaine (10 mg/kg)."( Olanzapine attenuates the reinforcing effects of cocaine.
Meil, WM; Schechter, MD, 1997
)
"Pretreatment with olanzapine (0.25 and 0.5 mg/kg) inhibited the dizocilpine (0.5 mg/kg)-induced hyperlocomotion but not the stereotypy."( Preferential inhibition of dizocilpine-induced hyperlocomotion by olanzapine.
Kulkarni, SK; Ninan, I, 1999
)
"When treated with olanzapine and levomepromazine, the patient had a fulminant NMS which was complicated with pneumonia. "( Neuroleptic malignant syndrome during olanzapine and levomepromazine treatment.
Järventausta, K; Leinonen, E, 2000
)

Toxicity

Olanzapine is an atypical antipsychotic drug, whose chronic use has been associated with the development of potential adverse effects such as weight gain and cardio-metabolic disorders like hypercholesterolemia and diabetes.

ExcerptReference
" It does not appear to be free of adverse effects on liver function."( First clinical experience with olanzapine (LY 170053): results of an open-label safety and dose-ranging study in patients with schizophrenia.
Baldwin, DS; Montgomery, SA, 1995
)
" Considerable progress has been made in improving the motor side effect profile with the advent of clozapine and risperidone."( Side effect profiles of new antipsychotic agents.
Casey, DE, 1996
)
" Significant adverse events included somnolence, weight gain, and asymptomatic treatment-emergent transaminase elevation."( Safety of olanzapine.
Beasley, CM; Tollefson, GD; Tran, PV, 1997
)
"Most traditional neuroleptics have a narrow therapeutic-to-toxic index, and thus, the novel antipsychotics are the result of a search to substantially widen the distance between the dose that treats psychosis and the one that produces adverse effects."( The relationship of pharmacology to side effects.
Casey, DE, 1997
)
" Neutrophils from two patients with a history of clozapine-induced agranulocytosis seemed to be more sensitive to the toxic effects of the clozapine reactive metabolite; however, the numbers are too small to draw any definite conclusions."( A comparison of the oxidation of clozapine and olanzapine to reactive metabolites and the toxicity of these metabolites to human leukocytes.
Gardner, I; MacCrimmon, D; Uetrecht, JP; Zahid, N, 1998
)
" Thus, clinicians should address patients' concerns about adverse effects and attempt to choose medications that will improve their patients' quality of life as well as overall health."( Adverse effects of the atypical antipsychotics. Collaborative Working Group on Clinical Trial Evaluations.
, 1998
)
" The side effects associated with traditional antipsychotic treatment are generally minimal in patients who take risperidone, a combined 5-HT2/D2 antagonist, but the literature is sparse on adverse events among the newer atypical antipsychotics."( Risperidone side effects.
Conley, RR, 2000
)
" Compared with traditional agents, olanzapine shows only a few adverse events such as dry mouth, sedation, and increase in appetite."( Adverse events related to olanzapine.
Conley, RR; Meltzer, HY, 2000
)
" Their adverse effects, which include extrapyramidal side effects, tardive dyskinesia, weight gain, sedation, and sexual dysfunction, often lead to non-compliance; their use may have a negative impact on the overall course of illness; and they may not be as effective as lithium in treating the core manic symptoms over the long term."( Antipsychotic drug side effect issues in bipolar manic patients.
Zarate, CA, 2000
)
" Safety was evaluated through the collection of spontaneous adverse events and a specific questionnaire for extrapyramidal symptoms."( The safety of olanzapine compared with other antipsychotic drugs: results of an observational prospective study in patients with schizophrenia (EFESO Study). Pharmacoepidemiologic Study of Olanzapine in Schizophrenia.
Antón Saiz, C; Breier, A; Fontova Carbonell, E; Gómez, JC; Hernández, J; Ruiz Carrasco, P; Sacristán, JA, 2000
)
" Overall incidence of adverse events was significantly lower in the olanzapine group compared with the control group (p < ."( The safety of olanzapine compared with other antipsychotic drugs: results of an observational prospective study in patients with schizophrenia (EFESO Study). Pharmacoepidemiologic Study of Olanzapine in Schizophrenia.
Antón Saiz, C; Breier, A; Fontova Carbonell, E; Gómez, JC; Hernández, J; Ruiz Carrasco, P; Sacristán, JA, 2000
)
"These results show that olanzapine is safe and effective in nonselected schizophrenic outpatients and are consistent with the efficacy and safety profile that olanzapine has shown in previous controlled clinical trials."( The safety of olanzapine compared with other antipsychotic drugs: results of an observational prospective study in patients with schizophrenia (EFESO Study). Pharmacoepidemiologic Study of Olanzapine in Schizophrenia.
Antón Saiz, C; Breier, A; Fontova Carbonell, E; Gómez, JC; Hernández, J; Ruiz Carrasco, P; Sacristán, JA, 2000
)
" Olanzapine seems to be safe in this patient, since no major decreases of haematological parameters were observed."( Olanzapine appears haematologically safe in patients who developed blood dyscrasia on clozapine and risperidone.
Dernovsek, MZ; Tavcar, R, 2000
)
" Although the incidence of serious adverse cardiac events in response to antipsychotic medications is relatively low, any possibility for the occurrence of cardiotoxicity warrants continued study."( Cardiac safety parameters of olanzapine: comparison with other atypical and typical antipsychotics.
Beasley, CM; Czekalla, J; Kollack-Walker, S, 2001
)
" These findings suggest that intramuscular olanzapine is a safe and effective treatment for reducing acute agitation in patients with bipolar mania."( A double-blind, randomized comparison of the efficacy and safety of intramuscular injections of olanzapine, lorazepam, or placebo in treating acutely agitated patients diagnosed with bipolar mania.
Breier, A; David, S; Janicak, P; Koch, M; Meehan, K; Rizk, R; Small, J; Tohen, M; Tran, P; Walker, D; Zhang, F, 2001
)
" We conducted a survey of Spanish psychiatrists in mental health centers and outpatient treatment units to assess the severity scores that they would assign to a list of the most common adverse events (AEs) that usually occur with antipsychotic treatment."( Global index of safety (GIS): a new instrument to assess drug safety.
Badía, X; Gómez, JC; Kind, P; Sacristán, JA, 2001
)
"In vitro receptor characterization methods, when done using physiologically relevant conditions allow accurate prediction of the relatively low rate of anticholinergic-like adverse events, extrapyramidal symptoms, and cardiovascular adverse events during treatment with OLZ."( A current review of olanzapine's safety in the geriatric patient: from pre-clinical pharmacology to clinical data.
Baker, RW; Beasley, CM; Bernauer, M; Breier, A; Bymaster, FP; Calligaro, DO; Dossenbach, M; Effron, MB; Felder, CC; Hay, D; Holcombe, JH; Kaiser, C; Kennedy, JS; Kinon, BJ; Nomikos, G; Roth, HJ; Schuh, L, 2001
)
"Converging evidence indicates that, in controlled drug trials, individuals receiving novel antipsychotic medications have fewer adverse effects than those receiving conventional antipsychotic medications."( Short report: comparison of patient satisfaction and burden of adverse effects with novel and conventional neuroleptics: a naturalistic study.
Bromet, EJ; Davidson, M; Rabinowitz, J, 2001
)
"Psychopharmacology research aims to expand the therapeutic ratio between efficacy, on the one hand, and adverse events and safety, on the other."( Psychotropic drugs and adverse events in the treatment of bipolar disorders revisited.
McIntyre, RS, 2002
)
" Relatively little information on adverse events (AEs), specifically in children or adolescents taking atypical antipsychotics, is available."( Effects of development on olanzapine-associated adverse events.
Martin, A; McGlashan, TH; Spector, SG; Woods, SW, 2002
)
" Safety was assessed through the collection of spontaneous adverse events and a specific extrapyramidal symptoms questionnaire (EPS)."( Safety of olanzapine versus conventional antipsychotics in the treatment of patients with acute schizophrenia. A naturalistic study.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M; Sacristán, JA, 2003
)
" Other safety and tolerability endpoints included spontaneous adverse event reporting and changes from baseline in laboratory measures and vital signs."( A comparison of the efficacy, safety, and tolerability of divalproex sodium and olanzapine in the treatment of bipolar disorder.
Sachs, G; Sommerville, KW; Swann, AC; Weisler, R; Wozniak, P; Zajecka, JM, 2002
)
"05) greater proportion of olanzapine-treated subjects experienced somnolence, weight gain, edema, rhinitis, and speech disorder (slurred speech); no adverse events were significantly greater in the divalproex group."( A comparison of the efficacy, safety, and tolerability of divalproex sodium and olanzapine in the treatment of bipolar disorder.
Sachs, G; Sommerville, KW; Swann, AC; Weisler, R; Wozniak, P; Zajecka, JM, 2002
)
" Divalproex was associated with a more favorable adverse event profile and significantly less weight gain than olanzapine."( A comparison of the efficacy, safety, and tolerability of divalproex sodium and olanzapine in the treatment of bipolar disorder.
Sachs, G; Sommerville, KW; Swann, AC; Weisler, R; Wozniak, P; Zajecka, JM, 2002
)
" Olanzapine is one of the atypical antipsychotics with efficacy for psychotic symptoms and a safer side-effect profile than typical antipsychotics."( The efficacy and safety of olanzapine for the treatment of geriatric psychosis.
Hwang, JP; Lee, TW; Tsai, SJ; Yang, CH, 2003
)
" Safety was evaluated in terms of the spontaneous adverse events reported and a specific questionnaire for extrapyramidal symptoms (EPS)."( Safety and effectiveness of olanzapine versus conventional antipsychotics in the acute treatment of first-episode schizophrenic inpatients.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Ciudad, A; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M, 2003
)
"The results of this observational, naturalistic study show that olanzapine is safe and effective in a nonselected sample of acute, first-episode schizophrenic inpatients."( Safety and effectiveness of olanzapine versus conventional antipsychotics in the acute treatment of first-episode schizophrenic inpatients.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Ciudad, A; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M, 2003
)
" This is because of their efficacy in the treatment of several psychiatric disorders, ease of administration, and absence of the well-known extrapyramidal adverse effects long-attributed to the standard dopamine blocking anti-psychotic medications."( Atypical psychotropic medications and their adverse effects: a review for the African-American primary care physician.
Bailey, RK, 2003
)
"To assess the adverse events associated with the appropriate use of oral risperidone and oral olanzapine in long-term care patients with behavioral and psychotic disturbances associated with dementia."( Safety profile assessment of risperidone and olanzapine in long-term care patients with dementia.
Cornacchione, MJ; Deymann, S; Martin, H; Slyk, MP,
)
" Adverse events of particular significance in the elderly population, including agitation/anxiety, laxative use, dry eyes, and falls, were collected from audited medical records."( Safety profile assessment of risperidone and olanzapine in long-term care patients with dementia.
Cornacchione, MJ; Deymann, S; Martin, H; Slyk, MP,
)
"Among long-term care residents with dementia who received low doses of risperidone or olanzapine, the incidence of adverse events was low."( Safety profile assessment of risperidone and olanzapine in long-term care patients with dementia.
Cornacchione, MJ; Deymann, S; Martin, H; Slyk, MP,
)
" Adverse events and scores on EPS rating scales were assessed."( A comparison of the efficacy and safety of olanzapine versus haloperidol during transition from intramuscular to oral therapy.
Birkett, M; Breier, A; Lindborg, SR; Meehan, K; Morris, P; Taylor, CC; Wright, P, 2003
)
" Although the nature of adverse events differed between the two agents, retention in the study was greater with olanzapine."( Comparative efficacy and safety of atypical and conventional antipsychotic drugs in first-episode psychosis: a randomized, double-blind trial of olanzapine versus haloperidol.
Green, AI; Gur, RE; Hamer, RM; Kahn, R; Lieberman, JA; McEvoy, J; Perkins, D; Sharma, T; Tohen, M; Tollefson, G; Wei, H; Zipursky, R, 2003
)
"Available toxicity data concerning olanzapine were obtained from the Offices of the Medical Examiners of Canada, the Canadian Adverse Drug Reaction Monitoring Program and a review of the literature."( A review of olanzapine-associated toxicity and fatality in overdose.
Chue, P; Singer, P, 2003
)
" Early signal detection and effective notification processes are crucial in the event that serious adverse effects do occur."( A review of olanzapine-associated toxicity and fatality in overdose.
Chue, P; Singer, P, 2003
)
" Divalproex loading was as well tolerated or better tolerated than the other active treatments as measured by adverse events and changes in laboratory parameters."( The safety and early efficacy of oral-loaded divalproex versus standard-titration divalproex, lithium, olanzapine, and placebo in the treatment of acute mania associated with bipolar disorder.
Baker, JD; Hirschfeld, RM; Sommerville, KW; Tracy, K; Wozniak, P, 2003
)
" Statistically significant differences of mean change of BAS total score from baseline to endpoint were noted between treatment groups Treatment--emergent adverse events occurred more frequently in patients receiving perphenazine (46%), than in patients receiving olanzapine (17%)."( [Safety and efficacy of olanzapine versus perphenazine in patients with schizophrenia: results of multicenter, 18-week, double-blind clinical trial].
Araszkiewicz, A; Bilikiewicz, A; Bomba, J; Chrzanowski, W; Debowska, G; Jarema, M; Landowski, J; Olajossy, M; Rybakowski, J,
)
" Safety was assessed via adverse events, vital signs, laboratory analytes, electrocardiography, and extrapyramidal symptom measures."( Long-term antidepressant efficacy and safety of olanzapine/fluoxetine combination: a 76-week open-label study.
Andersen, SW; Corya, SA; Detke, HC; Dubé, S; Kelly, LS; Sanger, TM; Van Campen, LE; Williamson, DJ, 2003
)
" The most frequently reported adverse events were somnolence, weight gain, dry mouth, increased appetite, and headache."( Long-term antidepressant efficacy and safety of olanzapine/fluoxetine combination: a 76-week open-label study.
Andersen, SW; Corya, SA; Detke, HC; Dubé, S; Kelly, LS; Sanger, TM; Van Campen, LE; Williamson, DJ, 2003
)
" The aim of this paper is to review literature about newer antipsychotics, focusing on their advantages in terms of efficacy and side effect profiles when compared to classical and older atypical antipsychotics, and to evaluate the efficacy of the different new antipsychotics when compared to one another."( New antipsychotics and schizophrenia: a review on efficacy and side effects.
Berardi, D; De Ronchi, D; Lorenzi, C; Serretti, A, 2004
)
" New compounds might show new or different adverse effects that arise in the post-marketing phase when a greater number of patients are treated."( Hyperglycemia associated with antipsychotic treatment in a multicenter drug safety project.
Degner, D; Grohmann, R; Hauser, U; Kropp, S; Rüther, E, 2004
)
"Olanzapine, an atypical antipsychotic, is often regarded as a safe choice for psychosis management."( Severe cardiovascular side effects of olanzapine in an elderly patient: case report.
Hwang, JP; Lee, TW; Tsai, SJ, 2003
)
" Safety measures included the recording of spontaneous adverse events and extrapyramidal symptoms (EPS)."( Safety and tolerability of olanzapine compared with other antipsychotics in the treatment of elderly patients with schizophrenia: a naturalistic study.
Ciudad, A; Gómez, JC; Montes, JM; Olivares, JM, 2004
)
"The incidence of overall adverse events and EPS was non-significantly lower in patients treated with olanzapine than in patients treated with other antipsychotics."( Safety and tolerability of olanzapine compared with other antipsychotics in the treatment of elderly patients with schizophrenia: a naturalistic study.
Ciudad, A; Gómez, JC; Montes, JM; Olivares, JM, 2004
)
"Results from this naturalistic study showed that olanzapine was as safe and effective as other antipsychotic drugs in the treatment of elderly patients with schizophrenia."( Safety and tolerability of olanzapine compared with other antipsychotics in the treatment of elderly patients with schizophrenia: a naturalistic study.
Ciudad, A; Gómez, JC; Montes, JM; Olivares, JM, 2004
)
"Five new antipsychotic drugs introduced in the United States in the last decade offer physicians the ability to treat patients with schizophrenia and bipolar mania without the adverse effects of the first-generation antipsychotics."( The promise of atypical antipsychotics: fewer side effects mean enhanced compliance and improved functioning.
Citrome, L; Volavka, J, 2004
)
"Common adverse effect measures in psychiatric trials are typically analysed with repeated measures ANOVA, despite having distributions which violate key assumptions of that method; moreover, some adverse effects may be concentrated in vulnerable subgroups of participants."( More powerful two-sample tests for differences in repeated measures of adverse effects in psychiatric trials when only some patients may be at risk.
Arndt, S; Conley, RR; McMahon, RP, 2005
)
"The global index of safety (GIS) is an adverse event (AE) based instrument designed to evaluate the safety profile of drugs."( The validity and reliability of the global index of safety (GIS).
Gómez, JC; Prieto, L; Sacristán, JA, 2004
)
"The data presented here on inter-rater reliability estimates of adverse events related to antipsychotic drugs indicate that GIS is a promising alternative for the evaluation of the safety profile of drugs."( The validity and reliability of the global index of safety (GIS).
Gómez, JC; Prieto, L; Sacristán, JA, 2004
)
" Olanzapine is potentially effective and safe in panic disorder."( Potential effectiveness and safety of olanzapine in refractory panic disorder.
Hollifield, M; Ruiz, JE; Thompson, PM; Uhlenhuth, EH, 2005
)
" However, there are still significant adverse effects and toxicities with this class of medications."( Toxicology and overdose of atypical antipsychotic medications in children: does newer necessarily mean safer?
Dubois, D, 2005
)
"Continued research to evaluate adverse effects and tolerability of atypical antipsychotics compared with first-generation antipsychotics and each other is reviewed."( Toxicology and overdose of atypical antipsychotic medications in children: does newer necessarily mean safer?
Dubois, D, 2005
)
"While new atypical antipsychotic medications may have a safer therapeutic and overdose profile than first-generation antipsychotic medications, many adverse and toxic effects still need to be considered in therapeutic monitoring and overdose management."( Toxicology and overdose of atypical antipsychotic medications in children: does newer necessarily mean safer?
Dubois, D, 2005
)
" Safety of antipsychotic therapy was assessed with an extrapyramidal symptoms questionnaire (based on the Udvalg for Kliniske Undersøgelser scale) and the report of spontaneous adverse events."( Safety, effectiveness, and patterns of use of olanzapine in acute schizophrenia: a multivariate analysis of a large naturalistic study in the hospital setting.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Ciudad, A; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M, 2005
)
"Olanzapine is a safe and effective treatment for patients with acute schizophrenia in the hospital setting, even for patients with prominent positive or agitation symptoms."( Safety, effectiveness, and patterns of use of olanzapine in acute schizophrenia: a multivariate analysis of a large naturalistic study in the hospital setting.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Ciudad, A; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M, 2005
)
" Data included safety assessments with an extrapyramidal symptoms (EPS) questionnaire and the report of spontaneous adverse events, plus clinical assessments with the Brief Psychiatric Rating Scale (BPRS) and the Clinical Global Impressions-Severity of Illness (CGI-S)."( Safety and effectiveness of olanzapine in monotherapy: a multivariate analysis of a naturalistic study.
Alvarez, E; Bobes, J; Cañas, F; Carrasco, JL; Ciudad, A; Gascón, J; Gibert, J; Gómez, JC; Gutiérrez, M, 2005
)
"Both drugs were well tolerated and their use was associated with fewer symptoms of schizophrenia and less adverse effects than were seen when the patients were taking a typical antipsychotic at baseline."( A comparison of the efficacy and safety of olanzapine and risperidone in the treatment of elderly patients with schizophrenia: an open study of six months duration.
Ames, D; Chiu, E; Hall, K; Halliday, G; Harrigan, S; Hassett, A; Hustig, H; MacFarlane, S; Mastwyk, M; Nagalingam, V; O'Connor, DW; Opie, J; Ritchie, CW; Snowdon, J, 2006
)
"These data agree with recent clinical reports concerning the direct or mediated toxic effects of olanzapine on progenitor and committed cells (GM-CFU) and suggest that the correlation between its plasma levels and clinical effects warrants further investigation."( In vitro toxicity of clozapine, olanzapine, and quetiapine on granulocyte-macrophage progenitors (GM-CFU).
Bareggi, S; Bonomi, A; Cavicchini, L; Croera, C; Guizzardi, F; Pessina, A; Turlizzi, E, 2006
)
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
" Several clinical trials have not shown efficacy, and there have been concerns about adverse events."( Efficacy and adverse effects of atypical antipsychotics for dementia: meta-analysis of randomized, placebo-controlled trials.
Dagerman, K; Insel, PS; Schneider, LS, 2006
)
" Clinical and trials characteristics, outcomes, and adverse events were extracted."( Efficacy and adverse effects of atypical antipsychotics for dementia: meta-analysis of randomized, placebo-controlled trials.
Dagerman, K; Insel, PS; Schneider, LS, 2006
)
" Adverse events were mainly somnolence and urinary tract infection or incontinence across drugs, and extrapyramidal symptoms or abnormal gait with risperidone or olanzapine."( Efficacy and adverse effects of atypical antipsychotics for dementia: meta-analysis of randomized, placebo-controlled trials.
Dagerman, K; Insel, PS; Schneider, LS, 2006
)
" Dropouts and adverse events further limit effectiveness."( Efficacy and adverse effects of atypical antipsychotics for dementia: meta-analysis of randomized, placebo-controlled trials.
Dagerman, K; Insel, PS; Schneider, LS, 2006
)
" Although antipsychotics may be efficacious in this population, elderly patients with dementia may be particularly vulnerable to adverse events."( A review of treatment-emergent adverse events during olanzapine clinical trials in elderly patients with dementia.
Carlson, JL; Cavazzoni, PA; Jansen, JF; Jeste, DV; Kryzhanovskaya, LA; Polzer, JP; Roddy, TE; Young, CA, 2006
)
"Data from 6 studies comparing olanzapine to placebo, risperidone, or conventional antipsychotics in elderly patients with dementia were analyzed for mortality, cerebrovascular adverse events (CVAEs), and other adverse events."( A review of treatment-emergent adverse events during olanzapine clinical trials in elderly patients with dementia.
Carlson, JL; Cavazzoni, PA; Jansen, JF; Jeste, DV; Kryzhanovskaya, LA; Polzer, JP; Roddy, TE; Young, CA, 2006
)
" Most people did not have any adverse effects; 5 patients (15."( Behavioral and psychological symptoms of dementia (BPSD) in elderly demented subjects: is the long lasting use of atypical antipsychotic drugs useful and safe?
Angelini, A; Bendini, C; Neri, M; Neviani, F, 2007
)
" Safety was evaluated by recording treatment-emergent adverse events, vital signs, body weight and, when available, laboratory parameters."( [Safety and tolerability of olanzapine versus risperidone: a one-year randomized study in outpatients with schizophrenia with prominent negative symptoms].
Alvarez, E; Bousoño, M; Ciudad, A; Gómez, JC; Olivares, JM,
)
"0292) and risperidone patients reported significantly more sexual adverse events (21."( [Safety and tolerability of olanzapine versus risperidone: a one-year randomized study in outpatients with schizophrenia with prominent negative symptoms].
Alvarez, E; Bousoño, M; Ciudad, A; Gómez, JC; Olivares, JM,
)
"Significantly less treatment-emergent extrapyramidal and sexual adverse events were observed in patients treated with olanzapine compared to those treated with risperidone."( [Safety and tolerability of olanzapine versus risperidone: a one-year randomized study in outpatients with schizophrenia with prominent negative symptoms].
Alvarez, E; Bousoño, M; Ciudad, A; Gómez, JC; Olivares, JM,
)
" Safety outcome measures were all new clinical adverse events between the start of treatment (which could be before April 2003) and 30 November 2004."( Safety and usage of atypical antipsychotic medicines in children: a nationwide prospective cohort study.
Ashton, J; Garcia-Quiroga, J; Harrison-Woolrych, M; Herbison, P, 2007
)
" A total of 131 (31%) children experienced an adverse event."( Safety and usage of atypical antipsychotic medicines in children: a nationwide prospective cohort study.
Ashton, J; Garcia-Quiroga, J; Harrison-Woolrych, M; Herbison, P, 2007
)
"Severely agitated patients responded rapidly after a single injection of olanzapine with mild levels of sedation and without serious treatment-emergent adverse events."( An observational study of the effectiveness and safety of intramuscular olanzapine in the treatment of acute agitation in patients with bipolar mania or schizophrenia/schizoaffective disorder.
Ahl, J; Centorrino, F; Cincotta, SL; Gulliver, AH; Houston, JP; Kinon, BJ; Meyers, AL; Zun, L, 2007
)
" Treatment-emergent adverse events occurring during the pivotal trials revealed statistically significant NNH versus placebo (or placebo equivalent) for aripiprazole for headache (NNH = 20, 95% CI = 11 to 170) and nausea (NNH = 17, 95% CI = 11 to 38), for ziprasidone in the treatment of headache (NNH = 15, 95% CI = 8 to 703), and for olanzapine in treatment-emergent hypotension (NNH = 50, 95% CI = 30 to 154)."( Comparison of intramuscular ziprasidone, olanzapine, or aripiprazole for agitation: a quantitative review of efficacy and safety.
Citrome, L, 2007
)
" There were 30 treatment-emergent adverse events with six serious cases, assessed as unrelated to study drug, reported."( Effectiveness and safety of olanzapine in the treatment of Asian outpatients with schizophrenia.
Budiman, R; Buenaventura, R; Chaudhry, HR; Gondoyoewono, H; Habil, MH; Hamid, AR; Hashmi, IT; Knowles, AG; Samanwongthai, U, 2007
)
" In addition, adverse events were also evaluated."( [A naturalistic, observational study of outpatients with schizophrenia: efficacy and safety results after 6 months. The International Schizophrenia Outpatient Health Outcomes study, IC-SOHO].
Agoston, T; István, S; Tamás, T; Zoltán, J, 2007
)
"A formalized policy was developed to warn of the potential for adverse events associated with the use of intramuscular olanzapine in combination with injectable benzodiazepines."( Optimizing patient safety by preventing combined use of intramuscular olanzapine and parenteral benzodiazepines.
Naso, AR, 2008
)
" Based on recent criteria for pediatric populations, patients were considered "at risk for adverse health outcome" if they met at least 1 of the following criteria: (1) > or = 85th BMI percentile plus presence of 1 or more negative weight-related clinical outcomes, or (2) > or = 95th BMI percentile."( Metabolic and hormonal side effects in children and adolescents treated with second-generation antipsychotics.
Arango, C; Cifuentes, A; Fraguas, D; Giráldez, M; Laita, P; Merchán-Naranjo, J; Moreno, D; Parellada, M; Ruiz-Sancho, A, 2008
)
" The number of patients at risk for adverse health outcome increased from 11 (16."( Metabolic and hormonal side effects in children and adolescents treated with second-generation antipsychotics.
Arango, C; Cifuentes, A; Fraguas, D; Giráldez, M; Laita, P; Merchán-Naranjo, J; Moreno, D; Parellada, M; Ruiz-Sancho, A, 2008
)
" Limited data is available concerning the toxic effects of olanzapine after deliberate overdose."( Prolonged toxicity after massive olanzapine overdose: two cases with confirmatory laboratory data.
Tse, GH; Waring, WS; Warner, MH, 2008
)
" Sample size was reduced from 311 to 156 patients, thereby decreasing the number of patients exposed to placebo from 54 to 30 and the number exposed to the active control with a known side effect from 126 to 60."( Bayesian adaptive non-inferiority with safety assessment: retrospective case study to highlight potential benefits and limitations of the approach.
Baker, R; Breier, A; Dunayevich, E; Lindborg, S; Seaman, J; Spann, M, 2009
)
" In the overall adolescent olanzapine exposure database, the most common adverse events included increased weight (31."( The safety of olanzapine in adolescents with schizophrenia or bipolar I disorder: a pooled analysis of 4 clinical trials.
Carlson, JL; Dittmann, RW; Kryzhanovskaya, LA; Merida, KM; Robertson-Plouch, CK; Xu, W, 2009
)
"The types of adverse events in olanzapine-treated adolescents appear to be similar to those of adults."( The safety of olanzapine in adolescents with schizophrenia or bipolar I disorder: a pooled analysis of 4 clinical trials.
Carlson, JL; Dittmann, RW; Kryzhanovskaya, LA; Merida, KM; Robertson-Plouch, CK; Xu, W, 2009
)
" Outcome measures included: treatment-emergent adverse events, concomitant psychotropic medication and the time taken to switch to oral medication."( Intramuscular olanzapine vs. intramuscular short-acting antipsychotics: safety, tolerability and the switch to oral antipsychotic medication in patients with schizophrenia or acute mania.
Chandrasena, R; Dvoráková, D; Karagianis, J; Lee, SI; Loza, N; Mosolov, SN; Osváth, P; Pregelj, P; Treuer, T; Walton, RJ, 2009
)
"Fewer patients in the IM olanzapine group experienced an adverse event than patients in the other IM antipsychotic group (34."( Intramuscular olanzapine vs. intramuscular short-acting antipsychotics: safety, tolerability and the switch to oral antipsychotic medication in patients with schizophrenia or acute mania.
Chandrasena, R; Dvoráková, D; Karagianis, J; Lee, SI; Loza, N; Mosolov, SN; Osváth, P; Pregelj, P; Treuer, T; Walton, RJ, 2009
)
" The toxic effects of cocaine can be attenuated by antagonists of serotonin, muscarinic cholinergic, and dopamine receptors."( The effect of olanzapine pretreatment on acute cocaine toxicity in mice.
Cleveland, NR; Heard, KJ; Krier, S, 2009
)
"A Lilly-maintained safety database was searched for all spontaneous adverse events (AEs) reported in temporal association with olanzapine IM treatment."( Case reports of postmarketing adverse event experiences with olanzapine intramuscular treatment in patients with agitation.
Baker, RW; Carlson, JL; Cavazzoni, PA; Dawe, IC; Dellva, MA; Dunayevich, E; Falk, DM; Karagianis, JL; Marder, SR; Sorsaburu, S, 2010
)
" Adverse effects (n = 15), inadequate efficacy (n = 14), or study nonadherence (n = 8) were the most common reasons for discontinuation."( Double-blind maintenance safety and effectiveness findings from the Treatment of Early-Onset Schizophrenia Spectrum (TEOSS) study.
Findling, RL; Frazier, JA; Hamer, RM; Hlastala, S; Johnson, JL; Kaufman, EM; Lieberman, JA; Lingler, J; Maloney, AE; McClellan, J; McNamara, NK; Noyes, N; Pierson, L; Puglia, M; Ritz, L; Sikich, L; Vitiello, B, 2010
)
"RLAI and OP show good short- and long-term safety when treating patients with schizophrenia, with uncommon discontinuation due to adverse effects."( Long-acting atypical injectable antipsychotics in the treatment of schizophrenia: safety and tolerability review.
Cañas, F; Möller, HJ, 2010
)
"5, and 5mg/kg/day) administration caused no observable adverse effects."( Two models for weight gain and hyperphagia as side effects of atypical antipsychotics in male rats: validation with olanzapine and ziprasidone.
Harada, K; Irie, M; Kayama, Y; Kondo, Y; Matsuoka, N; Mihara, T; Ni, K; Shobo, M; Yamada, H, 2011
)
" Safety measures included differences in the frequencies of adverse events along with measures of extrapyramidal symptoms, weight, glucose, and lipid changes over time."( Impact of race on efficacy and safety during treatment with olanzapine in schizophrenia, schizophreniform or schizoaffective disorder.
Conley, R; Durell, T; Gatz, J; Hoffmann, VP; Kollack-Walker, S; Piezer, KW; Sniadecki, JL; Stauffer, VL, 2010
)
"Analyses of several safety and efficacy parameters revealed significant associations with dose of olanzapine LAI, with the highest dose generally showing greater efficacy as well as greater adverse changes in metabolic safety measures."( Dose-associated changes in safety and efficacy parameters observed in a 24-week maintenance trial of olanzapine long-acting injection in patients with schizophrenia.
Hill, AL; Karagianis, JL; McDonnell, DP; Sun, B; Watson, SB, 2011
)
" Based on adverse drug reaction (ADR) reports of QT prolongation and torsades de pointes, regulatory agencies recommended the use of continuous telemetry or advising against the intravenous administration in general."( Comparative safety of antipsychotics in the WHO pharmacovigilance database: the haloperidol case.
Guglielmo, BJ; Meier, CR; Meyer-Massetti, C; Rätz Bravo, AE; Vaerini, S, 2011
)
"While regulatory agencies advise against the use of intravenous haloperidol, review of VigiBase does not reveal that the intravenous route is any more likely to be associated with cardiac adverse events."( Comparative safety of antipsychotics in the WHO pharmacovigilance database: the haloperidol case.
Guglielmo, BJ; Meier, CR; Meyer-Massetti, C; Rätz Bravo, AE; Vaerini, S, 2011
)
" The most common adverse events were sedation, self-reported weight gain, ≥7% increase in body weight, dizziness, and akathisia."( Safety and efficacy of olanzapine monotherapy in treatment-resistant bipolar mania: a 12-week open-label study.
Calabrese, JR; Chan, P; Chen, J; Conroy, C; Fang, Y; Ganocy, SJ; Gao, K; Kemp, DE; Muzina, DJ; Serrano, MB, 2011
)
"These preliminary results suggest that olanzapine monotherapy is effective and relatively safe in patients with treatment-resistant bipolar mania."( Safety and efficacy of olanzapine monotherapy in treatment-resistant bipolar mania: a 12-week open-label study.
Calabrese, JR; Chan, P; Chen, J; Conroy, C; Fang, Y; Ganocy, SJ; Gao, K; Kemp, DE; Muzina, DJ; Serrano, MB, 2011
)
" Safety measures included treatment-emergent adverse events (TEAEs), weight and extrapyramidal symptoms (EPSs)."( Efficacy and safety of olanzapine in the treatment of Japanese patients with bipolar I disorder in a current manic or mixed episode: a randomized, double-blind, placebo- and haloperidol-controlled study.
Higuchi, T; Kanba, S; Katagiri, H; Takahashi, M; Takita, Y; Tohen, M, 2012
)
" Safety was assessed by treatment-emergent adverse events (TEAEs), vital signs, weight, and extrapyramidal symptoms (EPSs)."( Safety and efficacy of olanzapine monotherapy and olanzapine with a mood stabilizer in 18-week treatment of manic/mixed episodes for Japanese patients with bipolar I disorder.
Higuchi, T; Kanba, S; Katagiri, H; Takahashi, M; Takita, Y; Tohen, M, 2012
)
"There were no deaths or serious adverse events considered potentially related to olanzapine in the monotherapy group (N = 100) or the combination-therapy group (N = 39)."( Safety and efficacy of olanzapine monotherapy and olanzapine with a mood stabilizer in 18-week treatment of manic/mixed episodes for Japanese patients with bipolar I disorder.
Higuchi, T; Kanba, S; Katagiri, H; Takahashi, M; Takita, Y; Tohen, M, 2012
)
" Adverse event (AE) incidence was lower during the extension (asenapine, 62%; olanzapine, 55%) than during the core study (78%, 80%)."( Long-term efficacy and safety of asenapine or olanzapine in patients with schizophrenia or schizoaffective disorder: an extension study.
Emsley, R; Naber, D; Panagides, J; Schoemaker, J; Stet, L; Vrijland, P, 2012
)
"This cross-sectional study aimed to compare the effects of treatment with an atypical antipsychotic drug (olanzapine or risperidone) on quality of life (QoL) and to document adverse effects in 115 patients diagnosed with schizophrenia who attended the ambulatory service of Hospital Dr."( Quality of life and adverse effects of olanzapine versus risperidone therapy in patients with schizophrenia.
Chaves, KM; de Araújo Júnior, RF; de Araújo, AA; de Paula Soares Rachetti, V; do Socorro Costa Feitosa Alves, M; Filgueira Júnior, A; Guerra, GC; Ribeiro, SB; Serrano-Blanco, A; Soares, LA, 2013
)
" They had similar safety profiles with respect to the total incidence of adverse events."( The efficacy and safety of 12 weeks of treatment with sertindole or olanzapine in patients with chronic schizophrenia who did not respond successfully to their previous treatments: a randomized, double-blind, parallel-group, flexible-dose study.
Cai, ZJ; Hwang, JY; Kwon, JS; Mittoux, A; Ong, A; Su, TP, 2012
)
"Atypical antipsychotic agents have been associated with cerebrovascular adverse events, particularly in elderly dementia patients."( Comparative risk of cerebrovascular adverse events in community-dwelling older adults using risperidone, olanzapine and quetiapine: a multiple propensity score-adjusted retrospective cohort study.
Aparasu, RR; Chatterjee, S; Chen, H; Johnson, ML, 2012
)
"16) was associated with a decrease in the risk of cerebrovascular adverse events compared with olanzapine."( Comparative risk of cerebrovascular adverse events in community-dwelling older adults using risperidone, olanzapine and quetiapine: a multiple propensity score-adjusted retrospective cohort study.
Aparasu, RR; Chatterjee, S; Chen, H; Johnson, ML, 2012
)
" Prescribers should closely monitor the patients treated with atypical agents for the incidence of cerebrovascular adverse events."( Comparative risk of cerebrovascular adverse events in community-dwelling older adults using risperidone, olanzapine and quetiapine: a multiple propensity score-adjusted retrospective cohort study.
Aparasu, RR; Chatterjee, S; Chen, H; Johnson, ML, 2012
)
"Primary metabolic markers (body mass index, blood pressure, fasting blood glucose, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides), percentage of patients who stay on the randomly assigned atypical antipsychotic for at least 6 months, psychopathology, percentage of patients who develop metabolic syndrome, and percentage of patients who develop serious and nonserious adverse events."( Comparison of longer-term safety and effectiveness of 4 atypical antipsychotics in patients over age 40: a trial using equipoise-stratified randomization.
Arndt, S; Glorioso, DK; Golshan, S; Henry, R; Jeste, DV; Jin, H; Kraemer, HC; Mudaliar, S; Shih, PA, 2013
)
"Because of a high incidence of serious adverse events, quetiapine was discontinued midway through the trial."( Comparison of longer-term safety and effectiveness of 4 atypical antipsychotics in patients over age 40: a trial using equipoise-stratified randomization.
Arndt, S; Glorioso, DK; Golshan, S; Henry, R; Jeste, DV; Jin, H; Kraemer, HC; Mudaliar, S; Shih, PA, 2013
)
" Double-blind, randomized, controlled trials investigating the metabolic adverse effects (weight gain, lipid, glucose, and prolactin level abnormalities) associated with atypical antipsychotic use in children and adolescents aged ≤ 18 years were included, irrespective of whether the investigation of adverse effects was a primary or secondary endpoint."( Weight gain and other metabolic adverse effects associated with atypical antipsychotic treatment of children and adolescents: a systematic review and meta-analysis.
Aitchison, KJ; Almandil, NB; Besag, FM; Liu, Y; Murray, ML; Wong, IC, 2013
)
"As part of the FP7 ARITMO (Arrhythmogenic Potential of Drugs) project, we explored the publicly available US FDA Adverse Event Reporting System (FAERS) database to detect signals of torsadogenicity for antipsychotics (APs)."( Antipsychotics and torsadogenic risk: signals emerging from the US FDA Adverse Event Reporting System database.
Behr, ER; De Ponti, F; Koci, A; Moretti, U; Poluzzi, E; Raschi, E; Spina, E; Sturkenboom, M, 2013
)
" The aim of this study was to identify genetic markers predictive of pharmacokinetics, pharmacodynamics, and adverse effects of olanzapine."( Polymorphisms influencing olanzapine metabolism and adverse effects in healthy subjects.
Abad-Santos, F; Cabaleiro, T; López-Rodríguez, R; Novalbos, J; Ochoa, D; Román, M, 2013
)
" The relationship of gender and polymorphisms with olanzapine pharmacokinetics, the change in prolactin levels, and the incidence of adverse effects were evaluated by multiple regression analysis."( Polymorphisms influencing olanzapine metabolism and adverse effects in healthy subjects.
Abad-Santos, F; Cabaleiro, T; López-Rodríguez, R; Novalbos, J; Ochoa, D; Román, M, 2013
)
" Polymorphisms in CYP2C9, TPMT, UGT1A1, MDR1, and 5-HTR2A were related to some adverse effects of olanzapine."( Polymorphisms influencing olanzapine metabolism and adverse effects in healthy subjects.
Abad-Santos, F; Cabaleiro, T; López-Rodríguez, R; Novalbos, J; Ochoa, D; Román, M, 2013
)
" A greater proportion of olanzapine-treated patients reported treatment- emergent adverse events (87."( Efficacy and safety of olanzapine for treatment of patients with bipolar depression: Japanese subpopulation analysis of a randomized, double-blind, placebo-controlled study.
Case, M; Fujikoshi, S; Gomez, JC; Kanba, S; Katagiri, H; McDonnell, DP; Takahashi, M; Tohen, M, 2013
)
"5%) in the SOC group discontinued due to adverse events (physician and subject decision combined, P = ."( A long-term, phase 2, multicenter, randomized, open-label, comparative safety study of pomaglumetad methionil (LY2140023 monohydrate) versus atypical antipsychotic standard of care in patients with schizophrenia.
Adams, DH; Baygani, S; Kinon, BJ; Kollack-Walker, S; Millen, BA; Velona, I; Walling, DP, 2013
)
"These data provide further evidence that the potential antipsychotic LY2140023 monohydrate, with a glutamatergic mechanism of action, may have a unique tolerability profile characterized by a low association with some adverse events such as extrapyramidal symptoms and weight gain that may characterize currently available dopaminergic antipsychotics."( A long-term, phase 2, multicenter, randomized, open-label, comparative safety study of pomaglumetad methionil (LY2140023 monohydrate) versus atypical antipsychotic standard of care in patients with schizophrenia.
Adams, DH; Baygani, S; Kinon, BJ; Kollack-Walker, S; Millen, BA; Velona, I; Walling, DP, 2013
)
" In these infants, the most commonly reported adverse events were somnolence (3."( Olanzapine in pregnancy and breastfeeding: a review of data from global safety surveillance.
Brunner, E; Dey, DK; Falk, DM; Jones, M; Shatapathy, CC, 2013
)
"Rats are used as animal models in the study of antipsychotic-induced metabolic adverse effects, with oral drug administration yielding hyperphagia, weight gain and, in some cases, lipogenic effects."( Olanzapine depot formulation in rat: a step forward in modelling antipsychotic-induced metabolic adverse effects.
Berge, RK; Fernø, J; López, M; Martins, L; Skrede, S; Steen, VM, 2014
)
" The safety was evaluated by the Udvalg Kliniske Undersogelser side effect rating scale."( Efficacy and safety of haloperidol versus atypical antipsychotic medications in the treatment of delirium.
Choi, SH; Choi, WJ; Kim, JJ; Park, JY; Park, KM; Seok, JH; Yoon, HJ, 2013
)
" Fifteen subjects experienced a few adverse events, but there were no significant differences in adverse event profiles among the four groups."( Efficacy and safety of haloperidol versus atypical antipsychotic medications in the treatment of delirium.
Choi, SH; Choi, WJ; Kim, JJ; Park, JY; Park, KM; Seok, JH; Yoon, HJ, 2013
)
"Haloperidol, risperidone, olanzapine, and quetiapine were equally efficacious and safe in the treatment of delirium."( Efficacy and safety of haloperidol versus atypical antipsychotic medications in the treatment of delirium.
Choi, SH; Choi, WJ; Kim, JJ; Park, JY; Park, KM; Seok, JH; Yoon, HJ, 2013
)
" Spontaneously reported adverse events were recorded at each visit."( Single- and multiple-dose pharmacokinetic, safety, and tolerability profiles of olanzapine long-acting injection: an open-label, multicenter, nonrandomized study in patients with schizophrenia.
Bergstrom, R; Jen, KY; Johnson, J; Kothare, P; McDonnell, D; Mitchell, M; Walker, D; Zhao, F, 2013
)
" The common adverse events were injection site pain, anxiety, sedation, insomnia, somnolence, and headache, and the safety profile for olanzapine LAI was comparable to that of oral olanzapine, except for injection site-related adverse events."( Single- and multiple-dose pharmacokinetic, safety, and tolerability profiles of olanzapine long-acting injection: an open-label, multicenter, nonrandomized study in patients with schizophrenia.
Bergstrom, R; Jen, KY; Johnson, J; Kothare, P; McDonnell, D; Mitchell, M; Walker, D; Zhao, F, 2013
)
" Six additional criteria were applied in order to target the subgroup of patients most likely to have experienced an adverse event due to treatment with olanzapine."( Adverse effects associated with high-dose olanzapine therapy in patients admitted to inpatient psychiatric care.
Andersen, SE; Christensen, M; Larsen, HL; Petersen, AB, 2014
)
" Extrapyramidal symptoms and sedation were the most frequent adverse events with frequencies of 27% and 25%, respectively."( Adverse effects associated with high-dose olanzapine therapy in patients admitted to inpatient psychiatric care.
Andersen, SE; Christensen, M; Larsen, HL; Petersen, AB, 2014
)
" In order to prevent harmful outcomes, the clinicians should be ready to act appropriately if toxic effects of olanzapine occur."( Adverse effects associated with high-dose olanzapine therapy in patients admitted to inpatient psychiatric care.
Andersen, SE; Christensen, M; Larsen, HL; Petersen, AB, 2014
)
"The purpose of this project was to provide evidence-based guidance concerning when and how it is appropriate to undertake elective changes in antipsychotic medications in order to reduce adverse effects, with a focus on those adverse effects associated with increased long-term health risks."( Switching antipsychotic medications to reduce adverse event burden in schizophrenia: establishing evidence-based practice.
Buchanan, RW; Newcomer, JW; Weiden, PJ, 2013
)
" Mice treated with PGW5 (25 and 50mg/kg/d) for 28 days did not show toxic effects in terms of weight gain and blood-chemistry analysis."( A novel analog of olanzapine linked to sarcosinyl moiety (PGW5) demonstrates high efficacy and good safety profile in mouse models of schizophrenia.
Bidder, M; Gil-Ad, I; Kramer, M; Portnoy, M; Taler, M; Tarasenko, I; Weizman, A, 2014
)
"PGW5 is a novel and safe antipsychotic, efficacious against schizophrenia-like positive and negative symptoms at nonsedative doses."( A novel analog of olanzapine linked to sarcosinyl moiety (PGW5) demonstrates high efficacy and good safety profile in mouse models of schizophrenia.
Bidder, M; Gil-Ad, I; Kramer, M; Portnoy, M; Taler, M; Tarasenko, I; Weizman, A, 2014
)
" Safety outcomes included treatment-emergent adverse events and changes in metabolic parameters."( Safety and efficacy of olanzapine in the long-term treatment of Japanese patients with bipolar I disorder, depression: an integrated analysis.
Case, M; Fujikoshi, S; Gomez, JC; Kanba, S; Katagiri, H; McDonnell, DP; Takahashi, M; Tohen, M, 2014
)
" The most common treatment-emergent adverse event was weight increased (47."( Safety and efficacy of olanzapine in the long-term treatment of Japanese patients with bipolar I disorder, depression: an integrated analysis.
Case, M; Fujikoshi, S; Gomez, JC; Kanba, S; Katagiri, H; McDonnell, DP; Takahashi, M; Tohen, M, 2014
)
" We report here the results of a pooled analysis of injection site-related adverse events (AEs) collected during treatment with the olanzapine long-acting injection (olanzapine LAI)."( A pooled analysis of injection site-related adverse events in patients with schizophrenia treated with olanzapine long-acting injection.
Atkins, S; Case, MG; Detke, HC; McDonnell, DP; Wang, S, 2014
)
"More than 50 % of individuals affected by adverse drug events (ADEs) are older adults."( Quantitative drug benefit-risk assessment: utility of modeling and simulation to optimize drug safety in older adults.
Crentsil, V; Jackson, A; Lee, J, 2014
)
"Our study introduces a real-world approach for finding the safe drug dosing regimen without extensive exposure of a vulnerable and older population to drugs."( Quantitative drug benefit-risk assessment: utility of modeling and simulation to optimize drug safety in older adults.
Crentsil, V; Jackson, A; Lee, J, 2014
)
" Both groups reported insomnia as the most common treatment-emergent adverse event, and no serious adverse event was reported."( A double-blind, randomized comparison study of efficacy and safety of intramuscular olanzapine and intramuscular haloperidol in patients with schizophrenia and acute agitated behavior.
Chan, HY; Chen, CK; Chen, JJ; Chen, YS; Chou, SY; Ree, SC; Su, LW, 2014
)
"Olanzapine is an atypical antipsychotic drug, whose chronic use has been associated with the development of potential adverse effects such as weight gain and cardio-metabolic disorders like hypercholesterolemia and diabetes."( Nanoencapsulation of olanzapine increases its efficacy in antipsychotic treatment and reduces adverse effects.
Burger, ME; Dimer, FA; Friedrich, RB; Guterres, SS; Ortiz, M; Pase, CS; Pohlmann, AR; Roversi, K, 2014
)
" The five-dimension EuroQoL (EQ-5D) was used to evaluate QoL, and side effects were assessed using the Udvalg for Kliniske Undersøgelser (UKU) Side Effect Rating Scale and the Simpson-Angus Scale."( Quality of life in patients with schizophrenia: the impact of socio-economic factors and adverse effects of atypical antipsychotics drugs.
Chaves, KM; de Araújo Dantas, D; de Araújo, AA; de Araújo, RF; de Lima Silva, V; de Medeiros, CA; de Souza, DL; do Nascimento, GG; Ribeiro, SB, 2014
)
"The primary aim of the present study was to assess the possible associations between dopaminergic, serotonergic, and glutamatergic system-related genes and adverse events after antipsychotic treatment in paranoid schizophrenia patients."( Pharmacogenetics of adverse events in schizophrenia treatment: comparison study of ziprasidone, olanzapine and perazine.
Beszlej, A; Bienkowski, P; Frydecka, D; Grzywacz, A; Mierzejewski, P; Samochowiec, A; Samochowiec, J; Trześniowska-Drukała, B; Tybura, P, 2014
)
" Clozapine and olanzapine have the safest therapeutic effect, while the side effect of neutropenia must be controlled by 3 weekly blood controls."( Safety of antipsychotic drugs: focus on therapeutic and adverse effects.
Coveñas, R; Werner, FM, 2014
)
" All studies in English reporting adverse effects associated with olanzapine use in children younger than 13 years or with a mean/median age less than 13 years were included."( The safety of olanzapine in young children: a systematic review and meta-analysis.
Dupuis, LL; Dvorak, CC; Flank, J; Spettigue, W; Sung, L, 2014
)
"No studies were identified with a primary focus on evaluating safety, and the adverse effects reported in the included studies were heterogeneous."( The safety of olanzapine in young children: a systematic review and meta-analysis.
Dupuis, LL; Dvorak, CC; Flank, J; Spettigue, W; Sung, L, 2014
)
"Most adverse events associated with olanzapine use in children less than 13 years of age are of minor clinical significance."( The safety of olanzapine in young children: a systematic review and meta-analysis.
Dupuis, LL; Dvorak, CC; Flank, J; Spettigue, W; Sung, L, 2014
)
"The aim of this study was to compare the efficacy and side-effect profile of the typical antipsychotic haloperidol with that of the atypical antipsychotics risperidone, olanzapine, and aripiprazole in the management of delirium."( Haloperidol, risperidone, olanzapine and aripiprazole in the management of delirium: A comparison of efficacy, safety, and side effects.
Boettger, S; Breitbart, W; Jenewein, J, 2015
)
"The Memorial Delirium Assessment Scale (MDAS), the Karnofsky Performance Status (KPS) scale, and a side-effect rating were recorded at baseline (T1), after 2-3 days (T2), and after 4-7 days (T3)."( Haloperidol, risperidone, olanzapine and aripiprazole in the management of delirium: A comparison of efficacy, safety, and side effects.
Boettger, S; Breitbart, W; Jenewein, J, 2015
)
"Haloperidol, risperidone, aripiprazole, and olanzapine were equally effective in the management of delirium; however, they differed in terms of their side-effect profile."( Haloperidol, risperidone, olanzapine and aripiprazole in the management of delirium: A comparison of efficacy, safety, and side effects.
Boettger, S; Breitbart, W; Jenewein, J, 2015
)
"The reports submitted to the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) from 1997 to 2011 were reviewed to assess serious adverse events induced by the administration of antipsychotics to children."( Antipsychotics-associated serious adverse events in children: an analysis of the FAERS database.
Brown, JB; Kadoyama, K; Kimura, G; Miki, I; Nakamura, T; Nisiguchi, K; Okuno, Y; Sakaeda, T, 2015
)
" Signals in the data that signified a drug-associated adverse event were detected via quantitative data mining algorithms."( Antipsychotics-associated serious adverse events in children: an analysis of the FAERS database.
Brown, JB; Kadoyama, K; Kimura, G; Miki, I; Nakamura, T; Nisiguchi, K; Okuno, Y; Sakaeda, T, 2015
)
" Significant signals of the QT prolongation adverse event were detected only for ziprasidone and risperidone."( Antipsychotics-associated serious adverse events in children: an analysis of the FAERS database.
Brown, JB; Kadoyama, K; Kimura, G; Miki, I; Nakamura, T; Nisiguchi, K; Okuno, Y; Sakaeda, T, 2015
)
"It was suggested that there is a level of diversity in the strength of the association between various first- and second-generation antipsychotics with associated serious adverse events, which possibly lead to fatal outcomes."( Antipsychotics-associated serious adverse events in children: an analysis of the FAERS database.
Brown, JB; Kadoyama, K; Kimura, G; Miki, I; Nakamura, T; Nisiguchi, K; Okuno, Y; Sakaeda, T, 2015
)
" There were no grade 3 or 4 adverse events."( Efficacy and safety of olanzapine combined with aprepitant, palonosetron, and dexamethasone for preventing nausea and vomiting induced by cisplatin-based chemotherapy in gynecological cancer: KCOG-G1301 phase II trial.
Abe, M; Hihara, H; Hirakawa, T; Hirashima, Y; Ichikawa, Y; Ito, K; Itonaga, Y; Kado, N; Kasamatsu, Y; Komeda, S; Kuji, S; Miyagi, K; Murakami, J; Nasu, K; Takahashi, N; Takekuma, M; Tanaka, A, 2016
)
" EPS were assessed at baseline and 4, 8, and 12 weeks after naturalistic SGA initiation for schizophrenia, mood, disruptive behavior, and autism spectrum disorders using the Simpson-Angus Scale (SAS), Barnes Akathisia Scale, Abnormal Involuntary Movement Scale (AIMS), and Treatment Emergent Side Effect Scale."( Neuromotor Adverse Effects in 342 Youth During 12 Weeks of Naturalistic Treatment With 5 Second-Generation Antipsychotics.
Al-Jadiri, A; Azzo, S; Carbon, M; Correll, CU; Kane, JM; Kapoor, S; Saito, E; Sarkaria, T; Sheridan, E, 2015
)
"The aim of this study was to evaluate demographic, clinical, and treatment factors that may impact on neurological adverse effects in naive and quasi-naive children and adolescents treated with antipsychotics."( Neurological Adverse Effects of Antipsychotics in Children and Adolescents.
Alda, JA; Andrés Nestares, P; Arango, C; Baeza, I; Cantarero, CM; Castro-Fornieles, J; de la Serna, E; Garcia-Amador, M; Merchán-Naranjo, J; Moreno, C; Muñoz, D; Tapia, C, 2015
)
" Total dyskinesia score (DyskinesiaS) and total Parkinson score (ParkinsonS) were calculated from the Maryland Psychiatric Research Center Involuntary Movement Scale, total UKU-Cognition score was calculated from the UKU Side Effect Rating Scale."( Neurological Adverse Effects of Antipsychotics in Children and Adolescents.
Alda, JA; Andrés Nestares, P; Arango, C; Baeza, I; Cantarero, CM; Castro-Fornieles, J; de la Serna, E; Garcia-Amador, M; Merchán-Naranjo, J; Moreno, C; Muñoz, D; Tapia, C, 2015
)
"Antipsychotics increased neurological adverse effects in a naive and quasi-naive pediatric population and should be carefully monitored."( Neurological Adverse Effects of Antipsychotics in Children and Adolescents.
Alda, JA; Andrés Nestares, P; Arango, C; Baeza, I; Cantarero, CM; Castro-Fornieles, J; de la Serna, E; Garcia-Amador, M; Merchán-Naranjo, J; Moreno, C; Muñoz, D; Tapia, C, 2015
)
"Olanzapine is efficacious and safe when used as a prophylaxis for CINV."( Efficacy and safety of olanzapine for the prophylaxis of chemotherapy-induced nausea and vomiting (CINV) as reported in phase I and II studies: a systematic review.
Chiu, L; Chiu, N; Chow, E; Chow, R; DeAngelis, C; Lam, H; Navari, R; Pasetka, M; Passik, S; Popovic, M, 2016
)
"Data were assessed from an ongoing, multinational, prospective, observational post-authorisation safety study being conducted to evaluate post-injection delirium/sedation syndrome (PDSS), an adverse reaction that can occur following injection of olanzapine LAI."( Baseline characteristics and hospitalizations in patients with schizophrenia receiving olanzapine long-acting injection: an interim analysis from a non-interventional, prospective observational safety study.
Andrews, JS; Chhabra-Khanna, R; Detke, HC; Faries, DE; Jones, ME; Landry, J; McDonnell, DP; Xu, J, 2015
)
" Case reports, case series, and prospective or cross-sectional studies including relevant data such as relative infant dose (RID), milk-to-plasma ratio (M/P ratio), infant drug plasma levels, and adverse events were identified."( Second-Generation Antipsychotics During the Lactation Period: A Comparative Systematic Review on Infant Safety.
Uguz, F, 2016
)
" Other than clozapine, adverse events were rarely reported in infants exposed to SGAs."( Second-Generation Antipsychotics During the Lactation Period: A Comparative Systematic Review on Infant Safety.
Uguz, F, 2016
)
"The current data suggest that SGAs seem to be relatively safe in the exposed breastfed infants for short-term usage."( Second-Generation Antipsychotics During the Lactation Period: A Comparative Systematic Review on Infant Safety.
Uguz, F, 2016
)
" However, when the patient switched to olanzapine, she developed the ocular side effect as described for chlorpromazine-induced ocular toxicity, with pigmentary depositions on both corneas and the anterior lens surface and decrease in vision."( A Case Report: Anti-Psychotic Agents Related Ocular Toxicity.
Choy, BNK; Fan, MCY; Lai, JSM; Ng, ALK; Shum, JWH, 2016
)
" Efficacy measures, including the Positive and Negative Syndrome Scale (PANSS) and other scales, safety measures, side effect measures, and quality of life were assessed regularly."( A randomized, double-blind, comparison of the efficacy and safety of low-dose olanzapine plus low-dose trifluoperazine versus full-dose olanzapine in the acute treatment of schizophrenia.
Chen, CC; Huang, YH; Lin, CH; Lin, SC; Wang, FC, 2017
)
"Both groups were similar in: 1) baseline characteristics, 2) score changes in all efficacy measures, safety measures, side effect measures, and quality of life, and 3) response rates at each visit."( A randomized, double-blind, comparison of the efficacy and safety of low-dose olanzapine plus low-dose trifluoperazine versus full-dose olanzapine in the acute treatment of schizophrenia.
Chen, CC; Huang, YH; Lin, CH; Lin, SC; Wang, FC, 2017
)
"Polypharmacy is as efficacious and safe as, but cheaper than, monotherapy in the acute treatment of schizophrenia."( A randomized, double-blind, comparison of the efficacy and safety of low-dose olanzapine plus low-dose trifluoperazine versus full-dose olanzapine in the acute treatment of schizophrenia.
Chen, CC; Huang, YH; Lin, CH; Lin, SC; Wang, FC, 2017
)
" The safety outcomes were the adverse events associated with olanzapine according to Common Terminology Criteria for Adverse Events (CTCAE)."( Efficacy and safety of olanzapine for the prevention of chemotherapy-induced nausea and vomiting: A systematic review and meta-analysis.
Nimworapan, M; Permsuwan, U; Yoodee, J, 2017
)
" Drowsiness and constipation were the most reported adverse events."( Efficacy and safety of olanzapine for the prevention of chemotherapy-induced nausea and vomiting: A systematic review and meta-analysis.
Nimworapan, M; Permsuwan, U; Yoodee, J, 2017
)
"Olanzapine is effective and safe at reducing during the delayed and overall phase of the CINV prevention."( Efficacy and safety of olanzapine for the prevention of chemotherapy-induced nausea and vomiting: A systematic review and meta-analysis.
Nimworapan, M; Permsuwan, U; Yoodee, J, 2017
)
"Weight gain is an important side effect of most atypical antipsychotic drugs such as olanzapine."( Metabolic side effects induced by olanzapine treatment are neutralized by CB1 receptor antagonist compounds co-administration in female rats.
Lazzari, P; Marcello, S; Mastinu, A; Pira, M; Serra, V, 2017
)
"The present paper discusses the design, characterization and in vivo evaluation of glyceryl monostearate nanoparticles of Olanzapine, an atypical antipsychotic drug for acute schizophrenia treatment, during which hospitalization is mandatory and adverse effects are at its peak."( Design and in vivo evaluation of solid lipid nanoparticulate systems of Olanzapine for acute phase schizophrenia treatment: Investigations on antipsychotic potential and adverse effects.
Balwani, G; Joseph, E; Reddi, S; Rinwa, V; Saha, R, 2017
)
"Our findings provide evidence suggesting that the metabolic adverse effects of olanzapine may aggravate cognitive dysfunction in patients with schizophrenia through an interaction between BDNF and TNF-alpha."( Metabolic adverse effects of olanzapine on cognitive dysfunction: A possible relationship between BDNF and TNF-alpha.
Cai, J; Chen, M; Fan, W; Fang, X; Mao, Y; Song, L; Tang, W; Yao, P; Zhang, C; Zhang, Y, 2017
)
"There is strong evidence from randomized controlled trials (RCTs) that second-generation antipsychotic (SGA) medications are associated with metabolic adverse events."( Second-Generation Antipsychotics and Metabolic Side Effects: A Systematic Review of Population-Based Studies.
Bresee, L; Hirsch, L; Jette, N; Patten, S; Pringsheim, T; Yang, J, 2017
)
" However, clozapine and olanzapine were consistently more strongly associated with metabolic adverse events than were other SGAs currently available."( Second-Generation Antipsychotics and Metabolic Side Effects: A Systematic Review of Population-Based Studies.
Bresee, L; Hirsch, L; Jette, N; Patten, S; Pringsheim, T; Yang, J, 2017
)
"Olanzapine seems safe when used for a variety of conditions in pediatric emergency patients."( The Use, Safety, and Efficacy of Olanzapine in a Level I Pediatric Trauma Center Emergency Department Over a 10-Year Period.
Blanchard, SR; Cole, JB; Klein, LR; Martel, ML; Nahum, R; Strobel, AM, 2020
)
" This paper provides a review of the principles of antipsychotic switching and discusses pharmacological principles underlying adverse events that occur while switching olanzapine to another antipsychotic medication."( Switch-associated adverse events: focus on olanzapine.
Krishnaswamy, S; Xu, L, 2018
)
"Few publications explore olanzapine switch-related adverse events, the underlying pharmacological principles and appropriate switching strategies to minimise the risk of adverse events."( Switch-associated adverse events: focus on olanzapine.
Krishnaswamy, S; Xu, L, 2018
)
"With the second-generation antipsychotics (SGAs) widely applied to treat patients with schizophrenia, adverse effects, especially the metabolic syndrome (MetS), were paid more attention following by the efficacy of SGAs."( Efficacy and safety of electroacupuncture on metabolic syndrome due to olanzapine and risperidone: Study protocol for a randomized controlled pilot trial.
Chen, P; Jia, H; Ning, Y; Yin, D; Zhu, H, 2019
)
" The effect size, remission/response rate, and risk for discontinuation due to adverse events (AEs), weight gain (WG), nervous systems and gastrointestinal AEs were assessed and compared between two regions with Cohen's d or number needed to treat/harm."( Do Asian and North American patients with bipolar disorder have similar efficacy, tolerability, and safety profile during clinical trials with atypical antipsychotics?
Bai, Y; Chen, G; Gao, K; Yang, H, 2020
)
"The addition of olanzapine to ondansetron and dexamethasone significantly improved CINV prevention and was safe in patients receiving HEC."( The efficacy and safety of the addition of olanzapine to ondansetron and dexamethasone for prevention of chemotherapy-induced nausea and vomiting in patients receiving highly emetogenic chemotherapy.
Angspatt, P; Chenaksara, P; Parinyanitikun, N; Poovorawan, N; Sakdejayont, S; Sriuranpong, V; Sukprakun, S; Tanasanvimon, S; Thawinwisan, W; Vimolchalao, V; Vinayanuwatikun, C; Wongchanapai, P, 2020
)
" Although the olanzapine treatment is associated with disturbed electrical heart activity, the exact mechanism underlying this severe adverse effect remains unclear."( Olanzapine-mediated cardiotoxicity is associated with altered energy metabolism in isolated rat hearts.
Arnold, M; Carrel, T; Grman, M; Gulac, P; Longnus, S; Stankovicova, T; Tomasova, L, 2020
)
" Adverse events (AEs) occurred in 54."( Efficacy and Safety of a Combination of Olanzapine and Samidorphan in Adult Patients With an Acute Exacerbation of Schizophrenia: Outcomes From the Randomized, Phase 3 ENLIGHTEN-1 Study.
DiPetrillo, L; Jiang, Y; Kunovac, J; McDonnell, D; Potkin, SG; Silverman, BL; Simmons, A, 2020
)
" Assessments included adverse events (AEs), weight, vital signs, Positive and Negative Syndrome Scale (PANSS), and Clinical Global Impression-Severity (CGI-S) scores."( Long-term safety and durability of effect with a combination of olanzapine and samidorphan in patients with schizophrenia: results from a 1-year open-label extension study.
Arevalo, C; Graham, C; Jiang, Y; McDonnell, D; Simmons, A; Yagoda, S, 2021
)
" The incidence of treatment-emergent adverse events with INP105 5 mg, 10 mg, and 15 mg was 80%, 66."( The SNAP 101 Double-Blind, Placebo/Active-Controlled, Safety, Pharmacokinetic, and Pharmacodynamic Study of INP105 (Nasal Olanzapine) in Healthy Adults.
Craig, KL; Hocevar-Trnka, J; Hoekman, J; Lickliter, JD; Satterly, KH; Shrewsbury, SB, 2020
)
"To assess adverse events (AEs) and safety of aripiprazole (ARI) and olanzapine (OLA) treatment."( Safety and cardiovascular effects of multiple-dose administration of aripiprazole and olanzapine in a randomised clinical trial.
Abad-Santos, F; Almenara, S; Koller, D; Martín, S; Mejía, G; Navares-Gómez, M; Ochoa, D; Román, M; Romero-Palacián, D; Saiz-Rodríguez, M; Wojnicz, A; Zubiaur, P, 2021
)
" The most frequent adverse drug reactions (ADRs) to ARI were somnolence, headache, insomnia, dizziness, restlessness, palpitations, akathisia and nausea while were somnolence, dizziness, asthenia, constipation, dry mouth, headache and nausea to OLA."( Safety and cardiovascular effects of multiple-dose administration of aripiprazole and olanzapine in a randomised clinical trial.
Abad-Santos, F; Almenara, S; Koller, D; Martín, S; Mejía, G; Navares-Gómez, M; Ochoa, D; Román, M; Romero-Palacián, D; Saiz-Rodríguez, M; Wojnicz, A; Zubiaur, P, 2021
)
" Adverse events for 6-36% patients were reported in all 20 drug arms."( Safety and effectiveness of olanzapine and droperidol for chemical restraint for non-consenting adults: a systematic review and meta-analysis.
Bastiampillai, T; Gerace, A; Grimmer, K; Muir-Cochrane, E; Oster, C, 2021
)
"5 mg intravenous olanzapine is recommended for quick, safe emergency management of people with acute behavioural disturbances associated with mental illness."( Safety and effectiveness of olanzapine and droperidol for chemical restraint for non-consenting adults: a systematic review and meta-analysis.
Bastiampillai, T; Gerace, A; Grimmer, K; Muir-Cochrane, E; Oster, C, 2021
)
" A disproportionality analysis was performed to detect a signal for reporting "infective-pneumonia" and "pneumonia-aspiration" and antipsychotics using reports submitted between 2004 and 2019 to the FDA adverse events spontaneous reporting system (FAERS) database."( Exploring a Safety Signal of Antipsychotic-Associated Pneumonia: A Pharmacovigilance-Pharmacodynamic Study.
Cepaityte, D; Egberts, T; Kouvelas, D; Leucht, S; Papazisis, G; Siafis, S, 2021
)
" We Propose a text mining approach to detect adverse events and medication episodes from the clinical text to enhance our understanding of adverse effects related to Clozapine, the most effective antipsychotic drug for the management of treatment-resistant schizophrenia, but underutilised due to concerns over its side effects."( The side effect profile of Clozapine in real world data of three large mental health hospitals.
Broadbent, M; Dobson, RJB; Dzahini, O; Govind, R; Ibrahim, ZM; Iqbal, E; Kim, CH; MacCabe, JH; Romero, A; Smith, T; Stewart, R; Werbeloff, N, 2020
)
" We explored the prevalence of 33 adverse effects by age, gender, ethnicity, smoking status and admission type three months before and after the patients started Clozapine treatment."( The side effect profile of Clozapine in real world data of three large mental health hospitals.
Broadbent, M; Dobson, RJB; Dzahini, O; Govind, R; Ibrahim, ZM; Iqbal, E; Kim, CH; MacCabe, JH; Romero, A; Smith, T; Stewart, R; Werbeloff, N, 2020
)
"Sedation, fatigue, agitation, dizziness, hypersalivation, weight gain, tachycardia, headache, constipation and confusion were amongst the highest recorded Clozapine adverse effect in the three months following the start of treatment."( The side effect profile of Clozapine in real world data of three large mental health hospitals.
Broadbent, M; Dobson, RJB; Dzahini, O; Govind, R; Ibrahim, ZM; Iqbal, E; Kim, CH; MacCabe, JH; Romero, A; Smith, T; Stewart, R; Werbeloff, N, 2020
)
"Olanzapine is an atypical antipsychotic widely used for the treatment of schizophrenia, which often causes serious adverse drug reactions."( Impact of polymorphisms in transporter and metabolizing enzyme genes on olanzapine pharmacokinetics and safety in healthy volunteers.
Abad-Santos, F; Almenara, S; Koller, D; Martín-Vílchez, S; Mejía-Abril, G; Navares-Gómez, M; Ochoa, D; Román, M; Saiz-Rodríguez, M; Soria-Chacartegui, P; Villapalos-García, G; Zubiaur, P, 2021
)
" Secondary outcomes included the proportion of patients who required rescue medications for agitation within 4 hours of initial IV olanzapine or IV haloperidol administration, incidence of adverse events and ICU length of stay."( A Retrospective Comparison of the Effectiveness and Safety of Intravenous Olanzapine Versus Intravenous Haloperidol for Agitation in Adult Intensive Care Unit Patients.
Abdallah, GT; Eche, IJ; Eche, IM; Hsu, D; Knoph, KN; Patel, P; Wang, M; Wong, A; Yankama, TT, 2022
)
" Safety endpoints analyzed included the following adverse drug events (ADEs): hypotension, bradycardia, cardiac arrhythmias, extrapyramidal adverse effects, and respiratory depressive events."( Safety of Intravenous Olanzapine Administration at a Tertiary Academic Medical Center.
Dube, KM; Hunt, NF; Kovacevic, MP; Lupi, KE; McLaughlin, KC, 2021
)
" All other adverse events were rare (<1%)."( Safety of Intravenous Olanzapine Administration at a Tertiary Academic Medical Center.
Dube, KM; Hunt, NF; Kovacevic, MP; Lupi, KE; McLaughlin, KC, 2021
)
" IVP olanzapine appears to be a safe route of administration in hospitalized patients, including those receiving multiple doses."( Safety of Intravenous Olanzapine Administration at a Tertiary Academic Medical Center.
Dube, KM; Hunt, NF; Kovacevic, MP; Lupi, KE; McLaughlin, KC, 2021
)
"Although it is reported that olanzapine (OLZ), which is an atypical antipsychotic drug, causes sexual dysfunction in men, it is noteworthy that there is not any study evaluating the toxic effects of OLZ on the male reproductive system."( Olanzapine induced reproductive toxicity in male rats.
Ardıç, CM; Atlı-Eklioğlu, Ö; Aydoğan-Kılıç, G; Baysal, M; Ilgın, S; Karaduman, AB; Kılıç, V; Uçarcan, Ş, 2021
)
"The World Health Organization pharmacovigilance database (VigiBase), comprising >18 million adverse events, was queried."( A safety signal of somnambulism with the use of antipsychotics and lithium: A pharmacovigilance disproportionality analysis.
Ferreira, A; Gouverneur, A; Morival, C; Pageot, C; Pariente, A; Tournier, M, 2021
)
" Assessments included adverse events (AEs; each visit), weight/waist circumference (every other week for the first 8 weeks, then every 4 weeks thereafter), metabolic laboratory parameters (weeks 4, 12, 24, 36, and 52), Positive and Negative Syndrome Scale (PANSS) scores (weeks 2, 4, 8, 12, 24, 36, and 52), and Clinical Global Impression-Severity (CGI-S) scores (weeks 2 and 4, then every 4 weeks thereafter through week 48, and at week 52)."( A phase 3, multicenter study to assess the 1-year safety and tolerability of a combination of olanzapine and samidorphan in patients with schizophrenia: Results from the ENLIGHTEN-2 long-term extension.
Bhupathi, V; DiPetrillo, L; Graham, C; Hopkinson, C; Jiang, Y; Kahn, RS; McDonnell, D; Silverman, BL; Simmons, A; Yagoda, S; Yin, J; Yu, B, 2021
)
" No treatment-related adverse events of grade 3 or higher were observed."( Efficacy and safety of 5 mg olanzapine for nausea and vomiting management in cancer patients receiving carboplatin: integrated study of three prospective multicenter phase II trials.
Abe, M; Fujita, Y; Hayasaki, Y; Hirose, C; Iihara, H; Imai, H; Inui, N; Karayama, M; Kawazoe, H; Morishige, KI; Nakamura, K; Ohno, Y; Suda, T; Suzuki, A; Tanaka, K; Uozumi, R; Yamamoto, S, 2021
)
"The findings suggest that antiemetic regimens containing low-dose (5 mg) olanzapine could be effective and safe for patients receiving carboplatin-based chemotherapy."( Efficacy and safety of 5 mg olanzapine for nausea and vomiting management in cancer patients receiving carboplatin: integrated study of three prospective multicenter phase II trials.
Abe, M; Fujita, Y; Hayasaki, Y; Hirose, C; Iihara, H; Imai, H; Inui, N; Karayama, M; Kawazoe, H; Morishige, KI; Nakamura, K; Ohno, Y; Suda, T; Suzuki, A; Tanaka, K; Uozumi, R; Yamamoto, S, 2021
)
" SGAs used for approved indications are associated with significant metabolic adverse effects, including weight gain."( Metabolic adverse effects of off-label use of second-generation antipsychotics in the adult population: a systematic review and meta-analysis.
Agarwal, SM; Asgariroozbehani, R; Bowden, S; Hahn, MK; McIntyre, WB; Remington, G; Siskind, D; Smith, E; Stogios, N; Tran, V, 2022
)
"In this systematic literature review (SLR), we qualitatively synthesized evidence on the comparative efficacy (based on neuropsychiatric inventory), tolerability (weight gain), and safety (cerebrovascular adverse events [CVAE], cardiovascular events, mortality, somnolence, extrapyramidal symptoms [EPS]) of AAPs used to treat DRP."( Comparative Efficacy, Safety, Tolerability, and Effectiveness of Antipsychotics in The Treatment of Dementia-Related Psychosis (DRP): A Systematic Literature Review.
Abler, V; Rajagopalan, K; Rashid, N; Yunusa, I, 2021
)
" Patients treated with these agents may be at higher risk for adverse events such as QTc prolongation and arrhythmias."( Atypical Antipsychotic Safety in the CICU.
Abdul-Aziz, AA; Adie, SK; Deshmukh, A; Gondi, K; Hanna, MP; Ketcham, SW; Konerman, MC; Prescott, HC; Thomas, MP, 2022
)
" Most APs were as safe as oral olanzapine."( Comparative effectiveness and safety of antipsychotic drugs in patients with schizophrenia initiating or reinitiating treatment: A Real-World Observational Study.
Brodeur, S; Courteau, J; Courteau, M; Fleury, MJ; Lesage, A; Roy, MA; Stip, E; Vanasse, A, 2022
)
"The effectiveness of LAI SGAs and clozapine appears to justify their use and are as safe as a recognized treatment (oral olanzapine) in Quebec (Canada)."( Comparative effectiveness and safety of antipsychotic drugs in patients with schizophrenia initiating or reinitiating treatment: A Real-World Observational Study.
Brodeur, S; Courteau, J; Courteau, M; Fleury, MJ; Lesage, A; Roy, MA; Stip, E; Vanasse, A, 2022
)
" Secondary outcomes included psychopathology, remission, all-cause-discontinuation, inefficacy-related discontinuation, and adverse events."( Efficacy and safety/tolerability of antipsychotics in the treatment of adult patients with major depressive disorder: a systematic review and meta-analysis.
Correll, CU; Hagi, K; Kane, JM; Kishimoto, T; Kurokawa, S, 2023
)
" Our study investigated the FDA Adverse Event Reporting System and the pharmacodynamic CHEMBL database to further characterize TGA-induced ICDs."( Impulse Control Disorders by Dopamine Partial Agonists: A Pharmacovigilance-Pharmacodynamic Assessment Through the FDA Adverse Event Reporting System.
De Ponti, F; Fusaroli, M; Giunchi, V; Menchetti, M; Poluzzi, E; Raschi, E; Rimondini Giorgini, R, 2022
)
"We downloaded and pre-processed the FDA Adverse Event Reporting System up to December 2020."( Impulse Control Disorders by Dopamine Partial Agonists: A Pharmacovigilance-Pharmacodynamic Assessment Through the FDA Adverse Event Reporting System.
De Ponti, F; Fusaroli, M; Giunchi, V; Menchetti, M; Poluzzi, E; Raschi, E; Rimondini Giorgini, R, 2022
)
"Retrospective studies using spontaneous reporting system databases have provided a great understanding of adverse drug reactions (ADRs) in the real world, complementing the data obtained from randomized controlled trials."( Characteristics of adverse reactions among antipsychotic drugs using the Korean Adverse Event Reporting System database from 2010 to 2019.
Byeon, SJ; Chung, SJ; Oh, S, 2022
)
"Data were collected from the Korea Adverse Event Reporting System database between 2010 and 2019."( Characteristics of adverse reactions among antipsychotic drugs using the Korean Adverse Event Reporting System database from 2010 to 2019.
Byeon, SJ; Chung, SJ; Oh, S, 2022
)
"In total, 5067 adverse events associated with antipsychotic drugs were reported."( Characteristics of adverse reactions among antipsychotic drugs using the Korean Adverse Event Reporting System database from 2010 to 2019.
Byeon, SJ; Chung, SJ; Oh, S, 2022
)
"Olanzapine and clozapine have similar efficacy when treating mental and behavioral disorders in patients with senile dementia, in which olanzapine is more effective in improving the symptoms of patients with Alzheimer's disease (AD), with less adverse reactions and high safety, which is worth popularizing in clinical practice."( Meta-Analysis of the Efficacy and Safety of Olanzapine versus Clozapine when Treating Senile Dementia.
Feng, Y; Li, M; Lv, L; Qiu, H; Rui, Z; Wang, Y; Wang, Z, 2022
)
" The most common adverse events with Lu AF35700 were increased weight and headache."( Efficacy and safety of Lu AF35700 in treatment-resistant schizophrenia: A randomized, active-controlled trial with open-label extension.
Forray, C; Hertel, P; Howes, OD; Kane, JM; Kinon, BJ; Lemming, OM; Mittoux, A; Such, P, 2022
)
"Current methods are not designed to relate the incidence of individual adverse events reported in clinical trials to the plurality of adverse events accumulated in spontaneous reporting databases during real-world use."( Depicting Risperidone Safety Profiles in Clinical Trials Across Different Diagnoses Using a Dopamine D
Hopkins, SC; Koblan, KS; Ogirala, A; Worden, M; Zeni, C, 2022
)
"Patient-level adverse event data (n = 4400) from controlled clinical trials of the antipsychotic risperidone in schizophrenia, bipolar disorder, Alzheimer's disease psychosis, and autism were obtained through the Yale University Open Data Access (YODA) project."( Depicting Risperidone Safety Profiles in Clinical Trials Across Different Diagnoses Using a Dopamine D
Hopkins, SC; Koblan, KS; Ogirala, A; Worden, M; Zeni, C, 2022
)
"In pooled data from seven trials of adult schizophrenia, class-specific adverse events were identified in 49% of patients treated with risperidone; in 49% of risperidone-treated patients in two trials in adolescent schizophrenia; in 65% of risperidone-treated patients in four trials in adult bipolar disorder; in 50% of risperidone-treated patients in two trials in adolescent schizophrenia; in 36% of risperidone-treated patients in one trial in Alzheimer's disease; and in 94% of risperidone-treated patients in one trial in autism."( Depicting Risperidone Safety Profiles in Clinical Trials Across Different Diagnoses Using a Dopamine D
Hopkins, SC; Koblan, KS; Ogirala, A; Worden, M; Zeni, C, 2022
)
"The cumulative curves of class-specific adverse events in risperidone clinical trials of schizophrenia were similar to those first reported for other atypical antipsychotic drugs."( Depicting Risperidone Safety Profiles in Clinical Trials Across Different Diagnoses Using a Dopamine D
Hopkins, SC; Koblan, KS; Ogirala, A; Worden, M; Zeni, C, 2022
)
" The primary outcome was the overall complete response (defined as the absence of vomiting and of the use of rescue drugs from 0 to 120 hrs since chemotherapy); secondary outcomes were acute (absence of vomiting and use of rescue medicine 0-24 hrs after chemotherapy) and delayed (24-120 hrs) response and adverse events."( Efficacy and safety of antiemetic regimens for highly emetogenic chemotherapy-induced nausea and vomiting: A systematic review and network meta-analysis.
Altamura, V; Carcagnì, A; Daniele, G; Falcone, R; Filetti, M; Giannarelli, D; Giusti, R; Lombardi, P; Scambia, G; Scotte, F, 2023
)
" The secondary outcomes were nausea control, the need for rescue medications, and adverse events of olanzapine."( Efficacy and Safety of Olanzapine for the Prevention of Chemotherapy-induced Nausea and Vomiting in Children: A Systematic Review and Meta-analysis of Randomized Controlled Trials.
Anandani, G; Gupta, AK; Jat, KR; Meena, JP; Sasidharan, A; Tanwar, P, 2023
)
" The adverse effects were headache, insomnia, restlessness, tremor, and akathisia."( Efficacy and Safety of Aripiprazole in Borderline Personality Disorder: A Systematic Review.
Benites-Zapata, VA; Campos-Rodriguez, SK; Fernández, MF; Ortiz-Saavedra, B; Pino-Zavaleta, DA; Valdivieso-Jiménez, G, 2023
)
"To compare the risk for in-hospital adverse events associated with oral haloperidol, olanzapine, quetiapine, and risperidone in older patients after major surgery."( Comparative Safety Analysis of Oral Antipsychotics for In-Hospital Adverse Clinical Events in Older Adults After Major Surgery : A Nationwide Cohort Study.
Bateman, BT; Ely, EW; Inouye, SK; Jones, RN; Kim, DH; Lee, SB; Levin, R; Marcantonio, ER; Metzger, E; Pandharipande, PP; Park, CM; Pisani, MA, 2023
)
"These results suggest that atypical antipsychotics and haloperidol have similar rates of in-hospital adverse clinical events in older patients with postoperative delirium who receive an oral low-to-moderate dose antipsychotic drug."( Comparative Safety Analysis of Oral Antipsychotics for In-Hospital Adverse Clinical Events in Older Adults After Major Surgery : A Nationwide Cohort Study.
Bateman, BT; Ely, EW; Inouye, SK; Jones, RN; Kim, DH; Lee, SB; Levin, R; Marcantonio, ER; Metzger, E; Pandharipande, PP; Park, CM; Pisani, MA, 2023
)
" We analyzed the rank order of the association of antipsychotic agents for schizophrenia with DKA using the Japanese Adverse Drug Event Report database, a spontaneous reporting system database."( Risk evaluation of diabetic ketoacidosis associated with antipsychotics among patients with schizophrenia in the Japanese adverse event report database.
Shimoda, K; Sugawara, N; Yasui-Furukori, N, 2023
)
"We performed a retrospective pharmacovigilance disproportionality analysis using adverse event reports submitted to the Pharmaceuticals and Medical Devices Agency between April 2004 and March 2021."( Risk evaluation of diabetic ketoacidosis associated with antipsychotics among patients with schizophrenia in the Japanese adverse event report database.
Shimoda, K; Sugawara, N; Yasui-Furukori, N, 2023
)

Pharmacokinetics

The literature lacks a pharmacodynamic model to allow for gender-based clinical trial simulations from modelling parameters for Olanzapine and dopamine D2 receptor occupancy. There are limited studies providing sufficient pharmacokinetic data, thus the variability of concentrations of olanzapine used in Chinese paediatric patients aged 10 to 17 years remains to be evaluated. Polymorphisms in CYP2C9, SLC22A1, ABCB1,ABCC2, and APOC3 were related to olanZapine pharmacokinetics variability.

ExcerptReference
" The purpose of the present study was to assess the potential for a pharmacokinetic interaction between olanzapine and carbamazepine, since these agents are likely to be used concomitantly in the treatment of manic psychotic disorder."( A pharmacokinetic interaction between carbamazepine and olanzapine: observations on possible mechanism.
Bergstrom, RF; Gilfillan, DJ; Lucas, RA, 1998
)
" Olanzapine pharmacokinetic values for Cmax and AUC were significantly lower after the second dose, the elimination half-life was significantly shorter, and the clearance and volume of distribution were significantly increased."( A pharmacokinetic interaction between carbamazepine and olanzapine: observations on possible mechanism.
Bergstrom, RF; Gilfillan, DJ; Lucas, RA, 1998
)
" Its mean half-life in healthy individuals was 33 hours, ranging from 21 to 54 hours."( Olanzapine. Pharmacokinetic and pharmacodynamic profile.
Beasley, CM; Bergstrom, RF; Callaghan, JT; Ptak, LR, 1999
)
" Blood samples, collected during dose titration and at a steady state provided pharmacokinetic data."( Olanzapine pharmacokinetics in pediatric and adolescent inpatients with childhood-onset schizophrenia.
Bergstrom, RF; Calis, KA; DeVane, CL; Grothe, DR; Jacobsen, L; Kumra, S; Kurtz, DL; Rapoport, JL, 2000
)
" Its pharmacokinetic properties are comparable to those of classical antipsychotics."( [Olanzapine: pharmacology, pharmacokinetics and therapeutic drug monitoring].
Baumann, P; Grasmäder, K; Hiemke, C; Rao, ML, 2001
)
" The purpose of this study was to assess the potential for pharmacokinetic interaction between olanzapine and fluoxetine, a popular antidepressant that is a selective serotonin reuptake inhibitor."( Influence of fluoxetine on olanzapine pharmacokinetics.
de Suray, JM; Gangji, D; Gossen, D; Onkelinx, C; Vandenhende, F, 2002
)
" We compared olanzapine noncompartmental pharmacokinetic parameter values before and after ritonavir with a paired Student t test."( Influence of ritonavir on olanzapine pharmacokinetics in healthy volunteers.
Hon, YY; Jann, MW; Lawhorn, WD; Penzak, SR; Shirley, KL; Spratlin, V, 2002
)
" In this study, pharmacokinetic interactions and clinical effects of adding the CYP1A2 inhibitor fluvoxamine to steady-state olanzapine was examined in patients suffering from schizophrenia."( Fluvoxamine augmentation of olanzapine in chronic schizophrenia: pharmacokinetic interactions and clinical effects.
Hadjez, J; Härtter, S; Hiemke, C; Jabarin, M; Modai, I; Peled, A; Ritsner, M; Silver, H; Weigmann, H, 2002
)
"To compare the pharmacokinetic profiles and dose proportionality of olanzapine in Chinese and Caucasian subjects."( Olanzapine pharmacokinetics are similar in Chinese and Caucasian subjects.
Bergstrom, RF; Chan, C; Sathirakul, K; Teng, L; Wise, SD; Yeo, KP, 2003
)
" Noncompartmental pharmacokinetic parameters were derived."( Olanzapine pharmacokinetics are similar in Chinese and Caucasian subjects.
Bergstrom, RF; Chan, C; Sathirakul, K; Teng, L; Wise, SD; Yeo, KP, 2003
)
" However, pharmacokinetic interactions between the two classes of drugs remain to be explored."( The differential effects of steady-state fluvoxamine on the pharmacokinetics of olanzapine and clozapine in healthy volunteers.
Cai, ZJ; Li, WB; Wang, CY; Weng, YZ; Zhai, YM; Zhang, ZJ; Zhao, JP; Zhou, HH; Zhu, RH, 2004
)
" This study investigated the pharmacokinetic interactions between olanzapine and fluvoxamine in patients with schizophrenia."( Dose-dependent alternations in the pharmacokinetics of olanzapine during coadministration of fluvoxamine in patients with schizophrenia.
Chang, WH; Chiu, CC; Hon, YY; Huang, MC; Jann, MW; Lane, HY; Liu, HC; Lu, ML, 2004
)
" However, there were no statistically significant differences observed between any of the OLZ exposures for observed pharmacokinetic parameters (C(max), T(max), AUC(0-8h))."( Pharmacokinetics of olanzapine after single-dose oral administration of standard tablet versus normal and sublingual administration of an orally disintegrating tablet in normal volunteers.
DeVane, CL; Donovan, JL; Gefroh, HA; Malcolm, RJ; Markowitz, JS; Wang, JS; Zhu, HJ, 2006
)
"To assess the pharmacokinetic effect and tolerability of lamotrigine 200 mg day(-1) and olanzapine 15 mg day(-1) coadministration in healthy male volunteers."( Pharmacokinetics and tolerability of lamotrigine and olanzapine coadministered to healthy subjects.
Abbott, R; Ascher, J; Bullman, J; Francis, E; Job, S; Sidhu, J; Theis, JG, 2006
)
" Steady state (0-24 h) pharmacokinetic profiles were determined on day 56 in each group."( Pharmacokinetics and tolerability of lamotrigine and olanzapine coadministered to healthy subjects.
Abbott, R; Ascher, J; Bullman, J; Francis, E; Job, S; Sidhu, J; Theis, JG, 2006
)
"Among these subjects with psychiatric illnesses, olanzapine at doses of 30 and 40 mg/d displayed a pharmacokinetic profile consistent with that of 20 mg/d."( A double-blind, randomized trial to evaluate the pharmacokinetics and tolerability of 30 or 40 mg/d oral olanzapine relative to 20 mg/d oral olanzapine in stable psychiatric subjects.
Bari, MA; Cavazzoni, P; Falk, D; Hardy, T; Kurtz, D; Marquez, E; Mitchell, CP; Mitchell, M; Riesenberg, R; Taylor, CC, 2006
)
"The plasma concentration curve of olanzapine following a single oral dose conformed to the two compartment open model."( [Reversed phase high-performance liquid chromatography for determination of plasma olanzapine and pharmacokinetics of olanzapine in healthy Chinese volunteers].
Liu, WZ; Yang, H; Zhu, J, 2006
)
" This article reports results from 3 studies examining the potential for cytochrome P450-dependent pharmacokinetic interactions between STS and 3 psychotropic medications that might be coadministered."( Selegiline transdermal system: an examination of the potential for CYP450-dependent pharmacokinetic interactions with 3 psychotropic medications.
Azzaro, AJ; Campbell, BJ; Kemper, E; VanDenBerg, C; Ziemniak, J, 2007
)
" These long-term effects would not be captured by a standard 5-day pharmacokinetic TDM developmental testing model for antipsychotics, and a new model for characterizing variation in C/D by time course is therefore proposed."( Long-term therapeutic drug monitoring of risperidone and olanzapine identifies altered steady-state pharmacokinetics: a clinical, two-group, naturalistic study.
Darby, JK; Herbert, J; Pasta, DJ; Wilson, MG, 2008
)
" The pharmacokinetic parameters were calculated by the non-compartment method using WinNonlin software."( Pharmacokinetics of olanzapine in Chinese male schizophrenic patients with various smoking behaviors.
Chen, HY; Chiu, CC; Lin, FW; Lu, ML; Shen, WW; Wang, LH; Wu, TH, 2008
)
" In addition, olanzapine pharmacokinetic parameters in adolescents were compared with those in adults to guide appropriate dosing recommendations for adolescent patients."( Oral olanzapine disposition in adolescents with schizophrenia or bipolar I disorder: a population pharmacokinetic model.
Bergstrom, RF; Hong, Q; Lobo, ED; Quinlan, T; Robertson-Plouch, C, 2010
)
"A population pharmacokinetic modeling study was performed."( Oral olanzapine disposition in adolescents with schizophrenia or bipolar I disorder: a population pharmacokinetic model.
Bergstrom, RF; Hong, Q; Lobo, ED; Quinlan, T; Robertson-Plouch, C, 2010
)
"The pharmacokinetics of oral olanzapine in adolescent patients were described by a one-compartment pharmacokinetic model."( Oral olanzapine disposition in adolescents with schizophrenia or bipolar I disorder: a population pharmacokinetic model.
Bergstrom, RF; Hong, Q; Lobo, ED; Quinlan, T; Robertson-Plouch, C, 2010
)
" A two-compartment pharmacokinetic model was used to describe the plasma pharmacokinetic profile."( Mechanism-based pharmacokinetic-pharmacodynamic modeling of the dopamine D2 receptor occupancy of olanzapine in rats.
Danhof, M; de Greef, R; Grimwood, S; Groothuis, GM; Johnson, M; Kozielska, M; Li, C; Pilla Reddy, V; Proost, JH; Vermeulen, A, 2011
)
" The objective of this review was to determine whether olanzapine warrants clinical pharmacokinetic monitoring in patients with schizophrenia, using a previously published decision-making algorithm."( Does olanzapine warrant clinical pharmacokinetic monitoring in schizophrenia?
Dumontet, J; Ensom, MH; Schwenger, E, 2011
)
" Statistical analysis of the pharmacokinetic parameters Cmax, AUC0-144, and AUC0-∞ was conducted to determine bioequivalence."( Pharmacokinetics and bioequivalence of 2 tablet formulations of olanzapine in healthy Chinese volunteers: a randomized, open-label, single-dose study.
Chen, Q; Jia, JY; Li, SJ; Liu, GY; Liu, Y; Liu, YM; Lu, C; Qi, YL; Yu, C; Zhang, MQ, 2012
)
" The present study aims to improve our understanding of antipsychotic-related adverse reactions (ARs) and their possible association with common genetic variants of pharmacodynamic proteins such as neurotransmitter receptors/transporters."( Pharmacodynamic genetic variants related to antipsychotic adverse reactions in healthy volunteers.
Abad-Santos, F; Ayuso, C; Borobia, AM; Cabaleiro, T; Carcas, AJ; López-Rodríguez, R; Novalbos, J; Ochoa, D; Román, M, 2013
)
"Genetic variants in pharmacodynamic genes could represent valuable markers of AR risk and antipsychotic safety."( Pharmacodynamic genetic variants related to antipsychotic adverse reactions in healthy volunteers.
Abad-Santos, F; Ayuso, C; Borobia, AM; Cabaleiro, T; Carcas, AJ; López-Rodríguez, R; Novalbos, J; Ochoa, D; Román, M, 2013
)
"This study assessed the safety profile, tolerability, and pharmacokinetic (PK) properties of olanzapine after single and multiple administrations of olanzapine LAI and evaluated maintenance of symptom control."( Single- and multiple-dose pharmacokinetic, safety, and tolerability profiles of olanzapine long-acting injection: an open-label, multicenter, nonrandomized study in patients with schizophrenia.
Bergstrom, R; Jen, KY; Johnson, J; Kothare, P; McDonnell, D; Mitchell, M; Walker, D; Zhao, F, 2013
)
" The objective of this study was to use pharmacokinetic and pharmacodynamic modeling tools to relate CAT with D2RO in rats and to compare that with the relationship between D2RO and EPS in humans."( Dopamine D2 receptor occupancy as a predictor of catalepsy in rats: a pharmacokinetic-pharmacodynamic modeling approach.
Barton, HA; Danhof, M; de Greef, R; Grimwood, S; Groothuis, GM; Johnson, M; Kozielska, M; Pilla Reddy, V; Proost, JH; Vermeulen, A, 2014
)
" Half-life was ∼30 days, controlled by the slow rate of intramuscular absorption rather than the 30-h elimination rate-based half-life of oral olanzapine."( Pharmacokinetics of olanzapine long-acting injection: the clinical perspective.
Bergstrom, RF; Detke, HC; Heres, S; Kraemer, S, 2014
)
" Pharmacodynamic assessments (apomorphine - induced compulsive behavior and spontaneous locomotor activity) were performed using mice."( Evaluation of brain targeting efficiency of intranasal microemulsion containing olanzapine: pharmacodynamic and pharmacokinetic consideration.
Bhatt, KK; Gaikwad, RV; Patel, BG; Patel, MR; Patel, RB, 2016
)
" Standard pharmacokinetic models do not fit to the toxic concentration data."( Abnormal olanzapine toxicokinetic profiles--population pharmacokinetic analysis.
Anand, JS; Ciszowski, K; Jawień, W; Tylutki, Z; Wilimowska, J, 2015
)
"One-hundred thirty-five plasma concentration data from 21 patients hospitalized for acute olanzapine poisoning were analyzed with the use of the population pharmacokinetic approach."( Abnormal olanzapine toxicokinetic profiles--population pharmacokinetic analysis.
Anand, JS; Ciszowski, K; Jawień, W; Tylutki, Z; Wilimowska, J, 2015
)
" This validated method was successfully applied to a pharmacokinetic study in which 10-mg OLZ tablets were administered to healthy volunteers and their plasma OLZ levels were monitored over time."( The development and validation of a method for quantifying olanzapine in human plasma by liquid chromatography tandem mass spectrometry and its application in a pharmacokinetic study.
Bastos Leal, L; Cavalcanti Bedor, NC; da Mota Castelo Branco, D; Galindo Bedor, DC; Miranda de Sousa, CE; Nunes Bonifácio, F; Pereira de Santana, D, 2015
)
" We characterized the impact of sertraline co-administration on olanzapine clearance in psychotic depression using population pharmacokinetic methods."( The Impact of Sertraline Co-Administration on the Pharmacokinetics of Olanzapine: A Population Pharmacokinetic Analysis of the STOP-PD.
Bies, RR; Davies, SJ; Flint, AJ; Kirshner, MM; Meyers, BS; Mulsant, BH; Pollock, BG; Rothschild, AJ; Sorisio, D; Whyte, EM, 2015
)
" We used NONMEM (Version VII) for population pharmacokinetic analysis, assessing effects of the covariates sex, African American origin, smoking, age, and sertraline co-administration."( The Impact of Sertraline Co-Administration on the Pharmacokinetics of Olanzapine: A Population Pharmacokinetic Analysis of the STOP-PD.
Bies, RR; Davies, SJ; Flint, AJ; Kirshner, MM; Meyers, BS; Mulsant, BH; Pollock, BG; Rothschild, AJ; Sorisio, D; Whyte, EM, 2015
)
"Population pharmacokinetic analysis comprised 336 samples from 175 individuals."( The Impact of Sertraline Co-Administration on the Pharmacokinetics of Olanzapine: A Population Pharmacokinetic Analysis of the STOP-PD.
Bies, RR; Davies, SJ; Flint, AJ; Kirshner, MM; Meyers, BS; Mulsant, BH; Pollock, BG; Rothschild, AJ; Sorisio, D; Whyte, EM, 2015
)
" The validated UPLC method was successfully applied to the pharmacokinetic study of RIS and 9-OHRIS in human plasma."( Concurrent determination of olanzapine, risperidone and 9-hydroxyrisperidone in human plasma by ultra performance liquid chromatography with diode array detection method: application to pharmacokinetic study.
Ramanathan, M; Siva Selva Kumar, M, 2016
)
"Due to high inter-individual variability in peripheral pharmacokinetic parameters, dosing of antipsychotics currently relies on clinical trial-and-error, and predicting antipsychotic plasma concentrations before changing a dose has been a challenge."( Predicting Plasma Olanzapine Concentration Following a Change in Dosage: A Population Pharmacokinetic Study.
Bies, RR; Caravaggio, F; Graff-Guerrero, A; Mamo, DC; Mimura, M; Nakajima, S; Plitman, E; Pollock, BG; Suzuki, T; Takeuchi, H; Tsuboi, T; Uchida, H, 2015
)
" Half-life and sex effect on sertraline apparent clearance (males averaging 50% higher (p < 0."( SSRI-antipsychotic combination in psychotic depression: sertraline pharmacokinetics in the presence of olanzapine, a brief report from the STOP-PD study.
Bies, RR; Davies, SJ; Flint, AJ; Kirshner, MM; Meyers, BS; Mulsant, BH; Pollock, BG; Rothschild, AJ; Sorisio, D; Whyte, EM, 2016
)
"The aim of this study was to build an eligible population pharmacokinetic (PK) model for olanzapine in Chinese psychotic patients based on therapeutic drug monitoring (TDM) data, with assistance of meta-analysis, to facilitate individualized therapy."( Population pharmacokinetics analysis of olanzapine for Chinese psychotic patients based on clinical therapeutic drug monitoring data with assistance of meta-analysis.
Li, L; Lu, W; Shang, D; Wen, Y; Yin, A; Zhou, T, 2016
)
" However, the literature lacks a pharmacodynamic model to allow for gender-based clinical trial simulations from modelling parameters for Olanzapine and dopamine D2 receptor occupancy."( A pharmacodynamic modelling and simulation study identifying gender differences of daily olanzapine dose and dopamine D2-receptor occupancy.
Eugene, AR; Masiak, J, 2017
)
"Population pharmacodynamic modelling was performed using non-linear mixed effects modelling in MONOLIX, while the Clinical Trial Simulations were performed using R for statistical programming."( A pharmacodynamic modelling and simulation study identifying gender differences of daily olanzapine dose and dopamine D2-receptor occupancy.
Eugene, AR; Masiak, J, 2017
)
"The aim of the present study was to predict olanzapine (OLZ) exposure in individual patients using physiologically based pharmacokinetic modelling and simulation (PBPK M&S)."( Prediction of olanzapine exposure in individual patients using physiologically based pharmacokinetic modelling and simulation.
Korprasertthaworn, P; Mohan, T; Perera, V; Polasek, TM; Rostami-Hodjegan, A; Rowland, A; Sorich, MJ; Tucker, GT; Wiese, MD, 2018
)
"1) and validated against pharmacokinetic studies and data from therapeutic drug monitoring (TDM)."( Prediction of olanzapine exposure in individual patients using physiologically based pharmacokinetic modelling and simulation.
Korprasertthaworn, P; Mohan, T; Perera, V; Polasek, TM; Rostami-Hodjegan, A; Rowland, A; Sorich, MJ; Tucker, GT; Wiese, MD, 2018
)
" Studies reporting the pharmacokinetic parameters of CYP1A2-metabolized antipsychotic drugs in individuals who were genotyped for CYP1A2 genetic polymorphisms were retrieved."( Impact of CYP1A2 genetic polymorphisms on pharmacokinetics of antipsychotic drugs: a systematic review and meta-analysis.
Hanprasertpong, N; Koonrungsesomboon, N; Na Takuathung, M; Teekachunhatean, S, 2019
)
" Pharmacokinetic parameters were calculated according to noncompartmental analysis."( Pharmacokinetics and Short-term Safety of ALKS 3831, a Fixed-dose Combination of Olanzapine and Samidorphan, in Adult Subjects with Schizophrenia.
McDonnell, D; Sun, L; von Moltke, L, 2018
)
" At steady state, exposure to olanzapine increased dose proportionally from 10 mg (ALKS 3831 10/10) to 20 mg (ALKS 3831 20/10), and exposure to samidorphan was similar between the 2 ALKS 3831 dose groups, indicating that different dose levels of olanzapine in ALKS 3831 had no impact on the pharmacokinetic profile of samidorphan."( Pharmacokinetics and Short-term Safety of ALKS 3831, a Fixed-dose Combination of Olanzapine and Samidorphan, in Adult Subjects with Schizophrenia.
McDonnell, D; Sun, L; von Moltke, L, 2018
)
" The present data indicate that combining olanzapine with samidorphan does not affect the pharmacokinetic profile of either drug and support continued clinical evaluation of ALKS 3831."( Pharmacokinetics and Short-term Safety of ALKS 3831, a Fixed-dose Combination of Olanzapine and Samidorphan, in Adult Subjects with Schizophrenia.
McDonnell, D; Sun, L; von Moltke, L, 2018
)
" Olanzapine and samidorphan pharmacokinetic parameters were determined after OLZ/SAM dosing on days 1 and 22."( A Phase I Open-Label Study to Evaluate the Effects of Rifampin on the Pharmacokinetics of Olanzapine and Samidorphan Administered in Combination in Healthy Human Subjects.
Kumar, V; McDonnell, D; Sun, L; von Moltke, L; Yu, M, 2019
)
" Pharmacokinetic parameters of lithium and valproate, including maximum plasma concentration and area under the plasma concentration-time curve over a 12-h dosing interval, were calculated."( Combination of Olanzapine and Samidorphan Has No Clinically Significant Effect on the Pharmacokinetics of Lithium or Valproate.
Graham, C; Sun, L; von Moltke, L; Yagoda, S; Yao, B, 2020
)
" This open-label, randomized, single-dose, 2-sequence, 2-period crossover, comparative pharmacokinetic study assessed the bioequivalence of 5 mg of olanzapine administered in tablet (R) or disintegrating tablet (T) formulation in healthy Chinese volunteers under both fasting and fed conditions."( Open-Label, Randomized, Single-Dose, 2-Period, 2-Sequence Crossover, Comparative Pharmacokinetic Study to Evaluate Bioequivalence of 2 Oral Formulations of Olanzapine Under Fasting and Fed Conditions.
Du, P; Li, P; Liu, H; Liu, L; Yu, W; Zhao, R; Zhao, Z; Zhou, X, 2020
)
" As cytochrome P450 (CYP) 1A2 and CYP3A4 are the major enzymes involved in metabolism of olanzapine and samidorphan, respectively, physiologically-based pharmacokinetic (PBPK) modeling was applied to predict any drug-drug interaction (DDI) potential between olanzapine and samidorphan or between OLZ/SAM and CYP3A4/CYP1A2 inhibitors/inducers."( Physiologically-Based Pharmacokinetic Modeling for Predicting Drug Interactions of a Combination of Olanzapine and Samidorphan.
Rowland Yeo, K; Sun, L; von Moltke, L, 2020
)
" Population pharmacokinetic approach, based on nonlinear mixed effects modeling, is a useful tool to identify covariates explaining pharmacokinetic variability, as well as to characterize and distinguish unexplained residual and between-subject (interindividual) variability."( Understanding variability in the pharmacokinetics of atypical antipsychotics - focus on clozapine, olanzapine and aripiprazole population models.
Jovanović, M; Miljković, B; Vučićević, K, 2020
)
" The analysis was restricted to pharmacokinetic (PK) samples collected following enteral administration (oral and feeding tube)."( Population pharmacokinetics of olanzapine in children.
Al-Uzri, A; Autmizguine, J; Cohen-Wolkowiez, M; Erinjeri, J; Goldstein, SL; Hornik, CP; Kalra, R; Maharaj, AR; Payne, EH; Sherwin, CMT; Watt, K; Wu, H; Zimmerman, KO, 2021
)
"At equivalent doses, INP105 provided similar area under the drug concentration-time curve (AUC) from time 0 to the last measurable concentration, AUC from time 0 to infinity, and maximum observed concentration (Cmax) as OLZ IM and greater Cmax than but similar AUCs to OLZ ODT."( The SNAP 101 Double-Blind, Placebo/Active-Controlled, Safety, Pharmacokinetic, and Pharmacodynamic Study of INP105 (Nasal Olanzapine) in Healthy Adults.
Craig, KL; Hocevar-Trnka, J; Hoekman, J; Lickliter, JD; Satterly, KH; Shrewsbury, SB, 2020
)
"INP105 has rapid absorption and pharmacodynamic effects and may represent an effective, convenient, noninvasive, and well-tolerated alternative for treating acutely agitated patients by self- or caregiver administration in the home, community, or hospital environments."( The SNAP 101 Double-Blind, Placebo/Active-Controlled, Safety, Pharmacokinetic, and Pharmacodynamic Study of INP105 (Nasal Olanzapine) in Healthy Adults.
Craig, KL; Hocevar-Trnka, J; Hoekman, J; Lickliter, JD; Satterly, KH; Shrewsbury, SB, 2020
)
" Complementary to the clinical findings, physiologically based pharmacokinetic modeling was used to assess the effects of varying degrees of renal impairment on the pharmacokinetics of olanzapine and samidorphan."( Application of Physiologically Based Pharmacokinetic Modeling to Predict the Effect of Renal Impairment on the Pharmacokinetics of Olanzapine and Samidorphan Given in Combination.
Rowland Yeo, K; Sun, L; von Moltke, L, 2021
)
"A physiologically based pharmacokinetic model for OLZ/SAM was developed and validated by comparing model-simulated data with observed clinical data."( Application of Physiologically Based Pharmacokinetic Modeling to Predict the Effect of Renal Impairment on the Pharmacokinetics of Olanzapine and Samidorphan Given in Combination.
Rowland Yeo, K; Sun, L; von Moltke, L, 2021
)
"Physiologically based pharmacokinetic modeling extended the findings from a clinical study in severe renal impairment to other untested clinical scenarios; these data could be of interest to clinicians treating patients with renal impairment."( Application of Physiologically Based Pharmacokinetic Modeling to Predict the Effect of Renal Impairment on the Pharmacokinetics of Olanzapine and Samidorphan Given in Combination.
Rowland Yeo, K; Sun, L; von Moltke, L, 2021
)
" Polymorphisms in CYP2C9, SLC22A1, ABCB1, ABCC2, and APOC3 were related to olanzapine pharmacokinetic variability."( Impact of polymorphisms in transporter and metabolizing enzyme genes on olanzapine pharmacokinetics and safety in healthy volunteers.
Abad-Santos, F; Almenara, S; Koller, D; Martín-Vílchez, S; Mejía-Abril, G; Navares-Gómez, M; Ochoa, D; Román, M; Saiz-Rodríguez, M; Soria-Chacartegui, P; Villapalos-García, G; Zubiaur, P, 2021
)
" Population pharmacokinetic models for olanzapine and samidorphan were developed using data from 11 clinical studies in healthy subjects or patients with schizophrenia."( Population Pharmacokinetics of Olanzapine and Samidorphan When Administered in Combination in Healthy Subjects and Patients With Schizophrenia.
Mills, R; Rege, B; Sadler, BM; Sun, L, 2021
)
" With this review, we aim to provide an overview of the pharmacodynamic interactions between ketamine and mood stabilizers, benzodiazepines, monoamine oxidase-inhibitors, antipsychotics, and psychostimulants."( Pharmacodynamic Interactions Between Ketamine and Psychiatric Medications Used in the Treatment of Depression: A Systematic Review.
Bakker, IM; Kamphuis, J; Schoevers, RA; Smith-Apeldoorn, SY; Touw, DJ; Veraart, JKE; Visser, BAE, 2021
)
" More studies are needed to provide insight into pharmacodynamic interactions with ketamine."( Pharmacodynamic Interactions Between Ketamine and Psychiatric Medications Used in the Treatment of Depression: A Systematic Review.
Bakker, IM; Kamphuis, J; Schoevers, RA; Smith-Apeldoorn, SY; Touw, DJ; Veraart, JKE; Visser, BAE, 2021
)
" Physiologically-based pharmacokinetic (PBPK) modeling was used to extend the clinical findings to predict the effects of varying degrees of hepatic impairment on the PKs of olanzapine and samidorphan."( Using physiologically-based pharmacokinetic modeling for predicting the effects of hepatic impairment on the pharmacokinetics of olanzapine and samidorphan given as a combination tablet.
Barter, Z; Rowland Yeo, K; Sun, L; von Moltke, L, 2021
)
" The rate of removal of LAIs is regulated by the slow rate of absorption in the site of injection and the phenomenon of their increased half-life is called flip-flop pharmacokinetics."( [Clinical pharmacokinetics and pharmaceutical forms of long-acting injectable antipsychotics].
Kyziridis, TC, 2022
)
" Our study investigated the FDA Adverse Event Reporting System and the pharmacodynamic CHEMBL database to further characterize TGA-induced ICDs."( Impulse Control Disorders by Dopamine Partial Agonists: A Pharmacovigilance-Pharmacodynamic Assessment Through the FDA Adverse Event Reporting System.
De Ponti, F; Fusaroli, M; Giunchi, V; Menchetti, M; Poluzzi, E; Raschi, E; Rimondini Giorgini, R, 2022
)
" There are limited studies providing sufficient pharmacokinetic data, thus the variability of concentrations of olanzapine used in Chinese paediatric patients aged 10 to 17 years remains to be evaluated."( Population pharmacokinetics and dosing optimization of olanzapine in Chinese paediatric patients: Based on the impact of sex and concomitant valproate on clearance.
Hu, JQ; Huang, SQ; Kong, W; Li, XL; Liu, SJ; Lu, HQ; Lu, HY; Ni, XJ; Shang, DW; Wen, YG; Xiao, T; Yang, HL; Zhang, M; Zhu, XQ, 2022
)
" Due to its high pharmacokinetic variability, several population pharmacokinetic studies have been performed to identify factors contributing to the variability and thus facilitate individualized dosing."( Significant predictors for olanzapine pharmacokinetics: a systematic review of population pharmacokinetic studies.
Han, L; Jiao, Z; Liu, XQ; Mao, JH,
)
"A total of 10 population pharmacokinetic and three population pharmacokinetic/pharmacodynamic studies involving infants, children, adolescents, and adults were finally included."( Significant predictors for olanzapine pharmacokinetics: a systematic review of population pharmacokinetic studies.
Han, L; Jiao, Z; Liu, XQ; Mao, JH,
)

Compound-Compound Interactions

Olanzapine and other antipsychotics in combination with selective serotonin uptake inhibitors fluoxetine or sertraline on neurotransmitter release in rat prefrontal cortex (PFC) using microdialysis.

ExcerptReference
"To understand the mechanism of the clinical efficacy of olanzapine and fluoxetine combination therapy for treatment-resistant depression (TRD), we studied the effects of olanzapine and other antipsychotics in combination with the selective serotonin uptake inhibitors fluoxetine or sertraline on neurotransmitter release in rat prefrontal cortex (PFC) using microdialysis."( Synergistic effects of olanzapine and other antipsychotic agents in combination with fluoxetine on norepinephrine and dopamine release in rat prefrontal cortex.
Bao, J; Bymaster, FP; Perry, KW; Potts, BD; Tollefson, GD; Wong, DT; Zhang, W, 2000
)
"This study examined the short-term efficacy of electroconvulsive therapy (ECT) combined with antipsychotic medication in treatment-resistant schizophrenia (TRS)."( Efficacy of electroconvulsive therapy combined with antipsychotic medication in treatment-resistant schizophrenia: a prospective, open trial.
Tang, WK; Ungvari, GS, 2002
)
" Treatment with divalproex in combination with an atypical antipsychotic agent resulted in earlier improvements in a range of psychotic symptoms among acutely hospitalized patients with schizophrenia."( Effect of divalproex combined with olanzapine or risperidone in patients with an acute exacerbation of schizophrenia.
Casey, DE; Daniel, DG; Sommerville, KW; Tracy, KA; Wassef, AA; Wozniak, P, 2003
)
"To evaluate the efficacy of olanzapine, in combination with lithium or valproate, for treating depressive symptoms associated with mania."( Efficacy of olanzapine combined with valproate or lithium in the treatment of dysphoric mania.
Akiskal, HS; Baker, RW; Brown, E; Calabrese, JR; Ketter, TA; Schuh, LM; Tohen, M; Trzepacz, PT; Watkin, JG, 2004
)
"Secondary analysis of a 6-week, double-blind, randomised study of olanzapine (5-20 mg/day) or placebo combined with ongoing valproate or lithium open treatment for 344 patients in mixed or manic episodes."( Efficacy of olanzapine combined with valproate or lithium in the treatment of dysphoric mania.
Akiskal, HS; Baker, RW; Brown, E; Calabrese, JR; Ketter, TA; Schuh, LM; Tohen, M; Trzepacz, PT; Watkin, JG, 2004
)
"Patients with major depressive disorder (MDD) treated with olanzapine in combination with fluoxetine (OFC) demonstrate robust improvement in their depressive symptoms."( Long-term weight gain in patients treated with open-label olanzapine in combination with fluoxetine for major depressive disorder.
Andersen, SW; Clemow, DB; Corya, SA, 2005
)
" It highlights three features: first, MHN can safely prescribe psychiatric medication in combination with concordance therapy."( Pharmacological management of akathisia in combination with psychological interventions by a mental health nurse consultant.
Arya, P; Bennett, J; Gray, R; Jones, M; Lucas, B, 2006
)
"To identify symptoms associated with suicidality in bipolar I disorder patients, and to assess suicide risk during treatment with olan-zapine in combination with lithium or divalproex."( Reduced suicidal ideation in bipolar I disorder mixed-episode patients in a placebo-controlled trial of olanzapine combined with lithium or divalproex.
Ahl, J; Baldessarini, RJ; Houston, JP; Kaiser, CJ; Meyers, AL; Tohen, M, 2006
)
" Olanzapine (orally disintegrating tablets) in combination with alprazolam was used successfully to relieve this terminally ill patient's anxiety and tension improving his relationship with his physicians and his daily life."( Sublingual use of olanzapine in combination with alprazolam to treat agitation in a terminally ill patient receiving parenteral nutrition.
Douzenis, A; Economopoulos, T; Lykouras, L; Michopoulos, I; Soldatos, CR, 2007
)
" This study evaluates the effects of treatment with lithium, alone or in combination with antipsychotic olanzapine, on oxidant-antioxidant status and atherogenic character in patients with BD."( Treatment with lithium, alone or in combination with olanzapine, relieves oxidative stress but increases atherogenic lipids in bipolar disorder.
Aliyazicioğlu, R; Ayvaz, S; Colak, M; Değer, O; Karahan, SC; Kural, B, 2007
)
"The objective of this study was to evaluate the efficacy and safety of divalproex sodium extended release (divalproex ER) vs placebo in combination with olanzapine or risperidone for the treatment of acute exacerbations of schizophrenia."( Divalproex ER combined with olanzapine or risperidone for treatment of acute exacerbations of schizophrenia.
Abi-Saab, W; Baker, J; Casey, DE; Daniel, DG; Greco, N; Kane, JM; Redden, L; Saltarelli, M; Tamminga, C; Tran-Johnson, T; Wozniak, P, 2009
)
" In this study, we sought to further examine this mechanism using a novel drug-drug conditioning procedure."( An investigation of the behavioral mechanisms of antipsychotic action using a drug-drug conditioning paradigm.
He, W; Li, M; Mead, A, 2009
)
" We reexamined all his possible medical conditions and found that the patient had an abnormally enlarged cavus septum pellucidum (CSP) combined with cavum vergae (CV) (maximum length >30 mm)."( A case report on the relationship between treatment-resistant childhood-onset schizophrenia and an abnormally enlarged cavum septum pellucidum combined with cavum vergae.
Hu, SH; Liao, ZL; Xu, Y, 2012
)
" This practice of polypharmacy increases the possibility for drug-drug interactions."( Drug-drug conditioning between citalopram and haloperidol or olanzapine in a conditioned avoidance response model: implications for polypharmacy in schizophrenia.
Li, M; Sparkman, NL, 2012
)
"The objective of this study is to compare the effectiveness of olanzapine combined with ondansetron or ondansetron alone in preventing chemotherapy-induced nausea and vomiting (CINV) of non-small cell lung cancer (NSCLC)."( Effectiveness of Olanzapine Combined with Ondansetron in Prevention of Chemotherapy-Induced Nausea and Vomiting of Non-small Cell Lung Cancer.
Wang, H; Wang, L; Wang, X; Zhang, H, 2015
)
" Oral olanzapine (5 mg) was administered with triplet therapy a day prior to cisplatin administration and on days 1-5."( Efficacy and safety of olanzapine combined with aprepitant, palonosetron, and dexamethasone for preventing nausea and vomiting induced by cisplatin-based chemotherapy in gynecological cancer: KCOG-G1301 phase II trial.
Abe, M; Hihara, H; Hirakawa, T; Hirashima, Y; Ichikawa, Y; Ito, K; Itonaga, Y; Kado, N; Kasamatsu, Y; Komeda, S; Kuji, S; Miyagi, K; Murakami, J; Nasu, K; Takahashi, N; Takekuma, M; Tanaka, A, 2016
)
"Preventive use of olanzapine combined with triplet therapy gives better results than those from previously reported studies of triplet therapy."( Efficacy and safety of olanzapine combined with aprepitant, palonosetron, and dexamethasone for preventing nausea and vomiting induced by cisplatin-based chemotherapy in gynecological cancer: KCOG-G1301 phase II trial.
Abe, M; Hihara, H; Hirakawa, T; Hirashima, Y; Ichikawa, Y; Ito, K; Itonaga, Y; Kado, N; Kasamatsu, Y; Komeda, S; Kuji, S; Miyagi, K; Murakami, J; Nasu, K; Takahashi, N; Takekuma, M; Tanaka, A, 2016
)
"To investigate the efficacy and safety of olanzapine in combination with palonosetron and dexamethasone for patients receiving cisplatin (≥50 mg/m(2) ), because this antiemetic therapy has not been sufficiently examined in patients receiving cisplatin."( A phase II trial of prophylactic olanzapine combined with palonosetron and dexamethasone for preventing nausea and vomiting induced by cisplatin.
Asano, C; Haegawa, I; Horio, Y; Kadowaki, S; Kajita, M; Komori, A; Maeda, A; Mizutani, A; Muro, K; Narita, Y; Nomura, M; Oze, I; Taniguchi, H; Ura, T; Yoshida, T, 2016
)
"Olanzapine combined with palonosetron and dexamethasone did not prevent chemotherapy-induced nausea and vomiting induced by cisplatin as expected."( A phase II trial of prophylactic olanzapine combined with palonosetron and dexamethasone for preventing nausea and vomiting induced by cisplatin.
Asano, C; Haegawa, I; Horio, Y; Kadowaki, S; Kajita, M; Komori, A; Maeda, A; Mizutani, A; Muro, K; Narita, Y; Nomura, M; Oze, I; Taniguchi, H; Ura, T; Yoshida, T, 2016
)
"Atypical antipsychotics are used for the treatment of acute mania, either as monotherapy or in combination with lithium or divalproex, which have a better tolerability profile as compared with typical antipsychotics."( Efficacy and Safety of Asenapine Versus Olanzapine in Combination With Divalproex for Acute Mania: A Randomized Controlled Trial.
Arora, M; Gillani, Z; Mahajan, V; Praharaj, SK; Tandon, VR,
)
"One hundred twenty patients aged 18 to 55 years, diagnosed with manic episode, were randomized to receive either flexible dose of sublingual asenapine (10-20 mg/d) or tablet olanzapine (10-20 mg/d), in combination with valproate 20 mg/kg per day for a period of 6 weeks."( Efficacy and Safety of Asenapine Versus Olanzapine in Combination With Divalproex for Acute Mania: A Randomized Controlled Trial.
Arora, M; Gillani, Z; Mahajan, V; Praharaj, SK; Tandon, VR,
)
"This study found that asenapine was an effective and well-tolerated atypical antipsychotic alternative to olanzapine in combination with divalproex for the short-term management of acute mania."( Efficacy and Safety of Asenapine Versus Olanzapine in Combination With Divalproex for Acute Mania: A Randomized Controlled Trial.
Arora, M; Gillani, Z; Mahajan, V; Praharaj, SK; Tandon, VR,
)
" 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
)
" As cytochrome P450 (CYP) 1A2 and CYP3A4 are the major enzymes involved in metabolism of olanzapine and samidorphan, respectively, physiologically-based pharmacokinetic (PBPK) modeling was applied to predict any drug-drug interaction (DDI) potential between olanzapine and samidorphan or between OLZ/SAM and CYP3A4/CYP1A2 inhibitors/inducers."( Physiologically-Based Pharmacokinetic Modeling for Predicting Drug Interactions of a Combination of Olanzapine and Samidorphan.
Rowland Yeo, K; Sun, L; von Moltke, L, 2020
)
"Preventive use of OLZ combined with standard triplet therapy had promising activity with manageable safety, suggesting that this combination could be an effective standard treatment option for patients with AUC ≥4 mg/mL/min CBDCA combination therapy."( Efficacy and safety of 5 mg olanzapine combined with aprepitant, granisetron and dexamethasone to prevent carboplatin-induced nausea and vomiting in patients with gynecologic cancer: A multi-institution phase II study.
Abe, M; Arai, T; Fujita, Y; Hayasaki, Y; Iihara, H; Kado, N; Mori, M; Morishige, KI; Murase, S; Nakamura, K; Sakurai, M; Shimaoka, R; Shimokawa, M; Suzuki, A; Takenaka, M; Yamamoto, S, 2020
)
"We performed a pooled analysis to evaluate the efficacy and adverse events (AEs) of olanzapine combined with dexamethasone plus 5-hydroxytryptamine type 3 receptor antagonist (5-HT3 RA) compared with 5-HT3 RA plus dexamethasone for the prevention and treatment of chemotherapy-induced nausea and vomiting (CINV) in high and moderate emetogenic chemotherapy based on randomised controlled trials (RCTs)."( Olanzapine combined with 5-hydroxytryptamine type 3 receptor antagonist (5-HT3 RA) plus dexamethasone for prevention and treatment of chemotherapy-induced nausea and vomiting in high and moderate emetogenic chemotherapy: a systematic review and meta-analy
Frey, B; Gaipl, US; Huang, L; Jin, SH; Ma, H; Xu, C; Zhou, JG, 2020
)
" Although our multicentre randomised double-blind comparative study verified non-inferiority of sparing DEX after day 2 of chemotherapy when combined with neurokinin-1 receptor antagonist (NK1-RA) and palonosetron (Palo) for patients receiving HEC regimen, DEX sparing was not non-inferior in patients receiving cisplatin (CDDP)-based HEC regimens in subgroup analysis."( Study protocol for SPARED trial: randomised non-inferiority phase III trial comparing dexamethasone on day 1 with dexamethasone on days 1-4, combined with neurokinin-1 receptor antagonist, palonosetron and olanzapine (5 mg) in patients receiving cisplatin
Arioka, H; Hida, N; Iihara, H; Inada, Y; Ishida, H; Izawa, N; Katada, C; Kawaguchi, T; Kazunori, H; Minatogawa, H; Miyaji, T; Morita, H; Nakajima, TE; Nawata, S; Ohno, Y; Shimomura, K; Sugawara, M; Tsuboya, A; Tsuda, T; Yamaguchi, T, 2020
)
" Here, we retrospectively analyze CINV data of 100 patients who received either SEAM (semustine, etoposide, cytarabine, melphalan) or MEL140-200 (high-dose melphalan) before ASCT, evaluate the efficacy and safety of multiple-day administration of fosaprepitant combined with tropisetron and olanzapine (FTO), and compare the results to those of patients who received a standard regimen of aprepitant, tropisetron, and dexamethasone (ATD)."( Multiple-day administration of fosaprepitant combined with tropisetron and olanzapine improves the prevention of nausea and vomiting in patients receiving chemotherapy prior to autologous hematopoietic stem cell transplant: a retrospective study.
Cao, J; Chen, D; Du, X; Hu, Y; Jiang, L; Li, S; Liu, X; Lu, Y; Pei, R; Tang, S; Wang, T; Ye, P; Zhang, P, 2022
)
"Polypharmacy increases the risk of potential drug-drug interactions (pDDIs)."( Clinical significance of potential drug-drug interactions in older adults with psychiatric disorders: a retrospective study.
Cui, Y; Ding, Y; Ji, M; Liu, Y; Wang, D; Wang, H; Yang, M; Zhang, H; Zhuang, T, 2022
)

Bioavailability

The intranasal nanocubic vesicles were significantly more efficient in targeting olanzapine to the brain compared to the liposomal vesicle with drug targeting efficiency values of 100% and 80%, respectively, and absolute bioavailability of 37%.

ExcerptReference
" After oral administration, OLZ was well absorbed in dogs (absolute bioavailability of 73%) and to the extent of at least 55% in monkeys and 32% in mice."( Disposition and metabolism of olanzapine in mice, dogs, and rhesus monkeys.
Bernstein, J; Chiu, A; Franklin, R; Gillespie, T; Hotten, T; Kassahun, K; Mattiuz, E; Murphy, A, 1997
)
" The drug is well absorbed from the GI tract; food has no effect."( Olanzapine: a serotonin-dopamine-receptor antagonist for antipsychotic therapy.
Bever, KA; Perry, PJ, 1998
)
"The quantitative structure-bioavailability relationship of 232 structurally diverse drugs was studied to evaluate the feasibility of constructing a predictive model for the human oral bioavailability of prospective new medicinal agents."( QSAR model for drug human oral bioavailability.
Topliss, JG; Yoshida, F, 2000
)
" It may be less well absorbed and/or less effective than Clozaril, although evidence is conflicting."( Advances in atypical antipsychotics for the treatment of schizophrenia: new formulations and new agents.
Albert, MJ; Baldessarini, RJ; Centorrino, F; Kelleher, JP, 2002
)
" The validated method has been successfully used to analyze human plasma samples for application in pharmacokinetic, bioavailability or bioequivalence studies."( Development and validation of a sensitive liquid chromatography/electrospray tandem mass spectrometry assay for the quantification of olanzapine in human plasma.
Boosi, R; Kandikere, VN; Maurya, S; Mudigonda, K; Nirogi, RV; Shukla, M; Yerramilli, A, 2006
)
" We found that RG-15 showed a good oral bioavailability (54%) and high brain levels (approx."( Subnanomolar dopamine D3 receptor antagonism coupled to moderate D2 affinity results in favourable antipsychotic-like activity in rodent models: II. behavioural characterisation of RG-15.
Agai Csongor, E; Domány, G; Elekes, O; Gémesi, LI; Gyertyán, I; Kapás, M; Kedves, R; Kiss, B; Laszy, J; Pásztor, G; Sághy, K; Szombathelyi, Z; Zájer-Balázs, M, 2008
)
" Both formulations were apparently well absorbed from the gastrointestinal tract (ie, no specific gastrointestinal tract-related adverse events were reported)."( A single-dose, randomized, two-way crossover study comparing two olanzapine tablet products in healthy adult male volunteers under fasting conditions.
Elshafeey, AH; Elsherbiny, MA; Fathallah, MM, 2009
)
" Bioavailability parameters including C(max), T(max), and AUC(0-48 h) of both tablets were compared."( Controlled release matrix tablets of olanzapine: influence of polymers on the in vitro release and bioavailability.
Badshah, A; Rauf, K; Subhan, F, 2010
)
" The validated method was successfully applied to analyzing human plasma samples in bioavailability study."( Development and validation of a liquid chromatography-isotope dilution tandem mass spectrometry for determination of olanzapine in human plasma and its application to bioavailability study.
Gui, YZ; Jia, JY; Li, SJ; Liu, GY; Liu, Y; Liu, YM; Lu, C; Wang, W; Yu, C; Yu, CY; Zhang, MQ, 2010
)
" It has poor bioavailability due to hepatic first-pass metabolism and low permeability into the brain due to efflux by P-glycoproteins."( Development and evaluation of olanzapine-loaded PLGA nanoparticles for nose-to-brain delivery: in vitro and in vivo studies.
Kumar, A; Sawant, KK; Seju, U, 2011
)
" The calculated relative bioavailability of TDDS was 113."( Natural oils as skin permeation enhancers for transdermal delivery of olanzapine: in vitro and in vivo evaluation.
Aggarwal, G; Dhawan, S; HariKumar, SL, 2012
)
" The intranasal nanocubic vesicles were significantly more efficient in targeting olanzapine to the brain compared to the liposomal vesicles with drug targeting efficiency values of 100% and 80%, respectively, and absolute bioavailability of 37."( Phospholipid based colloidal poloxamer-nanocubic vesicles for brain targeting via the nasal route.
Abdel Hady, M; Awad, GA; Kamel, AO; Mahmoud, AA; Salama, HA, 2012
)
" Values for absolute drug bioavailability in rat plasma for transfersomes containing SDC and those containing Span 60 were 24."( Brain delivery of olanzapine by intranasal administration of transfersomal vesicles.
Abdel Hady, M; Awad, GA; Kamel, AO; Mahmoud, AA; Salama, HA, 2012
)
"We describe the discovery of potent and orally bioavailable tetrahydropyridopyrimidine inhibitors of phosphodiesterase 10A by systematic optimization of a novel HTS lead."( Discovery of tetrahydropyridopyrimidine phosphodiesterase 10A inhibitors for the treatment of schizophrenia.
Breslin, MJ; Coleman, PJ; Cox, CD; Fandozzi, C; Fuerst, J; Hill, N; Huszar, S; Kandebo, M; Kim, SH; Ma, B; McGaughey, G; Raheem, IT; Renger, JJ; Schreier, JD; Sharma, S; Smith, S; Uslaner, J; Yan, Y, 2012
)
" The relative bioavailability of the test formulation to reference formulation was 100."( Pharmacokinetics and bioequivalence of 2 tablet formulations of olanzapine in healthy Chinese volunteers: a randomized, open-label, single-dose study.
Chen, Q; Jia, JY; Li, SJ; Liu, GY; Liu, Y; Liu, YM; Lu, C; Qi, YL; Yu, C; Zhang, MQ, 2012
)
"This single dose, randomized, open label, 2-period and crossover study in healthy Iranian adult volunteers was conducted to compare the bioavailability of 2 branded formulations of olanzapine 10 mg tablets."( Single dose bioequivalence study of two brands of olanzapine 10 mg tablets in Iranian healthy volunteers.
Ghanbarzadeh, S; Islambulchilar, Z; Valizadeh, H; Zakeri-Milani, P, 2013
)
" Some evidence suggestive of variations in bioavailability and clinical effectiveness between different formulations make policy decisions occasionally difficult."( Mental state deterioration after switching from brand-name to generic olanzapine in an adolescent with bipolar affective disorder, autism and intellectual disability: a case study.
Attard, A; Kyriakopoulos, M; Samuel, R, 2013
)
" This multifunctional drug candidate is orally bioavailable and exhibits good antipsychotic efficacy in vivo."( Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
Beard, JD; Davis, RE; Hendrick, JP; Lee, T; Li, P; Mates, S; Peng, Y; Robichaud, AJ; Snyder, GL; Tomesch, J; Vanover, KE; Wennogle, LP; Yao, W; Zhang, Q; Zhu, H, 2014
)
"The aim of this study was to investigate olanzapine (OZ) systemic absolute bioavailability after intranasal (i."( Intranasal drug delivery of olanzapine-loaded chitosan nanoparticles.
Al-Ghananeem, AM; Baltzley, S; Malkawi, AH; Mohammad, A, 2014
)
" Higher olanzapine concentrations and AUC(0-12 h) were found in plasma and tissues evaluated after the administration of OLA-LNC compared to the drug in the free form, resulting in a relative bioavailability of 226."( Nanoencapsulation Improves Relative Bioavailability and Antipsychotic Effect of Olanzapine in Rats.
Boque, CA; Burger, ME; Dalla Costa, T; Dimer, FA; Guterres, SS; Pase, CS; Pigatto, MC; Pohlmann, AR; Rates, MK; Roversi, K, 2015
)
" Though OLZ is an effective agent in the treatment of Schizophrenia, but it exhibits poor bioavailability (57%) due to extensive first-pass metabolism resulted in high dose is required to achieve therapeutic concentration in brain."( Enhanced brain targeting efficacy of Olanzapine through solid lipid nanoparticles.
Baskaran, M; Humtsoe, LC; Justin, A; Natarajan, J; Vadivelan, R, 2017
)
"Solid dispersion technology represents a successful approach to addressing the bioavailability issues caused by the low aqueous solubility of many Biopharmaceutics Classification System (BCS) Class II drugs."( Development of micro-fibrous solid dispersions of poorly water-soluble drugs in sucrose using temperature-controlled centrifugal spinning.
Barker, SA; Craig, DQM; Marano, S; Missaghi, S; Raimi-Abraham, BT; Rajabi-Siahboomi, A, 2016
)
" Overall, this study successfully generated OLZ loaded SMD films with improved in vitro dissolution rates which is highly likely to result in improved oral bioavailability in vivo."( Solid microcrystalline dispersion films as a new strategy to improve the dissolution rate of poorly water soluble drugs: A case study using olanzapine.
de Fátima Pina, M; Modica de Mohac, L; Raimi-Abraham, BT, 2016
)
" So, in order to increase the bioavailability of drug and possibly reducing some of side effects, this paper proposes a new material able to controllably release the drug in the body."( Bionanocomposite systems based on montmorillonite and biopolymers for the controlled release of olanzapine.
Alcântara, ACS; Oliveira, AS; Pergher, SBC, 2017
)
" Bioavailability studies indicate that there was more than 5½-fold increase in oral bioavailability in case of NLCs (F6) compared to olanzapine suspension which indicates that NLCs provided sustained release of the drugs, and these systems can be the preferred as drug carriers for lipophilic drugs in long term disease conditions such as schizophrenia for enhanced bioavailability."( Enhanced oral bioavailability of an antipsychotic drug through nanostructured lipid carriers.
Anbarasan, A; Arun, R; G, N; Hingarh, PK; Jawahar, N; S, S; Selvaraj, J, 2018
)
"The objective of this study was to evaluate the relative bioavailability of olanzapine in 3 olanzapine-containing tablet formulations."( Bioequivalence of Olanzapine Given in Combination With Samidorphan as a Bilayer Tablet (ALKS 3831) Compared With Olanzapine-Alone Tablets: Results From a Randomized, Crossover Relative Bioavailability Study.
Liu, J; McDonnell, D; Sun, L; von Moltke, L, 2019
)
"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
)
" As olanzapine has shown poor bioavailability and permeability in the brain, the sustained release of olanzapine from the designed carriers could enhance pharmacokinetic effectiveness."( Sustained delivery of olanzapine from sunflower oil-based polyol-urethane nanoparticles synthesised through a cyclic carbonate ring-opening reaction.
Babanejad, N; Dorkoosh, F; Farhadian, A; Mozafari, M; Nabid, MR; Saeb, MR; Zarrintaj, P, 2019
)
" Poor solubility is a major issue, and 40% of marketed and about 75% of new active pharmaceutical ingredients are poorly water soluble which significantly affect the bioavailability and therapeutic effects of these drugs."( Poloxamer-407-Co-Poly (2-Acrylamido-2-Methylpropane Sulfonic Acid) Cross-linked Nanogels for Solubility Enhancement of Olanzapine: Synthesis, Characterization, and Toxicity Evaluation.
Akhtar, N; Khan, KU; Minhas, MU, 2020
)
"Amorphous and co-amorphous formulations have been used to enhance the solubility and bioavailability of poorly water-soluble drugs."( Measurement of the amorphous fraction of olanzapine incorporated in a co-amorphous formulation.
da Costa, NF; Fernandes, AI; Pinto, JF, 2020
)
"In this study, we evaluated whether changes in the gut microbiota of male Sprague Dawley rats, as a result of either antibiotic or probiotic administration, influenced the oral bioavailability of two commonly prescribed antipsychotics, olanzapine and risperidone."( The gut microbiome influences the bioavailability of olanzapine in rats.
Clarke, G; Cryan, JF; Cussotto, S; Dinan, TG; Fouhy, F; Golubeva, AV; Griffin, BT; Hyland, NP; Stanton, C; Strain, CR; Walsh, J; Zhdanov, AV, 2021
)
"The bioavailability of olanzapine, was significantly increased (1."( The gut microbiome influences the bioavailability of olanzapine in rats.
Clarke, G; Cryan, JF; Cussotto, S; Dinan, TG; Fouhy, F; Golubeva, AV; Griffin, BT; Hyland, NP; Stanton, C; Strain, CR; Walsh, J; Zhdanov, AV, 2021
)
" The gut microbiome might be an important variable determining the systemic bioavailability of orally administered olanzapine."( The gut microbiome influences the bioavailability of olanzapine in rats.
Clarke, G; Cryan, JF; Cussotto, S; Dinan, TG; Fouhy, F; Golubeva, AV; Griffin, BT; Hyland, NP; Stanton, C; Strain, CR; Walsh, J; Zhdanov, AV, 2021
)
" Modifications to model parameters, including absorption rate constant and fraction unbound to plasma protein, were made to recover the observed change in the PKs of olanzapine and samidorphan in individuals with moderate hepatic impairment."( Using physiologically-based pharmacokinetic modeling for predicting the effects of hepatic impairment on the pharmacokinetics of olanzapine and samidorphan given as a combination tablet.
Barter, Z; Rowland Yeo, K; Sun, L; von Moltke, L, 2021
)
" The rate of removal of LAIs is regulated by the slow rate of absorption in the site of injection and the phenomenon of their increased half-life is called flip-flop pharmacokinetics."( [Clinical pharmacokinetics and pharmaceutical forms of long-acting injectable antipsychotics].
Kyziridis, TC, 2022
)
"The preparation of amorphous and co-amorphous systems (CAMs) effectively addresses the solubility and bioavailability issues of poorly water-soluble chemical entities."( Amorphous and Co-Amorphous Olanzapine Stability in Formulations Intended for Wet Granulation and Pelletization.
da Costa, NF; Daniels, R; Fernandes, AI; Pinto, JF, 2022
)

Dosage Studied

Eleven patients with schizophrenia stabilized on oral olanzapine (mean dosage 12.5 mg/d) The aim of this study was to evaluate the time-dependent effects of olanZapine depot administration at clinically relevant dosing.

ExcerptReference
" However, risperidone induced a U-shaped dose-response curve."( Differential effects of repeated administration of novel antipsychotic drugs on the activity of midbrain dopamine neurons in the rat.
Skarsfeldt, T, 1995
)
" Detailed evaluation of the dose-response characteristics of olanzapine and direct clinical comparison to clozapine will thus provide valuable leads to the clarification of atypical antipsychotic action."( A PET study of 5-HT2 and D2 dopamine receptor occupancy induced by olanzapine in healthy subjects.
Farde, L; Halldin, C; Nyberg, S, 1997
)
" Analyses indicated that an increasing dose-response curve was observed across the range of all olanzapine dose groups."( Olanzapine versus haloperidol: acute phase results of the international double-blind olanzapine trial.
Beasley, CM; Beuzen, JN; Blin, O; Crawford, AM; Dellva, MA; Hamilton, SH; Tollefson, GD; Tran, PV, 1997
)
" Olanzapine exhibits linear kinetics over the dosage range studied and is extensively metabolized in humans."( Olanzapine: a new antipsychotic agent with efficacy in the management of schizophrenia.
Green, AI; Kando, JC; Patel, JK; Reams, SG; Satterlee, W; Shepski, JC, 1997
)
" After a 2- to 9-day placebo lead-in, 79 inpatients with schizophrenia according to DSM-III-R criteria were placed on an olanzapine dosage of 10 mg/day or 1 mg/day for up to 6 weeks."( Olanzapine plasma concentrations and clinical response in acutely ill schizophrenic patients.
Beasley, C; Perry, PJ; Sanger, T, 1997
)
" In conclusion, the present studies demonstrate that in the case of sequential dosing olanzapine more effectively enhances DA and NE release in the Pfc than in the subcortical areas, which may have an impact on its atypical antipsychotic actions."( Olanzapine increases in vivo dopamine and norepinephrine release in rat prefrontal cortex, nucleus accumbens and striatum.
Bymaster, FP; Li, XM; Perry, KW; Wong, DT, 1998
)
"The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, drug interactions, dosage and administration, and cost of olanzapine are reviewed."( Olanzapine: a serotonin-dopamine-receptor antagonist for antipsychotic therapy.
Bever, KA; Perry, PJ, 1998
)
"The 14 patients received olanzapine at a mean (SD dosage of 14."( Olanzapine in treatment-resistant bipolar disorder.
Altshuler, L; Denicoff, K; Frye, M; Keck, PE; Kmetz, GF; Kupka, R; Leverich, GS; McElroy, SL; Nolen, W; Post, RM; Suppes, T, 1998
)
" There are others who are unable to tolerate a high dosage of clozapine."( Olanzapine augmentation of clozapine.
Frank, B; Gupta, S; Sonnenberg, SJ, 1998
)
"Olanzapine was given to five patients with idiopathic Parkinson's disease and the dosage was titrated until a clinically meaningful reduction in hallucinosis was achieved."( Olanzapine in the treatment of hallucinosis in idiopathic Parkinson's disease: a cautionary note.
Ford, KS; Graham, JM; Sagar, HJ; Sussman, JD, 1998
)
" Proper dosing has emerged as a vital factor in the effective use of these newer drugs."( Risperidone and olanzapine: optimal dosing for efficacy and tolerability in patients with schizophrenia.
Kasper, S, 1998
)
" Dosing requirements for elderly patients tend to be much lower than those for younger adults."( Conventional vs. newer antipsychotics in elderly patients.
Harris, MJ; Jeste, DV; Lacro, J; Lohr, JB; Rockwell, E, 1999
)
" To provide the therapeutic benefits of maintenance medication without its drawbacks, intermittent dosing and long-term therapy with reduced doses of conventional medications have been explored."( Olanzapine in the long-term treatment of schizophrenia.
Kane, J, 1999
)
" The atypical properties of first-line atypical antipsychotics as well as clozapine are reviewed here, with clinical pearls and dosing tips for each based upon a consensus of information from both clinical trials and clinical practice."( Selecting an atypical antipsychotic by combining clinical experience with guidelines from clinical trials.
Stahl, SM, 1999
)
" Published studies have drawn criticism in terms of inappropriate titration schedules, nonequivalent dosing between treatment groups, short treatment duration, and inadequate sample sizes."( Clozapine: a comparison with other novel antipsychotics.
Fleischhacker, WW, 1999
)
" The decreased D(2)/D(3) receptor availability revealed an exponential dose-response relationship (r=-0."( In vivo effects of olanzapine on striatal dopamine D(2)/D(3) receptor binding in schizophrenic patients: an iodine-123 iodobenzamide single-photon emission tomography study.
Dresel, S; Hahn, K; Mager, T; Meisenzahl, E; Möller, HJ; Rossmüller, B; Tatsch, K, 1999
)
" The withdrawal symptoms disappeared rapidly with an increase in olanzapine dosage and with anticholinergic started at the beginning of the switch."( Clozapine-olanzapine: a potentially dangerous switch. A report of two cases.
Delassus-Guenault, N; Jegouzo, A; Odou, P; Robert, H; Seguret, T; Vignole, E; Zangerlin, H, 1999
)
" Assessments of attention, memory and motor control were made prior to dosing on each day, at 2, 4, 6 and 8 h after dosing on days 1 and 4, and at 24 and 48 h following the last dose."( A comparison of the effects of olanzapine, haloperidol and placebo on cognitive and psychomotor functions in healthy elderly volunteers.
Beuzen, JN; Taylor, N; Wesnes, K; Wood, A, 1999
)
" The pharmacokinetics of olanzapine are linear and dose-proportional within the approved dosage range."( Olanzapine. Pharmacokinetic and pharmacodynamic profile.
Beasley, CM; Bergstrom, RF; Callaghan, JT; Ptak, LR, 1999
)
" Dosing was 12."( Differential olanzapine plasma concentrations by sex in a fixed-dose study.
Conley, RR; Kelly, DL; Tamminga, CA, 1999
)
" Surprisingly, there has been little relationship between the pivotal trials designed for FDA approval and current dosing strategies in broader clinical settings."( New antipsychotic medications: more than old wine and new bottles.
Schulz, SC, 2000
)
" Without such data, clinicians have difficulty designing appropriate dosage regimens for patients in these age groups."( Olanzapine pharmacokinetics in pediatric and adolescent inpatients with childhood-onset schizophrenia.
Bergstrom, RF; Calis, KA; DeVane, CL; Grothe, DR; Jacobsen, L; Kumra, S; Kurtz, DL; Rapoport, JL, 2000
)
"Thirty adult patients with acute schizophrenia were included into six-week open-labelled, non-comparative trial of olanzapine with free dosing from 5 to 20 mg per day."( [The experience of application of olanzapine: an atypical neuroleptic in acute schizophrenia].
Beniashvili, AG; Morozova, MA; Zharkova, NB, 2000
)
" Cases admitted in the first semester received a significantly higher daily dosage of antipsychotic drugs and more frequently received anticholinergics."( Second-generation antipsychotics in the emergency care setting. A prospective naturalistic study.
Azzoni, A; Raja, M,
)
" Longitudinal study is required because this relationship may have implications for dosing strategies."( Subjective experience and striatal dopamine D(2) receptor occupancy in patients with schizophrenia stabilized by olanzapine or risperidone.
Booij, J; de Haan, L; Dingemans, PM; Lavalaye, J; Linszen, D, 2000
)
" Initial dosage was 10 mg/day with a maximum dosage of 20 mg/day."( Effective open-label treatment of tourette's disorder with olanzapine.
Aschauer, HN; De Zwaan, M; Kasper, S; Resinger, E; Schindler, SD; Stamenkovic, M; Willinger, U, 2000
)
" A dose-response relationship was not consistently confirmed with any of the drug treatments."( The effects of olanzapine, risperidone, and haloperidol on plasma prolactin levels in patients with schizophrenia.
Breier, A; David, SR; Kinon, BJ; Taylor, CC, 2000
)
" No consistent dose-response relationship was observed, and the time course and sex-dependency of the response differed between the 3 agents."( The effects of olanzapine, risperidone, and haloperidol on plasma prolactin levels in patients with schizophrenia.
Breier, A; David, SR; Kinon, BJ; Taylor, CC, 2000
)
" In addition, psychiatrists' clinical preference of antipsychotic medication and dosage for patient subtypes were examined by the national survey."( Comparison of cost, dosage and clinical preference for risperidone and olanzapine.
Kaplan, Z; Lichtenberg, P; Rabinowitz, J, 2000
)
" Taking into account drug costs and dosage requirements, the average daily retail price was US $6."( Comparison of cost, dosage and clinical preference for risperidone and olanzapine.
Kaplan, Z; Lichtenberg, P; Rabinowitz, J, 2000
)
"In this open case series, the dose-response relationship of atypical antipsychotic augmentation in the treatment of obsessive compulsive disorder (OCD), and the dose-severity relationship in atypical anti psychotic-induced OC symptoms were examined."( Serotonin and dopamine antagonism in obsessive-compulsive disorder: effect of atypical antipsychotic drugs.
Lapierre, Y; Ramasubbu, R; Ravindran, A, 2000
)
"Case 1: A linear dose-response relationship between increasing doses of olanzapine and improvement in OC symptoms was observed in an OCD patient resistant to 5-HT reuptake inhibitors."( Serotonin and dopamine antagonism in obsessive-compulsive disorder: effect of atypical antipsychotic drugs.
Lapierre, Y; Ramasubbu, R; Ravindran, A, 2000
)
"Controlled studies are needed to investigate the dose-response or dose-severity relationships between OCD and atypical antipsychotics."( Serotonin and dopamine antagonism in obsessive-compulsive disorder: effect of atypical antipsychotic drugs.
Lapierre, Y; Ramasubbu, R; Ravindran, A, 2000
)
" Olanzapine concentrations were found to be a function of olanzapine dose (in milligrams per day) and gender such that prospective olanzapine dosing is feasible."( Olanzapine plasma concentrations and clinical response: acute phase results of the North American Olanzapine Trial.
Beasley, C; Lund, BC; Perry, PJ; Sanger, T, 2001
)
" clozapine, Clo) in 3 aspects: 1) the multiple receptor pharmacodynamics involving D1/D2, 5-HT2 and M-ACh receptors; 2) dose-response separation between the block of conditioned avoidance response and catalepsy induction; and 3) the specificity of action sites of firing rates upon acute drug challenge."( Behavioral characteristics of olanzapine: an atypical neuroleptic.
Chen, LJ; Fu, Y; Jin, GZ; Yu, LP; Zhu, ZT, 2000
)
"Ten adult patients aged 20 to 44 years with Tourette's disorder were treated using an open-label, flexible dosing schedule for 8 weeks."( An open-label study of the treatment efficacy of olanzapine for Tourette's disorder.
Bruun, RD; Budman, CL; Gayer, A; Lesser, M; Shi, Q, 2001
)
" The initial dosage was 5 mg/day and was titrated to a maximum of 20 mg/day."( Olanzapine in the treatment of post-traumatic stress disorder: a pilot study.
Becker, ME; Butterfield, MI; Churchill, LE; Connor, KM; Davidson, JR; Sutherland, S, 2001
)
" Olanzapine typically alleviated pain within 20 minutes after oral dosing and treatment response was consistent across multiple treated attacks."( Olanzapine as an abortive agent for cluster headache.
Rozen, TD, 2001
)
" The trial was divided into two periods: eight weeks during which the dosage was escalated and then fixed, and six weeks during which variable dosages were used."( Effects of clozapine, olanzapine, risperidone, and haloperidol on hostility among patients with schizophrenia.
Chakos, M; Citrome, L; Cooper, TB; Czobor, P; Lieberman, JA; Lindenmayer, JP; McEvoy, J; Sheitman, B; Volavka, J, 2001
)
" Subjective impairment, as assessed with the subscale 'mental functioning', was significantly correlated with greater conventional neuroleptic dosage after controlling for psychopathology (P<0."( Relationship between neuroleptic dosage and subjective cognitive dysfunction in schizophrenic patients treated with either conventional or atypical neuroleptic medication.
Krausz, M; Moritz, S; Naber, D; Woodward, TS, 2002
)
" Among the group receiving novel antipsychotics, dosage was not related to satisfaction or burden of adverse effects."( Short report: comparison of patient satisfaction and burden of adverse effects with novel and conventional neuroleptics: a naturalistic study.
Bromet, EJ; Davidson, M; Rabinowitz, J, 2001
)
" Risk factors are a high dosage of antipsychotics, akathisia in a previous treatment, and diabetes mellitus."( [Drug-induced akathisia].
van Harten, PN, 2002
)
"A 27-year-old white woman was observed to have a seizure while receiving a stable dosage of olanzapine 15 mg/d, with the addition of quetiapine 100 mg in the evening 1 day before the occurrence of the seizure."( New-onset seizure associated with quetiapine and olanzapine.
Hedges, DW; Jeppson, KG, 2002
)
"Current dosing regimens of psychotropic drugs are based on plasma kinetic considerations, although it is unclear whether plasma levels faithfully reflect brain kinetics of drugs."( Significant dissociation of brain and plasma kinetics with antipsychotics.
Jones, C; Kapur, S; Remington, G; Tauscher, J; Zipursky, RB, 2002
)
" The manuscript describes the pharmacology, efficacy and tolerability studies, adverse effects and dosing considerations in the elderly."( Use of olanzapine for elderly patients with psychotic disorders: a review.
Bogunovic, O; Brenner, R; Gupta, S; Madhusoodanan, S; Sinha, S, 2001
)
" No serious side effects were reported at the maximum dosage reached (7."( Treatment of patients with tardive dystonia with olanzapine.
Bellini, G; Bernardini, S; Bonuccelli, U; Dell'Agnello, G; Lucetti, C; Maggi, L; Manca, L; Nuti, A; Piccinni, A,
)
" A dose-response relationship for IM olanzapine in the reduction of agitation was assessed by measuring the reduction in Positive and Negative Syndrome Scale Excited Component (PANSS-EC) scores 2 hours after the first injection."( A double-blind, placebo-controlled dose-response comparison of intramuscular olanzapine and haloperidol in the treatment of acute agitation in schizophrenia.
Birkett, M; Breier, A; Brook, S; David, S; Dossenbach, M; Ferchland, I; Kiesler, G; Meehan, K; Palmer, R; Sutton, V; Taylor, CC; Wright, P, 2002
)
"Olanzapine exhibited a dose-response relationship for reduction in agitation (F(1,179)= 14."( A double-blind, placebo-controlled dose-response comparison of intramuscular olanzapine and haloperidol in the treatment of acute agitation in schizophrenia.
Birkett, M; Breier, A; Brook, S; David, S; Dossenbach, M; Ferchland, I; Kiesler, G; Meehan, K; Palmer, R; Sutton, V; Taylor, CC; Wright, P, 2002
)
"0 mg per injection exhibits a dose-response relationship in the rapid treatment of acute agitation in patients with schizophrenia and demonstrates a favorable safety profile."( A double-blind, placebo-controlled dose-response comparison of intramuscular olanzapine and haloperidol in the treatment of acute agitation in schizophrenia.
Birkett, M; Breier, A; Brook, S; David, S; Dossenbach, M; Ferchland, I; Kiesler, G; Meehan, K; Palmer, R; Sutton, V; Taylor, CC; Wright, P, 2002
)
" In the case presented, the good efficacy of olanzapine in low dosage over an extended period of time is described."( [Delusional ectoparasitic infestation in multiple system atrophy].
Kornhuber, M; Kumbier, E, 2002
)
"A 3-week, randomized, double-blind trial compared flexibly dosed olanzapine (5-20 mg/day) to divalproex (500-2500 mg/day in divided doses) for the treatment of patients hospitalized for acute bipolar manic or mixed episodes."( Olanzapine versus divalproex in the treatment of acute mania.
Altshuler, LL; Baker, RW; Breier, A; Gilmore, JA; Ketter, TA; Milton, DR; Risser, R; Suppes, T; Tohen, M; Tollefson, GA; Zarate, CA, 2002
)
" When olanzapine was discontinued or the dosage decreased, 78% of patients had improved glycemic control."( Olanzapine-associated diabetes mellitus.
Doraiswamy, PM; Koller, EA, 2002
)
" The present TDM-based follow-up suggests that the influence of gender, smoking habits, and certain drug interactions may need to be considered for optimal dosage of OLA."( Therapeutic drug monitoring data on olanzapine and its N-demethyl metabolite in the naturalistic clinical setting.
Bengtsson, F; Dahl, ML; Lundmark, J; Reis, M; Skogh, E, 2002
)
" Whole brain and plasma P and 3alpha,5alpha-THP concentrations were increased with olanzapine or P dosing and were greatest with coadministration."( Olanzapine and progesterone have dose-dependent and additive effects to enhance lordosis and progestin concentrations of rats.
Frye, C; Seliga, A, 2002
)
" This double-blind, randomized controlled trial, comparing flexible dosing of olanzapine (5-20 mg/day, n = 234) to haloperidol (3-15 mg/day, n = 219), consisted of a 6-week acute phase, followed by a 6-week continuation phase."( Olanzapine versus haloperidol in the treatment of acute mania: clinical outcomes, health-related quality of life and work status.
Breier, A; Edgell, ET; Gandhi, G; Haro, JM; Namjoshi, MA; Shi, L; Tohen, M; Zhang, F, 2002
)
"Eleven patients with schizophrenia stabilized on oral olanzapine (mean dosage 12."( Dissolution profile, tolerability, and acceptability of the orally disintegrating olanzapine tablet in patients with schizophrenia.
Chue, P; Dickson, R; Jones, B; Taylor, CC, 2002
)
" Divalproex was initiated at 15 mg/kg/day and titrated over 12 days to a maximum dosage of 30 mg/kg/day."( Effect of divalproex combined with olanzapine or risperidone in patients with an acute exacerbation of schizophrenia.
Casey, DE; Daniel, DG; Sommerville, KW; Tracy, KA; Wassef, AA; Wozniak, P, 2003
)
" The mean daily dosage of olanzapine in the fourth week was 10."( The efficacy and safety of olanzapine for the treatment of geriatric psychosis.
Hwang, JP; Lee, TW; Tsai, SJ; Yang, CH, 2003
)
" The patients were treated with conventional antipsychotics for seven days after admission and were then randomised to the treatment arms with risperidone (4 mg/day) or with olanzapine (10 mg/day) at a fixed dosage in the first week and thereafter in flexible dosages for the remaining seven weeks."( Measurement of simple reaction time in antipsychotic treatment of patients with schizophrenia.
Kores Plesnicar, B; Krajnc, I; Tomori, M; Zalar, B, 2003
)
"This 47-week, randomized, double-blind study compared flexibly dosed olanzapine (5-20 mg/day) to divalproex (500-2500 mg/day) for manic or mixed episodes of bipolar disorder (N=251)."( Olanzapine versus divalproex sodium for the treatment of acute mania and maintenance of remission: a 47-week study.
Altshuler, L; Baker, RW; Brown, E; Frye, M; Ketter, TA; Risser, RC; Schuh, LM; Suppes, T; Tohen, M; Zajecka, J; Zarate, CA, 2003
)
" At a higher dosage (0."( The atypical antipsychotics risperidone, clozapine and olanzapine differ regarding their sedative potency in rats.
Ahnaou, A; Drinkenburg, WH; Megens, AA, 2003
)
"This was a double-blind, randomized, parallel-groups, placebo-controlled trial with fixed-flexible dosing conducted at four sites."( Randomized trial of olanzapine versus placebo in the symptomatic acute treatment of the schizophrenic prodrome.
Addington, J; Breier, A; Hawkins, KA; Lindborg, SR; Marquez, E; McGlashan, TH; Miller, TJ; Perkins, DO; Tohen, M; Woods, SW; Zipursky, RB, 2003
)
" A new approach to olanzapine dosing that expands the initial dose range up to 40 mg/d may offer superior efficacy in rapidly and effectively controlling the symptoms of agitation."( Effectiveness of rapid initial dose escalation of up to forty milligrams per day of oral olanzapine in acute agitation.
Baker, RW; Hill, AL; Kinon, BJ; Liu, H; Maguire, GA, 2003
)
" Daily dosage was subsequently adjusted between 5 and 20 mg/d based on individual clinical status."( A Canadian multicenter trial assessing memory and executive functions in patients with schizophrenia spectrum disorders treated with olanzapine.
Chokka, PR; Dickson, RA; Dursun, SM; Jones, B; MacEwan, GW; Reiss, JP; Remington, GJ; Rotstein, E; Stip, E, 2003
)
"Previous studies have examined the safety and tolerability of oral-loaded divalproex sodium in the treatment of acute mania, but not the early efficacy of this dosing strategy."( The safety and early efficacy of oral-loaded divalproex versus standard-titration divalproex, lithium, olanzapine, and placebo in the treatment of acute mania associated with bipolar disorder.
Baker, JD; Hirschfeld, RM; Sommerville, KW; Tracy, K; Wozniak, P, 2003
)
" However, no correlation between prolactin levels and dosage could be found."( [Plasma prolactin level and incidence of adverse endocrinologic effects during therapy with atypical neuroleptics].
Fric, M; Laux, G, 2003
)
" The diagnosis of rhabdomyolysis was confirmed by myoglobinemia dosage and ortholuidine test."( [Rhabdomyolysis associated with respiratory infection in chronic psychiatric patients during neuroleptic treatment].
Busiello, L; Cascella, M; De Robertis, E; Di Domenico, MG; Palmese, S; Pezza, M, 2003
)
" Mean duration of olanzapine treatment was 289 days (SD +/- 139) and the mean olanzapine dosage at the end of the study was 12."( Effects of olanzapine on lipid abnormalities in elderly psychotic patients.
Aizenberg, D; Barak, Y, 2003
)
" The starting dose was 10 mg/day, with dosage adjustments based on physician judgment."( Switching treatment-resistant patients with schizophrenia or schizoaffective disorder to olanzapine: a one-year open-label study with five-year follow-up.
Karagianis, JL; LeDrew, KK; Walker, DJ, 2003
)
"Double-blind data on patients age > or =60 randomized to 5 mg/d OLZ (n=83) or 5 mg/d HAL (n=34) (Week 1) then flexibly dosed to 5-20 mg/d over six weeks, with a 48-week extension for responders, were analyzed post-hoc."( Olanzapine vs haloperidol in geriatric schizophrenia: analysis of data from a double-blind controlled trial.
Breier, A; Bymaster, FP; Dossenbach, M; Gilmore, JA; Golshan, S; Jeste, D; Kaiser, CJ; Kennedy, JS; Kinon, BJ; Maguire, GA; Sanger, T; Tollefson, G, 2003
)
" The mean dosage of olanzapine was 11."( Pilot study: access to fitness facility and exercise levels in olanzapine-treated patients.
Archie, S; Hobbs, H; McNiven, J; Osborne, S; Wilson, JH, 2003
)
" We suggest that plasma olanzapine monitoring can be used for dose-response optimization, but only to complement the normal clinical evaluation process."( Investigation of target plasma concentration-effect relationships for olanzapine in schizophrenia.
Ahmad, F; Bulsara, MK; Castle, DJ; Dusci, LJ; Fellows, L; Ilett, KF, 2003
)
" The treating clinician was free to vary or discontinue dosing and use additional medications."( A 1-year open-label trial of olanzapine in school-age children with schizophrenia.
Adler, LE; Farley, GK; Novins, D; Ross, RG, 2003
)
"Patients were randomly assigned to receive flexibly dosed olanzapine, 5 to 20 mg/d, with prophylactic benztropine, 1 to 4 mg/d (n = 159); or haloperidol, 5 to 20 mg/d (n = 150), for 12 months."( Effectiveness and cost of olanzapine and haloperidol in the treatment of schizophrenia: a randomized controlled trial.
Allan, E; Bingham, S; Campbell, EC; Caroff, S; Collins, J; Corwin, J; Davis, L; Douyon, R; Dunn, L; Evans, D; Frecska, E; Grabowski, J; Graeber, D; Herz, L; Kwon, K; Lawson, W; Leslie, D; Liu-Mares, W; Mena, F; Perlick, D; Rosenheck, R; Sheikh, J; Smelson, D; Smith-Gamble, V; Warren, S, 2003
)
"The design consisted of 2 successive, 6-week, double-blind periods and compared flexible dosing of olanzapine (5-20 mg/d, n = 234) with haloperidol (3-15 mg/d, n = 219)."( A 12-week, double-blind comparison of olanzapine vs haloperidol in the treatment of acute mania.
Azorin, JM; Baker, RW; Breier, A; Emsley, RA; Evans, AR; Goldberg, JF; Gonzalez-Pinto Arrillaga, AM; Hardy-Bayle, MC; Lawson, WB; Namjoshi, MA; Risser, RC; Tohen, M; Vieta, E; Zhang, F, 2003
)
" In the present study, blood samples were collected for 24 h after dosing rats orally with a 5 mg/kg dose of olanzapine (OLAN)."( An automated blood sampler for simultaneous sampling of systemic blood and brain microdialysates for drug absorption, distribution, metabolism, and elimination studies.
Gitzen, JF; Gunaratna, PC; Kissinger, CB; Kissinger, PT,
)
" Unfortunately, this type of drugs cannot block the D2 receptors only in the mesolimbic dopaminergic pathway (which mediates their therapeutic effects), because of their non-selective D2 receptor blockage in both the mesolimbic and striatal regions, and the consequent appearance of side effects related to striatal interaction in the same dosage range as is needed for the therapeutical effects."( New antipsychotics and schizophrenia: a review on efficacy and side effects.
Berardi, D; De Ronchi, D; Lorenzi, C; Serretti, A, 2004
)
"These data indicate that the dosage of these medications, found to be effective in the treatment of schizophrenia, reduces DA stimulation of D2 receptors to levels slightly lower than those found in unmedicated healthy subjects."( Occupancy of dopamine D2 receptors by the atypical antipsychotic drugs risperidone and olanzapine: theoretical implications.
Abi-Dargham, A; Cangiano, C; Frankle, WG; Gil, R; Gorman, JM; Hackett, E; Kochan, LD; Laruelle, M; Mawlawi, O; Slifstein, M; Zea-Ponce, Y; Zhu, Z, 2004
)
" To estimate the dose-response relationship as a guide for the provision of optimal management of olanzapine intoxicated patients."( The clinical picture of olanzapine poisoning with special reference to fluctuating mental status.
Kupferschmidt, H; Meier, PJ; Palenzona, S; Rauber-Luethy, C, 2004
)
" The doses of each CPM were converted into dosage equivalents of standard reference drugs."( Patterns of concomitant psychotropic medication use during a 2-year study comparing clozapine and olanzapine for the prevention of suicidal behavior.
Glick, ID; Gunay, I; Hsu, C; Kumar, V; Weiss, L; Young, FK; Zaninelli, R, 2004
)
" The mean dosage at the end of the trial was 14."( Olanzapine in the treatment of aggression and tics in children with Tourette's syndrome--a pilot study.
Bassel, C; Sandor, P; Stephens, RJ, 2004
)
" Food and Drug Administration-approved dosing range of 10 to 20 mg/day but is often used at doses exceeding this range."( Variables associated with high olanzapine dosing in a state hospital.
Botts, S; de Leon, J; Littrell, R, 2004
)
" Therefore, patients who smoke should be closely monitored for their cigarette consumption when the dosage of olanzapine is adjusted."( Heavy smoking, reduced olanzapine levels, and treatment effects: a case report.
Chen, KP; Chiu, CC; Huang, MC; Lu, ML, 2004
)
"5 mg/kg dosing paradigm suggesting differences in tolerability rates as a function of olanzapine dose."( Weight loss dynamics during combined fluoxetine and olanzapine treatment.
Chabla, JM; Hallas, BH; Horowitz, JM; Perrone, JA; Torres, G, 2004
)
"Additional studies comparing intramuscular olanzapine with combination antipsychotic/benzodiazepine therapy in more severely ill patients and patients with concomitant medical illnesses are needed to determine the most effective dosing regimen, use of adjunctive medications, and to obtain a comprehensive safety profile."( Intramuscular olanzapine in the management of acute agitation.
Tulloch, KJ; Zed, PJ, 2004
)
" This paper focuses on hypothesis testing in a dose-response framework and shows that increased power is possible by using a mixture model where both the logit of the response rate and the response mean are linear functions of the dose level."( Score tests for dose effect in the presence of non-responders.
Boos, DD; Luo, X; Tamura, RN, 2004
)
" The failure to confirm previous claims of greater improvement on either risperidone or olanzapine in patients with a first episode of psychosis may be the result of methodological bias introduced by unequal dosing between the two drugs or the use of chronically ill and treatment-refractory patients in previous studies."( A comparison of two novel antipsychotics in first episode non-affective psychosis: one-year outcome on symptoms, motor side effects and cognition.
Haricharan, R; Malla, A; Manchanda, R; Norman, R; Scholten, D; Takhar, J; Townsend, L, 2004
)
"The primary objective was to demonstrate non-inferiority of olanzapine, mean dosage 16."( Randomized double blind comparison of olanzapine vs. clozapine on subjective well-being and clinical outcome in patients with schizophrenia.
Bandelow, B; Bender, S; Dittmann, RW; Klimke, A; Kühn, KU; Lambert, M; Lemmer, W; Moritz, S; Naber, D; Riedel, M; Vorbach, EU, 2005
)
" However, for this variable, there was a clear dose-response curve, with the maximal effect at the highest dose (4 mg/kg)."( A parametric analysis of olanzapine-induced weight gain in female rats.
Cooper, GD; Goudie, AJ; Halford, JC; Pickavance, LC; Wilding, JP, 2005
)
" Mice were acclimated to individual housing, given ad libitum access to chow and water, dosed with placebo peanut butter pills for 1 week, and then dosed daily with AAPD-laced peanut butter pills for 4 weeks."( Antipsychotic drug-induced weight gain: development of an animal model.
Allison, DB; Casey, DE; Cope, MB; Fernández, JR; Geary, N; Nagy, TR, 2005
)
") is an atypical antipsychotic medication with once-daily dosing that was originally developed for the treatment of schizophrenia."( Use of olanzapine in the treatment of bipolar I disorder.
Goodwin, FK; Lieberman, DZ, 2004
)
"OXC, at a dosage of 900-1,200 mg/day, was administered for 5 consecutive weeks to 25 outpatients, 10 men and 15 women, aged 25 to 64 years, with bipolar or schizoaffective disorder."( Plasma concentrations of risperidone and olanzapine during coadministration with oxcarbazepine.
Cacciola, M; D'Arrigo, C; La Torre, D; Migliardi, G; Pacetti, M; Rosaria Muscatello, M; Spina, E; Zoccali, R, 2005
)
" Dosage alterations of olanzapine and clozapine, dependent on cytochrome P450 1A2 (CYP1A2) for clearance, and quetiapine, dependent on cytochrome P450 3A (CYP3A), may be necessary when used with other drugs that inhibit or induce their metabolic enzymes."( The dosing of atypical antipsychotics.
Armstrong, SC; Cozza, KL; de Leon, J,
)
" Among the classes of medications that are H1 antagonists we point out that atypical antipsychotic medications such as olanzapine and quetiapine are among the most potent H1 antagonists, and can have simple daily dosing schedules and thus may be particularly useful in ACD."( Using histamine (H1) antagonists, in particular atypical antipsychotics, to treat anemia of chronic disease via interleukin-6 suppression.
Altschuler, EL; Kast, RE, 2005
)
" Olanzapine might be useful for delusion of PD in patients not responded to quetiapine, although it should be started at a very low dosage to ameliorate worsening parkinsonism."( [The efficacy of olanzapine for delusion in patients with Parkinson's disease].
Atsuta, N; Hirayama, M; Ito, M; Sobue, G; Watanabe, H, 2005
)
" When OCSs appear with clozapine, dosage can be reduced and a serotonin reuptake inhibitor treatment added."( [Obsessive-compulsive symptoms treatment in: schizophrenia].
Dardennes, R; Faucher, S; Ghaëm, O; Guelfi, JD, 2005
)
" According to response, dosage was then adjusted to a maximum dosage of 20 mg daily of either drug."( Treatment response to olanzapine and haloperidol and its association with dopamine D receptor occupancy in first-episode psychosis.
Christensen, BK; Daskalakis, Z; Epstein, I; Furimsky, I; Kapur, S; Roy, P; Sanger, T; Zipursky, RB, 2005
)
" When patients were rescanned following dosage adjustment, mean D2 receptor occupancies were greater than 70% in both groups."( Treatment response to olanzapine and haloperidol and its association with dopamine D receptor occupancy in first-episode psychosis.
Christensen, BK; Daskalakis, Z; Epstein, I; Furimsky, I; Kapur, S; Roy, P; Sanger, T; Zipursky, RB, 2005
)
" Patients were initiated with quetiapine to 400 mg/day over 7 days, and then flexibly dosed (300-750 mg/day) for 11 weeks."( Efficacy and tolerability of quetiapine in patients with schizophrenia who switched from haloperidol, olanzapine or risperidone.
Altman, C; de Nayer, A; Jones, AM; Larmo, I; Lindenbauer, B; Platz, T; Rittmannsberger, H; Windhager, E, 2005
)
" Among parameters analyzed were chlorpromazine equivalent dosage of antipsychotic, metabolic parameters, body mass index (BMI), level of concurrent medications, and concomitant dietary restrictions."( Metabolic effects associated with atypical antipsychotic treatment in the developmentally disabled.
Ball, MP; Bodfish, JW; Heeth, WL; Mahorney, SL; McKee, JR, 2005
)
" Treatment was naturalistic, and dosing was based on the discretion of the treating physician."( Olanzapine versus risperidone in newly admitted acutely ill psychotic patients.
Cook, A; Kraus, JE; Lieberman, JA; Reviere, R; Sheitman, BB, 2005
)
" Results of the sensitivity analysis confirmed that the results were robust to a wide variation of different input variables (effectiveness, dosing distribution, patient status according to healthcare system)."( Long-acting risperidone compared with oral olanzapine and haloperidol depot in schizophrenia: a Belgian cost-effectiveness analysis.
Caleo, S; De Graeve, D; Lecompte, D; Mehnert, A; Miadi-Fargier, H; Mosqueda, GJ; Peuskens, J; Smet, A, 2005
)
"Olanzapine (OLZ) is a second-generation antipsychotic agent available in 2 solid oral dosage forms, a standard oral tablet (SOT) and an orally disintegrating tablet (ODT)."( Pharmacokinetics of olanzapine after single-dose oral administration of standard tablet versus normal and sublingual administration of an orally disintegrating tablet in normal volunteers.
DeVane, CL; Donovan, JL; Gefroh, HA; Malcolm, RJ; Markowitz, JS; Wang, JS; Zhu, HJ, 2006
)
"6%) with a higher mean daily dosage in the public care setting."( [Neuroleptic drug utilization among schizophrenic outpatients].
Blin, P; Cialdella, P; Gérard, A; Hanssens, L; Olié, JP; Petitjean, F; Sechter, D; Westerloppe, J, 2005
)
" Lamotrigine dosing schedules are recommended to remain unchanged when combined with olanzapine therapy."( Pharmacokinetics and tolerability of lamotrigine and olanzapine coadministered to healthy subjects.
Abbott, R; Ascher, J; Bullman, J; Francis, E; Job, S; Sidhu, J; Theis, JG, 2006
)
" We used the Dosage Record Treatment Emergent Symptom Scale (DOTES) in a supplemented version to measure the presence and severity of side effects."( Clinical drug monitoring in child and adolescent psychiatry: side effects of atypical neuroleptics.
Fleischhaker, C; Heiser, P; Hennighausen, K; Herpertz-Dahlmann, B; Holtkamp, K; Mehler-Wex, C; Rauh, R; Remschmidt, H; Schulz, E; Warnke, A, 2006
)
"Fifty-one schizophrenic inpatients were randomly assigned to receive OLZ at 5 mg/d (26 patients, group 1) or 20 mg/d (25 patients, group 2) as a starting dosage during an exacerbation phase."( A single-blind, randomized comparison of olanzapine at a starting dose of 5 mg versus 20 mg in acute schizophrenia.
Baldi, ML; Colasanti, A; Mauri, MC; Moliterno, D; Papa, P; Rossattini, M,
)
" Atypical antipsychotics are an alternative treatment, and this 12-week, randomised, flexibly dosed study compared the efficacy, safety and tolerability of quetiapine and olanzapine in this regard."( Quetiapine versus olanzapine for the treatment of negative symptoms in patients with schizophrenia.
Koren, A; Pannet, I; Sirota, P; Tchernichovsky, E, 2006
)
" Dosage could be modified during the study according to clinical criteria."( Improvement in social functioning in outpatients with schizophrenia with prominent negative symptoms treated with olanzapine or risperidone in a 1 year randomized, open-label trial.
Alvarez, E; Bousoño, M; Ciudad, A; Gómez, JC; Olivares, JM, 2006
)
" On days 10, 20, and 30, blood samples were collected before dosing and at 1, 2, 5, 6, 10, 14, 18, and 24 hours after dosing."( A double-blind, randomized trial to evaluate the pharmacokinetics and tolerability of 30 or 40 mg/d oral olanzapine relative to 20 mg/d oral olanzapine in stable psychiatric subjects.
Bari, MA; Cavazzoni, P; Falk, D; Hardy, T; Kurtz, D; Marquez, E; Mitchell, CP; Mitchell, M; Riesenberg, R; Taylor, CC, 2006
)
" IMS analysis of tissues from 8 mg/kg olanzapine dosed rats revealed temporal distribution of the drug and metabolites that correlate to previous quantitative whole-body autoradiography studies."( Direct molecular analysis of whole-body animal tissue sections by imaging MALDI mass spectrometry.
Andersson, M; Caprioli, RM; Gillespie, TA; Herman, JL; Khatib-Shahidi, S, 2006
)
" Also discussed are findings concerning the continuation of acute treatments, including antidepressants, into the maintenance phase; dosage adjustments for maintenance treatment; the rationale for combination treatments; and implications of comorbid substance abuse and strategies for its management."( Maintenance treatment of bipolar disorder: Applying research to clinical practice.
Chou, JC; Fazzio, L, 2006
)
" CLOZ also induced profound insulin resistance after dosing 10 mg/kg/day for 5 days (P<0."( Acute effects of atypical antipsychotics on whole-body insulin resistance in rats: implications for adverse metabolic effects.
Gibbs, EM; Houseknecht, KL; Johnson, DE; Robertson, AS; Rollema, H; Zavadoski, W, 2007
)
" Lamotrigine was titrated up to a final dosage of 200 mg/day over 8 weeks, and pharmacokinetic assessments were made at baseline and during treatment weeks 6 and 10, at lamotrigine dosages of 100 and 200 mg/day respectively."( Effect of adjunctive lamotrigine treatment on the plasma concentrations of clozapine, risperidone and olanzapine in patients with schizophrenia or bipolar disorder.
D'Amico, G; D'Arrigo, C; Micò, U; Migliardi, G; Muscatello, MR; Perucca, E; Santoro, V; Spina, E, 2006
)
" Additional analysis revealed a significant positive correlation between baseline thalamic volume and dosage of typical antipsychotic medication."( Reduced thalamic volume in patients with chronic schizophrenia after switching from typical antipsychotic medications to olanzapine.
Goghari, VM; Honer, WG; Khorram, B; Kopala, LC; Lang, DJ; Rui, Q; Smith, GN; Vandorpe, RA, 2006
)
"In 73 schizophrenic patients recruited from psychiatric nursing homes, patient characteristics, smoking habits, drug dosing and serum concentrations of clozapine (n=33) and olanzapine (n=40) were registered."( The effect of variable cigarette consumption on the interaction with clozapine and olanzapine.
Eikeseth, PH; Haslemo, T; Molden, E; Refsum, H; Tanum, L, 2006
)
" Dosing was determined by clinical judgment."( Switching to olanzapine after unsuccessful treatment with risperidone during the first episode of schizophrenia: an open-label trial.
Higuchi, H; Ishigooka, J; Kamata, M; Takahashi, H; Yoshida, K, 2006
)
" The mean dosage of olanzapine was 15."( Switching to olanzapine after unsuccessful treatment with risperidone during the first episode of schizophrenia: an open-label trial.
Higuchi, H; Ishigooka, J; Kamata, M; Takahashi, H; Yoshida, K, 2006
)
"A 57-year-old man with a 30 year history of schizophrenia had been taking olanzapine for 4 years, with the dosage titrated to 20 mg/day, to control the psychosis."( Efficacy with high-dose aripiprazole after olanzapine-related metabolic disturbances.
Chavez, B; Poveda, RA, 2006
)
", dosage adjustments, behavioral or psychosocial interventions) before switching medications."( Effectiveness of switching antipsychotic medications.
Covell, NH; Davis, SM; Essock, SM; Lieberman, JA; Rosenheck, RA; Stroup, TS, 2006
)
" Dosing between children and adolescents significantly differed in the olanzapine group, whereas dosing was comparable in the ziprasidone group."( A naturalistic evaluation of intramuscular ziprasidone versus intramuscular olanzapine for the management of acute agitation and aggression in children and adolescents.
Khan, SS; Mican, LM, 2006
)
"Thirty-eight outpatients on long-term treatment with clozapine (250-500 mg/d, n = 10), olanzapine (10-20 mg/d, n = 12), risperidone (3-6 mg/d, n = 9), or quetiapine (200-600 mg/d, n = 7) received adjunctive topiramate, gradually titrated up to a final dosage of 200 mg/d for 6 weeks."( Effect of topiramate on plasma concentrations of clozapine, olanzapine, risperidone, and quetiapine in patients with psychotic disorders.
Bruno, A; Cacciola, M; Campolo, D; Cortese, L; D'Arrigo, C; Migliardi, G; Santoro, V; Spina, E,
)
" However, supplemental oral olanzapine or another dosing strategy may be necessary to maintain adequate therapeutic response during the first few injection cycles."( D2 receptor occupancy of olanzapine pamoate depot using positron emission tomography: an open-label study in patients with schizophrenia.
Barsoum, P; Kapur, S; Keshavan, M; Kothare, PA; Laruelle, M; Mamo, D; McDonnell, D; Taylor, CC, 2008
)
"There is no evidence that haloperidol in low dosage has different efficacy in comparison with the atypical antipsychotics olanzapine and risperidone in the management of delirium or has a greater frequency of adverse drug effects than these drugs."( Antipsychotics for delirium.
Britton, AM; Lonergan, E; Luxenberg, J; Wyller, T, 2007
)
" The pharmacokinetics of olanzapine has been described as linear and dose-proportional throughout the therapeutic dosing range."( Serum levels of olanzapine in a non-fatal overdose.
Asplund, C; Hägg, S; Lakso, HA; Lennestål, R; Mjörndal, T; Nilsson, M, 2007
)
"Children, ages 10-18 years, who met DSM-IV criteria for schizophrenia and who were resistant or intolerant to at least two antipsychotic drugs were randomized to receive 12 weeks of double-blind flexibly dosed treatment with clozapine (n = 18) or "high-dose" olanzapine (up to 30 mg/day) (n = 21)."( Clozapine and "high-dose" olanzapine in refractory early-onset schizophrenia: a 12-week randomized and double-blind comparison.
Correll, CU; De Thomas, C; Gerbino-Rosen, G; Kafantaris, V; Kane, JM; Kester, HM; Kranzler, H; Kumra, S, 2008
)
" Conversely, upon smoking cessation, smokers may require a reduction in the dosage of an interacting medication."( Drug interactions with smoking.
Kroon, LA, 2007
)
" Future prospective studies are necessary to clarify whether the prescribed dosage should be different in young and older patients."( Age and gender effects on olanzapine and risperidone plasma concentrations in children and adolescents.
Aichhorn, W; Hinterhuber, H; Kemmler, G; Marksteiner, J; Stuppaeck, C; Walch, T; Zernig, G, 2007
)
"The trial was a prospective, open-label, single-center one with a flexible dosing of SGAs."( Differences in the effect of second-generation antipsychotics on prolactinaemia: six weeks open-label trial in female in-patients.
Cejpková, A; Rodáková, I; Svestka, J; Synek, O; Tomanová, J, 2007
)
" Haloperidol (mean dosage 4,1 mg daily) was administered to 17 patients and trifluoperazine (mean dosage 7,1 mg daily) to 14 patients."( [Prescription of traditional neuroleptics in the remission period for schizophrenic patients with excess of body mass caused by atypical antipsychotics].
Danilov, DS; Tiul'pin, IuG, 2007
)
" Neuroleptic drugs can produce severe side effects and need careful dosage and monitoring."( [Delusion in the critical patient].
Palencia-Herrejón, E; Romera, MA; Silva, JA, 2008
)
" Olanzapine treatment was started with a daily dosage of 15 mg."( Olanzapine treatment during breast feeding: a case report.
Bartels, M; Gaertner, HJ; Lutz, UC; Orlikowsky, T; Wiatr, G, 2008
)
" The fourth patient showed RLS symptoms that were initially caused by a 20-mg daily olanzapine dosage and were later mitigated when olanzapine was reduced and ropinirole was administered."( Restless legs syndrome and periodic limb movements during sleep probably associated with olanzapine.
Kang, SG; Kim, L; Lee, HJ, 2009
)
"The objective of this study was to assess the dose-response relationship of standard and higher doses of olanzapine in a randomized, double-blind, 8-week, fixed-dose study comparing olanzapine 10 (n = 199), 20 (n = 200), and 40 mg/d (n = 200) for patients with schizophrenia or schizoaffective disorder and suboptimal response to current treatment."( Standard and higher dose of olanzapine in patients with schizophrenia or schizoaffective disorder: a randomized, double-blind, fixed-dose study.
Adams, DH; Buckley, PF; Chen, L; Citrome, L; Edwards, SE; Kinon, BJ; Lieberman, JA; Lindenmayer, JP; Liu-Seifert, H; McEvoy, JP; Meltzer, HY; Stauffer, V; Volavka, J; Wilson, DR, 2008
)
" However, the question whether olanzapine treats, ameliorates, or masks preexisting tardive dyskinesia was difficult to answer, as no dosage reduction or withdrawal was undertaken."( The impact of olanzapine on tardive dyskinetic symptoms in a state hospital population.
Appel, N; Brar, JS; Chalasani, L; Chengappa, KN; Gopalani, A; Parepally, H,
)
" Daily dosage of olanzapine was adjusted to the clinical condition of the patient and it varied from 5 to 20 mg a day."( Statistical evaluation of olanzapine efficacy in catamnesticly investigated patients.
Djedjibegovic, J; Jovanovic-Gmaz, M; Kapetanovic, D; Sahović, D; Skrbo, A; Todorovic, L, 2008
)
" Deficits were unrelated to drug dosage and clinical ratings."( Effects of second-generation antipsychotic medication on smooth pursuit performance in antipsychotic-naive schizophrenia.
Harris, MS; Keshavan, MS; Lencer, R; Reilly, JL; Sprenger, A; Sweeney, JA, 2008
)
" This 5-day, randomized, double-blind trial evaluated relative improvements in agitation in hospitalized patients who received orally dosed olanzapine (n = 306, 20 mg/d) or aripiprazole (n = 298, 15 mg/d, increasing to 30 mg/d as needed)."( Olanzapine versus aripiprazole for the treatment of agitation in acutely ill patients with schizophrenia.
Chen, L; Kinon, BJ; Kollack-Walker, S; Sniadecki, J; Stauffer, VL, 2008
)
" Treatment was at the psychiatrist's discretion, including flexible dosing and use of concomitant therapies and medications, with assessments at 0, 3, 6, 12, 18, 24, 30, and 36 months."( Long-term antipsychotic monotherapy for schizophrenia: disease burden and comparative outcomes for patients treated with olanzapine, quetiapine, risperidone, or haloperidol monotherapy in a pan-continental observational study.
Anders, M; Dossenbach, M; Irimia, V; Kotler, M; Logozar-Perkovic, D; Lowry, AJ; Pecenak, J; Peciukaitiene, D; Smulevich, AB; Szulc, A; Treuer, T; West, TM, 2008
)
"To evaluate treatment with variably dosed olanzapine in individuals with borderline personality disorder."( Olanzapine for the treatment of borderline personality disorder: variable dose 12-week randomised double-blind placebo-controlled study.
Bateman, A; Bohus, M; Corya, S; Deberdt, W; Detke, HC; Lin, D; Schulz, SC; Tanaka, Y; Trzaskoma, Q; Zanarini, MC, 2008
)
" Divalproex ER was initiated on day 1 at 20 mg/kg per day q AM and was titrated to clinical effect on days 3, 7, and 10, not to exceed a maximum dosage of 35 mg/kg per day."( Divalproex ER combined with olanzapine or risperidone for treatment of acute exacerbations of schizophrenia.
Abi-Saab, W; Baker, J; Casey, DE; Daniel, DG; Greco, N; Kane, JM; Redden, L; Saltarelli, M; Tamminga, C; Tran-Johnson, T; Wozniak, P, 2009
)
"The mean daily dosage of olanzapine was 10."( The safety of olanzapine in adolescents with schizophrenia or bipolar I disorder: a pooled analysis of 4 clinical trials.
Carlson, JL; Dittmann, RW; Kryzhanovskaya, LA; Merida, KM; Robertson-Plouch, CK; Xu, W, 2009
)
"The primary objective of this observational research was to study the evolution of the olanzapine dosage under naturalistic settings."( [Pattern and evolution of the prescription of olanzapine during one year: Results of the cohort study ECOL].
Chartier, F; Deal, C; Flandre, P; Fourrier-Réglat, A; Gasquet, I; Heurtebize, N; Perrin, E, 2009
)
" At second month of treatment clinicians were requested to very well document any changes in olanzapine dosage as well as reasons for the dosage modifications and potential coprescriptions."( [Pattern and evolution of the prescription of olanzapine during one year: Results of the cohort study ECOL].
Chartier, F; Deal, C; Flandre, P; Fourrier-Réglat, A; Gasquet, I; Heurtebize, N; Perrin, E, 2009
)
" In the first case report, the patient was switched to olanzapine ODT in daily dosage of 20 mg, while in the second case report, the patient was switched to olanzapine ODT in daily dosage of 15 mg, and weight loss was similar (14 kg vs."( Weight loss during therapy with olanzapine orally disintegrating tablets: two case reports.
Jakovljević, M; Kozumplik, O; Uzun, S, 2009
)
" The patient improved with olanzapine at a dosage of 20 mg daily."( Psychosis secondary to traumatic brain injury.
Carvalho, M; Gois, C; Guerreiro, DF; Navarro, R; Silva, M, 2009
)
" Prompt dosage of CK should be performed."( [Olanzapine induced rhabdomyolysis and serum creatine kinase increase].
Cathébras, P; Guy, C; Koenig, M; Ribeyron, S, 2009
)
"The aim of this study was to assess the bioequivalence of 2 commercial 10-mg tablet formulations of olanzapine by statistical analysis of the pharmacokinetic parameters C(max), AUC from 0 to 72 hours after dosing (AUC(0-72)), and AUC(0-infinity) as required by the Egyptian health authority for the marketing of a generic product."( A single-dose, randomized, two-way crossover study comparing two olanzapine tablet products in healthy adult male volunteers under fasting conditions.
Elshafeey, AH; Elsherbiny, MA; Fathallah, MM, 2009
)
" However the impact of their high dose related side effects on their low dosage related neuroprotectivity is still unknown."( Olanzapine does not aggrevate ischemic neuronal injury by focal cerebral ischemia: a dose related restriction of the neuroprotective effect?
Kilic, E; Yuluğ, B, 2009
)
" The preferred switch strategy was immediate discontinuation, and the preferred dosing regimen was 120 mg/day."( Efficacy and tolerability of switching to ziprasidone from olanzapine, risperidone or haloperidol: an international, multicenter study.
Akkaya, C; Alptekin, K; Brook, S; Danaci, AE; El Tallawy, H; Hafez, J; Karayal, ON; Lowe, W; Tzebelikos, E; Ucok, A, 2009
)
" In conclusion, dosing of olanzapine in clinical practice is higher than what has been established in the registration program for schizophrenia or bipolar disorder."( Olanzapine dosing above the licensed range is more efficacious than lower doses: fact or fiction?
Citrome, L; Kantrowitz, JT, 2009
)
"3 times higher after controlling for dosing potency)."( Short- and long-term effects on prolactin of risperidone and olanzapine treatments in children and adolescents.
D'Arrigo, C; de Leon, J; Diaz, FJ; Gagliano, A; Germanò, E; Migliardi, G; Siracusano, R; Spina, E, 2009
)
" The products formed in marketed tablet dosage forms are similar to those formed in standard drug solutions under similar stress conditions."( Development of a stability-indicating HPLC method for simultaneous determination of olanzapine and fluoxetine in combined dosage forms.
Pathak, A; Rajput, SJ, 2009
)
" If the patient is currently taking other mood stabilizers, their dosage should be optimized, and the clinician should consider adding or switching to lithium, quetiapine, or lamotrigine."( The psychopharmacology algorithm project at the Harvard South Shore Program: an update on bipolar depression.
Ansari, A; Osser, DN,
)
" Plasma samples were collected before the medications were given and 12h after the bedtime dosing each week."( Gender-specific prolactin response to antipsychotic treatments with risperidone and olanzapine and its relationship to drug concentrations in patients with acutely exacerbated schizophrenia.
Furukori, H; Kaneko, S; Nakagami, T; Saito, M; Sato, Y; Sugawara, N; Tsuchimine, S; Yasui-Furukori, N, 2010
)
" Reports that included serum concentrations consistently found elevations following smoking cessation, and dosage reductions of 30-40% were required to achieve pre-cessation concentrations."( Impact of tobacco smoking cessation on stable clozapine or olanzapine treatment.
Ackman, ML; Lowe, EJ, 2010
)
" Measurement of baseline serum clozapine concentrations and/or empiric dosage adjustment in patients expected to have a prolonged hospital stay with forced smoking cessation may be appropriate."( Impact of tobacco smoking cessation on stable clozapine or olanzapine treatment.
Ackman, ML; Lowe, EJ, 2010
)
" In addition, olanzapine pharmacokinetic parameters in adolescents were compared with those in adults to guide appropriate dosing recommendations for adolescent patients."( Oral olanzapine disposition in adolescents with schizophrenia or bipolar I disorder: a population pharmacokinetic model.
Bergstrom, RF; Hong, Q; Lobo, ED; Quinlan, T; Robertson-Plouch, C, 2010
)
" Patients treated with greater amounts of chlorpromazine-equivalent daily dosage had smaller anterior internal capsule volumes at baseline (r = -0."( Anterior internal capsule volumes increase in patients with schizophrenia switched from typical antipsychotics to olanzapine.
Barr, AM; Goghari, VM; Götz, J; Honer, WG; Khorram, B; Kopala, LC; Lang, DJ; Smith, GN; Vandorpe, RA, 2011
)
" Prolactin concentrations before dosing during risperidone treatment were significantly higher than during treatment with olanzapine and perospirone in females."( Prolactin fluctuation over the course of a day during treatments with three atypical antipsychotics in schizophrenic patients.
Fujii, A; Furukori, H; Inoue, Y; Kaneko, S; Sugawara, N; Tsuchimine, S; Yasui-Furukori, N, 2010
)
" In order to provide a dosing comparison to a therapeutically relevant endpoint, both drugs were tested against amphetamine-induced disruption of prepulse inhibition as well."( Disruption of conditioned reward association by typical and atypical antipsychotics.
Danna, CL; Elmer, GI, 2010
)
" Further investigations are warranted to identify patient characteristics and antipsychotic dosage regimens that are not associated with a greater risk of mortality in elderly patients with dementia."( Are all commonly prescribed antipsychotics associated with greater mortality in elderly male veterans with dementia?
Dysken, MW; Lederle, FA; Rector, TS; Rossom, RC, 2010
)
" In the first experiment, rats dosed only with olanzapine gained a statistically significant amount of weight."( Selective glucocorticoid receptor (type II) antagonist prevents and reverses olanzapine-induced weight gain.
Belanoff, JK; Blasey, CM; Clark, RD; Roe, RL, 2010
)
"Manufacturing irregularities, improper drug reconstitution, and inappropriate dosing were ruled out as possible causes of PDSS."( Post-injection delirium/sedation syndrome in patients with schizophrenia treated with olanzapine long-acting injection, II: investigations of mechanism.
Bergstrom, RF; Detke, HC; Johnson, J; Kothare, P; McDonnell, DP; Mitchell, MI; Sanchez-Felix, MV; Sorsaburu, S; Stickelmeyer, M, 2010
)
" The three protocols differ in many aspects (routes of administration, extent of the chronic treatment, diets, and dosage regimen), and the pros and cons of each procedure are systematically detailed throughout."( A murine model of atypical antipsychotic-induced weight gain and metabolic dysregulation.
Coccurello, R; Moles, A, 2010
)
"Individuals in the extended dosing group were not at greater risk of symptom exacerbation, relapse, or rehospitalization; indeed, more rehospitalizations occurred in those receiving regular dosing."( "Extended" antipsychotic dosing in the maintenance treatment of schizophrenia: a double-blind, placebo-controlled trial.
Feingold, A; Kapur, S; Mann, S; Remington, G; Seeman, P; Shammi, C, 2011
)
" After the OGTT, the medication was switched to another by decreasing the previous dosage gradually over 2 to 8 months after the initiation of the second medicine."( A crossover study on the glucose metabolism between treatment with olanzapine and risperidone in schizophrenic patients.
Furukori, H; Kaneko, S; Nakagami, T; Saito, M; Sato, Y; Yasui-Furukori, N, 2010
)
" Pharmacokinetic modeling was conducted to evaluate the resulting dosing recommendations."( Dose correspondence between olanzapine long-acting injection and oral olanzapine: recommendations for switching.
Carlson, J; Detke, HC; Garhyan, P; McDonnell, D; Zhao, F, 2011
)
" Previous animal model studies have utilised a range of olanzapine dosages, however the dosage that better mimics the human scenario of olanzapine-induced weight gain is unclear."( Olanzapine treatment and metabolic dysfunction: a dose response study in female Sprague Dawley rats.
Deng, C; Huang, XF; Weston-Green, K, 2011
)
"A simple, sensitive and reproducible ultra performance liquid chromatography (UPLC) coupled with a photodiode array detector method was developed for the quantitative determination of olanzapine (OLN) in API and pharmaceutical dosage forms."( Development of a stability-indicating UPLC method for determining olanzapine and its associated degradation products present in active pharmaceutical ingredients and pharmaceutical dosage forms.
Krishnaiah, Ch; Kumar, R; Mukkanti, K; Vishnu Murthy, M, 2011
)
" Side effects were assessed with Dosage Record and Treatment Emergent Symptoms Scale, other symptom-specific scales, laboratory and instrumental tests."( Olanzapine vs. risperidone in treating aggressive behaviours in adults with intellectual disability: a single blind study.
Amore, M; Bertelli, M; Rossi, M; Tamborini, S; Villani, D, 2011
)
" Psychiatry was consulted, and a monthlong cross-taper to discontinue olanzapine and initiate aripiprazole with a target dosage of 20 mg daily was recommended."( Olanzapine-induced parkinsonism associated with smoking cessation.
Arnoldi, J; Repking, N, 2011
)
" This previously unreported sensitization phenomenon represents a novel finding that may have clinical implications for patients receiving intermittent antipsychotic drug dosing or with variable adherence to treatment."( Intermittent treatment with olanzapine causes sensitization of the metabolic side-effects in rats.
Barr, AM; Boyda, HN; Honer, WG; Pang, CC; Procyshyn, RM; Tse, L; Wong, D, 2012
)
"Two bioequivalence studies were carried out in healthy volunteers in order to compare the rate and extent of absorption of two dosage forms (film-coated tablet and orodispersible tablet) of oral olanzapine (CAS 132539-06-1) 10 mg test formulations and the respective brand formulations as reference."( Bioequivalence evaluation of two dosage forms of olanzapine 10 mg formulations in healthy volunteers.
Arcabell, M; Cabré, F; Cánovas, M; Cebrecos, J; Domenech, G; Manríquez, M; Martínez, G; Pelagio, P; Torres, F, 2011
)
" The sensitivity of olanzapine dosage to predict EEG changes was 66."( EEG alterations during treatment with olanzapine.
Bias, F; Degner, D; Nitsche, MA; Reulbach, U; Rüther, E, 2011
)
"OCS were significantly more prevalent and severe in group I, in which OCS severity correlated with dosage of clozapine and duration of treatment."( Antiserotonergic antipsychotics are associated with obsessive-compulsive symptoms in schizophrenia.
Englisch, S; Esslinger, C; Meyer-Lindenberg, A; Rausch, F; Schirmbeck, F; Zink, M, 2011
)
"The aim of this study was to examine the effects of dipyridamole monotherapy of 200 mg/day on positive and negative symptoms, with the goal of determining dosing for future adjunctive studies in schizophrenia."( Dipyridamole monotherapy in schizophrenia: pilot of a novel treatment approach by modulation of purinergic signaling.
Adami, H; Allen-Emerson, R; Gopinath, HV; Hong, LE; Liu, J; McMahon, RP; Thaker, GK; Wonodi, I, 2011
)
" Olanzapine was added to milnacipran, and its dosage was adjusted according to each patient."( Olanzapine augmentation of milnacipran for stage 2 treatment-resistant major depression: an open study.
Boku, S; Honma, H; Inoue, T; Koyama, T; Nakagawa, S, 2011
)
"Participants, who were recently admitted inpatients with schizophrenia with an acute exacerbation of psychotic symptoms, were randomly assigned to 6 weeks of double-blind treatment with 40 mg of lurasidone, 120 mg of lurasidone, 15 mg of olanzapine (included to test for assay sensitivity), or placebo, dosed once daily."( Lurasidone in the treatment of schizophrenia: a randomized, double-blind, placebo- and olanzapine-controlled study.
Cucchiaro, J; Kalali, AH; Loebel, A; Meltzer, HY; Ogasa, M; Phillips, D; Pikalov, A; Schweizer, E; Silva, R; Xu, J, 2011
)
" Next, training was suspended and the mice received a maintenance dosing regimen in which they were injected twice daily with 10 mg/kg N-desmethylclozapine for 10 days."( The metabolites N-desmethylclozapine and N-desmethylolanzapine produce cross-tolerance to the discriminative stimulus of the atypical antipsychotic clozapine in C57BL/6 mice.
Meltzer, HY; Porter, JH; Webster, KA; Wiebelhaus, JM, 2011
)
"Patients with schizophrenia or schizoaffective disorder with a body mass index ≥ 27 and non-high-density lipoprotein (non-HDL) cholesterol ≥ 130 mg/dl who were on a stable treatment dosage of olanzapine, quetiapine, or risperidone were randomly assigned to switch to ari-piprazole (N=109) for 24 weeks or stay on their current medication (N=106)."( A randomized trial examining the effectiveness of switching from olanzapine, quetiapine, or risperidone to aripiprazole to reduce metabolic risk: comparison of antipsychotics for metabolic problems (CAMP).
Hamer, RH; LaVange, LM; Lieberman, JA; McEvoy, JP; Nussbaum, AM; Perkins, DO; Ring, KD; Rosenheck, RA; Stroup, TS; Swartz, MS, 2011
)
" Thus, developed formulation of olanzapine is expected to improve the patient compliance, form better dosage regimen, and provide maintenance therapy to psychotic patients."( Formulation, in vitro, and in vivo evaluation of matrix-type transdermal patches containing olanzapine.
Aggarwal, G; Dhawan, S; Harikumar, SL,
)
" The FGA group demonstrated that extrapyramidal syndrome (EPS) worsened under an increased dosage of anti-EPS drugs."( Risperidone and olanzapine versus another first generation antipsychotic in patients with schizophrenia inadequately responsive to first generation antipsychotics.
Chan, HY; Chen, CH; Chen, JJ; Gau, SS; Hwu, HG, 2012
)
" Propensity-stratified and propensity-weighted models as well as analyses controlling for site of care and medication dosage revealed similar patterns."( Risk of mortality among individual antipsychotics in patients with dementia.
Blow, FC; Chiang, C; Cunningham, F; Kales, HC; Kim, HM; Schneider, LS; Seyfried, LS; Valenstein, M; Zivin, K, 2012
)
" Also, data from the three active dosing arms were combined and compared to placebo data."( Effects of olanzapine long-acting injection on levels of functioning among acutely ill patients with schizophrenia.
Ascher-Svanum, H; Case, MG; Schuh, KJ; Witte, MM, 2012
)
" The dosage of pre-existing atypical antipsychotics was fixed, while the dosage of aripiprazole ranged from 5 to 20 mg/day during the study period."( Adjunctive effects of aripiprazole on metabolic profiles: comparison of patients treated with olanzapine to patients treated with other atypical antipsychotic drugs.
Chen, CK; Hsiao, CC; Huang, YS; Ree, SC; Wang, LJ, 2013
)
"All trials were industry supported, with some variability in dosage of haloperidol."( Lower rate of depressive switch following antimanic treatment with second-generation antipsychotics versus haloperidol.
Capapey, J; Colom, F; Goikolea, JM; Grande, I; Sanchez-Moreno, J; Torres, I; Undurraga, J; Valentí, M; Vieta, E, 2013
)
" We wonder if we should have kept olanzapine and strengthen its dosage like Cassidy et al."( [Acute catatonia: Questions, diagnosis and prognostics, and the place of atypical antipsychotics].
Belaizi, M; Bichra, MZ; Bouchikhi Idrissi, ML; Mehssani, J; Yahia, A, 2013
)
" This compound is efficacious when dosed orally in an olanzapine-induced weight gain model in rats."( Discovery of a novel non-steroidal GR antagonist with in vivo efficacy in the olanzapine-induced weight gain model in the rat.
Ahmed, S; Belanoff, J; Blasey, C; Buckley, G; Clark, RD; Daly, S; Hunt, HJ; Hynd, G; Lockey, P; O'Connor, E; Ray, NC; Roe, R; Sajad, M; Sutton, J, 2012
)
"OFC trades simplicity of administration for loss of flexibility of dosing and lack of a generic preparation, both of which are available for olanzapine and fluoxetine separately."( Pharmacokinetic evaluation of olanzapine + fluoxetine for the treatment of bipolar depression.
Dubovsky, SL, 2013
)
" We treated adolescent, male rats with olanzapine (Ola) on post-natal days 28-49, under dosing conditions that approximate those employed therapeutically in humans."( Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function.
Bailey, AM; Burke, JS; Cheer, JF; Elnabawi, A; Frost, DO; Kallevang, JK; Kolb, B; Lansink, CS; Merchenthaler, I; Milstein, JA; Turek, KC; Vinish, M, 2013
)
"To examine the effectiveness of switching patients to lurasidone using 3 different dosing strategies."( Effectiveness of lurasidone in patients with schizophrenia or schizoaffective disorder switched from other antipsychotics: a randomized, 6-week, open-label study.
Citrome, L; Cucchiaro, J; Hernandez, D; Hsu, J; Loebel, A; McEvoy, JP; Pikalov, A, 2013
)
"Adults with DSM-IV-defined schizophrenia or schizoaffective disorder in a nonacute phase of illness were randomized to 1 of 3 lurasidone dosing regimens for the initial 2 weeks of the study: (1) 40 mg/d for 2 weeks; (2) 40 mg/d for 1 week, increased to 80 mg/d on day 8 for week 2 (up-titration group); and (3) 80 mg/d for 2 weeks."( Effectiveness of lurasidone in patients with schizophrenia or schizoaffective disorder switched from other antipsychotics: a randomized, 6-week, open-label study.
Citrome, L; Cucchiaro, J; Hernandez, D; Hsu, J; Loebel, A; McEvoy, JP; Pikalov, A, 2013
)
"Patients who completed a 6-week, double-blind, placebo-controlled study evaluating the efficacy of fixed doses of once-daily lurasidone (40 or 120 mg) or olanzapine 15 mg (to confirm assay sensitivity) were eligible to receive flexibly dosed lurasidone 40 to 120 mg/d in this 6-month, open-label extension study (conducted from March 2008 to December 2009)."( Effectiveness of lurasidone for patients with schizophrenia following 6 weeks of acute treatment with lurasidone, olanzapine, or placebo: a 6-month, open-label, extension study.
Cucchiaro, J; Hsu, J; Loebel, A; Pikalov, A; Simonelli, D; Stahl, SM, 2013
)
"Open-label treatment with flexibly dosed lurasidone (40-120 mg/d) was generally safe, well tolerated, and effective over a 6-month period in patients who had completed a preceding 6-week, double-blind study."( Effectiveness of lurasidone for patients with schizophrenia following 6 weeks of acute treatment with lurasidone, olanzapine, or placebo: a 6-month, open-label, extension study.
Cucchiaro, J; Hsu, J; Loebel, A; Pikalov, A; Simonelli, D; Stahl, SM, 2013
)
" The effect size-dose relationship showed a typical dose-response curve with minimal rise in slope for doses higher than 10 mg/d."( Olanzapine: a systematic review and meta-regression of the relationships between dose, plasma concentration, receptor occupancy, and response.
Bishara, D; Kapur, S; Olofinjana, O; Patel, MX; Sparshatt, A; Taylor, D, 2013
)
" This implies that neither the incorrect drug nor the optimal dosage for that patient is achieved."( Considering CYP1A2 phenotype and genotype for optimizing the dose of olanzapine in the management of schizophrenia.
Forrest, A; Gross, AS; McLachlan, AJ; Perera, V; Polasek, TM; Qin, Y; Rao, G; Xu, J, 2013
)
" Furthermore, the authors discuss the utilization of phenotyping and genotyping of CYP1A2 and their potential utility in clinical practice for olanzapine dosing regimens."( Considering CYP1A2 phenotype and genotype for optimizing the dose of olanzapine in the management of schizophrenia.
Forrest, A; Gross, AS; McLachlan, AJ; Perera, V; Polasek, TM; Qin, Y; Rao, G; Xu, J, 2013
)
" The method was successfully used for the analysis of samples from nonsmoking patients (n = 48) treated with OLZ in the dosage range of 5-20 mg per day."( Determination of olanzapine and N-desmethyl-olanzapine in plasma using a reversed-phase HPLC coupled with coulochemical detection: correlation of olanzapine or N-desmethyl-olanzapine concentration with metabolic parameters.
Chen, YC; Lin, CH; Lu, ML; Wu, TH; Yang, HC, 2013
)
" All values were more than 30 ng/mL after 11-16 h from dosing to sample collection, and the mean value was 47."( The possibility that requiring high-dose olanzapine cannot be explained by pharmacokinetics in the treatment of acute-phase schizophrenia.
Hatta, K; Hirata, T; Ito, S; Kasuya, M; Katayama, S; Kuga, H; Morikawa, F; Nakamura, H; Nakamura, M; Nakase, R; Ohnuma, T; Sawa, Y; Shirai, Y; Sudo, Y; Takebayashi, H; Usui, C, 2013
)
" This variation in turn gives rise to the need for individualized dosing in order to avoid concentration-dependent adverse effects or therapeutic failure."( Pharmacogenetics of olanzapine metabolism.
Dahl, ML; Söderberg, MM, 2013
)
" One-third of children and adolescents had abnormal serum triglycerides and cholesterol; however, a dose-response was not demonstrated."( Metabolic changes in first-episode early-onset schizophrenia with second-generation antipsychotics.
Amminger, GP; Becker, J; O'Donoghue, B; Papageorgiou, K; Schäfer, MR, 2014
)
" This analysis evaluated the dosing and interval patterns to compare the actual dosing patterns with the recommended dosing strategy."( Real-world use patterns of olanzapine long-acting injection in the United States: comparison to the recommended dosing strategy.
Case, MG; Hoffmann, VP; Karagianis, JL; Schuh, KJ, 2013
)
" The study is limited by a database that does not include reasons for dose and dosing interval decisions or reasons for delaying or discontinuing treatment."( Real-world use patterns of olanzapine long-acting injection in the United States: comparison to the recommended dosing strategy.
Case, MG; Hoffmann, VP; Karagianis, JL; Schuh, KJ, 2013
)
" Dosing of olanzapine was established based on inhibition of amphetamine-induced locomotion."( Effects of intracerebroventricular (ICV) olanzapine on insulin sensitivity and secretion in vivo: an animal model.
Arenovich, T; Chintoh, A; Cohn, T; Fletcher, P; Giacca, A; Guenette, M; Hahn, MK; Lam, L; Mann, S; Nobrega, J; Remington, G; Teo, C, 2014
)
" The PK properties suggested prolonged release providing sustained olanzapine plasma concentrations and supporting a dosing interval ≤4 weeks."( Single- and multiple-dose pharmacokinetic, safety, and tolerability profiles of olanzapine long-acting injection: an open-label, multicenter, nonrandomized study in patients with schizophrenia.
Bergstrom, R; Jen, KY; Johnson, J; Kothare, P; McDonnell, D; Mitchell, M; Walker, D; Zhao, F, 2013
)
" Establishing a drug dosing regimen that balances benefit and risk, and minimizes ADEs in older populations can be challenging."( Quantitative drug benefit-risk assessment: utility of modeling and simulation to optimize drug safety in older adults.
Crentsil, V; Jackson, A; Lee, J, 2014
)
"The aim of this study is to evaluate the use of modeling, simulation, and risk-benefit acceptability methods to establish a drug dosing regimen that balances benefit and risk."( Quantitative drug benefit-risk assessment: utility of modeling and simulation to optimize drug safety in older adults.
Crentsil, V; Jackson, A; Lee, J, 2014
)
"Our study introduces a real-world approach for finding the safe drug dosing regimen without extensive exposure of a vulnerable and older population to drugs."( Quantitative drug benefit-risk assessment: utility of modeling and simulation to optimize drug safety in older adults.
Crentsil, V; Jackson, A; Lee, J, 2014
)
" All patients were titrated on iloperidone to 6mg BID by Day 4, then flexibly dosing between 6 and 12mg BID, as needed."( A trial evaluating gradual- or immediate-switch strategies from risperidone, olanzapine, or aripiprazole to iloperidone in patients with schizophrenia.
Alva, G; Brams, M; Citrome, L; Glick, ID; Hochfeld, M; Jackson, R; Kianifard, F; Mattingly, G; Meng, X; Pestreich, L; Weiden, PJ; Winseck, A, 2014
)
" Dosing thereafter was flexible (150-405 mg/4 weeks of LAI vs 5-20 mg/d of oral)."( Comparison of olanzapine long-acting injection and oral olanzapine: a 2-year, randomized, open-label study in outpatients with schizophrenia.
Ascher-Svanum, H; Brunner, E; Choukour, M; Detke, HC; Llorca, PM; Watson, SB; Weiden, PJ, 2014
)
" Renal dosing for topiramate, reduction in PIMs/anticholinergic burden, and substituting haloperidol for olanzapine resolved his violent behavior and CD."( Capgras delusion with violent behavior in Alzheimer dementia: case analysis with literature review.
Dawood, A; Kaufman, KR; Newman, NB, 2014
)
" Peak-to-trough fluctuation was greater for the 4-week dosing interval than the 2-week one, with no apparent clinical ramifications for these differences."( Pharmacokinetics of olanzapine long-acting injection: the clinical perspective.
Bergstrom, RF; Detke, HC; Heres, S; Kraemer, S, 2014
)
" Patients received flexibly dosed (45-405 mg) olanzapine LAI every 2-4 weeks."( Long-term safety and efficacy of olanzapine long-acting injection in patients with schizophrenia or schizoaffective disorder: a 6-year, multinational, single-arm, open-label study.
Detke, HC; Landry, J; McDonnell, DP, 2014
)
" We therefore propose a 50% dosage increase of olanzapine when combining with a ritonavir-boosted protease inhibitor."( Effect of fosamprenavir/ritonavir on the pharmacokinetics of single-dose olanzapine in healthy volunteers.
Burger, DM; Colbers, AP; Jacobs, BS; Schouwenberg, BJ; Velthoven-Graafland, K, 2014
)
" Further and larger studies are needed before genotype-based dosage recommendations can help patients treated with CYP1A2 metabolized drugs."( CYP1A2*1D and *1F polymorphisms have a significant impact on olanzapine serum concentrations.
Czerwensky, F; Leucht, S; Steimer, W, 2015
)
"Results provide some support for the notion that dosage is an important consideration in relation to effectiveness; however, the cost-benefit balance does not support the clinical utility of olanzapine in treating alcohol dependence."( Dose specific effects of olanzapine in the treatment of alcohol dependence.
Arenella, P; Bogenschutz, M; Bryan, AD; Claus, ED; Ewing, SW; Hutchison, KE; Karoly, H; Littlewood, RA, 2015
)
" Indeed, we and others have previously reported that treatment of adolescent rats with olanzapine (OLA; a widely prescribed AAPD) on postnatal days 28-49, under dosing conditions that approximate those employed therapeutically in humans, causes long-term behavioral and neurobiological perturbations."( Olanzapine antipsychotic treatment of adolescent rats causes long term changes in glutamate and GABA levels in the nucleus accumbens.
Frost, DO; Gullapalli, RP; Xu, S, 2015
)
" Patients were given a dosage of either 210 or 300 or 405 mg of OLZ-LAI every 28 days."( "Long-acting" olanzapine in maintenance therapy of schizophrenia: A study with plasma levels.
Altamura, CA; Di Pace, C; Maffini, M; Mauri, MC; Moliterno, D; Paletta, S; Reggiori, A; Rovera, C, 2015
)
"The objective of this study was to evaluate the effectiveness and impact of once- versus twice-daily dosing of risperidone and olanzapine on clinical outcomes in patients with schizophrenia."( Effectiveness of different dosing regimens of risperidone and olanzapine in schizophrenia.
Agid, O; Fervaha, G; Lee, J; Remington, G; Takeuchi, H, 2015
)
" The incremental dosage of olanzapine from 5 to 20 mg/day was given but failed to control her psychotic symptoms during the first week, and was therefore switched to risperidone."( Chemotherapy-induced acute psychosis in a patient with malignant germ cell tumour.
Pongpirul, K; Puangthong, U, 2015
)
" They received 100 mg dehydroepiandrosterone (DHEA) or placebo as an augmentation of olanzapine treatment (an average dosage 15 mg/day)."( [The stabilizing effect of dehydroepiandrosterone on clinical parameters of metabolic syndrome in patients with schizophrenia treated with olanzapine - a randomized, double-blind trial].
Holka-Pokorska, JA; Jarema, M; Radzio, R; Wichniak, A,
)
" There was no support for a dose-response relationship for any drug combination."( Skating on thin ice: pragmatic prescribing for medication refractory schizophrenia.
Joyce, DW; Mateos Fernandez, MJ; Sarkar, SN; Shergill, SS; Tracy, DK, 2015
)
" This may be typically taken only for a few days, at a dosage range of 5-50 mg/day."( Olanzapine as the ideal "trip terminator"? Analysis of online reports relating to antipsychotics' use and misuse following occurrence of novel psychoactive substance-related psychotic symptoms.
Bersani, FS; Bersani, G; Corazza, O; Melcore, C; Metastasio, A; Schifano, F; Valeriani, G, 2015
)
"Population pharmacokinetics can predict antipsychotic blood concentrations at a given time point prior to a dosage change."( Dopamine D2/3 Receptor Occupancy Following Dose Reduction Is Predictable With Minimal Plasma Antipsychotic Concentrations: An Open-Label Clinical Trial.
Bies, RR; Caravaggio, F; Gerretsen, P; Graff-Guerrero, A; Mamo, DC; Mar, W; Mulsant, BH; Nakajima, S; Plitman, E; Pollock, BG; Suzuki, T; Uchida, H, 2016
)
"D2/3R occupancy levels can be predicted from blood drug concentrations collected prior to dosage change."( Dopamine D2/3 Receptor Occupancy Following Dose Reduction Is Predictable With Minimal Plasma Antipsychotic Concentrations: An Open-Label Clinical Trial.
Bies, RR; Caravaggio, F; Gerretsen, P; Graff-Guerrero, A; Mamo, DC; Mar, W; Mulsant, BH; Nakajima, S; Plitman, E; Pollock, BG; Suzuki, T; Uchida, H, 2016
)
"Due to high inter-individual variability in peripheral pharmacokinetic parameters, dosing of antipsychotics currently relies on clinical trial-and-error, and predicting antipsychotic plasma concentrations before changing a dose has been a challenge."( Predicting Plasma Olanzapine Concentration Following a Change in Dosage: A Population Pharmacokinetic Study.
Bies, RR; Caravaggio, F; Graff-Guerrero, A; Mamo, DC; Mimura, M; Nakajima, S; Plitman, E; Pollock, BG; Suzuki, T; Takeuchi, H; Tsuboi, T; Uchida, H, 2015
)
" At least 7 days after a dosage change of olanzapine, a third sample was collected."( Predicting Plasma Olanzapine Concentration Following a Change in Dosage: A Population Pharmacokinetic Study.
Bies, RR; Caravaggio, F; Graff-Guerrero, A; Mamo, DC; Mimura, M; Nakajima, S; Plitman, E; Pollock, BG; Suzuki, T; Takeuchi, H; Tsuboi, T; Uchida, H, 2015
)
"Plasma olanzapine concentrations following an actual dosage change can be predicted in advance with a high degree of certainty."( Predicting Plasma Olanzapine Concentration Following a Change in Dosage: A Population Pharmacokinetic Study.
Bies, RR; Caravaggio, F; Graff-Guerrero, A; Mamo, DC; Mimura, M; Nakajima, S; Plitman, E; Pollock, BG; Suzuki, T; Takeuchi, H; Tsuboi, T; Uchida, H, 2015
)
" Moreover, available tools that guide dosing in neuropsychiatric pediatric patients are scant, leading to the possibility of reduced efficacy and/or increased risks of toxicity."( Therapeutic drug monitoring of second-generation antipsychotics in pediatric patients: an observational study in real-life settings.
Auricchio, F; Baldelli, S; Bernardini, R; Bertella, S; Bravaccio, C; Capuano, A; Carnovale, C; Cattaneo, D; Clementi, E; Ferrajolo, C; Fucile, S; Guastella, G; Mani, E; Molteni, M; Pascotto, A; Pisano, S; Pozzi, M; Radice, S; Rafaniello, C; Riccio, MP; Rizzo, R; Rossi, F; Scuderi, MG; Sperandeo, S; Sportiello, L; Villa, L, 2016
)
" Analyses were conducted assuming pooled dosing from randomised clinical trials included in the MTCs."( Cost-effectiveness Analysis of Aripiprazole Once-Monthly for the Treatment of Schizophrenia in the UK.
Beillat, M; Robinson, P; Sapin, C; Tempest, M; Treur, M, 2015
)
" The dosage of olanzapine, treatment duration, and duration from initial use until death were collected from the medical records."( Use of olanzapine for the relief of nausea and vomiting in patients with advanced cancer: a multicenter survey in Japan.
Imai, K; Iwase, S; Kaneishi, K; Maeda, I; Matsuo, N; Morita, T; Nishimura, K; Nishina, H; Okamoto, K; Sakurai, N; Sano, H; Suga, A; Takahashi, N; Yamaguchi, T, 2016
)
" TDM of both OLZ and DMO levels could assist clinical practice when individualizing OLZ dosage adjustments for patients with schizophrenia."( Application of Plasma Levels of Olanzapine and N-Desmethyl-Olanzapine to Monitor Clinical Efficacy in Patients with Schizophrenia.
Chen, CH; Chen, YH; Kuo, PT; Lin, CH; Lu, ML; Wu, TH; Wu, YX, 2016
)
" The safety, efficacy, and appropriate dosage of olanzapine for the rescue of breakthrough CINV should be prospectively evaluated in a randomized controlled trial (RCT)."( Olanzapine for the prophylaxis and rescue of chemotherapy-induced nausea and vomiting (CINV): a retrospective study.
Chiu, L; Chiu, N; Chow, E; Chow, R; DeAngelis, C; Lechner, B; Pasetka, M; Pulenzas, N; Stinson, J; Verma, S; Zhang, L, 2016
)
" The study provided an understanding of the conversion pathways of the different forms when they were exposed to humid air or aqueous environments, resembling the transformations that might occur during processing, storage or during the persecution of dissolution tests to assess the quality of dosage forms delivering olanzapine."( Role of moisture on the physical stability of polymorphic olanzapine.
Paisana, MC; Pinto, JF; Wahl, MA, 2016
)
" This open-label, parallel-group study was performed to compare finger-stick-based capillary with corresponding venous plasma concentrations for risperidone, paliperidone, quetiapine, olanzapine, and aripiprazole and their major metabolites after repeated dosing in patients with schizophrenia or related illnesses."( Comparison of Capillary and Venous Plasma Drug Concentrations After Repeated Administration of Risperidone, Paliperidone, Quetiapine, Olanzapine, or Aripiprazole.
Ariyawansa, J; De Meulder, M; Remmerie, B; Savitz, A, 2016
)
" Despite estimates being robust following sensitivity analyses, limitations include the potential for residual confounding and ascertainment bias and an inability to examine dosage effects."( Adverse Renal, Endocrine, Hepatic, and Metabolic Events during Maintenance Mood Stabilizer Treatment for Bipolar Disorder: A Population-Based Cohort Study.
Geddes, JR; Hayes, JF; King, M; Marston, L; Osborn, DP; Walters, K, 2016
)
"The aim of this study was to evaluate the time-dependent effects of olanzapine depot administration at clinically relevant dosing on the regulation of energy homeostasis, glucose and lipid metabolism, gastrointestinal and adipose tissue-derived hormones involved in energy balance regulations in female Sprague-Dawley rats."( Olanzapine-depot administration induces time-dependent changes in adipose tissue endocrine function in rats.
Babinska, Z; Demlova, R; Horska, K; Karpisek, M; Kotolova, H; Opatrilova, R; Ruda-Kucerova, J; Suchy, P, 2016
)
" This work aimed at developing an innovative solid dosage form for oral administration based on tableting nanostructured lipid carriers (NLC), coated with conventional polymer agents."( Can lipid nanoparticles improve intestinal absorption?
Arnaut, LG; Mendes, M; Pais, AACC; Soares, HT; Sousa, JJ; Vitorino, C, 2016
)
" Prolactin levels could assist in the determination of appropriate antipsychotic dosing to minimize adverse effects."( Threshold of Dopamine D2/3 Receptor Occupancy for Hyperprolactinemia in Older Patients With Schizophrenia.
Caravaggio, F; Chung, JK; Gerretsen, P; Graff-Guerrero, A; Iwata, Y; Mamo, DC; Mar, W; Mulsant, BH; Nakajima, S; Plitman, E; Pollock, BG; Rajji, TK; Suzuki, T; Uchida, H, 2016
)
"The pharmacometrics analysis and model-based dosing simulations suggest that, in order to achieve 70% D2RO, women require a 10 mg/day dose and men require approximately a 20 mg/day dose of Olanzapine."( A pharmacodynamic modelling and simulation study identifying gender differences of daily olanzapine dose and dopamine D2-receptor occupancy.
Eugene, AR; Masiak, J, 2017
)
" The duration of each adequate antipsychotic treatment at optimal dosage was 4 weeks or more."( Algorithm-based pharmacotherapy for first-episode schizophrenia involuntarily hospitalized: A retrospective analysis of real-world practice.
Sato, K; Takaki, M; Yamada, N; Yoshimura, B, 2019
)
"5 mg/day dosage of olanzapine is sufficient to prevent from CINV in Japanese patients receiving continuous five-day chemotherapy."( Feasibility of olanzapine, multi acting receptor targeted antipsychotic agent, for the prevention of emesis caused by continuous cisplatin- or ifosfamide-based chemotherapy.
Akagi, T; Bun, S; Fujiwara, Y; Hayashi, Y; Makino, Y; Noguchi, E; Shimizu, C; Shimoi, T; Shimomura, A; Tamura, K; Yonemori, K; Yunokawa, M, 2018
)
" Participants were assessed at baseline and after 12 weeks with the following instruments: the Clinical Global Impression Scale, Severity item (CGI-S), Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scale (HAM-A), Social Occupational Functioning Assessment Scale (SOFAS), Borderline Personality Disorder Severity Index (BPDSI), Barratt Impulsiveness Scale, version 11 (BIS-11), Modified Overt Aggression Scale (MOAS), Self-Harm Inventory (SHI), and Dosage Record and Treatment Emergent Symptom Scale (DOTES)."( Efficacy and Tolerability of Asenapine Compared with Olanzapine in Borderline Personality Disorder: An Open-Label Randomized Controlled Trial.
Bellino, S; Bozzatello, P; Rocca, P; Uscinska, M, 2017
)
" Plasma samples were drawn at 11 (SD, 1) hours after dosing and analyzed with high-performance liquid chromatography/tandem mass spectrometry."( A Pilot Study of the Usefulness of a Single Olanzapine Plasma Concentration as an Indicator of Early Drug Effect in a Small Sample of First-Episode Psychosis Patients.
Alonso, M; Bustillo, M; González-Pinto, A; Gutiérrez, M; Meana, JJ; Mentxaka, O; Querejeta, I; Segarra, R; Ugarte, A; Zabala, A, 2017
)
"Second-generation long-acting injectable therapies (SGA-LAIs) may reduce health care resource utilization (HRU) and health care costs compared with daily oral atypical antipsychotics (OAAs) in patients with schizophrenia due to reduced dosing frequency, delivery/monitoring by a health care provider, and improved adherence."( Treatment Patterns, Health Care Resource Utilization, and Spending in Medicaid Beneficiaries Initiating Second-generation Long-acting Injectable Agents Versus Oral Atypical Antipsychotics.
Emond, B; Joshi, K; Kamstra, R; Lafeuille, MH; Lefebvre, P; Pilon, D; Tandon, N, 2017
)
" Repurposing of available PBPK M&S platforms is an option for model-informed precision dosing and requires further study to examine clinical potential."( Prediction of olanzapine exposure in individual patients using physiologically based pharmacokinetic modelling and simulation.
Korprasertthaworn, P; Mohan, T; Perera, V; Polasek, TM; Rostami-Hodjegan, A; Rowland, A; Sorich, MJ; Tucker, GT; Wiese, MD, 2018
)
" Patients received OLAI in dosage between 210-405 mg (287±62 (mean ± SD)) every 2-4 weeks."( Occurrence of post-injection delirium/sedation syndrome after application of olanzapine long-acting injection during one year period.
Ćelić, I; Kozumplik, O; Mimica, N; Pivac, N; Uzun, S, 2017
)
" We sought to determine the change in cognitive function and symptomatology after reducing risperidone or olanzapine dosage in stable schizophrenic patients."( Dose reduction of risperidone and olanzapine can improve cognitive function and negative symptoms in stable schizophrenic patients: A single-blinded, 52-week, randomized controlled study.
Cui, H; Li, D; Li, G; Ning, Y; Zhou, Y, 2018
)
" The duration of each adequate antipsychotic treatment at an optimal dosage was 4 weeks or more."( Predictors of remission during acute treatment of first-episode schizophrenia patients involuntarily hospitalized and treated with algorithm-based pharmacotherapy: Secondary analysis of an observational study.
Sakamoto, S; Sato, K; Takaki, M; Yamada, N; Yoshimura, B, 2019
)
" There were no differences in first-line antipsychotics, dosage of antipsychotics at time of response and adherence rates to algorithm-based pharmacotherapy between remitters and non-remitters."( Predictors of remission during acute treatment of first-episode schizophrenia patients involuntarily hospitalized and treated with algorithm-based pharmacotherapy: Secondary analysis of an observational study.
Sakamoto, S; Sato, K; Takaki, M; Yamada, N; Yoshimura, B, 2019
)
" Insulin therapy was practiced, with progressive dosage reduction, until complete cessation of treatment after 13 months."( Second-generation antipsychotic and diabetes mellitus in children and adolescents.
Nurchi, AM; Pinna, AP; Podda, F; Ripoli, C; Tronci, MG; Zanni, R, 2017
)
" CYP1A2 genotyping may have no clinical implications for personalized dosing of CYP1A2-metabolized antipsychotic drugs."( Impact of CYP1A2 genetic polymorphisms on pharmacokinetics of antipsychotic drugs: a systematic review and meta-analysis.
Hanprasertpong, N; Koonrungsesomboon, N; Na Takuathung, M; Teekachunhatean, S, 2019
)
" For patients who maintained long-acting treatment, they received a dosage of 25mg oral olanzapine (min=7."( [Cost-effectiveness study of olanzapine pamoate: Mirror-image analysis after one year].
Burgot, G; Drapier, D; Langrée, B; Marie, N; Potaufeu, J, 2019
)
" Olanzapine and samidorphan pharmacokinetic parameters were determined after OLZ/SAM dosing on days 1 and 22."( A Phase I Open-Label Study to Evaluate the Effects of Rifampin on the Pharmacokinetics of Olanzapine and Samidorphan Administered in Combination in Healthy Human Subjects.
Kumar, V; McDonnell, D; Sun, L; von Moltke, L; Yu, M, 2019
)
"During a period of inflammation in patients taking quetiapine, according to our results, attention in dosing strategies is required to prevent toxic plasma concentrations."( Pathological Concentration of C-reactive Protein is Correlated to Increased Concentrations of Quetiapine, But Not of Risperidone, Olanzapine and Aripiprazole in a Naturalistic Setting.
Deckert, J; Menke, A; Scherf-Clavel, M; Unterecker, S; Weidner, A, 2020
)
"Modeling dose-response relationships of drugs is essential to understanding their safety effects on patients under realistic circumstances."( Bayesian Meta-analysis of Multiple Continuous Treatments with Individual Participant-Level Data: An Application to Antipsychotic Drugs.
Horvitz-Lennon, M; Normand, ST; Spertus, J, 2019
)
"Both acute and chronic dosing of olanzapine resulted in decreased perfusion in the sensorimotor cortex, while no effect was observed in the piriform cortex or hippocampus."( Olanzapine exposure diminishes perfusion and decreases volume of sensorimotor cortex in rats.
Babinska, Z; Buchtova, M; Drazanova, E; Horska, K; Kotolova, H; Kratka, L; Ruda-Kucerova, J; Skoupy, R; Starcuk, Z; Vaskovicova, N; Vrlikova, L, 2019
)
" TDM is also useful in assessing adherence and may have a role in limiting olanzapine dosage geared at minimizing the risk of long-term toxicity."( Therapeutic Drug Monitoring of Olanzapine and Cytochrome P450 Genotyping in Nonsmoking Subjects.
Baymeeva, NV; Ivanova, SA; Miroshnichenko, II; Pozhidaev, IV, 2020
)
" At the time of randomization, the median dosage of sertraline was 150 mg/d (interquartile range [IQR], 150-200 mg/d) and the median dosage of olanzapine was 15 mg/d (IQR, 10-20 mg/d)."( Effect of Continuing Olanzapine vs Placebo on Relapse Among Patients With Psychotic Depression in Remission: The STOP-PD II Randomized Clinical Trial.
Alexopoulos, GS; Banerjee, S; Flint, AJ; Marino, P; Meyers, BS; Mulsant, BH; Pollari, CD; Rothschild, AJ; Rudorfer, MV; Voineskos, AN; Whyte, EM; Wu, Y, 2019
)
" A randomized, double-blind controlled trial is performed at 16 German centers comparing flexibly dosed monotherapy of oral amisulpride (400-800 mg/day), and olanzapine (10-20 mg/day) and amisulpride-olanzapine co-treatment."( A randomized double-blind controlled trial to assess the benefits of amisulpride and olanzapine combination treatment versus each monotherapy in acutely ill schizophrenia patients (COMBINE): methods and design.
Baumgärtner, J; Brockhaus-Dumke, A; Cordes, J; Correll, CU; Engelke, C; Englisch, S; Feyerabend, S; Gaebel, W; Gouzoulis-Mayfrank, E; Gründer, G; Hasan, A; Heres, S; Jäger, M; Kluge, M; Kolbe, H; Lange, C; Langguth, B; Leucht, S; Makiol, C; Meisenzahl-Lechner, E; Neff, A; Poeppl, T; Reske, D; Riesbeck, M; Schmidt-Kraepelin, C; Verde, PE; Wobrock, T; Zink, M, 2020
)
" Multiple daily doses of olanzapine do not affect the pharmacokinetics of lithium or valproate; therefore, concomitant olanzapine administration does not require dosage adjustment of lithium or valproate."( Combination of Olanzapine and Samidorphan Has No Clinically Significant Effect on the Pharmacokinetics of Lithium or Valproate.
Graham, C; Sun, L; von Moltke, L; Yagoda, S; Yao, B, 2020
)
" Pharmacokinetic parameters of lithium and valproate, including maximum plasma concentration and area under the plasma concentration-time curve over a 12-h dosing interval, were calculated."( Combination of Olanzapine and Samidorphan Has No Clinically Significant Effect on the Pharmacokinetics of Lithium or Valproate.
Graham, C; Sun, L; von Moltke, L; Yagoda, S; Yao, B, 2020
)
" absence of OLZ/SAM, were within the equivalence interval of 80-125% for both maximum plasma concentration and area under the plasma concentration-time curve over a 12-h dosing interval of lithium and of valproate."( Combination of Olanzapine and Samidorphan Has No Clinically Significant Effect on the Pharmacokinetics of Lithium or Valproate.
Graham, C; Sun, L; von Moltke, L; Yagoda, S; Yao, B, 2020
)
" Particularly, impact associated with dosage has been barely studied."( Effects of long-term antipsychotics treatment on body weight: A population-based cohort study.
Bazo-Alvarez, JC; Carpenter, JR; Hayes, JF; Morris, TP; Petersen, I, 2020
)
"The dose-response relationships of antipsychotic drugs for schizophrenia are not well defined, but such information would be important for decision making by clinicians."( Dose-Response Meta-Analysis of Antipsychotic Drugs for Acute Schizophrenia.
Crippa, A; Davis, JM; Leucht, S; Orsini, N; Patel, MX; Siafis, S, 2020
)
" Dose-response curves were constructed with random-effects dose-response meta-analyses and a spline model."( Dose-Response Meta-Analysis of Antipsychotic Drugs for Acute Schizophrenia.
Crippa, A; Davis, JM; Leucht, S; Orsini, N; Patel, MX; Siafis, S, 2020
)
" For some drugs, higher than currently licensed doses might be tested in further trials, because their dose-response curves did not plateau."( Dose-Response Meta-Analysis of Antipsychotic Drugs for Acute Schizophrenia.
Crippa, A; Davis, JM; Leucht, S; Orsini, N; Patel, MX; Siafis, S, 2020
)
" In the present study, we showed that with an inverted U-shape dose-response curve, olanzapine increased NPY expression in the NPY-GFP hypothalamic neurons; however, this was not the case in the hypothalamic neurons of H1R knockout mice."( Olanzapine increases AMPK-NPY orexigenic signaling by disrupting H1R-GHSR1a interaction in the hypothalamic neurons of mice.
Chen, X; He, M; Huang, XF; Jin, T; Jones, A; Song, X; Yu, Y; Zheng, M; Zheng, P, 2020
)
" Various factors may influence their pharmacokinetics, particularly elimination, leading to highly variable drug concentrations between individual patients following the same dosing regimen."( Understanding variability in the pharmacokinetics of atypical antipsychotics - focus on clozapine, olanzapine and aripiprazole population models.
Jovanović, M; Miljković, B; Vučićević, K, 2020
)
" We used the Generalized Propensity Score method to evaluate the dose-response risk of Parkinsonism associated with SGAs."( Comparative risk of Parkinsonism associated with olanzapine, risperidone and quetiapine in older adults-a propensity score matched cohort study.
Chyou, TY; Nishtala, PS; Nishtala, R, 2020
)
"The aim of this study was to evaluate the population pharmacokinetics (PopPK) of olanzapine in children and devise a model-informed paediatric dosing scheme."( Population pharmacokinetics of olanzapine in children.
Al-Uzri, A; Autmizguine, J; Cohen-Wolkowiez, M; Erinjeri, J; Goldstein, SL; Hornik, CP; Kalra, R; Maharaj, AR; Payne, EH; Sherwin, CMT; Watt, K; Wu, H; Zimmerman, KO, 2021
)
" Simulations from the developed PopPK model were used to devise a paediatric dosing scheme that targeted comparable plasma exposures to adolescents and adults."( Population pharmacokinetics of olanzapine in children.
Al-Uzri, A; Autmizguine, J; Cohen-Wolkowiez, M; Erinjeri, J; Goldstein, SL; Hornik, CP; Kalra, R; Maharaj, AR; Payne, EH; Sherwin, CMT; Watt, K; Wu, H; Zimmerman, KO, 2021
)
" Developed dosing schemes used weight-normalized doses for children ≤6 months postnatal age or <15 kg and fixed doses for children ≥15 kg."( Population pharmacokinetics of olanzapine in children.
Al-Uzri, A; Autmizguine, J; Cohen-Wolkowiez, M; Erinjeri, J; Goldstein, SL; Hornik, CP; Kalra, R; Maharaj, AR; Payne, EH; Sherwin, CMT; Watt, K; Wu, H; Zimmerman, KO, 2021
)
" The development of tools capable of quantifying and monitoring the recrystallization of amorphous materials is required to ensure the delivery of solid dosage forms with improved performance."( Measurement of the amorphous fraction of olanzapine incorporated in a co-amorphous formulation.
da Costa, NF; Fernandes, AI; Pinto, JF, 2020
)
"In Iran, the most important challenges these patients faced with are as follows: the absence of a specific referral center, patients resort to self-treatment or traditional methods, and lack of a certain duration and dosage of antipsychotic for these cases."( A comprehensive entomological survey and evaluation of the efficacy of different therapies on a suspected delusional parasitosis case.
Soltan-Alinejad, P; Soltani, A; Turki, H; Vahedi, M, 2021
)
"The primary aim of this study was to standardize the correlated effective dosage of the antidiabetic drug empagliflozin (EMPA) and the antipsychotic drug olanzapine (Ola)."( Standardizing the Effective Correlated Dosage of Olanzapine and Empagliflozin in Female Wistar Rats.
Alam, MZ; Alghamdi, BS; Alshehri, FS; Ashraf, GM; Tarazi, FI; Tayeb, HO, 2021
)
"The objective of this study was to standardize the correlated effective dosage of EMPA and Ola."( Standardizing the Effective Correlated Dosage of Olanzapine and Empagliflozin in Female Wistar Rats.
Alam, MZ; Alghamdi, BS; Alshehri, FS; Ashraf, GM; Tarazi, FI; Tayeb, HO, 2021
)
"We conclude that Ola-4 and EMPA-20 were the most effective dosage for experimental purposes in female Wistar rats."( Standardizing the Effective Correlated Dosage of Olanzapine and Empagliflozin in Female Wistar Rats.
Alam, MZ; Alghamdi, BS; Alshehri, FS; Ashraf, GM; Tarazi, FI; Tayeb, HO, 2021
)
" Additional prospective studies with accurate dosage information are needed to validate our findings."( Occurrence of metabolic diseases associated with antipsychotic use among Korean patients with schizophrenia.
Kim, BH; Kim, E; Kim, S; Kuk, S; Lee, W; Park, SI, 2021
)
" Dosing strategies, discontinuation considerations, and side effects are discussed."( The Psychopharmacology Algorithm Project at the Harvard South Shore Program: An update on management of behavioral and psychological symptoms in dementia.
Chen, A; Cloutier, A; Copeli, F; Metzger, E; Osser, DN, 2021
)
" Avoiding amisulpride and warning against increasing the dosage in renal failure is the only recommendation by drug manufacturers and clinical guidelines."( Antipsychotics and hemodialysis: A systematic review.
Atlani, MK; Chaudhary, P; Sutar, R, 2021
)
"Findings of the review reveals modest evidence favoring multiple dosing regimens of oral aripiprazole, ziprasidone, olanzapine, and risperidone."( Antipsychotics and hemodialysis: A systematic review.
Atlani, MK; Chaudhary, P; Sutar, R, 2021
)
" Olanzapine dosing was increased to 10 mg daily on hospital day 34 and 15 mg daily on hospital day 45."( Extrapyramidal Symptoms Induced by Treatment for Delirium: A Case Report.
Rose, MQ; Santos, CD, 2021
)
" No significant differences were found in the rate of violent behavior and antipsychotic dosage at discharge."( Olanzapine intramuscular shows better efficacy than zuclopenthixol acetate intramuscular in reducing the need for restraint, but not in comparison to haloperidol intramuscular.
Bloemhof-Bris, E; Shelef, A; Sinai, O; Stryjer, R; Weizman, S, 2022
)
" The determination of the CYP2C19 genotypes may be useful for dosing adjustment in schizophrenia patients on valproic acid therapy."( Effect of CYP2C19 polymorphisms on serum valproic level acid in Chinese Han patients with schizophrenia.
Ju, X; Li, J; Liu, J; Shi, J; Song, M; Wang, C; Wang, S; Yan, P, 2021
)
"This review details the pharmacologic, pharmacokinetic, associated dosing and indications, and adverse effects for the drug combination olanzapine/samidorphan."( Olanzapine/Samidorphan: New Drug Approved for Treating Bipolar I Disorder and Schizophrenia.
Gums, JG; McCoy, L; Monahan, C; Powell, J, 2022
)
" Participants in the olanzapine group received olanzapine once daily on days 1 and 2, while those in the control group received a placebo in the same dosage and schedule."( Efficacy and Safety of Olanzapine in Children Receiving Highly Emetogenic Chemotherapy: A Randomized, Double-blind Placebo-controlled Phase 3 Trial.
Gupta, AK; Meena, JP; Moothedath, AW; Pandey, RM; Seth, R; Velpandian, T, 2022
)
" We aimed to fill this gap with a dose-response meta-analysis."( Antipsychotic-Induced Weight Gain: Dose-Response Meta-Analysis of Randomized Controlled Trials.
Davis, JM; Hamza, T; Leucht, S; Salanti, G; Schneider-Thoma, J; Siafis, S; Wu, H, 2022
)
" We estimated the dose-response curves by conducting random-effects dose-response meta-analyses."( Antipsychotic-Induced Weight Gain: Dose-Response Meta-Analysis of Randomized Controlled Trials.
Davis, JM; Hamza, T; Leucht, S; Salanti, G; Schneider-Thoma, J; Siafis, S; Wu, H, 2022
)
" For most drugs, dose-response curves showed an initial dose-related increase in weight which plateaued at higher doses, while for others there was no plateau and some even had bell-shaped curves, meaning less weight gain to be associated with higher doses."( Antipsychotic-Induced Weight Gain: Dose-Response Meta-Analysis of Randomized Controlled Trials.
Davis, JM; Hamza, T; Leucht, S; Salanti, G; Schneider-Thoma, J; Siafis, S; Wu, H, 2022
)
"Second-generation antipsychotics do not only differ in their propensity to produce weight gain, but also in the shapes of their dose-response curves."( Antipsychotic-Induced Weight Gain: Dose-Response Meta-Analysis of Randomized Controlled Trials.
Davis, JM; Hamza, T; Leucht, S; Salanti, G; Schneider-Thoma, J; Siafis, S; Wu, H, 2022
)
" Flexibly dosed monotherapy of oral amisulpride (amisulpride plus placebo, 200-800 mg per day) or olanzapine (olanzapine plus placebo, 5-20 mg per day) was compared with a combination of amisulpride plus olanzapine."( Amisulpride and olanzapine combination treatment versus each monotherapy in acutely ill patients with schizophrenia in Germany (COMBINE): a double-blind randomised controlled trial.
Baumgärtner, J; Brockhaus-Dumke, A; Cordes, J; Correll, CU; Engelke, C; Englisch, S; Feyerabend, S; Gouzoulis-Mayfrank, E; Gründer, G; Hasan, A; Jäger, M; Kluge, M; Lange, C; Langguth, B; Leucht, S; Makiol, C; Meisenzahl-Lechner, E; Neff, A; Poeppl, TB; Reske, D; Riesbeck, M; Schmidt-Kraepelin, C; Verde, PE; Zink, M, 2022
)
" The acute cognitive effects were predicted by olanzapine dosage and serum levels (i."( Serum levels of olanzapine are associated with acute cognitive effects in bipolar disorder.
Almeida, NL; Fars, J; Fernandes, TP; Oliveira, MEC; Santos, NA; Shoshina, II; Silva, GM; Trombetta, BNT, 2022
)
"To compare the efficacy and safety of two different dosage levels of olanzapine for the prevention of chemotherapy-induced nausea and vomiting (CINV) in patients receiving high emetic risk chemotherapy."( Efficacy of Olanzapine 5 mg versus 10 mg for the Prophylaxis of Chemotherapy-Induced Nausea and Vomiting in Patients Receiving High Emetic Risk Chemotherapy without Neurokinin-1 Receptor Antagonist.
Ketkaew, C; Othaganont, N; Pichaya, P; Promsuwan, P; Sukauichai, S, 2022
)
"The two dosage levels of olanzapine were not different in terms of the efficacy and AE in the prophylaxis of CINV."( Efficacy of Olanzapine 5 mg versus 10 mg for the Prophylaxis of Chemotherapy-Induced Nausea and Vomiting in Patients Receiving High Emetic Risk Chemotherapy without Neurokinin-1 Receptor Antagonist.
Ketkaew, C; Othaganont, N; Pichaya, P; Promsuwan, P; Sukauichai, S, 2022
)
" Both the presence of EPS as well as the dosage of antipsychotic medication seem to be of particular relevance in this regard."( Driving fitness in clinically stable outpatients with chronic schizophrenia.
Biedermann, F; Haibach, M; Hofer, A; Holzner, B; Kemmler, G; Kurzthaler, I; Pardeller, S; Pichler, T, 2022
)
"The effects of antipsychotic drugs are dose-dependent, which is particularly true for their efficacy, each antipsychotic having a specific dose-response curve."( Comorbidities and the right dose: antipsychotics.
Azorin, JM; Simon, N; Torrents, R,
)
"Factors liable to impact antipsychotic dosage are numerous and their subsequent effects often hard to predict, due to multilevel interactions and compensatory phenomena."( Comorbidities and the right dose: antipsychotics.
Azorin, JM; Simon, N; Torrents, R,
)
"Due to its effect, simple dosage and a good safety profile, olanzapine is a useful drug for the routine clinical practice of an oncologist - a non-psychiatrist."( Olanzapine in oncology palliative care.
Šoukalová, Z, 2022
)
" Our model may be a useful tool for recommending dosage adjustments for physicians."( Population pharmacokinetics and dosing optimization of olanzapine in Chinese paediatric patients: Based on the impact of sex and concomitant valproate on clearance.
Hu, JQ; Huang, SQ; Kong, W; Li, XL; Liu, SJ; Lu, HQ; Lu, HY; Ni, XJ; Shang, DW; Wen, YG; Xiao, T; Yang, HL; Zhang, M; Zhu, XQ, 2022
)
" Moreover, there were insufficient studies to conduct meta-analyses on many outcome measures; to compare efficacy across and within major categories of interventions; to explore dosage effects; or to examine effects beyond post-treatment."( Pharmacological interventions for the treatment of disordered and problem gambling.
Bowden-Jones, H; Cowlishaw, S; Dowling, N; Lubman, D; Merkouris, S; Thomas, S, 2022
)
" Besides resistance under the processing conditions of the dosage forms considered, OLZ-CAMs presented a higher solubility and dissolution rate than the respective crystalline counterpart."( Amorphous and Co-Amorphous Olanzapine Stability in Formulations Intended for Wet Granulation and Pelletization.
da Costa, NF; Daniels, R; Fernandes, AI; Pinto, JF, 2022
)
" Our patient developed neuroleptic malignant syndrome (NMS) after his neuroleptic drug dosage was increased."( Neuroleptic malignant syndrome secondary to olanzapine, a presentation with severe acute kidney injury requiring hemodialysis: a case report.
Chang, CK; Lansing, MG; Lu, SJA; Noh, MM; Payus, AO; Sumpat, D; Yew, BT, 2022
)
" The dosage forms currently on the market for OZP are administered via oral or intramuscular routes."( Development and evaluation of a drug-in-adhesive transdermal delivery system for delivery of olanzapine.
Banga, AK; Vora, D, 2022
)
"Data on sex, age, and OLA dosage and steady-state plasma concentrations of 386 patients with schizophrenia (who have received OLA or a comedication of OLA with a psychotherapeutic drug) were collected and analyzed."( Effects of Age, Sex, and Comedication on the Plasma Concentrations of Olanzapine in Chinese Patients With Schizophrenia Based on Therapeutic Drug Monitoring Data.
Cui, X; Ding, J; Li, Y; Meng, Z; Xing, H; Yang, L; Zhang, S; Zhang, Y,
)
" Evidence of brain insulin resistance induced by acute AP dosing can inform the early use of adjunctive insulin sensitizers for the treatment of metabolic comorbidities associated with AP treatment in severe mental illness."( Investigating the effects of antipsychotics on brain insulin action: Study protocol for a multi-modality magnetic resonance imaging (MRI) study in healthy controls.
Agarwal, SM; Dash, S; Graff-Guerrero, A; Hahn, M; Hamel, L; Remington, G; Sanches, M; Smith, E; Stogios, N; Voineskos, A, 2022
)
" Our survey showed that many analytical techniques were carried out using UV spectrophotometry, MS, LC-MS/MS techniques, and chromatographic techniques like HPLC and high-performance thin layer chromatography in both bulk and solid dosage forms."( A review of various analytical methods for the estimation of olanzapine: An antipsychotic drug.
Almalki, WH; Kesharwani, P; S, R; Sheikh, A; Thanikachalam, PV, 2023
)
" Our data favor the addition of olanzapine in the antiemetic cocktail considering the low incidence of metabolic adverse effects for the period and dosage analyzed in male and female rats."( Coadministration of olanzapine causes minor impacts on the diabetogenic outcomes induced by dexamethasone treatment in rats.
da Silva, FN; do Amaral, TA; Martins, JRN; Rafacho, A; Zimath, PL, 2023
)
"A higher dosage may be required for men or heavy smokers than for women or nonsmokers to reach the same exposure."( Significant predictors for olanzapine pharmacokinetics: a systematic review of population pharmacokinetic studies.
Han, L; Jiao, Z; Liu, XQ; Mao, JH,
)
"Expert consensus-based clinically equivalent dose estimates and dosing recommendations can provide valuable support for the use of drugs for psychosis in clinical practice and research."( Second International Consensus Study of Antipsychotic Dosing (ICSAD-2).
Baldessarini, RJ; Gardner, DM; McAdam, MK; Murphy, AL, 2023
)
"This second International Consensus Study of Antipsychotic Dosing provides dosing equivalencies and recommendations for newer drugs for psychosis and previously reported drugs with low consensus."( Second International Consensus Study of Antipsychotic Dosing (ICSAD-2).
Baldessarini, RJ; Gardner, DM; McAdam, MK; Murphy, AL, 2023
)
"We used a two-step Delphi survey process to establish and update consensus with a broad, international sample of clinical and research experts regarding 26 drug formulations to obtain dosing recommendations (start, target range, and maximum) and estimates of clinically equivalent doses for the treatment of schizophrenia."( Second International Consensus Study of Antipsychotic Dosing (ICSAD-2).
Baldessarini, RJ; Gardner, DM; McAdam, MK; Murphy, AL, 2023
)
"As randomized, controlled, fixed, multiple-dose trials to optimize the dosing of drugs for psychosis remain rare, expert consensus remains a useful alternative for estimating clinical dosing equivalents."( Second International Consensus Study of Antipsychotic Dosing (ICSAD-2).
Baldessarini, RJ; Gardner, DM; McAdam, MK; Murphy, AL, 2023
)
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (7)

RoleDescription
histamine antagonistHistamine antagonists are the drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists.
muscarinic antagonistA drug that binds to but does not activate muscarinic cholinergic receptors, thereby blocking the actions of endogenous acetylcholine or exogenous agonists.
serotonergic antagonistDrugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or serotonergic agonists.
dopaminergic antagonistA drug that binds to but does not activate dopamine receptors, thereby blocking the actions of dopamine or exogenous agonists.
antiemeticA drug used to prevent nausea or vomiting. An antiemetic may act by a wide range of mechanisms: it might affect the medullary control centres (the vomiting centre and the chemoreceptive trigger zone) or affect the peripheral receptors.
second generation antipsychoticAntipsychotic drugs which can have different modes of action but which tend to be less likely than first generation antipsychotics to cause extrapyramidal motor control disabilities such as body rigidity or Parkinson's disease-type movements.
serotonin uptake inhibitorA compound that specifically inhibits the reuptake of serotonin in the brain. This increases the serotonin concentration in the synaptic cleft which then activates serotonin receptors to a greater extent.
[role 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]

Drug Classes (3)

ClassDescription
benzodiazepineA group of heterocyclic compounds with a core structure containing a benzene ring fused to a diazepine ring.
N-methylpiperazine
N-arylpiperazine
[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 (81)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
GLS proteinHomo sapiens (human)Potency8.91250.35487.935539.8107AID624170
TDP1 proteinHomo sapiens (human)Potency28.23200.000811.382244.6684AID686978; AID686979
GLI family zinc finger 3Homo sapiens (human)Potency4.46620.000714.592883.7951AID1259392
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency8.06080.001022.650876.6163AID1224838; AID1224893
peroxisome proliferator-activated receptor deltaHomo sapiens (human)Potency13.33220.001024.504861.6448AID743212
aryl hydrocarbon receptorHomo sapiens (human)Potency33.49150.000723.06741,258.9301AID743085; AID743122
v-jun sarcoma virus 17 oncogene homolog (avian)Homo sapiens (human)Potency25.82220.057821.109761.2679AID1159528
lysosomal alpha-glucosidase preproproteinHomo sapiens (human)Potency5.62340.036619.637650.1187AID2100
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency89.12510.354828.065989.1251AID504847
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency18.83360.000323.4451159.6830AID743065; AID743067
mitogen-activated protein kinase 1Homo sapiens (human)Potency3.20480.039816.784239.8107AID1454; AID995
ubiquitin carboxyl-terminal hydrolase 2 isoform aHomo sapiens (human)Potency19.95260.65619.452025.1189AID927
gemininHomo sapiens (human)Potency0.25290.004611.374133.4983AID624296; AID624297
lamin isoform A-delta10Homo sapiens (human)Potency25.11890.891312.067628.1838AID1487
Cellular tumor antigen p53Homo sapiens (human)Potency5.95570.002319.595674.0614AID651631
Spike glycoproteinSevere acute respiratory syndrome-related coronavirusPotency17.78280.009610.525035.4813AID1479145
Disintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)Potency19.95261.584913.004325.1189AID927
Inositol monophosphatase 1Rattus norvegicus (Norway rat)Potency8.91251.000010.475628.1838AID1457
[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)
5-hydroxytryptamine receptor 3EHomo sapiens (human)Ki0.19950.00100.88359.9000AID298488
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
5-hydroxytryptamine receptor 4Cavia porcellus (domestic guinea pig)IC50 (µMol)0.09700.00011.00768.7800AID625218; AID63866
5-hydroxytryptamine receptor 4Cavia porcellus (domestic guinea pig)Ki0.01100.00000.887110.0000AID625218
5-hydroxytryptamine receptor 3BHomo sapiens (human)Ki0.19950.00100.87119.9000AID298488
Bile salt export pumpHomo sapiens (human)IC50 (µMol)93.78500.11007.190310.0000AID1449628; AID1473738
Muscarinic acetylcholine receptor M2Homo sapiens (human)Ki0.02600.00000.690210.0000AID141100
Muscarinic acetylcholine receptor M4Homo sapiens (human)IC50 (µMol)0.15500.00001.15467.5858AID625154
Muscarinic acetylcholine receptor M4Homo sapiens (human)Ki0.02020.00000.79519.1201AID141100; AID298491; AID625154
Cytochrome P450 3A4Homo sapiens (human)Ki0.00600.00011.41629.9000AID599884
5-hydroxytryptamine receptor 1AHomo sapiens (human)Ki3.07340.00010.532610.0000AID1128459; AID1169862; AID1185959; AID1393366; AID342783; AID3657; AID694795
5-hydroxytryptamine receptor 2CRattus norvegicus (Norway rat)IC50 (µMol)0.04700.00040.629810.0000AID4782
5-hydroxytryptamine receptor 2CRattus norvegicus (Norway rat)Ki0.01260.00020.667710.0000AID5090
Muscarinic acetylcholine receptor M5Homo sapiens (human)IC50 (µMol)0.04000.00010.99178.0000AID625155
Muscarinic acetylcholine receptor M5Homo sapiens (human)Ki0.02750.00000.72926.9183AID141100; AID625155
Alpha-2A adrenergic receptorHomo sapiens (human)IC50 (µMol)0.54100.00001.44217.3470AID625201
Alpha-2A adrenergic receptorHomo sapiens (human)Ki0.19130.00010.807410.0000AID238989; AID36197; AID36199; AID625201
Muscarinic acetylcholine receptor M1Homo sapiens (human)Ki0.01070.00000.59729.1201AID141100; AID141174; AID298490; AID342774
Glucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)Ki497.20001.19105.12919.9410AID1802951
Polyunsaturated fatty acid lipoxygenase ALOX15Oryctolagus cuniculus (rabbit)IC50 (µMol)2.76800.11003.26419.0330AID625146
Angiotensin-converting enzymeOryctolagus cuniculus (rabbit)IC50 (µMol)100.00000.00001.612910.0000AID625171
D(2) dopamine receptorHomo sapiens (human)IC50 (µMol)0.11800.00000.74728.0000AID625253
D(2) dopamine receptorHomo sapiens (human)Ki0.03290.00000.651810.0000AID1125020; AID1125021; AID1152652; AID1169860; AID1185963; AID1281952; AID1353520; AID1393368; AID1413420; AID1568825; AID1677161; AID1760279; AID1823826; AID239052; AID298478; AID342777; AID458632; AID458633; AID625253; AID63060; AID63070; AID694797
5-hydroxytryptamine receptor 2ARattus norvegicus (Norway rat)IC50 (µMol)0.04700.00040.908610.0000AID4782
5-hydroxytryptamine receptor 2ARattus norvegicus (Norway rat)Ki0.00580.00010.601710.0000AID1172030; AID238882; AID410335; AID492640; AID5090
Alpha-1B adrenergic receptorRattus norvegicus (Norway rat)Ki1.81920.00010.949010.0000AID1128464; AID238991; AID298478; AID3657
Alpha-2B adrenergic receptorHomo sapiens (human)IC50 (µMol)0.42100.00001.23808.1590AID625202
Alpha-2B adrenergic receptorHomo sapiens (human)Ki0.18730.00020.725710.0000AID36197; AID36199; AID625202
Alpha-2C adrenergic receptorHomo sapiens (human)IC50 (µMol)0.53100.00001.47257.8980AID625203
Alpha-2C adrenergic receptorHomo sapiens (human)Ki0.13230.00030.483410.0000AID238990; AID36197; AID36199; AID625203
DRattus norvegicus (Norway rat)Ki0.07110.00010.610010.0000AID238855; AID238940; AID410331; AID492643; AID61517; AID61675; AID61679
D(3) dopamine receptorRattus norvegicus (Norway rat)Ki0.03900.00010.25675.8000AID65622
5-hydroxytryptamine receptor 1ARattus norvegicus (Norway rat)Ki0.50000.00010.739610.0000AID4066
Alpha-2B adrenergic receptorRattus norvegicus (Norway rat)Ki0.01000.00000.929610.0000AID298490
Muscarinic acetylcholine receptor M3Homo sapiens (human)IC50 (µMol)0.39200.00011.01049.9280AID625153
Muscarinic acetylcholine receptor M3Homo sapiens (human)Ki0.05450.00000.54057.7600AID141100; AID625153
D(1A) dopamine receptorHomo sapiens (human)IC50 (µMol)0.07200.00031.84739.2250AID625252
D(1A) dopamine receptorHomo sapiens (human)Ki0.07450.00010.836310.0000AID1185962; AID1677162; AID342775; AID625252; AID63345; AID63347
D(4) dopamine receptorHomo sapiens (human)IC50 (µMol)0.17300.00011.14239.3280AID63866
D(4) dopamine receptorHomo sapiens (human)Ki0.03050.00000.436210.0000AID1128466; AID298480; AID342779; AID61808; AID63537; AID64005
Alpha-2C adrenergic receptorRattus norvegicus (Norway rat)Ki0.01000.00000.970810.0000AID298490
Alpha-2A adrenergic receptorRattus norvegicus (Norway rat)Ki0.01000.00000.937510.0000AID298490
Alpha-1D adrenergic receptorRattus norvegicus (Norway rat)Ki2.40260.00000.575110.0000AID238991; AID298478; AID3657
Sodium-dependent noradrenaline transporter Homo sapiens (human)Ki0.00400.00031.465610.0000AID1799301
Adenosine receptor A1Rattus norvegicus (Norway rat)Ki0.08500.00011.20929.9700AID238940
Alpha-1D adrenergic receptorHomo sapiens (human)IC50 (µMol)0.09200.00020.75688.8970AID625200
Alpha-1D adrenergic receptorHomo sapiens (human)Ki0.02910.00000.360910.0000AID1682829; AID36113; AID36116; AID36118; AID625200
5-hydroxytryptamine receptor 2AHomo sapiens (human)IC50 (µMol)0.03800.00010.88018.8500AID1242912; AID5171; AID625192
5-hydroxytryptamine receptor 2AHomo sapiens (human)Ki0.00360.00000.385510.0000AID1128452; AID1169863; AID1185960; AID1393364; AID1430532; AID1520007; AID1556425; AID1570059; AID1595144; AID1601980; AID1677158; AID1799301; AID1823823; AID239010; AID298482; AID342784; AID452390; AID5196; AID5197; AID5199; AID625192
5-hydroxytryptamine receptor 2CHomo sapiens (human)IC50 (µMol)0.02100.00011.03029.0000AID625218
5-hydroxytryptamine receptor 2CHomo sapiens (human)Ki0.00830.00010.954910.0000AID1128453; AID1169864; AID239069; AID298485; AID342781; AID5614; AID5616; AID599883; AID625218
D(4) dopamine receptorRattus norvegicus (Norway rat)Ki0.05000.00020.18872.0000AID1185965
5-hydroxytryptamine receptor 2BRattus norvegicus (Norway rat)IC50 (µMol)0.04700.00040.615610.0000AID4782
5-hydroxytryptamine receptor 2BRattus norvegicus (Norway rat)Ki0.01260.00020.590910.0000AID5090
Histamine H1 receptorCavia porcellus (domestic guinea pig)Ki0.01260.00261.783210.0000AID298491
Sodium-dependent serotonin transporterHomo sapiens (human)IC50 (µMol)1.03300.00010.86458.7096AID625222
Sodium-dependent serotonin transporterHomo sapiens (human)Ki7.77450.00000.70488.1930AID342787; AID625222
5-hydroxytryptamine receptor 7Homo sapiens (human)Ki0.20890.00030.380610.0000AID1393367; AID239149; AID298487; AID694794
Alpha-1A adrenergic receptorHomo sapiens (human)Ki0.02900.00000.272610.0000AID1128462; AID1682829; AID36113; AID36116; AID36118
Histamine H1 receptorHomo sapiens (human)IC50 (µMol)0.01300.00000.44365.1768AID625269
Histamine H1 receptorHomo sapiens (human)Ki0.00340.00000.511010.0000AID1128460; AID1682828; AID239091; AID342782; AID625269; AID87242; AID87244
Alpha-1B adrenergic receptorHomo sapiens (human)Ki0.02510.00000.471310.0000AID1682829; AID36113; AID36116; AID36118
D(3) dopamine receptorHomo sapiens (human)IC50 (µMol)0.07800.00011.01788.7960AID625254
D(3) dopamine receptorHomo sapiens (human)Ki0.04000.00000.602010.0000AID1169861; AID1185964; AID239150; AID239151; AID298479; AID342778; AID410333; AID625254; AID65121; AID65785
5-hydroxytryptamine receptor 2BHomo sapiens (human)IC50 (µMol)0.05700.00011.18738.9125AID625217
5-hydroxytryptamine receptor 2BHomo sapiens (human)Ki0.02120.00030.769310.0000AID298483; AID625217
Alpha-1A adrenergic receptorRattus norvegicus (Norway rat)Ki2.40260.00000.965010.0000AID238991; AID298478; AID3657
5-hydroxytryptamine receptor 3AHomo sapiens (human)Ki0.19950.00000.74119.9000AID298488
5-hydroxytryptamine receptor 6Homo sapiens (human)IC50 (µMol)0.01300.00170.83815.4200AID625221
5-hydroxytryptamine receptor 6Homo sapiens (human)Ki0.01010.00020.522910.0000AID1126945; AID1172031; AID1393365; AID1430530; AID1520006; AID1556427; AID1568824; AID1570060; AID1595145; AID1601981; AID1760276; AID238747; AID298486; AID342773; AID599884; AID625221; AID694796
3-hydroxy-3-methylglutaryl-coenzyme A reductase Rattus norvegicus (Norway rat)Ki0.01400.00100.01630.0330AID599883
D(2) dopamine receptorRattus norvegicus (Norway rat)IC50 (µMol)0.15800.00010.54948.4000AID61415
D(2) dopamine receptorRattus norvegicus (Norway rat)Ki0.05620.00000.437510.0000AID1128454; AID1172033; AID238941; AID410332; AID492642; AID63809; AID63824; AID65563
Potassium voltage-gated channel subfamily H member 2Homo sapiens (human)IC50 (µMol)11.29140.00091.901410.0000AID161281; AID243151; AID386536; AID397743; AID408340; AID576612; AID625171
Potassium voltage-gated channel subfamily H member 2Homo sapiens (human)Ki36.00000.00211.840710.0000AID410338; AID492638
Sigma non-opioid intracellular receptor 1Cavia porcellus (domestic guinea pig)Ki0.00900.00000.338510.0000AID1353520
TransporterRattus norvegicus (Norway rat)Ki2.00000.00010.76295.5000AID342786
Nuclear receptor subfamily 3 group C member 3 Bos taurus (cattle)IC50 (µMol)100.00000.10482.83988.3173AID625171
5-hydroxytryptamine receptor 3DHomo sapiens (human)Ki0.19950.00100.88359.9000AID298488
5-hydroxytryptamine receptor 3CHomo sapiens (human)Ki0.19950.00100.88359.9000AID298488
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
TransporterRattus norvegicus (Norway rat)Ki0.95800.00010.866710.0000AID238962
[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)
5-hydroxytryptamine receptor 1AHomo sapiens (human)Kd1.25890.00010.95285.0119AID438555
Muscarinic acetylcholine receptor M1Homo sapiens (human)EC50 (µMol)100.00000.00161.304310.0000AID1757456
Histamine H1 receptorHomo sapiens (human)Kd0.00010.00010.40215.4000AID692513
[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)
FAD-linked sulfhydryl oxidase ALRHomo sapiens (human)AC500.36900.00503.212622.7870AID493248
ATP-dependent translocase ABCB1Homo sapiens (human)Km8.30000.01403.717210.0000AID681619
UDP-glucuronosyltransferase 1A4Homo sapiens (human)Km227.00007.00007.00007.0000AID624633
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (585)

Processvia Protein(s)Taxonomy
serotonin receptor signaling pathway5-hydroxytryptamine receptor 3EHomo sapiens (human)
monoatomic ion transmembrane transport5-hydroxytryptamine receptor 3EHomo sapiens (human)
excitatory postsynaptic potential5-hydroxytryptamine receptor 3EHomo sapiens (human)
inorganic cation transmembrane transport5-hydroxytryptamine receptor 3EHomo sapiens (human)
regulation of membrane potential5-hydroxytryptamine receptor 3EHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 3EHomo sapiens (human)
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 3BHomo sapiens (human)
monoatomic ion transmembrane transport5-hydroxytryptamine receptor 3BHomo sapiens (human)
excitatory postsynaptic potential5-hydroxytryptamine receptor 3BHomo sapiens (human)
inorganic cation transmembrane transport5-hydroxytryptamine receptor 3BHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 3BHomo sapiens (human)
regulation of membrane potential5-hydroxytryptamine receptor 3BHomo sapiens (human)
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)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
phospholipase C-activating G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
nervous system developmentMuscarinic acetylcholine receptor M2Homo sapiens (human)
regulation of heart contractionMuscarinic acetylcholine receptor M2Homo sapiens (human)
response to virusMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
presynaptic modulation of chemical synaptic transmissionMuscarinic acetylcholine receptor M2Homo sapiens (human)
regulation of smooth muscle contractionMuscarinic acetylcholine receptor M2Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M2Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M2Homo sapiens (human)
signal transductionMuscarinic acetylcholine receptor M4Homo sapiens (human)
cell surface receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
regulation of locomotionMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M4Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M4Homo sapiens (human)
G2/M transition of mitotic cell cycleATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic metabolic processATP-dependent translocase ABCB1Homo sapiens (human)
response to xenobiotic stimulusATP-dependent translocase ABCB1Homo sapiens (human)
phospholipid translocationATP-dependent translocase ABCB1Homo sapiens (human)
terpenoid transportATP-dependent translocase ABCB1Homo sapiens (human)
regulation of response to osmotic stressATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
transepithelial transportATP-dependent translocase ABCB1Homo sapiens (human)
stem cell proliferationATP-dependent translocase ABCB1Homo sapiens (human)
ceramide translocationATP-dependent translocase ABCB1Homo sapiens (human)
export across plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
positive regulation of anion channel activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
regulation of chloride transportATP-dependent translocase ABCB1Homo sapiens (human)
lipid hydroxylationCytochrome P450 3A4Homo sapiens (human)
lipid metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid catabolic processCytochrome P450 3A4Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid metabolic processCytochrome P450 3A4Homo sapiens (human)
cholesterol metabolic processCytochrome P450 3A4Homo sapiens (human)
androgen metabolic processCytochrome P450 3A4Homo sapiens (human)
estrogen metabolic processCytochrome P450 3A4Homo sapiens (human)
alkaloid catabolic processCytochrome P450 3A4Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 3A4Homo sapiens (human)
calcitriol biosynthetic process from calciolCytochrome P450 3A4Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D metabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D catabolic processCytochrome P450 3A4Homo sapiens (human)
retinol metabolic processCytochrome P450 3A4Homo sapiens (human)
retinoic acid metabolic processCytochrome P450 3A4Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 3A4Homo sapiens (human)
aflatoxin metabolic processCytochrome P450 3A4Homo sapiens (human)
oxidative demethylationCytochrome P450 3A4Homo sapiens (human)
behavioral fear response5-hydroxytryptamine receptor 1AHomo sapiens (human)
G protein-coupled receptor signaling pathway5-hydroxytryptamine receptor 1AHomo sapiens (human)
adenylate cyclase-inhibiting serotonin receptor signaling pathway5-hydroxytryptamine receptor 1AHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 1AHomo sapiens (human)
gamma-aminobutyric acid signaling pathway5-hydroxytryptamine receptor 1AHomo sapiens (human)
positive regulation of cell population proliferation5-hydroxytryptamine receptor 1AHomo sapiens (human)
regulation of serotonin secretion5-hydroxytryptamine receptor 1AHomo sapiens (human)
regulation of vasoconstriction5-hydroxytryptamine receptor 1AHomo sapiens (human)
exploration behavior5-hydroxytryptamine receptor 1AHomo sapiens (human)
regulation of dopamine metabolic process5-hydroxytryptamine receptor 1AHomo sapiens (human)
serotonin metabolic process5-hydroxytryptamine receptor 1AHomo sapiens (human)
regulation of hormone secretion5-hydroxytryptamine receptor 1AHomo sapiens (human)
regulation of behavior5-hydroxytryptamine receptor 1AHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 1AHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 1AHomo sapiens (human)
gastric acid secretionMuscarinic acetylcholine receptor M5Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M5Homo sapiens (human)
dopamine transportMuscarinic acetylcholine receptor M5Homo sapiens (human)
transmission of nerve impulseMuscarinic acetylcholine receptor M5Homo sapiens (human)
regulation of phosphatidylinositol dephosphorylationMuscarinic acetylcholine receptor M5Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M5Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M5Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M5Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M5Homo sapiens (human)
positive regulation of cytokine productionAlpha-2A adrenergic receptorHomo sapiens (human)
DNA replicationAlpha-2A adrenergic receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating G protein-coupled receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
Ras protein signal transductionAlpha-2A adrenergic receptorHomo sapiens (human)
Rho protein signal transductionAlpha-2A adrenergic receptorHomo sapiens (human)
female pregnancyAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of cell population proliferationAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of norepinephrine secretionAlpha-2A adrenergic receptorHomo sapiens (human)
regulation of vasoconstrictionAlpha-2A adrenergic receptorHomo sapiens (human)
actin cytoskeleton organizationAlpha-2A adrenergic receptorHomo sapiens (human)
platelet activationAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of cell migrationAlpha-2A adrenergic receptorHomo sapiens (human)
activation of protein kinase activityAlpha-2A adrenergic receptorHomo sapiens (human)
activation of protein kinase B activityAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of epinephrine secretionAlpha-2A adrenergic receptorHomo sapiens (human)
cellular response to hormone stimulusAlpha-2A adrenergic receptorHomo sapiens (human)
receptor transactivationAlpha-2A adrenergic receptorHomo sapiens (human)
vasodilationAlpha-2A adrenergic receptorHomo sapiens (human)
glucose homeostasisAlpha-2A adrenergic receptorHomo sapiens (human)
fear responseAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of potassium ion transportAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of MAP kinase activityAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of calcium ion-dependent exocytosisAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of insulin secretionAlpha-2A adrenergic receptorHomo sapiens (human)
intestinal absorptionAlpha-2A adrenergic receptorHomo sapiens (human)
thermoceptionAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of lipid catabolic processAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of membrane protein ectodomain proteolysisAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of calcium ion transportAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of insulin secretion involved in cellular response to glucose stimulusAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of uterine smooth muscle contractionAlpha-2A adrenergic receptorHomo sapiens (human)
adrenergic receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
adenylate cyclase-inhibiting adrenergic receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
phospholipase C-activating adrenergic receptor signaling pathwayAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of wound healingAlpha-2A adrenergic receptorHomo sapiens (human)
presynaptic modulation of chemical synaptic transmissionAlpha-2A adrenergic receptorHomo sapiens (human)
negative regulation of calcium ion transmembrane transporter activityAlpha-2A adrenergic receptorHomo sapiens (human)
positive regulation of monoatomic ion transportMuscarinic acetylcholine receptor M1Homo sapiens (human)
signal transductionMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
protein kinase C-activating G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
phospholipase C-activating G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
neuromuscular synaptic transmissionMuscarinic acetylcholine receptor M1Homo sapiens (human)
nervous system developmentMuscarinic acetylcholine receptor M1Homo sapiens (human)
regulation of locomotionMuscarinic acetylcholine receptor M1Homo sapiens (human)
saliva secretionMuscarinic acetylcholine receptor M1Homo sapiens (human)
cognitionMuscarinic acetylcholine receptor M1Homo sapiens (human)
regulation of postsynaptic membrane potentialMuscarinic acetylcholine receptor M1Homo sapiens (human)
regulation of glial cell proliferationMuscarinic acetylcholine receptor M1Homo sapiens (human)
positive regulation of intracellular protein transportMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
postsynaptic modulation of chemical synaptic transmissionMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M1Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M1Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M1Homo sapiens (human)
pentose-phosphate shuntGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
lipid metabolic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
cholesterol biosynthetic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
NADP metabolic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
NADPH regenerationGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
glutathione metabolic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
pentose-phosphate shunt, oxidative branchGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
response to iron(III) ionGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
negative regulation of protein glutathionylationGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
response to organic cyclic compoundGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
pentose biosynthetic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
substantia nigra developmentGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
response to foodGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
cellular response to oxidative stressGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
erythrocyte maturationGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
regulation of neuron apoptotic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
response to ethanolGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
ribose phosphate biosynthetic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
glucose 6-phosphate metabolic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
negative regulation of cell growth involved in cardiac muscle cell developmentGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
positive regulation of calcium ion transmembrane transport via high voltage-gated calcium channelGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
negative regulation of reactive oxygen species metabolic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
glucose metabolic processGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
phospholipase C-activating dopamine receptor signaling pathwayD(2) dopamine receptorHomo sapiens (human)
temperature homeostasisD(2) dopamine receptorHomo sapiens (human)
response to hypoxiaD(2) dopamine receptorHomo sapiens (human)
negative regulation of protein phosphorylationD(2) dopamine receptorHomo sapiens (human)
response to amphetamineD(2) dopamine receptorHomo sapiens (human)
nervous system process involved in regulation of systemic arterial blood pressureD(2) dopamine receptorHomo sapiens (human)
regulation of heart rateD(2) dopamine receptorHomo sapiens (human)
regulation of sodium ion transportD(2) dopamine receptorHomo sapiens (human)
G protein-coupled receptor internalizationD(2) dopamine receptorHomo sapiens (human)
positive regulation of neuroblast proliferationD(2) dopamine receptorHomo sapiens (human)
positive regulation of receptor internalizationD(2) dopamine receptorHomo sapiens (human)
autophagyD(2) dopamine receptorHomo sapiens (human)
adenylate cyclase-inhibiting dopamine receptor signaling pathwayD(2) dopamine receptorHomo sapiens (human)
neuron-neuron synaptic transmissionD(2) dopamine receptorHomo sapiens (human)
neuroblast proliferationD(2) dopamine receptorHomo sapiens (human)
axonogenesisD(2) dopamine receptorHomo sapiens (human)
synapse assemblyD(2) dopamine receptorHomo sapiens (human)
sensory perception of smellD(2) dopamine receptorHomo sapiens (human)
long-term memoryD(2) dopamine receptorHomo sapiens (human)
grooming behaviorD(2) dopamine receptorHomo sapiens (human)
locomotory behaviorD(2) dopamine receptorHomo sapiens (human)
adult walking behaviorD(2) dopamine receptorHomo sapiens (human)
protein localizationD(2) dopamine receptorHomo sapiens (human)
negative regulation of cell population proliferationD(2) dopamine receptorHomo sapiens (human)
associative learningD(2) dopamine receptorHomo sapiens (human)
visual learningD(2) dopamine receptorHomo sapiens (human)
response to xenobiotic stimulusD(2) dopamine receptorHomo sapiens (human)
response to light stimulusD(2) dopamine receptorHomo sapiens (human)
response to toxic substanceD(2) dopamine receptorHomo sapiens (human)
response to iron ionD(2) dopamine receptorHomo sapiens (human)
response to inactivityD(2) dopamine receptorHomo sapiens (human)
Wnt signaling pathwayD(2) dopamine receptorHomo sapiens (human)
striatum developmentD(2) dopamine receptorHomo sapiens (human)
orbitofrontal cortex developmentD(2) dopamine receptorHomo sapiens (human)
cerebral cortex GABAergic interneuron migrationD(2) dopamine receptorHomo sapiens (human)
adenohypophysis developmentD(2) dopamine receptorHomo sapiens (human)
negative regulation of cell migrationD(2) dopamine receptorHomo sapiens (human)
peristalsisD(2) dopamine receptorHomo sapiens (human)
auditory behaviorD(2) dopamine receptorHomo sapiens (human)
regulation of synaptic transmission, GABAergicD(2) dopamine receptorHomo sapiens (human)
positive regulation of cytokinesisD(2) dopamine receptorHomo sapiens (human)
circadian regulation of gene expressionD(2) dopamine receptorHomo sapiens (human)
negative regulation of dopamine secretionD(2) dopamine receptorHomo sapiens (human)
response to histamineD(2) dopamine receptorHomo sapiens (human)
response to nicotineD(2) dopamine receptorHomo sapiens (human)
positive regulation of urine volumeD(2) dopamine receptorHomo sapiens (human)
positive regulation of renal sodium excretionD(2) dopamine receptorHomo sapiens (human)
positive regulation of multicellular organism growthD(2) dopamine receptorHomo sapiens (human)
response to cocaineD(2) dopamine receptorHomo sapiens (human)
negative regulation of circadian sleep/wake cycle, sleepD(2) dopamine receptorHomo sapiens (human)
dopamine metabolic processD(2) dopamine receptorHomo sapiens (human)
drinking behaviorD(2) dopamine receptorHomo sapiens (human)
regulation of potassium ion transportD(2) dopamine receptorHomo sapiens (human)
response to morphineD(2) dopamine receptorHomo sapiens (human)
pigmentationD(2) dopamine receptorHomo sapiens (human)
phosphatidylinositol 3-kinase/protein kinase B signal transductionD(2) dopamine receptorHomo sapiens (human)
positive regulation of G protein-coupled receptor signaling pathwayD(2) dopamine receptorHomo sapiens (human)
negative regulation of blood pressureD(2) dopamine receptorHomo sapiens (human)
negative regulation of innate immune responseD(2) dopamine receptorHomo sapiens (human)
positive regulation of transcription by RNA polymerase IID(2) dopamine receptorHomo sapiens (human)
negative regulation of insulin secretionD(2) dopamine receptorHomo sapiens (human)
acid secretionD(2) dopamine receptorHomo sapiens (human)
behavioral response to cocaineD(2) dopamine receptorHomo sapiens (human)
behavioral response to ethanolD(2) dopamine receptorHomo sapiens (human)
regulation of long-term neuronal synaptic plasticityD(2) dopamine receptorHomo sapiens (human)
response to axon injuryD(2) dopamine receptorHomo sapiens (human)
branching morphogenesis of a nerveD(2) dopamine receptorHomo sapiens (human)
arachidonic acid secretionD(2) dopamine receptorHomo sapiens (human)
epithelial cell proliferationD(2) dopamine receptorHomo sapiens (human)
negative regulation of epithelial cell proliferationD(2) dopamine receptorHomo sapiens (human)
negative regulation of protein secretionD(2) dopamine receptorHomo sapiens (human)
release of sequestered calcium ion into cytosolD(2) dopamine receptorHomo sapiens (human)
dopamine uptake involved in synaptic transmissionD(2) dopamine receptorHomo sapiens (human)
regulation of dopamine uptake involved in synaptic transmissionD(2) dopamine receptorHomo sapiens (human)
positive regulation of dopamine uptake involved in synaptic transmissionD(2) dopamine receptorHomo sapiens (human)
regulation of synapse structural plasticityD(2) dopamine receptorHomo sapiens (human)
negative regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionD(2) dopamine receptorHomo sapiens (human)
negative regulation of synaptic transmission, glutamatergicD(2) dopamine receptorHomo sapiens (human)
excitatory postsynaptic potentialD(2) dopamine receptorHomo sapiens (human)
positive regulation of growth hormone secretionD(2) dopamine receptorHomo sapiens (human)
prepulse inhibitionD(2) dopamine receptorHomo sapiens (human)
negative regulation of dopamine receptor signaling pathwayD(2) dopamine receptorHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeD(2) dopamine receptorHomo sapiens (human)
regulation of locomotion involved in locomotory behaviorD(2) dopamine receptorHomo sapiens (human)
postsynaptic modulation of chemical synaptic transmissionD(2) dopamine receptorHomo sapiens (human)
presynaptic modulation of chemical synaptic transmissionD(2) dopamine receptorHomo sapiens (human)
negative regulation of cellular response to hypoxiaD(2) dopamine receptorHomo sapiens (human)
positive regulation of glial cell-derived neurotrophic factor productionD(2) dopamine receptorHomo sapiens (human)
positive regulation of long-term synaptic potentiationD(2) dopamine receptorHomo sapiens (human)
hyaloid vascular plexus regressionD(2) dopamine receptorHomo sapiens (human)
negative regulation of neuron migrationD(2) dopamine receptorHomo sapiens (human)
negative regulation of cytosolic calcium ion concentrationD(2) dopamine receptorHomo sapiens (human)
regulation of dopamine secretionD(2) dopamine receptorHomo sapiens (human)
negative regulation of adenylate cyclase activityD(2) dopamine receptorHomo sapiens (human)
phospholipase C-activating dopamine receptor signaling pathwayD(2) dopamine receptorHomo sapiens (human)
negative regulation of voltage-gated calcium channel activityD(2) dopamine receptorHomo sapiens (human)
positive regulation of MAPK cascadeD(2) dopamine receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayD(2) dopamine receptorHomo sapiens (human)
MAPK cascadeAlpha-2B adrenergic receptorHomo sapiens (human)
angiogenesisAlpha-2B adrenergic receptorHomo sapiens (human)
regulation of vascular associated smooth muscle contractionAlpha-2B adrenergic receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-2B adrenergic receptorHomo sapiens (human)
cell-cell signalingAlpha-2B adrenergic receptorHomo sapiens (human)
female pregnancyAlpha-2B adrenergic receptorHomo sapiens (human)
negative regulation of norepinephrine secretionAlpha-2B adrenergic receptorHomo sapiens (human)
platelet activationAlpha-2B adrenergic receptorHomo sapiens (human)
activation of protein kinase B activityAlpha-2B adrenergic receptorHomo sapiens (human)
negative regulation of epinephrine secretionAlpha-2B adrenergic receptorHomo sapiens (human)
receptor transactivationAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of neuron differentiationAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of blood pressureAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of uterine smooth muscle contractionAlpha-2B adrenergic receptorHomo sapiens (human)
adrenergic receptor signaling pathwayAlpha-2B adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-2B adrenergic receptorHomo sapiens (human)
regulation of smooth muscle contractionAlpha-2C adrenergic receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-2C adrenergic receptorHomo sapiens (human)
cell-cell signalingAlpha-2C adrenergic receptorHomo sapiens (human)
negative regulation of norepinephrine secretionAlpha-2C adrenergic receptorHomo sapiens (human)
regulation of vasoconstrictionAlpha-2C adrenergic receptorHomo sapiens (human)
platelet activationAlpha-2C adrenergic receptorHomo sapiens (human)
activation of protein kinase B activityAlpha-2C adrenergic receptorHomo sapiens (human)
negative regulation of epinephrine secretionAlpha-2C adrenergic receptorHomo sapiens (human)
receptor transactivationAlpha-2C adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-2C adrenergic receptorHomo sapiens (human)
positive regulation of neuron differentiationAlpha-2C adrenergic receptorHomo sapiens (human)
adrenergic receptor signaling pathwayAlpha-2C adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-2C adrenergic receptorHomo sapiens (human)
negative regulation of insulin secretionAlpha-2C adrenergic receptorHomo sapiens (human)
calcium-mediated signalingMuscarinic acetylcholine receptor M3Homo sapiens (human)
regulation of monoatomic ion transmembrane transporter activityMuscarinic acetylcholine receptor M3Homo sapiens (human)
smooth muscle contractionMuscarinic acetylcholine receptor M3Homo sapiens (human)
signal transductionMuscarinic acetylcholine receptor M3Homo sapiens (human)
G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
phospholipase C-activating G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
synaptic transmission, cholinergicMuscarinic acetylcholine receptor M3Homo sapiens (human)
nervous system developmentMuscarinic acetylcholine receptor M3Homo sapiens (human)
positive regulation of insulin secretionMuscarinic acetylcholine receptor M3Homo sapiens (human)
protein modification processMuscarinic acetylcholine receptor M3Homo sapiens (human)
positive regulation of smooth muscle contractionMuscarinic acetylcholine receptor M3Homo sapiens (human)
saliva secretionMuscarinic acetylcholine receptor M3Homo sapiens (human)
acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
ion channel modulating, G protein-coupled receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
ligand-gated ion channel signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
regulation of smooth muscle contractionMuscarinic acetylcholine receptor M3Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerMuscarinic acetylcholine receptor M3Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathwayMuscarinic acetylcholine receptor M3Homo sapiens (human)
chemical synaptic transmissionMuscarinic acetylcholine receptor M3Homo sapiens (human)
temperature homeostasisD(1A) dopamine receptorHomo sapiens (human)
conditioned taste aversionD(1A) dopamine receptorHomo sapiens (human)
behavioral fear responseD(1A) dopamine receptorHomo sapiens (human)
regulation of protein phosphorylationD(1A) dopamine receptorHomo sapiens (human)
synaptic transmission, dopaminergicD(1A) dopamine receptorHomo sapiens (human)
response to amphetamineD(1A) dopamine receptorHomo sapiens (human)
protein import into nucleusD(1A) dopamine receptorHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerD(1A) dopamine receptorHomo sapiens (human)
adenylate cyclase-activating G protein-coupled receptor signaling pathwayD(1A) dopamine receptorHomo sapiens (human)
activation of adenylate cyclase activityD(1A) dopamine receptorHomo sapiens (human)
adenylate cyclase-activating dopamine receptor signaling pathwayD(1A) dopamine receptorHomo sapiens (human)
synapse assemblyD(1A) dopamine receptorHomo sapiens (human)
memoryD(1A) dopamine receptorHomo sapiens (human)
mating behaviorD(1A) dopamine receptorHomo sapiens (human)
grooming behaviorD(1A) dopamine receptorHomo sapiens (human)
adult walking behaviorD(1A) dopamine receptorHomo sapiens (human)
visual learningD(1A) dopamine receptorHomo sapiens (human)
response to xenobiotic stimulusD(1A) dopamine receptorHomo sapiens (human)
astrocyte developmentD(1A) dopamine receptorHomo sapiens (human)
dopamine transportD(1A) dopamine receptorHomo sapiens (human)
transmission of nerve impulseD(1A) dopamine receptorHomo sapiens (human)
neuronal action potentialD(1A) dopamine receptorHomo sapiens (human)
dentate gyrus developmentD(1A) dopamine receptorHomo sapiens (human)
striatum developmentD(1A) dopamine receptorHomo sapiens (human)
cerebral cortex GABAergic interneuron migrationD(1A) dopamine receptorHomo sapiens (human)
positive regulation of cell migrationD(1A) dopamine receptorHomo sapiens (human)
peristalsisD(1A) dopamine receptorHomo sapiens (human)
operant conditioningD(1A) dopamine receptorHomo sapiens (human)
synaptic transmission, glutamatergicD(1A) dopamine receptorHomo sapiens (human)
regulation of dopamine metabolic processD(1A) dopamine receptorHomo sapiens (human)
vasodilationD(1A) dopamine receptorHomo sapiens (human)
dopamine metabolic processD(1A) dopamine receptorHomo sapiens (human)
maternal behaviorD(1A) dopamine receptorHomo sapiens (human)
positive regulation of potassium ion transportD(1A) dopamine receptorHomo sapiens (human)
glucose importD(1A) dopamine receptorHomo sapiens (human)
habituationD(1A) dopamine receptorHomo sapiens (human)
sensitizationD(1A) dopamine receptorHomo sapiens (human)
behavioral response to cocaineD(1A) dopamine receptorHomo sapiens (human)
positive regulation of release of sequestered calcium ion into cytosolD(1A) dopamine receptorHomo sapiens (human)
regulation of dopamine uptake involved in synaptic transmissionD(1A) dopamine receptorHomo sapiens (human)
positive regulation of synaptic transmission, glutamatergicD(1A) dopamine receptorHomo sapiens (human)
prepulse inhibitionD(1A) dopamine receptorHomo sapiens (human)
phospholipase C-activating dopamine receptor signaling pathwayD(1A) dopamine receptorHomo sapiens (human)
long-term synaptic potentiationD(1A) dopamine receptorHomo sapiens (human)
long-term synaptic depressionD(1A) dopamine receptorHomo sapiens (human)
cellular response to catecholamine stimulusD(1A) dopamine receptorHomo sapiens (human)
modification of postsynaptic structureD(1A) dopamine receptorHomo sapiens (human)
presynaptic modulation of chemical synaptic transmissionD(1A) dopamine receptorHomo sapiens (human)
positive regulation of neuron migrationD(1A) dopamine receptorHomo sapiens (human)
positive regulation of MAPK cascadeD(1A) dopamine receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayD(1A) dopamine receptorHomo sapiens (human)
dopamine receptor signaling pathwayD(1A) dopamine receptorHomo sapiens (human)
positive regulation of MAP kinase activityD(4) dopamine receptorHomo sapiens (human)
behavioral fear responseD(4) dopamine receptorHomo sapiens (human)
synaptic transmission, dopaminergicD(4) dopamine receptorHomo sapiens (human)
response to amphetamineD(4) dopamine receptorHomo sapiens (human)
intracellular calcium ion homeostasisD(4) dopamine receptorHomo sapiens (human)
adenylate cyclase-inhibiting dopamine receptor signaling pathwayD(4) dopamine receptorHomo sapiens (human)
dopamine receptor signaling pathwayD(4) dopamine receptorHomo sapiens (human)
adult locomotory behaviorD(4) dopamine receptorHomo sapiens (human)
positive regulation of sodium:proton antiporter activityD(4) dopamine receptorHomo sapiens (human)
positive regulation of kinase activityD(4) dopamine receptorHomo sapiens (human)
response to histamineD(4) dopamine receptorHomo sapiens (human)
social behaviorD(4) dopamine receptorHomo sapiens (human)
regulation of dopamine metabolic processD(4) dopamine receptorHomo sapiens (human)
dopamine metabolic processD(4) dopamine receptorHomo sapiens (human)
fear responseD(4) dopamine receptorHomo sapiens (human)
regulation of circadian rhythmD(4) dopamine receptorHomo sapiens (human)
positive regulation of MAP kinase activityD(4) dopamine receptorHomo sapiens (human)
behavioral response to cocaineD(4) dopamine receptorHomo sapiens (human)
behavioral response to ethanolD(4) dopamine receptorHomo sapiens (human)
rhythmic processD(4) dopamine receptorHomo sapiens (human)
arachidonic acid secretionD(4) dopamine receptorHomo sapiens (human)
negative regulation of protein secretionD(4) dopamine receptorHomo sapiens (human)
positive regulation of dopamine uptake involved in synaptic transmissionD(4) dopamine receptorHomo sapiens (human)
inhibitory postsynaptic potentialD(4) dopamine receptorHomo sapiens (human)
regulation of postsynaptic neurotransmitter receptor internalizationD(4) dopamine receptorHomo sapiens (human)
negative regulation of voltage-gated calcium channel activityD(4) dopamine receptorHomo sapiens (human)
adenylate cyclase-inhibiting serotonin receptor signaling pathwayD(4) dopamine receptorHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerD(4) dopamine receptorHomo sapiens (human)
chemical synaptic transmissionD(4) dopamine receptorHomo sapiens (human)
bilirubin conjugationUDP-glucuronosyltransferase 1A4Homo sapiens (human)
heme catabolic processUDP-glucuronosyltransferase 1A4Homo sapiens (human)
cellular glucuronidationUDP-glucuronosyltransferase 1A4Homo sapiens (human)
vitamin D3 metabolic processUDP-glucuronosyltransferase 1A4Homo sapiens (human)
monoamine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transportSodium-dependent noradrenaline transporter Homo sapiens (human)
chemical synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
response to xenobiotic stimulusSodium-dependent noradrenaline transporter Homo sapiens (human)
response to painSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine uptakeSodium-dependent noradrenaline transporter Homo sapiens (human)
neuron cellular homeostasisSodium-dependent noradrenaline transporter Homo sapiens (human)
amino acid transportSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine uptake involved in synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
sodium ion transmembrane transportSodium-dependent noradrenaline transporter Homo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-1D adrenergic receptorHomo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayAlpha-1D adrenergic receptorHomo sapiens (human)
positive regulation of cell population proliferationAlpha-1D adrenergic receptorHomo sapiens (human)
neuron-glial cell signalingAlpha-1D adrenergic receptorHomo sapiens (human)
cell-cell signalingAlpha-1D adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-1D adrenergic receptorHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathwayAlpha-1D adrenergic receptorHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationAlpha-1D adrenergic receptorHomo sapiens (human)
positive regulation of vasoconstrictionAlpha-1D adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-1D adrenergic receptorHomo sapiens (human)
temperature homeostasis5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of cytokine production involved in immune response5-hydroxytryptamine receptor 2AHomo sapiens (human)
glycolytic process5-hydroxytryptamine receptor 2AHomo sapiens (human)
intracellular calcium ion homeostasis5-hydroxytryptamine receptor 2AHomo sapiens (human)
activation of phospholipase C activity5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of cytosolic calcium ion concentration5-hydroxytryptamine receptor 2AHomo sapiens (human)
memory5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of cell population proliferation5-hydroxytryptamine receptor 2AHomo sapiens (human)
response to xenobiotic stimulus5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of phosphatidylinositol biosynthetic process5-hydroxytryptamine receptor 2AHomo sapiens (human)
regulation of dopamine secretion5-hydroxytryptamine receptor 2AHomo sapiens (human)
artery smooth muscle contraction5-hydroxytryptamine receptor 2AHomo sapiens (human)
urinary bladder smooth muscle contraction5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of heat generation5-hydroxytryptamine receptor 2AHomo sapiens (human)
negative regulation of potassium ion transport5-hydroxytryptamine receptor 2AHomo sapiens (human)
phosphatidylinositol 3-kinase/protein kinase B signal transduction5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of neuron apoptotic process5-hydroxytryptamine receptor 2AHomo sapiens (human)
protein localization to cytoskeleton5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of fat cell differentiation5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of glycolytic process5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of vasoconstriction5-hydroxytryptamine receptor 2AHomo sapiens (human)
symbiont entry into host cell5-hydroxytryptamine receptor 2AHomo sapiens (human)
sensitization5-hydroxytryptamine receptor 2AHomo sapiens (human)
behavioral response to cocaine5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of inflammatory response5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylation5-hydroxytryptamine receptor 2AHomo sapiens (human)
detection of temperature stimulus involved in sensory perception of pain5-hydroxytryptamine receptor 2AHomo sapiens (human)
detection of mechanical stimulus involved in sensory perception of pain5-hydroxytryptamine receptor 2AHomo sapiens (human)
release of sequestered calcium ion into cytosol5-hydroxytryptamine receptor 2AHomo sapiens (human)
negative regulation of synaptic transmission, glutamatergic5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascade5-hydroxytryptamine receptor 2AHomo sapiens (human)
G protein-coupled serotonin receptor signaling pathway5-hydroxytryptamine receptor 2AHomo sapiens (human)
presynaptic modulation of chemical synaptic transmission5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of execution phase of apoptosis5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of platelet aggregation5-hydroxytryptamine receptor 2AHomo sapiens (human)
positive regulation of DNA biosynthetic process5-hydroxytryptamine receptor 2AHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 2AHomo sapiens (human)
phospholipase C-activating serotonin receptor signaling pathway5-hydroxytryptamine receptor 2AHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 2AHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 2AHomo sapiens (human)
behavioral fear response5-hydroxytryptamine receptor 2CHomo sapiens (human)
intracellular calcium ion homeostasis5-hydroxytryptamine receptor 2CHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
phospholipase C-activating serotonin receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
locomotory behavior5-hydroxytryptamine receptor 2CHomo sapiens (human)
feeding behavior5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of phosphatidylinositol biosynthetic process5-hydroxytryptamine receptor 2CHomo sapiens (human)
cGMP-mediated signaling5-hydroxytryptamine receptor 2CHomo sapiens (human)
regulation of nervous system process5-hydroxytryptamine receptor 2CHomo sapiens (human)
regulation of appetite5-hydroxytryptamine receptor 2CHomo sapiens (human)
regulation of corticotropin-releasing hormone secretion5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of fat cell differentiation5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of calcium-mediated signaling5-hydroxytryptamine receptor 2CHomo sapiens (human)
release of sequestered calcium ion into cytosol5-hydroxytryptamine receptor 2CHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascade5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled serotonin receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 2CHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 2CHomo sapiens (human)
monoamine transportSodium-dependent serotonin transporterHomo sapiens (human)
response to hypoxiaSodium-dependent serotonin transporterHomo sapiens (human)
neurotransmitter transportSodium-dependent serotonin transporterHomo sapiens (human)
response to nutrientSodium-dependent serotonin transporterHomo sapiens (human)
memorySodium-dependent serotonin transporterHomo sapiens (human)
circadian rhythmSodium-dependent serotonin transporterHomo sapiens (human)
response to xenobiotic stimulusSodium-dependent serotonin transporterHomo sapiens (human)
response to toxic substanceSodium-dependent serotonin transporterHomo sapiens (human)
positive regulation of gene expressionSodium-dependent serotonin transporterHomo sapiens (human)
positive regulation of serotonin secretionSodium-dependent serotonin transporterHomo sapiens (human)
negative regulation of cerebellar granule cell precursor proliferationSodium-dependent serotonin transporterHomo sapiens (human)
negative regulation of synaptic transmission, dopaminergicSodium-dependent serotonin transporterHomo sapiens (human)
response to estradiolSodium-dependent serotonin transporterHomo sapiens (human)
social behaviorSodium-dependent serotonin transporterHomo sapiens (human)
vasoconstrictionSodium-dependent serotonin transporterHomo sapiens (human)
sperm ejaculationSodium-dependent serotonin transporterHomo sapiens (human)
negative regulation of neuron differentiationSodium-dependent serotonin transporterHomo sapiens (human)
positive regulation of cell cycleSodium-dependent serotonin transporterHomo sapiens (human)
negative regulation of organ growthSodium-dependent serotonin transporterHomo sapiens (human)
behavioral response to cocaineSodium-dependent serotonin transporterHomo sapiens (human)
enteric nervous system developmentSodium-dependent serotonin transporterHomo sapiens (human)
brain morphogenesisSodium-dependent serotonin transporterHomo sapiens (human)
serotonin uptakeSodium-dependent serotonin transporterHomo sapiens (human)
membrane depolarizationSodium-dependent serotonin transporterHomo sapiens (human)
platelet aggregationSodium-dependent serotonin transporterHomo sapiens (human)
cellular response to retinoic acidSodium-dependent serotonin transporterHomo sapiens (human)
cellular response to cGMPSodium-dependent serotonin transporterHomo sapiens (human)
regulation of thalamus sizeSodium-dependent serotonin transporterHomo sapiens (human)
conditioned place preferenceSodium-dependent serotonin transporterHomo sapiens (human)
sodium ion transmembrane transportSodium-dependent serotonin transporterHomo sapiens (human)
amino acid transportSodium-dependent serotonin transporterHomo sapiens (human)
smooth muscle contraction5-hydroxytryptamine receptor 7Homo sapiens (human)
circadian rhythm5-hydroxytryptamine receptor 7Homo sapiens (human)
blood circulation5-hydroxytryptamine receptor 7Homo sapiens (human)
vasoconstriction5-hydroxytryptamine receptor 7Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathway5-hydroxytryptamine receptor 7Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 7Homo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 7Homo sapiens (human)
MAPK cascadeAlpha-1A adrenergic receptorHomo sapiens (human)
negative regulation of heart rate involved in baroreceptor response to increased systemic arterial blood pressureAlpha-1A adrenergic receptorHomo sapiens (human)
norepinephrine-epinephrine vasoconstriction involved in regulation of systemic arterial blood pressureAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of heart rate by epinephrine-norepinephrineAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of the force of heart contraction by epinephrine-norepinephrineAlpha-1A adrenergic receptorHomo sapiens (human)
apoptotic processAlpha-1A adrenergic receptorHomo sapiens (human)
smooth muscle contractionAlpha-1A adrenergic receptorHomo sapiens (human)
signal transductionAlpha-1A adrenergic receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-1A adrenergic receptorHomo sapiens (human)
activation of phospholipase C activityAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationAlpha-1A adrenergic receptorHomo sapiens (human)
adult heart developmentAlpha-1A adrenergic receptorHomo sapiens (human)
negative regulation of cell population proliferationAlpha-1A adrenergic receptorHomo sapiens (human)
response to xenobiotic stimulusAlpha-1A adrenergic receptorHomo sapiens (human)
response to hormoneAlpha-1A adrenergic receptorHomo sapiens (human)
negative regulation of autophagyAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of cardiac muscle hypertrophyAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of synaptic transmission, GABAergicAlpha-1A adrenergic receptorHomo sapiens (human)
intracellular signal transductionAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of action potentialAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of vasoconstrictionAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of smooth muscle contractionAlpha-1A adrenergic receptorHomo sapiens (human)
calcium ion transport into cytosolAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of cardiac muscle contractionAlpha-1A adrenergic receptorHomo sapiens (human)
cell growth involved in cardiac muscle cell developmentAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeAlpha-1A adrenergic receptorHomo sapiens (human)
positive regulation of protein kinase C signalingAlpha-1A adrenergic receptorHomo sapiens (human)
pilomotor reflexAlpha-1A adrenergic receptorHomo sapiens (human)
neuron-glial cell signalingAlpha-1A adrenergic receptorHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathwayAlpha-1A adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-1A adrenergic receptorHomo sapiens (human)
cell-cell signalingAlpha-1A adrenergic receptorHomo sapiens (human)
inflammatory responseHistamine H1 receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayHistamine H1 receptorHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathwayHistamine H1 receptorHomo sapiens (human)
memoryHistamine H1 receptorHomo sapiens (human)
visual learningHistamine H1 receptorHomo sapiens (human)
regulation of vascular permeabilityHistamine H1 receptorHomo sapiens (human)
positive regulation of vasoconstrictionHistamine H1 receptorHomo sapiens (human)
regulation of synaptic plasticityHistamine H1 receptorHomo sapiens (human)
cellular response to histamineHistamine H1 receptorHomo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayHistamine H1 receptorHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerHistamine H1 receptorHomo sapiens (human)
chemical synaptic transmissionHistamine H1 receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-1B adrenergic receptorHomo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayAlpha-1B adrenergic receptorHomo sapiens (human)
regulation of vasoconstrictionAlpha-1B adrenergic receptorHomo sapiens (human)
intracellular signal transductionAlpha-1B adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-1B adrenergic receptorHomo sapiens (human)
regulation of cardiac muscle contractionAlpha-1B adrenergic receptorHomo sapiens (human)
neuron-glial cell signalingAlpha-1B adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-1B adrenergic receptorHomo sapiens (human)
cell-cell signalingAlpha-1B adrenergic receptorHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathwayAlpha-1B adrenergic receptorHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationAlpha-1B adrenergic receptorHomo sapiens (human)
response to ethanolD(3) dopamine receptorHomo sapiens (human)
synaptic transmission, dopaminergicD(3) dopamine receptorHomo sapiens (human)
G protein-coupled receptor internalizationD(3) dopamine receptorHomo sapiens (human)
intracellular calcium ion homeostasisD(3) dopamine receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayD(3) dopamine receptorHomo sapiens (human)
adenylate cyclase-activating dopamine receptor signaling pathwayD(3) dopamine receptorHomo sapiens (human)
adenylate cyclase-inhibiting dopamine receptor signaling pathwayD(3) dopamine receptorHomo sapiens (human)
learning or memoryD(3) dopamine receptorHomo sapiens (human)
learningD(3) dopamine receptorHomo sapiens (human)
locomotory behaviorD(3) dopamine receptorHomo sapiens (human)
visual learningD(3) dopamine receptorHomo sapiens (human)
response to xenobiotic stimulusD(3) dopamine receptorHomo sapiens (human)
regulation of dopamine secretionD(3) dopamine receptorHomo sapiens (human)
positive regulation of cytokinesisD(3) dopamine receptorHomo sapiens (human)
circadian regulation of gene expressionD(3) dopamine receptorHomo sapiens (human)
response to histamineD(3) dopamine receptorHomo sapiens (human)
social behaviorD(3) dopamine receptorHomo sapiens (human)
response to cocaineD(3) dopamine receptorHomo sapiens (human)
dopamine metabolic processD(3) dopamine receptorHomo sapiens (human)
response to morphineD(3) dopamine receptorHomo sapiens (human)
negative regulation of blood pressureD(3) dopamine receptorHomo sapiens (human)
positive regulation of mitotic nuclear divisionD(3) dopamine receptorHomo sapiens (human)
acid secretionD(3) dopamine receptorHomo sapiens (human)
behavioral response to cocaineD(3) dopamine receptorHomo sapiens (human)
negative regulation of oligodendrocyte differentiationD(3) dopamine receptorHomo sapiens (human)
arachidonic acid secretionD(3) dopamine receptorHomo sapiens (human)
negative regulation of protein secretionD(3) dopamine receptorHomo sapiens (human)
musculoskeletal movement, spinal reflex actionD(3) dopamine receptorHomo sapiens (human)
regulation of dopamine uptake involved in synaptic transmissionD(3) dopamine receptorHomo sapiens (human)
negative regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionD(3) dopamine receptorHomo sapiens (human)
prepulse inhibitionD(3) dopamine receptorHomo sapiens (human)
positive regulation of dopamine receptor signaling pathwayD(3) dopamine receptorHomo sapiens (human)
negative regulation of adenylate cyclase activityD(3) dopamine receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayD(3) dopamine receptorHomo sapiens (human)
negative regulation of voltage-gated calcium channel activityD(3) dopamine receptorHomo sapiens (human)
regulation of potassium ion transportD(3) dopamine receptorHomo sapiens (human)
phospholipase C-activating dopamine receptor signaling pathwayD(3) dopamine receptorHomo sapiens (human)
positive regulation of MAPK cascadeD(3) dopamine receptorHomo sapiens (human)
negative regulation of cytosolic calcium ion concentrationD(3) dopamine receptorHomo sapiens (human)
negative regulation of synaptic transmission, glutamatergicD(3) dopamine receptorHomo sapiens (human)
neural crest cell migration5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of cytokine production5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of endothelial cell proliferation5-hydroxytryptamine receptor 2BHomo sapiens (human)
G protein-coupled receptor internalization5-hydroxytryptamine receptor 2BHomo sapiens (human)
heart morphogenesis5-hydroxytryptamine receptor 2BHomo sapiens (human)
cardiac muscle hypertrophy5-hydroxytryptamine receptor 2BHomo sapiens (human)
intracellular calcium ion homeostasis5-hydroxytryptamine receptor 2BHomo sapiens (human)
G protein-coupled receptor signaling pathway5-hydroxytryptamine receptor 2BHomo sapiens (human)
activation of phospholipase C activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
protein kinase C-activating G protein-coupled receptor signaling pathway5-hydroxytryptamine receptor 2BHomo sapiens (human)
phospholipase C-activating serotonin receptor signaling pathway5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of cell population proliferation5-hydroxytryptamine receptor 2BHomo sapiens (human)
response to xenobiotic stimulus5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of phosphatidylinositol biosynthetic process5-hydroxytryptamine receptor 2BHomo sapiens (human)
neural crest cell differentiation5-hydroxytryptamine receptor 2BHomo sapiens (human)
intestine smooth muscle contraction5-hydroxytryptamine receptor 2BHomo sapiens (human)
phosphorylation5-hydroxytryptamine receptor 2BHomo sapiens (human)
calcium-mediated signaling5-hydroxytryptamine receptor 2BHomo sapiens (human)
cGMP-mediated signaling5-hydroxytryptamine receptor 2BHomo sapiens (human)
vasoconstriction5-hydroxytryptamine receptor 2BHomo sapiens (human)
negative regulation of apoptotic process5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of canonical NF-kappaB signal transduction5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of MAP kinase activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
phosphatidylinositol 3-kinase/protein kinase B signal transduction5-hydroxytryptamine receptor 2BHomo sapiens (human)
embryonic morphogenesis5-hydroxytryptamine receptor 2BHomo sapiens (human)
regulation of behavior5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of nitric-oxide synthase activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
release of sequestered calcium ion into cytosol5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of cell division5-hydroxytryptamine receptor 2BHomo sapiens (human)
ERK1 and ERK2 cascade5-hydroxytryptamine receptor 2BHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascade5-hydroxytryptamine receptor 2BHomo sapiens (human)
protein kinase C signaling5-hydroxytryptamine receptor 2BHomo sapiens (human)
cellular response to temperature stimulus5-hydroxytryptamine receptor 2BHomo sapiens (human)
G protein-coupled serotonin receptor signaling pathway5-hydroxytryptamine receptor 2BHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 2BHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 2BHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 2BHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 3AHomo sapiens (human)
monoatomic ion transmembrane transport5-hydroxytryptamine receptor 3AHomo sapiens (human)
excitatory postsynaptic potential5-hydroxytryptamine receptor 3AHomo sapiens (human)
inorganic cation transmembrane transport5-hydroxytryptamine receptor 3AHomo sapiens (human)
regulation of presynaptic membrane potential5-hydroxytryptamine receptor 3AHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 3AHomo sapiens (human)
regulation of membrane potential5-hydroxytryptamine receptor 3AHomo sapiens (human)
cerebral cortex cell migration5-hydroxytryptamine receptor 6Homo sapiens (human)
positive regulation of TOR signaling5-hydroxytryptamine receptor 6Homo sapiens (human)
G protein-coupled serotonin receptor signaling pathway5-hydroxytryptamine receptor 6Homo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 6Homo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathway5-hydroxytryptamine receptor 6Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger5-hydroxytryptamine receptor 6Homo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to hypoxiaDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
neutrophil mediated immunityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
germinal center formationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of leukocyte chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane protein ectodomain proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch receptor processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell population proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to xenobiotic stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of T cell chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
signal releaseDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
B cell differentiationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell growthDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to lipopolysaccharideDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of chemokine productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
regulation of mast cell apoptotic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
T cell differentiation in thymusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesion mediated by integrinDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
wound healing, spreading of epidermal cellsDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of blood vessel endothelial cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cyclin-dependent protein serine/threonine kinase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor-activated receptor activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
spleen developmentDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell motilityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
defense response to Gram-positive bacteriumDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cellular response to high density lipoprotein particle stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
commissural neuron axon guidanceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of cold-induced thermogenesisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycleDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor-mediated signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of vascular endothelial cell proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by hormonePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of DNA-templated transcriptionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion homeostasisPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cardiac muscle contractionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cellular response to xenobiotic stimulusPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane depolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of heart rate by cardiac conductionPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potentialPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
positive regulation of potassium ion transmembrane transportPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
negative regulation of potassium ion export across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
potassium ion import across plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 3DHomo sapiens (human)
monoatomic ion transmembrane transport5-hydroxytryptamine receptor 3DHomo sapiens (human)
excitatory postsynaptic potential5-hydroxytryptamine receptor 3DHomo sapiens (human)
inorganic cation transmembrane transport5-hydroxytryptamine receptor 3DHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 3DHomo sapiens (human)
regulation of membrane potential5-hydroxytryptamine receptor 3DHomo sapiens (human)
serotonin receptor signaling pathway5-hydroxytryptamine receptor 3CHomo sapiens (human)
monoatomic ion transmembrane transport5-hydroxytryptamine receptor 3CHomo sapiens (human)
excitatory postsynaptic potential5-hydroxytryptamine receptor 3CHomo sapiens (human)
inorganic cation transmembrane transport5-hydroxytryptamine receptor 3CHomo sapiens (human)
regulation of membrane potential5-hydroxytryptamine receptor 3CHomo sapiens (human)
chemical synaptic transmission5-hydroxytryptamine receptor 3CHomo sapiens (human)
xenobiotic metabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (166)

Processvia Protein(s)Taxonomy
serotonin-gated monoatomic cation channel activity5-hydroxytryptamine receptor 3EHomo sapiens (human)
excitatory extracellular ligand-gated monoatomic ion channel activity5-hydroxytryptamine receptor 3EHomo sapiens (human)
transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential5-hydroxytryptamine receptor 3EHomo sapiens (human)
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
serotonin-gated monoatomic cation channel activity5-hydroxytryptamine receptor 3BHomo sapiens (human)
transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential5-hydroxytryptamine receptor 3BHomo sapiens (human)
excitatory extracellular ligand-gated monoatomic ion channel activity5-hydroxytryptamine receptor 3BHomo sapiens (human)
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)
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M2Homo sapiens (human)
arrestin family protein bindingMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M2Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M4Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M4Homo sapiens (human)
protein bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATP bindingATP-dependent translocase ABCB1Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
efflux transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ATP hydrolysis activityATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ubiquitin protein ligase bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylcholine floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylethanolamine flippase activityATP-dependent translocase ABCB1Homo sapiens (human)
ceramide floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
steroid bindingCytochrome P450 3A4Homo sapiens (human)
iron ion bindingCytochrome P450 3A4Homo sapiens (human)
protein bindingCytochrome P450 3A4Homo sapiens (human)
steroid hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
retinoic acid 4-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
oxidoreductase activityCytochrome P450 3A4Homo sapiens (human)
oxygen bindingCytochrome P450 3A4Homo sapiens (human)
enzyme bindingCytochrome P450 3A4Homo sapiens (human)
heme bindingCytochrome P450 3A4Homo sapiens (human)
vitamin D3 25-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
caffeine oxidase activityCytochrome P450 3A4Homo sapiens (human)
quinine 3-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
testosterone 6-beta-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1-alpha,25-dihydroxyvitamin D3 23-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 8,9 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 11,12 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 14,15 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
aromatase activityCytochrome P450 3A4Homo sapiens (human)
vitamin D 24-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 16-alpha-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 2-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1,8-cineole 2-exo-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 1AHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 1AHomo sapiens (human)
receptor-receptor interaction5-hydroxytryptamine receptor 1AHomo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 1AHomo sapiens (human)
serotonin binding5-hydroxytryptamine receptor 1AHomo sapiens (human)
phosphatidylinositol phospholipase C activityMuscarinic acetylcholine receptor M5Homo sapiens (human)
protein bindingMuscarinic acetylcholine receptor M5Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M5Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M5Homo sapiens (human)
alpha2-adrenergic receptor activityAlpha-2A adrenergic receptorHomo sapiens (human)
protein bindingAlpha-2A adrenergic receptorHomo sapiens (human)
protein kinase bindingAlpha-2A adrenergic receptorHomo sapiens (human)
alpha-1B adrenergic receptor bindingAlpha-2A adrenergic receptorHomo sapiens (human)
alpha-2C adrenergic receptor bindingAlpha-2A adrenergic receptorHomo sapiens (human)
thioesterase bindingAlpha-2A adrenergic receptorHomo sapiens (human)
heterotrimeric G-protein bindingAlpha-2A adrenergic receptorHomo sapiens (human)
protein homodimerization activityAlpha-2A adrenergic receptorHomo sapiens (human)
protein heterodimerization activityAlpha-2A adrenergic receptorHomo sapiens (human)
epinephrine bindingAlpha-2A adrenergic receptorHomo sapiens (human)
norepinephrine bindingAlpha-2A adrenergic receptorHomo sapiens (human)
guanyl-nucleotide exchange factor activityAlpha-2A adrenergic receptorHomo sapiens (human)
phosphatidylinositol phospholipase C activityMuscarinic acetylcholine receptor M1Homo sapiens (human)
protein bindingMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M1Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M1Homo sapiens (human)
glucose-6-phosphate dehydrogenase activityGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
protein bindingGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
glucose bindingGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
identical protein bindingGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
protein homodimerization activityGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
NADP bindingGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
dopamine neurotransmitter receptor activity, coupled via Gi/GoD(2) dopamine receptorHomo sapiens (human)
G-protein alpha-subunit bindingD(2) dopamine receptorHomo sapiens (human)
protein bindingD(2) dopamine receptorHomo sapiens (human)
heterotrimeric G-protein bindingD(2) dopamine receptorHomo sapiens (human)
dopamine bindingD(2) dopamine receptorHomo sapiens (human)
ionotropic glutamate receptor bindingD(2) dopamine receptorHomo sapiens (human)
identical protein bindingD(2) dopamine receptorHomo sapiens (human)
heterocyclic compound bindingD(2) dopamine receptorHomo sapiens (human)
G protein-coupled receptor activityD(2) dopamine receptorHomo sapiens (human)
alpha2-adrenergic receptor activityAlpha-2B adrenergic receptorHomo sapiens (human)
protein bindingAlpha-2B adrenergic receptorHomo sapiens (human)
epinephrine bindingAlpha-2B adrenergic receptorHomo sapiens (human)
alpha2-adrenergic receptor activityAlpha-2C adrenergic receptorHomo sapiens (human)
protein bindingAlpha-2C adrenergic receptorHomo sapiens (human)
alpha-2A adrenergic receptor bindingAlpha-2C adrenergic receptorHomo sapiens (human)
protein homodimerization activityAlpha-2C adrenergic receptorHomo sapiens (human)
protein heterodimerization activityAlpha-2C adrenergic receptorHomo sapiens (human)
epinephrine bindingAlpha-2C adrenergic receptorHomo sapiens (human)
guanyl-nucleotide exchange factor activityAlpha-2C adrenergic receptorHomo sapiens (human)
phosphatidylinositol phospholipase C activityMuscarinic acetylcholine receptor M3Homo sapiens (human)
protein bindingMuscarinic acetylcholine receptor M3Homo sapiens (human)
G protein-coupled acetylcholine receptor activityMuscarinic acetylcholine receptor M3Homo sapiens (human)
signaling receptor activityMuscarinic acetylcholine receptor M3Homo sapiens (human)
acetylcholine bindingMuscarinic acetylcholine receptor M3Homo sapiens (human)
G protein-coupled serotonin receptor activityMuscarinic acetylcholine receptor M3Homo sapiens (human)
dopamine neurotransmitter receptor activity, coupled via GsD(1A) dopamine receptorHomo sapiens (human)
G-protein alpha-subunit bindingD(1A) dopamine receptorHomo sapiens (human)
dopamine neurotransmitter receptor activityD(1A) dopamine receptorHomo sapiens (human)
protein bindingD(1A) dopamine receptorHomo sapiens (human)
heterotrimeric G-protein bindingD(1A) dopamine receptorHomo sapiens (human)
dopamine bindingD(1A) dopamine receptorHomo sapiens (human)
arrestin family protein bindingD(1A) dopamine receptorHomo sapiens (human)
G protein-coupled receptor activityD(1A) dopamine receptorHomo sapiens (human)
dopamine neurotransmitter receptor activity, coupled via Gi/GoD(4) dopamine receptorHomo sapiens (human)
dopamine neurotransmitter receptor activityD(4) dopamine receptorHomo sapiens (human)
protein bindingD(4) dopamine receptorHomo sapiens (human)
potassium channel regulator activityD(4) dopamine receptorHomo sapiens (human)
SH3 domain bindingD(4) dopamine receptorHomo sapiens (human)
dopamine bindingD(4) dopamine receptorHomo sapiens (human)
identical protein bindingD(4) dopamine receptorHomo sapiens (human)
metal ion bindingD(4) dopamine receptorHomo sapiens (human)
epinephrine bindingD(4) dopamine receptorHomo sapiens (human)
norepinephrine bindingD(4) dopamine receptorHomo sapiens (human)
G protein-coupled serotonin receptor activityD(4) dopamine receptorHomo sapiens (human)
neurotransmitter receptor activityD(4) dopamine receptorHomo sapiens (human)
serotonin bindingD(4) dopamine receptorHomo sapiens (human)
retinoic acid bindingUDP-glucuronosyltransferase 1A4Homo sapiens (human)
glucuronosyltransferase activityUDP-glucuronosyltransferase 1A4Homo sapiens (human)
enzyme bindingUDP-glucuronosyltransferase 1A4Homo sapiens (human)
protein homodimerization activityUDP-glucuronosyltransferase 1A4Homo sapiens (human)
protein heterodimerization activityUDP-glucuronosyltransferase 1A4Homo sapiens (human)
actin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
protein bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
monoamine transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
alpha-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
metal ion bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
beta-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
protein bindingAlpha-1D adrenergic receptorHomo sapiens (human)
identical protein bindingAlpha-1D adrenergic receptorHomo sapiens (human)
alpha1-adrenergic receptor activityAlpha-1D adrenergic receptorHomo sapiens (human)
Gq/11-coupled serotonin receptor activity5-hydroxytryptamine receptor 2AHomo sapiens (human)
virus receptor activity5-hydroxytryptamine receptor 2AHomo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 2AHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 2AHomo sapiens (human)
protein tyrosine kinase activator activity5-hydroxytryptamine receptor 2AHomo sapiens (human)
identical protein binding5-hydroxytryptamine receptor 2AHomo sapiens (human)
protein-containing complex binding5-hydroxytryptamine receptor 2AHomo sapiens (human)
serotonin binding5-hydroxytryptamine receptor 2AHomo sapiens (human)
1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine binding5-hydroxytryptamine receptor 2AHomo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 2AHomo sapiens (human)
Gq/11-coupled serotonin receptor activity5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 2CHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
identical protein binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
serotonin binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine binding5-hydroxytryptamine receptor 2CHomo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 2CHomo sapiens (human)
integrin bindingSodium-dependent serotonin transporterHomo sapiens (human)
monoatomic cation channel activitySodium-dependent serotonin transporterHomo sapiens (human)
neurotransmitter transmembrane transporter activitySodium-dependent serotonin transporterHomo sapiens (human)
serotonin:sodium:chloride symporter activitySodium-dependent serotonin transporterHomo sapiens (human)
protein bindingSodium-dependent serotonin transporterHomo sapiens (human)
monoamine transmembrane transporter activitySodium-dependent serotonin transporterHomo sapiens (human)
antiporter activitySodium-dependent serotonin transporterHomo sapiens (human)
syntaxin-1 bindingSodium-dependent serotonin transporterHomo sapiens (human)
cocaine bindingSodium-dependent serotonin transporterHomo sapiens (human)
sodium ion bindingSodium-dependent serotonin transporterHomo sapiens (human)
identical protein bindingSodium-dependent serotonin transporterHomo sapiens (human)
nitric-oxide synthase bindingSodium-dependent serotonin transporterHomo sapiens (human)
actin filament bindingSodium-dependent serotonin transporterHomo sapiens (human)
serotonin bindingSodium-dependent serotonin transporterHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 7Homo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 7Homo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 7Homo sapiens (human)
alpha1-adrenergic receptor activityAlpha-1A adrenergic receptorHomo sapiens (human)
protein bindingAlpha-1A adrenergic receptorHomo sapiens (human)
protein heterodimerization activityAlpha-1A adrenergic receptorHomo sapiens (human)
histamine receptor activityHistamine H1 receptorHomo sapiens (human)
G protein-coupled serotonin receptor activityHistamine H1 receptorHomo sapiens (human)
neurotransmitter receptor activityHistamine H1 receptorHomo sapiens (human)
protein bindingAlpha-1B adrenergic receptorHomo sapiens (human)
protein heterodimerization activityAlpha-1B adrenergic receptorHomo sapiens (human)
alpha1-adrenergic receptor activityAlpha-1B adrenergic receptorHomo sapiens (human)
dopamine neurotransmitter receptor activity, coupled via Gi/GoD(3) dopamine receptorHomo sapiens (human)
protein bindingD(3) dopamine receptorHomo sapiens (human)
G protein-coupled receptor activityD(3) dopamine receptorHomo sapiens (human)
Gq/11-coupled serotonin receptor activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
G-protein alpha-subunit binding5-hydroxytryptamine receptor 2BHomo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
GTPase activator activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 2BHomo sapiens (human)
serotonin binding5-hydroxytryptamine receptor 2BHomo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 2BHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 3AHomo sapiens (human)
serotonin-gated monoatomic cation channel activity5-hydroxytryptamine receptor 3AHomo sapiens (human)
identical protein binding5-hydroxytryptamine receptor 3AHomo sapiens (human)
serotonin binding5-hydroxytryptamine receptor 3AHomo sapiens (human)
ligand-gated monoatomic ion channel activity involved in regulation of presynaptic membrane potential5-hydroxytryptamine receptor 3AHomo sapiens (human)
transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential5-hydroxytryptamine receptor 3AHomo sapiens (human)
excitatory extracellular ligand-gated monoatomic ion channel activity5-hydroxytryptamine receptor 3AHomo sapiens (human)
histamine receptor activity5-hydroxytryptamine receptor 6Homo sapiens (human)
protein binding5-hydroxytryptamine receptor 6Homo sapiens (human)
neurotransmitter receptor activity5-hydroxytryptamine receptor 6Homo sapiens (human)
G protein-coupled serotonin receptor activity5-hydroxytryptamine receptor 6Homo sapiens (human)
endopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
interleukin-6 receptor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
integrin bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
peptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metallopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
SH3 domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytokine bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
PDZ domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
tumor necrosis factor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metal ion bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activity involved in amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
transcription cis-regulatory region bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
delayed rectifier potassium channel activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
ubiquitin protein ligase bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
identical protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein homodimerization activityPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
C3HC4-type RING finger domain bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
scaffold protein bindingPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarizationPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
protein binding5-hydroxytryptamine receptor 3DHomo sapiens (human)
serotonin-gated monoatomic cation channel activity5-hydroxytryptamine receptor 3DHomo sapiens (human)
excitatory extracellular ligand-gated monoatomic ion channel activity5-hydroxytryptamine receptor 3DHomo sapiens (human)
transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential5-hydroxytryptamine receptor 3DHomo sapiens (human)
protein binding5-hydroxytryptamine receptor 3CHomo sapiens (human)
serotonin-gated monoatomic cation channel activity5-hydroxytryptamine receptor 3CHomo sapiens (human)
excitatory extracellular ligand-gated monoatomic ion channel activity5-hydroxytryptamine receptor 3CHomo sapiens (human)
transmitter-gated monoatomic ion channel activity involved in regulation of postsynaptic membrane potential5-hydroxytryptamine receptor 3CHomo sapiens (human)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (95)

Processvia Protein(s)Taxonomy
plasma membrane5-hydroxytryptamine receptor 3EHomo sapiens (human)
postsynaptic membrane5-hydroxytryptamine receptor 3EHomo sapiens (human)
serotonin-activated cation-selective channel complex5-hydroxytryptamine receptor 3EHomo sapiens (human)
neuron projection5-hydroxytryptamine receptor 3EHomo sapiens (human)
transmembrane transporter complex5-hydroxytryptamine receptor 3EHomo sapiens (human)
synapse5-hydroxytryptamine receptor 3EHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3EHomo sapiens (human)
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3BHomo sapiens (human)
postsynaptic membrane5-hydroxytryptamine receptor 3BHomo sapiens (human)
serotonin-activated cation-selective channel complex5-hydroxytryptamine receptor 3BHomo sapiens (human)
cell surface5-hydroxytryptamine receptor 3BHomo sapiens (human)
transmembrane transporter complex5-hydroxytryptamine receptor 3BHomo sapiens (human)
synapse5-hydroxytryptamine receptor 3BHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3BHomo sapiens (human)
neuron projection5-hydroxytryptamine receptor 3BHomo sapiens (human)
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)
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
clathrin-coated endocytic vesicle membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
asymmetric synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
symmetric synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
presynaptic membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
neuronal cell bodyMuscarinic acetylcholine receptor M2Homo sapiens (human)
axon terminusMuscarinic acetylcholine receptor M2Homo sapiens (human)
postsynaptic membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
glutamatergic synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
cholinergic synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M2Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M2Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M2Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M4Homo sapiens (human)
postsynaptic membraneMuscarinic acetylcholine receptor M4Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M4Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M4Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M4Homo sapiens (human)
cytoplasmATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
cell surfaceATP-dependent translocase ABCB1Homo sapiens (human)
membraneATP-dependent translocase ABCB1Homo sapiens (human)
apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
extracellular exosomeATP-dependent translocase ABCB1Homo sapiens (human)
external side of apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
cytoplasmCytochrome P450 3A4Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 3A4Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 3A4Homo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 1AHomo sapiens (human)
synapse5-hydroxytryptamine receptor 1AHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 1AHomo sapiens (human)
dendrite5-hydroxytryptamine receptor 1AHomo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M5Homo sapiens (human)
postsynaptic membraneMuscarinic acetylcholine receptor M5Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M5Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M5Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M5Homo sapiens (human)
cytoplasmAlpha-2A adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2A adrenergic receptorHomo sapiens (human)
basolateral plasma membraneAlpha-2A adrenergic receptorHomo sapiens (human)
neuronal cell bodyAlpha-2A adrenergic receptorHomo sapiens (human)
axon terminusAlpha-2A adrenergic receptorHomo sapiens (human)
presynaptic active zone membraneAlpha-2A adrenergic receptorHomo sapiens (human)
dopaminergic synapseAlpha-2A adrenergic receptorHomo sapiens (human)
postsynaptic density membraneAlpha-2A adrenergic receptorHomo sapiens (human)
glutamatergic synapseAlpha-2A adrenergic receptorHomo sapiens (human)
GABA-ergic synapseAlpha-2A adrenergic receptorHomo sapiens (human)
receptor complexAlpha-2A adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2A adrenergic receptorHomo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
presynaptic membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
axon terminusMuscarinic acetylcholine receptor M1Homo sapiens (human)
Schaffer collateral - CA1 synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
postsynaptic density membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
glutamatergic synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
cholinergic synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M1Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M1Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M1Homo sapiens (human)
cytoplasmGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
cytosolGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
cytoplasmic side of plasma membraneGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
membraneGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
centriolar satelliteGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
intracellular membrane-bounded organelleGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
extracellular exosomeGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
cytosolGlucose-6-phosphate 1-dehydrogenaseHomo sapiens (human)
Golgi membraneD(2) dopamine receptorHomo sapiens (human)
acrosomal vesicleD(2) dopamine receptorHomo sapiens (human)
plasma membraneD(2) dopamine receptorHomo sapiens (human)
ciliumD(2) dopamine receptorHomo sapiens (human)
lateral plasma membraneD(2) dopamine receptorHomo sapiens (human)
endocytic vesicleD(2) dopamine receptorHomo sapiens (human)
axonD(2) dopamine receptorHomo sapiens (human)
dendriteD(2) dopamine receptorHomo sapiens (human)
synaptic vesicle membraneD(2) dopamine receptorHomo sapiens (human)
sperm flagellumD(2) dopamine receptorHomo sapiens (human)
dendritic spineD(2) dopamine receptorHomo sapiens (human)
perikaryonD(2) dopamine receptorHomo sapiens (human)
axon terminusD(2) dopamine receptorHomo sapiens (human)
postsynaptic membraneD(2) dopamine receptorHomo sapiens (human)
ciliary membraneD(2) dopamine receptorHomo sapiens (human)
non-motile ciliumD(2) dopamine receptorHomo sapiens (human)
dopaminergic synapseD(2) dopamine receptorHomo sapiens (human)
GABA-ergic synapseD(2) dopamine receptorHomo sapiens (human)
G protein-coupled receptor complexD(2) dopamine receptorHomo sapiens (human)
glutamatergic synapseD(2) dopamine receptorHomo sapiens (human)
presynaptic membraneD(2) dopamine receptorHomo sapiens (human)
plasma membraneD(2) dopamine receptorHomo sapiens (human)
cytosolAlpha-2B adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2B adrenergic receptorHomo sapiens (human)
cell surfaceAlpha-2B adrenergic receptorHomo sapiens (human)
intracellular membrane-bounded organelleAlpha-2B adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2B adrenergic receptorHomo sapiens (human)
cytoplasmAlpha-2C adrenergic receptorHomo sapiens (human)
endosomeAlpha-2C adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2C adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2C adrenergic receptorHomo sapiens (human)
endoplasmic reticulum membraneMuscarinic acetylcholine receptor M3Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M3Homo sapiens (human)
basal plasma membraneMuscarinic acetylcholine receptor M3Homo sapiens (human)
basolateral plasma membraneMuscarinic acetylcholine receptor M3Homo sapiens (human)
postsynaptic membraneMuscarinic acetylcholine receptor M3Homo sapiens (human)
synapseMuscarinic acetylcholine receptor M3Homo sapiens (human)
plasma membraneMuscarinic acetylcholine receptor M3Homo sapiens (human)
dendriteMuscarinic acetylcholine receptor M3Homo sapiens (human)
nucleusD(1A) dopamine receptorHomo sapiens (human)
endoplasmic reticulum membraneD(1A) dopamine receptorHomo sapiens (human)
plasma membraneD(1A) dopamine receptorHomo sapiens (human)
ciliumD(1A) dopamine receptorHomo sapiens (human)
presynaptic membraneD(1A) dopamine receptorHomo sapiens (human)
dendritic spineD(1A) dopamine receptorHomo sapiens (human)
postsynaptic membraneD(1A) dopamine receptorHomo sapiens (human)
ciliary membraneD(1A) dopamine receptorHomo sapiens (human)
non-motile ciliumD(1A) dopamine receptorHomo sapiens (human)
glutamatergic synapseD(1A) dopamine receptorHomo sapiens (human)
GABA-ergic synapseD(1A) dopamine receptorHomo sapiens (human)
G protein-coupled receptor complexD(1A) dopamine receptorHomo sapiens (human)
plasma membraneD(1A) dopamine receptorHomo sapiens (human)
centrosomeD(4) dopamine receptorHomo sapiens (human)
plasma membraneD(4) dopamine receptorHomo sapiens (human)
membraneD(4) dopamine receptorHomo sapiens (human)
postsynapseD(4) dopamine receptorHomo sapiens (human)
glutamatergic synapseD(4) dopamine receptorHomo sapiens (human)
plasma membraneD(4) dopamine receptorHomo sapiens (human)
dendriteD(4) dopamine receptorHomo sapiens (human)
endoplasmic reticulumUDP-glucuronosyltransferase 1A4Homo sapiens (human)
endoplasmic reticulum membraneUDP-glucuronosyltransferase 1A4Homo sapiens (human)
endoplasmic reticulumUDP-glucuronosyltransferase 1A4Homo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
cell surfaceSodium-dependent noradrenaline transporter Homo sapiens (human)
membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
neuronal cell body membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
presynaptic membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
axonSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membraneAlpha-1D adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-1D adrenergic receptorHomo sapiens (human)
neurofilament5-hydroxytryptamine receptor 2AHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2AHomo sapiens (human)
caveola5-hydroxytryptamine receptor 2AHomo sapiens (human)
axon5-hydroxytryptamine receptor 2AHomo sapiens (human)
cytoplasmic vesicle5-hydroxytryptamine receptor 2AHomo sapiens (human)
presynaptic membrane5-hydroxytryptamine receptor 2AHomo sapiens (human)
neuronal cell body5-hydroxytryptamine receptor 2AHomo sapiens (human)
dendritic shaft5-hydroxytryptamine receptor 2AHomo sapiens (human)
postsynaptic membrane5-hydroxytryptamine receptor 2AHomo sapiens (human)
cell body fiber5-hydroxytryptamine receptor 2AHomo sapiens (human)
glutamatergic synapse5-hydroxytryptamine receptor 2AHomo sapiens (human)
G protein-coupled serotonin receptor complex5-hydroxytryptamine receptor 2AHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2AHomo sapiens (human)
dendrite5-hydroxytryptamine receptor 2AHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2CHomo sapiens (human)
synapse5-hydroxytryptamine receptor 2CHomo sapiens (human)
G protein-coupled serotonin receptor complex5-hydroxytryptamine receptor 2CHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2CHomo sapiens (human)
dendrite5-hydroxytryptamine receptor 2CHomo sapiens (human)
plasma membraneSodium-dependent serotonin transporterHomo sapiens (human)
focal adhesionSodium-dependent serotonin transporterHomo sapiens (human)
endosome membraneSodium-dependent serotonin transporterHomo sapiens (human)
endomembrane systemSodium-dependent serotonin transporterHomo sapiens (human)
presynaptic membraneSodium-dependent serotonin transporterHomo sapiens (human)
membrane raftSodium-dependent serotonin transporterHomo sapiens (human)
synapseSodium-dependent serotonin transporterHomo sapiens (human)
postsynaptic membraneSodium-dependent serotonin transporterHomo sapiens (human)
serotonergic synapseSodium-dependent serotonin transporterHomo sapiens (human)
synapseSodium-dependent serotonin transporterHomo sapiens (human)
plasma membraneSodium-dependent serotonin transporterHomo sapiens (human)
neuron projectionSodium-dependent serotonin transporterHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 7Homo sapiens (human)
trans-Golgi network membrane5-hydroxytryptamine receptor 7Homo sapiens (human)
synapse5-hydroxytryptamine receptor 7Homo sapiens (human)
dendrite5-hydroxytryptamine receptor 7Homo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 7Homo sapiens (human)
nucleusAlpha-1A adrenergic receptorHomo sapiens (human)
nucleoplasmAlpha-1A adrenergic receptorHomo sapiens (human)
cytoplasmAlpha-1A adrenergic receptorHomo sapiens (human)
cytosolAlpha-1A adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-1A adrenergic receptorHomo sapiens (human)
caveolaAlpha-1A adrenergic receptorHomo sapiens (human)
nuclear membraneAlpha-1A adrenergic receptorHomo sapiens (human)
intracellular membrane-bounded organelleAlpha-1A adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-1A adrenergic receptorHomo sapiens (human)
cytosolHistamine H1 receptorHomo sapiens (human)
plasma membraneHistamine H1 receptorHomo sapiens (human)
synapseHistamine H1 receptorHomo sapiens (human)
dendriteHistamine H1 receptorHomo sapiens (human)
plasma membraneHistamine H1 receptorHomo sapiens (human)
nucleusAlpha-1B adrenergic receptorHomo sapiens (human)
cytoplasmAlpha-1B adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-1B adrenergic receptorHomo sapiens (human)
caveolaAlpha-1B adrenergic receptorHomo sapiens (human)
nuclear membraneAlpha-1B adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-1B adrenergic receptorHomo sapiens (human)
plasma membraneD(3) dopamine receptorHomo sapiens (human)
synapseD(3) dopamine receptorHomo sapiens (human)
plasma membraneD(3) dopamine receptorHomo sapiens (human)
nucleoplasm5-hydroxytryptamine receptor 2BHomo sapiens (human)
cytoplasm5-hydroxytryptamine receptor 2BHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2BHomo sapiens (human)
synapse5-hydroxytryptamine receptor 2BHomo sapiens (human)
G protein-coupled serotonin receptor complex5-hydroxytryptamine receptor 2BHomo sapiens (human)
dendrite5-hydroxytryptamine receptor 2BHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 2BHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3AHomo sapiens (human)
cleavage furrow5-hydroxytryptamine receptor 3AHomo sapiens (human)
postsynaptic membrane5-hydroxytryptamine receptor 3AHomo sapiens (human)
serotonin-activated cation-selective channel complex5-hydroxytryptamine receptor 3AHomo sapiens (human)
synapse5-hydroxytryptamine receptor 3AHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3AHomo sapiens (human)
transmembrane transporter complex5-hydroxytryptamine receptor 3AHomo sapiens (human)
neuron projection5-hydroxytryptamine receptor 3AHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 6Homo sapiens (human)
cilium5-hydroxytryptamine receptor 6Homo sapiens (human)
synapse5-hydroxytryptamine receptor 6Homo sapiens (human)
dendrite5-hydroxytryptamine receptor 6Homo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 6Homo sapiens (human)
virion membraneSpike glycoproteinSevere acute respiratory syndrome-related coronavirus
cell-cell junctionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
focal adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
ruffle membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Golgi membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytoplasmDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
endoplasmic reticulum lumenDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytosolDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell surfaceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
actin cytoskeletonDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
apical plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane raftDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
cell surfacePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
perinuclear region of cytoplasmPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
voltage-gated potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
inward rectifier potassium channel complexPotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
plasma membranePotassium voltage-gated channel subfamily H member 2Homo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3DHomo sapiens (human)
postsynaptic membrane5-hydroxytryptamine receptor 3DHomo sapiens (human)
serotonin-activated cation-selective channel complex5-hydroxytryptamine receptor 3DHomo sapiens (human)
synapse5-hydroxytryptamine receptor 3DHomo sapiens (human)
transmembrane transporter complex5-hydroxytryptamine receptor 3DHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3DHomo sapiens (human)
neuron projection5-hydroxytryptamine receptor 3DHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3CHomo sapiens (human)
postsynaptic membrane5-hydroxytryptamine receptor 3CHomo sapiens (human)
serotonin-activated cation-selective channel complex5-hydroxytryptamine receptor 3CHomo sapiens (human)
synapse5-hydroxytryptamine receptor 3CHomo sapiens (human)
transmembrane transporter complex5-hydroxytryptamine receptor 3CHomo sapiens (human)
neuron projection5-hydroxytryptamine receptor 3CHomo sapiens (human)
plasma membrane5-hydroxytryptamine receptor 3CHomo sapiens (human)
plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (479)

Assay IDTitleYearJournalArticle
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.
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.
AID1601981Displacement of [3H]-LSD from recombinant human 5HT6 receptor expressed in HEK293 cells measured after 1 hr by microbeta scintillation counting analysis2019European journal of medicinal chemistry, Mar-15, Volume: 166Synthesis of novel pyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID298481Displacement of [3H]8-OH-DPAT from human 5HT1A receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID171680Effect of compound on apomorphine induced catalepsy, from rat brain striatum at 30 umol/kg upon subcutaneous administration; Catalepsy = 0/41998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
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).
AID114862Effective dose required for to antagonize apomorphine-induced climbing in mice after administration of 0.12 mg/kg dose subcutaneously2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID298486Displacement of [3H]LSD from human 5HT6 receptor expressed in HEK293 cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID3657Binding affinity towards human 5-hydroxytryptamine 1 receptor2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID298485Displacement of [3H]mesulergine from 5HT2C receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID238855Inhibition of [3H]SCH-23390 binding to rat Dopamine receptor D12005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1185962Displacement of [3H]SCH23390 from human dopamine D1 receptor by liquid scintillation counting2014Bioorganic & medicinal chemistry letters, Sep-01, Volume: 24, Issue:17
Further evaluation of the tropane analogs of haloperidol.
AID177351In vivo inhibition against catalepsy in rats after oral administration evaluated by metal bar2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID229416Selectivity ratio (D1/D2)2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID130696In vivo inhibitory activity against 5-MeO-DMT-Induced Head-Twitches in mouse after oral administration2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID458633Displacement of [3H]spiperone from human dopamine D2 receptor at high affinity state expressed in HEK293 cells2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID694795Displacement of [3H]-8-OH-DPAT from human 5-HT1A receptor expressed in HEK293 cells after 1 hr2012European journal of medicinal chemistry, Oct, Volume: 56The multiobjective based design, synthesis and evaluation of the arylsulfonamide/amide derivatives of aryloxyethyl- and arylthioethyl- piperidines and pyrrolidines as a novel class of potent 5-HT₇ receptor antagonists.
AID410338Binding affinity to human ERG expressed in HEK293 cells by whole cell patch clamp method2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID1169864Binding affinity to 5HT2C receptor (unknown origin)2014Journal of medicinal chemistry, Nov-26, Volume: 57, Issue:22
Targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors for developing effective antipsychotics: synthesis, biological characterization, and behavioral studies.
AID374351Antiviral activity against BKV Gardner ATCC VR837 infected in human WI38 cells assessed as reduction in viral DNA level preincubated for 2 hrs before viral infection measured after 7 days by real time PCR assay2007Antimicrobial agents and chemotherapy, Dec, Volume: 51, Issue:12
BK Virus replication in vitro: limited effect of drugs interfering with viral uptake and intracellular transport.
AID624633Drug glucuronidation reaction catalyzed by human recombinant UGT1A42005Pharmacology & therapeutics, Apr, Volume: 106, Issue:1
UDP-glucuronosyltransferases and clinical drug-drug interactions.
AID1393475Reversal of ketamine-induced cognitive flexibility in ip dosed Sprague-Dawley rat administered 30 mins prior to ketamine administration by attentional set-shifting test
AID1217705Time dependent inhibition of CYP2B6 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
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).
AID342781Binding affinity to human cloned 5HT2C receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID35289In vitro binding affinity towards alpha-1 adrenergic receptor in rat frontal cortex homogenate using of [3H]prazosin as radioligand2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID1393469Toxicity in ip dosed Sprague-Dawley rat assessed as sedation pretreated for 60 mins followed by PCP addition measured for 30 mins starting 15 min after rat reintroduction to auto-tracks
AID29359Ionization constant (pKa)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1152652Antagonist activity at human recombinant at D2S receptor assessed as inhibition of dopamine-induced cAMP accumulation2014Journal of medicinal chemistry, Jun-12, Volume: 57, Issue:11
Novel arylsulfonamide derivatives with 5-HT₆/5-HT₇ receptor antagonism targeting behavioral and psychological symptoms of dementia.
AID185010Effect of compound on apomorphine induced locomotor hyperactivity (APO-induced LMA), from rat brain striatum at 30 umol/kg upon subcutaneous administration; LMA (locomotor activity)1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
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
AID246865In vivo effective dose against spontaneous locomotor activity was determined in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1823823Displacement of [3H]-ketanserin from human human 5-HT2A receptor transfected in CHO-K1 cells measured after 60 mins by scintillation counting method
AID61679pKi value for Dopamine receptor D1 binding site1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID238990Inhibition of [3H]rauwolscine binding to Alpha-2C adrenergic receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1128453Displacement of [125]DOI from human recombinant full length 5HT2C receptor expressed in HEK293E cells2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID1169862Binding affinity to 5HT1A receptor (unknown origin)2014Journal of medicinal chemistry, Nov-26, Volume: 57, Issue:22
Targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors for developing effective antipsychotics: synthesis, biological characterization, and behavioral studies.
AID171545Effect of compound on apomorphine induced catalepsy, from rat brain striatum at 10 umol/kg upon subcutaneous administration; Catalepsy = 0/41998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID1185965Displacement of [3H]N-methylspiperone from rat dopamine D4 receptor by liquid scintillation counting2014Bioorganic & medicinal chemistry letters, Sep-01, Volume: 24, Issue:17
Further evaluation of the tropane analogs of haloperidol.
AID177349In vivo inhibition against MK-801 induced hyperactivity in rats after oral administration2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID1823833Displacement of [3H]-pyrilamine from human recombinant histamine H1 receptor expressed in human recombinant CHO-K1 cells at 1 uM incubated for 60 mins by solid scintillation counting method relative to control
AID1760276Displacement of [3H]LSD from human 5-HT6 receptor expressed in HEK293 cells incubated for 1 hr by microbeta counting method2020European journal of medicinal chemistry, Oct-01, Volume: 203Chlorine substituents and linker topology as factors of 5-HT
AID177353In vivo inhibition against conditioned avoidance response in rats after oral administration2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID576612Inhibition of human ERG2011European journal of medicinal chemistry, Feb, Volume: 46, Issue:2
Predicting hERG activities of compounds from their 3D structures: development and evaluation of a global descriptors based QSAR model.
AID330557Binding affinity to alphaMSH receptor at 10 nM2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID738112Displacement of [3H]raclopride from D2 receptor in human corpus striatum after 30 mins by scintillation counting2013Bioorganic & medicinal chemistry letters, Apr-01, Volume: 23, Issue:7
[11C]olanzapine, radiosynthesis and lipophilicity of a new potential PET 5-HT2 and D2 receptor radioligand.
AID301041Antipsychotic activity in orally dosed Wistar rat assessed as inhibition of conditioned avoidance response after 1 hr2007Bioorganic & medicinal chemistry letters, Oct-01, Volume: 17, Issue:19
Novel sulfonamides having dual dopamine D2 and D3 receptor affinity show in vivo antipsychotic efficacy with beneficial cognitive and EPS profile.
AID61675Half-maximal inhibition of [3H]-SCH- 23390 binding to Dopamine receptor D1 in rat striatal homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1393368Displacement of [3H]-raclopride from human D2LR expressed in HEK293 cell membranes after 1 hr at 37 degC by microbeta counting method
AID65253Binding affinity which represents concentration giving half-maximal inhibition of [3H]spiperone (Dopamine receptor D2) binding to rat tissue homogenate1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID1595145Displacement of [3H] LSD from human recombinant 5-HT6 receptor expressed in HEK293 cells measured after 1 hr by microbeta scintillation counting method
AID1128456Selectivity ratio of Ki for rat recombinant dopamine D2 short receptor to Ki for human recombinant full length 5HT2A receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID599883Displacement of [3H]mesulergine from human 5HT2C receptor in human tsA201 cells2010Bioorganic & medicinal chemistry letters, Sep-15, Volume: 20, Issue:18
Novel 7-phenylsulfanyl-1,2,3,4,10,10a-hexahydro-pyrazino[1,2-a]indoles as dual serotonin 5-HT2C and 5-HT6 receptor ligands.
AID243151Inhibitory concentration against potassium channel HERG2005Bioorganic & medicinal chemistry letters, Jun-02, Volume: 15, Issue:11
A discriminant model constructed by the support vector machine method for HERG potassium channel inhibitors.
AID161281Inhibition of human Potassium channel HERG expressed in mammalian cells2003Bioorganic & medicinal chemistry letters, Aug-18, Volume: 13, Issue:16
Prediction of hERG potassium channel affinity by traditional and hologram qSAR methods.
AID5250Binding affinity which represents concentration giving half-maximal inhibition of [3H]ketanserin binding to 5-hydroxytryptamine 2 receptor rat tissue homogenate1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID246836In vivo effective dose was determined against apomorphine climbing in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID64005Binding affinity towards human Dopamine receptor D4.2 in CHO cells1996Journal of medicinal chemistry, Sep-27, Volume: 39, Issue:20
Structure-activity relationships of a series of novel (piperazinylbutyl)thiazolidinone antipsychotic agents related to 3-[4-[4-(6-fluorobenzo[b]thien-3-yl)-1-piperazinyl]butyl]-2,5,5- trimethyl-4-thiazolidinone maleate.
AID1185959Displacement of [3H] 8-OH-DPAT from human 5-HT1A receptor by liquid scintillation counting2014Bioorganic & medicinal chemistry letters, Sep-01, Volume: 24, Issue:17
Further evaluation of the tropane analogs of haloperidol.
AID1823832Displacement of [3H]-scopolamine from human recombinant muscarinic M1 receptor expressed in human recombinant CHO-K1 cells at 1 uM incubated for 120 mins by solid scintillation counting method relative to control
AID342784Binding affinity to human cloned 5HT2A receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID1393473Reversal of ketamine-induced working social withdrawal in ip dosed Sprague-Dawley rat pretreated for 60 mins followed by ketamine administration
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]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
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).
AID1568824Displacement of [3H]-LSD from human 5-HT6R expressed in human HEK293 cells incubated for 1 hr by radioligand binding assay2019European journal of medicinal chemistry, Sep-15, Volume: 178Synthesis and computer-aided SAR studies for derivatives of phenoxyalkyl-1,3,5-triazine as the new potent ligands for serotonin receptors 5-HT
AID1677164In vivo receptor occupancy at human dopamine D2 receptor in schizophrenia patient brain at 10 mCi, iv by PET scanning
AID5614Binding affinity towards human serotonin 5-hydroxytryptamine 2C receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
AID1409608AUC (viral infection %) for SARS-CoV-2 in the Vero E6 cell line at 48 h by immunofluorescence-based assay (detecting the viral NP protein in the nucleus of the Vero E6 cells).2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID63347Binding affinity towards human Dopamine receptor D12004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
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).
AID63537Binding affinity towards human dopamine receptor D42001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID238941Inhibition of [3H]spiperone binding to rat dopamine D2 receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID1520007Binding affinity to human 5-HT2AR expressed in HEK293 cells by competitive binding assay
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1128468Selectivity ratio of Ki for adrenergic alpha1A receptor (unknown origin) to Ki for human recombinant full length 5HT2A receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID24452logY value was determined2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID230094Ratio of pKi of compound towards 5-HT2 receptor to that of D1 receptor1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID65620Half-maximal inhibition of [3H]-spiperone binding to Dopamine receptor D3 in rat tissue homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID342775Binding affinity to human cloned dopamine D1 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID298492Displacement of [3H]prazosin from adrenergic alpha1 receptor in rat cerebral cortex2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
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.
AID738353Displacement of [3H]mesulergine from 5-HT2C receptor in human frontal cortex after 30 mins by scintillation counting2013Bioorganic & medicinal chemistry letters, Apr-01, Volume: 23, Issue:7
[11C]olanzapine, radiosynthesis and lipophilicity of a new potential PET 5-HT2 and D2 receptor radioligand.
AID1185960Displacement of [3H]Ketanserin from human 5-HT2A receptor by liquid scintillation counting2014Bioorganic & medicinal chemistry letters, Sep-01, Volume: 24, Issue:17
Further evaluation of the tropane analogs of haloperidol.
AID1393467Toxicity in Wistar rat assessed as increase in prolactin level at 3 mg/kg, po after 60 mins by ELISA
AID1217707Time dependent inhibition of CYP2C19 in human liver microsomes at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID438555Binding affinity to 5HT1A receptor2009Journal of medicinal chemistry, Oct-08, Volume: 52, Issue:19
Physical binding pocket induction for affinity prediction.
AID298494Displacement of [3H]pyrilamine from histaminergic H1 receptor guinea pig cerebellum2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID246864In vivo effective dose against conditioned avoidance response was determined in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID239149Inhibition of [3H]5-HT binding to human 5-hydroxytryptamine 7 receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID87244Binding affinity towards human H1 receptor2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID238991Inhibition of [3H]prazosin binding to rat Alpha-1 adrenergic receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID298493Displacement of [3H]RX 821002 from adrenergic alpha-2 receptor in rat cerebral cortex2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1172033Displacement of [3H]-spiperone from dopamine D2 receptor in rat striatum2015Bioorganic & medicinal chemistry, Jan-01, Volume: 23, Issue:1
Antidepressant- and anxiolytic-like activity of 7-phenylpiperazinylalkyl-1,3-dimethyl-purine-2,6-dione derivatives with diversified 5-HT₁A receptor functional profile.
AID298482Displacement of [3H]ketanserin from human 5HT2A receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1677162Binding affinity to human dopamine D1 receptor
AID1125021Displacement of [3H]spiperone from human dopamine D2S receptor S5.43T/S5.46A mutant expressed in CHO-K1 cell membrane after 2 hrs by beta counting2014European journal of medicinal chemistry, Apr-22, Volume: 77Novel insights on the structural determinants of clozapine and olanzapine multi-target binding profiles.
AID298480Displacement of [3H]spiperone from human dopamine D4.4 receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID678713Inhibition of human CYP2C9 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-methoxy-4-trifluoromethylcoumarin-3-acetic acid as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1556427Displacement of [3H]LSD from human 5HT6 receptor expressed in HEK293 cells measured after 1 hr by liquid scintillation counter method2019European journal of medicinal chemistry, Oct-01, Volume: 1792-Aminoimidazole-based antagonists of the 5-HT
AID1204345Displacement of [3H]N-methylspiperone from dopamine D3 receptor (unknown origin) assessed as total radioligand binding at 1 uM incubated for 60 mins by microbeta plate reader based method2015European journal of medicinal chemistry, Jun-05, Volume: 97Structure-activity relationships and molecular studies of novel arylpiperazinylalkyl purine-2,4-diones and purine-2,4,8-triones with antidepressant and anxiolytic-like activity.
AID1128474Inhibition of quipazine-induced head twitches in po dosed rat head twitch model administered 25 mins prior to quipazine challenge measured after 30 mins2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID1823851Sedative activity in ip dosed Wistar rat assessed as effect on spontaneous locomotor activity measured for 10 mins by social interaction test
AID230935Ratio of the catalepsy to that of conditioned avoidance response in rats2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID1409613Selectivity ratio: ratio of AUC (viral infection %) of SARS-CoV-2 in the Vero E6 cell line compared to AUC (cytotoxicity %) of compound against Vero E6 cells by MTT assay.2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID330561Displacement of [3H]mepyramine from H1R in rat brain2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID1409607IC50 for antiviral activity against SARS-CoV-2 in the Vero E6 cell line at 48 h by immunofluorescence-based assay (detecting the viral NP protein in the nucleus of the Vero E6 cells).2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID395326Fraction unbound in rat brain2009Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6
Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID1677154Ratio of RO50 for in vivo receptor occupancy at dopamine D2 receptor in sc dosed rat brain by measuring free plasma concentration pretreated 1 hr in presence of raclopride to RO50 for in vivo receptor occupancy at dopamine D1 receptor in sc dosed rat brai
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1128452Displacement of [125]DOI from human recombinant full length 5HT2A receptor expressed in HEK293E cells2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID113515In vivo inhibitory activity tested in apomorphine climbing mice after oral administration2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID246931In vivo effective dose for reversal of tryptamine-induced backward locomotion in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID246835In vivo effective dose against catalepsy response was determined in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID298491Displacement of [3H]4-DAMP from human M4 receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID229417Selectivity ratio (D3/D1)2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1430530Displacement of [3H]-LSD from 5-HT6 receptor (unknown origin)
AID61502Binding affinity which represents concentration giving half-maximal inhibition of [3H]SCH-23390 (Dopamine receptor D1) binding to rat tissue homogenate1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID5326Half-maximal inhibition of [3H]- Ketanserin binding to 5-hydroxytryptamine 2A receptor in rat cerebral cortex homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID678714Inhibition of human CYP2C19 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 3-butyryl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID25470Area under curve (AUC) value of Dopamine level after second treatment (24.8 uM/Kg) in dialysates collected from rat striatum2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1281952Displacement of [3H]-Raclopride from human dopamine D2L receptor expressed in HEK293 cells2016European journal of medicinal chemistry, Apr-13, Volume: 112Rational design in search for 5-phenylhydantoin selective 5-HT7R antagonists. Molecular modeling, synthesis and biological evaluation.
AID61415Binding affinity towards Dopamine receptor D2 was determined in rat striatal homogenate using [3H]- spiperone as radioligand1996Journal of medicinal chemistry, Sep-27, Volume: 39, Issue:20
Structure-activity relationships of a series of novel (piperazinylbutyl)thiazolidinone antipsychotic agents related to 3-[4-[4-(6-fluorobenzo[b]thien-3-yl)-1-piperazinyl]butyl]-2,5,5- trimethyl-4-thiazolidinone maleate.
AID25466Area under curve (AUC) value of DOPAC level after first treatment (7.4 uM/Kg) in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
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).
AID298487Displacement of [3H]LSD from human 5HT7 receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID458640Reduction in 3,4-dihydroxyphenylacetic acid level in Sprague-Dawley rat striatum at 10.5 umol/kg, sc relative to saline treated control2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID410332Displacement of [3H]spiperone from dopamine D2 receptor in CRL:CD(SD)BR-COBS rat striatum by scintillation spectrometry2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID251584Relative binding affinity against 5-hydroxytryptamine 2A and dopamine D2 receptors2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
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.
AID1413420Displacement of [3H]-raclopride from human D2L receptor expressed in HEK293 cell membranes after 1 hr by microbeta counting method
AID1570061Displacement of [3H]-5-CT from human 5HT7 receptor expressed in HEK cells incubated for 1 hr by Cheng-Prusoff analysis based microbeta scintillation counting method2019European journal of medicinal chemistry, Oct-15, Volume: 180Synthesis of new 5,6,7,8-tetrahydropyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID36116Binding affinity towards human alpha-1 adrenergic receptor2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID239091Inhibition of [3H]pyrilamine binding to human Histamine H1 receptor 2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID298483Displacement of [3H]LSD from 5HT2B receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1682828Binding affinity to H1 histamine receptor (unknown origin)
AID395324Lipophilicity, log D at pH 7.4 by liquid chromatography2009Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6
Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID1823850Anxiolytic activity in stress-induced anxiety ip dosed Wistar rat model assessed as increase in open arm entry measured after 30 mins by elevated plus maze test
AID342782Binding affinity to human cloned histamine H1 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID1409611AUC (cytotoxicity %) of compound against Vero E6 cells by MTT assay.2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID171544Effect of compound on apomorphine induced catalepsy, from rat brain striatum at 1 umol/kg upon subcutaneous administration; Catalepsy = 0/41998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID395325Lipophilicity, log P by microemulsion electrokinetic chromatography2009Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6
Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID65121Binding affinity towards human dopamine receptor D32001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID678722Covalent binding affinity to human liver microsomes assessed per mg of protein at 10 uM after 60 mins presence of NADPH2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID298479Displacement of [3H]spiperone from human dopamine D3 receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1128459Inhibition of human 5HT1A receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID230095Ratio of pKi of compound towards 5-HT2 receptor to that of D2 receptor1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID247009In vivo effective dose to inhibit apomorphine induced agitation in rats upon subcutaneous administration2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID1125020Displacement of [3H]spiperone from wild-type human dopamine D2S receptor expressed in CHO-K1 cell membrane after 2 hrs by beta counting2014European journal of medicinal chemistry, Apr-22, Volume: 77Novel insights on the structural determinants of clozapine and olanzapine multi-target binding profiles.
AID238940Inhibition of [3H]-SCH- 23390 binding to rat dopamine D1 receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID25474Area under curve (AUC) value of HVA level after total treatment in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID397743Inhibition of human ERG channel2009Journal of medicinal chemistry, Jul-23, Volume: 52, Issue:14
Side chain flexibilities in the human ether-a-go-go related gene potassium channel (hERG) together with matched-pair binding studies suggest a new binding mode for channel blockers.
AID5196Binding affinity towards human 5-HT2A receptor in BEK cells1996Journal of medicinal chemistry, Sep-27, Volume: 39, Issue:20
Structure-activity relationships of a series of novel (piperazinylbutyl)thiazolidinone antipsychotic agents related to 3-[4-[4-(6-fluorobenzo[b]thien-3-yl)-1-piperazinyl]butyl]-2,5,5- trimethyl-4-thiazolidinone maleate.
AID781326pKa (acid-base dissociation constant) as determined by Avdeef ref: DOI: 10.1002/047145026X2014Pharmaceutical research, Apr, Volume: 31, Issue:4
Comparison of the accuracy of experimental and predicted pKa values of basic and acidic compounds.
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.
AID1393480Effect on failure incidence during conditioned avoidance response test in Sprague-Dawley rat at 2 mg/kg, ip administered 60 mins prior to testing
AID25469Area under curve (AUC) value of Dopamine level after first treatment (7.4 uM/Kg) in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
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).
AID238989Inhibition of [3H]rauwolscine binding to Alpha-2A adrenergic receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID65785Binding affinity towards human Dopamine receptor D32004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
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).
AID395329Dissociation constant, pKa by mass spectrometry2009Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6
Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID1217727Intrinsic clearance for reactive metabolites formation per mg of protein in human liver microsomes based on [3H]GSH adduct formation rate at 100 uM by [3H]GSH trapping assay2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID185006Effect of compound on apomorphine induced locomotor hyperactivity (APO-induced LMA), from rat brain striatum at 1 umol/kg upon subcutaneous administration; LMA (locomotor activity)1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID246918In vivo effective dose to inhibit tryptamine-induced bilateral convulsions in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID678716Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using diethoxyfluorescein as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID298478Displacement of [3H]spiperone from human dopamine D2 receptor short form expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1393366Displacement of [3H]-8-OH-DPAT from human 5-HT1AR expressed in HEK293 cell membranes after 1 hr by microbeta counting method
AID1204346Displacement of [3H]N-methylspiperone from dopamine D3 receptor (unknown origin) assessed as total radioligand binding at 1.66 x 10'-7 M incubated for 60 mins by microbeta plate reader based method2015European journal of medicinal chemistry, Jun-05, Volume: 97Structure-activity relationships and molecular studies of novel arylpiperazinylalkyl purine-2,4-diones and purine-2,4,8-triones with antidepressant and anxiolytic-like activity.
AID1393470Therapeutic index, ratio of MED for sedation in ip dosed Sprague-Dawley rat to MED for antipsychotic activity in ip dosed Sprague-Dawley rat assessed as reduction in PCP-induced hyper-locomotion
AID298490Displacement of [3H]pirenzepine from human M1 receptor expressed in CHO cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1677158Binding affinity to human 5HT2A receptor
AID230096Ratio of pKi of compound towards D1 receptor to that of D2 receptor1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID1823849Antipsychotic activity in ip dosed Wistar rat assessed as induction of MK801-induced hyperlocomotor activity by measuring minimum effective dose measured for 15 mins
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.
AID1677155In vivo receptor occupancy at dopamine D1 receptor in sc dosed rat brain by measuring free plasma concentration pretreated for 1 hr in presence of SCH-23390 by LC-MS/MS analysis
AID63345Binding affinity against dopamine receptor D12001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID177692In vivo inhibition of spontaneous locomotory activity tested in rats after oral administration2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID492638Binding affinity to human ERG expressed in HEK293 cells2010Journal of medicinal chemistry, Jun-24, Volume: 53, Issue:12
Discovery of bishomo(hetero)arylpiperazines as novel multifunctional ligands targeting dopamine D(3) and serotonin 5-HT(1A) and 5-HT(2A) receptors.
AID1217712Time dependent inhibition of CYP2C8 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID238747Binding affinity for human 5-hydroxytryptamine 6 receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Medicinal chemistry driven approaches toward novel and selective serotonin 5-HT6 receptor ligands.
AID458645Reduction in spontaneous locomotor activity in Sprague-Dawley rat striatum at 10.5 umol/kg, sc relative to control2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID239069Inhibition of [3H]mesulergine binding to human 5-hydroxytryptamine 2C receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID5199Binding affinity for human 5-hydroxytryptamine 2A receptor2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID374353Cytotoxicity against human WI38 cells assessed as reduction in cellular DNA level preincubated for 2 hrs before viral infection measured after 7 days by real time PCR assay2007Antimicrobial agents and chemotherapy, Dec, Volume: 51, Issue:12
BK Virus replication in vitro: limited effect of drugs interfering with viral uptake and intracellular transport.
AID61527In vitro binding affinity towards Dopamine receptor D1 in rat tissue homogenate using [3H]-SCH- 23390 as radioligand2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID298488Displacement of [3H]BLR-43694 from human 5HT3 receptor expressed in HEK293 cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID539464Solubility of the compound in 0.1 M phosphate buffer at 600 uM at pH 7.4 after 24 hrs by LC/MS/MS analysis2010Bioorganic & medicinal chemistry letters, Dec-15, Volume: 20, Issue:24
Experimental solubility profiling of marketed CNS drugs, exploring solubility limit of CNS discovery candidate.
AID458651Reduction in amphetamine-induced locomotor activity in Sprague-Dawley rat striatum at 10.5 umol/kg, sc relative to control2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID5197Binding affinity towards human serotonin 5-hydroxytryptamine 2A receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
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).
AID715349Toxicity in rat assessed as decrease in lean body mass at 4 mg/kg, po administered for 7 days relative to vehicle-treated control2012Bioorganic & medicinal chemistry letters, Sep-15, Volume: 22, Issue:18
Discovery of tetrahydropyridopyrimidine phosphodiesterase 10A inhibitors for the treatment of schizophrenia.
AID1570060Displacement of [3H]LSD from human 5-HT6 receptor expressed in HEK cells incubated for 1 hr by Cheng-Prusoff analysis based microbeta scintillation counting method2019European journal of medicinal chemistry, Oct-15, Volume: 180Synthesis of new 5,6,7,8-tetrahydropyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID1128469Selectivity ratio of Ki for adrenergic alpha1B receptor (unknown origin) to Ki for human recombinant full length 5HT2A receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID1677161Binding affinity to human dopamine D2 receptor
AID1393367Displacement of [3H]-5-CT from human 5-HT7R expressed in HEK293 cell membranes after 1 hr at 37 degC by microbeta counting method
AID1601983Displacement of [3H]-raclopride from recombinant human D2 receptor expressed in HEK293 cells measured after 1 hr by microbeta scintillation counting analysis2019European journal of medicinal chemistry, Mar-15, Volume: 166Synthesis of novel pyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID715351Toxicity in rat assessed as decrease in weight gain at 4 mg/kg, po administered for 7 days relative to vehicle-treated control2012Bioorganic & medicinal chemistry letters, Sep-15, Volume: 22, Issue:18
Discovery of tetrahydropyridopyrimidine phosphodiesterase 10A inhibitors for the treatment of schizophrenia.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
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).
AID61517Half-maximal inhibition of [3H]-SCH- 23390 binding to Dopamine receptor D1 in rat striatal homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID492642Displacement of [3H]spiperone from dopamine D2 receptor in CRL:CD(SD)BR-COBS rat striatum by scintillation spectrometry2010Journal of medicinal chemistry, Jun-24, Volume: 53, Issue:12
Discovery of bishomo(hetero)arylpiperazines as novel multifunctional ligands targeting dopamine D(3) and serotonin 5-HT(1A) and 5-HT(2A) receptors.
AID678715Inhibition of human CYP2D6 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 4-methylaminoethyl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID246894In vivo effective dose for reversal of RO-4-1284 induced hypothermia in mouse2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID330558Binding affinity to alphaMSH receptor at 100 nM2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID1128466Inhibition of human dopamine D4 receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID1760279Displacement of [3H]-raclopride from human D2L receptor expressed in HEK293 cells measured after 1 hr by microbeta counting method2020European journal of medicinal chemistry, Oct-01, Volume: 203Chlorine substituents and linker topology as factors of 5-HT
AID330539Increase in alpha-2AMPK activity in H1RKO mouse hyphalamic slices2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID65622In vitro binding affinity towards Dopamine receptor D3 in Sf9 cell membranes using [3H]7-OH-DPAT as radioligand2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID25471Area under curve (AUC) value of Dopamine level after total treatment in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID87242Binding affinity towards human histamine H1 receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
AID1169861Binding affinity to dopamine D3 receptor (unknown origin)2014Journal of medicinal chemistry, Nov-26, Volume: 57, Issue:22
Targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors for developing effective antipsychotics: synthesis, biological characterization, and behavioral studies.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID330551Increase in phospho-AMPK level in arcuate hyphalamic nuclei intact H1RKO mouse at 5 mg/kg after 3 hrs by immunohistochemistry2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID410334Displacement of [3H]8OH-DPAT from 5HT1A receptor in CRL:CD(SD)BR-COBS rat hippocampus by scintillation spectrometry2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID1601980Displacement of [3H]-ketanserin from recombinant human 5HT2A receptor expressed in HEK293 cells measured after 1.5 hrs by microbeta scintillation counting analysis2019European journal of medicinal chemistry, Mar-15, Volume: 166Synthesis of novel pyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID246883In vivo effective dose for reversal of tryptamine-induced cyanosis in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
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]
AID1601982Displacement of [3H]-5-CT from recombinant human 5HT7 receptor expressed in HEK293 cells measured after 1 hr by microbeta scintillation counting analysis2019European journal of medicinal chemistry, Mar-15, Volume: 166Synthesis of novel pyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
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]
AID1393471Reversal of PCP-induced cognitive impairment in ip dosed Sprague-Dawley rat assessed as reduction in time spent exploring novel object over familiar object pretreated for 60 mins followed by PCP addition by novel object recognition assay
AID681619TP_TRANSPORTER: ATP hydrolysis in membranes from MDR1-expressing insect cells2002Life sciences, May-31, Volume: 71, Issue:2
In vitro P-glycoprotein affinity for atypical and conventional antipsychotics.
AID1185964Displacement of [3H]N-methylspiperone from human dopamine D3 receptor by liquid scintillation counting2014Bioorganic & medicinal chemistry letters, Sep-01, Volume: 24, Issue:17
Further evaluation of the tropane analogs of haloperidol.
AID1409609Cytotoxicity of compound against Vero E6 cells by MTT assay.2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID25472Area under curve (AUC) value of HVA level after first treatment (7.4 uM/Kg) in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID410335Displacement of [3H]ketanserin from 5HT2A receptor in CRL:CD(SD)BR-COBS rat cortex by scintillation spectrometry2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID114868Effective dose required to antagonize apomorphine-induced climbing in mice after administration of 2.69 mg/kg dose through oral route2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID25473Area under curve (AUC) value of HVA level after second treatment (24.8 uM/Kg) in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1217729Intrinsic clearance for reactive metabolites formation assessed as summation of [3H]GSH adduct formation rate-based reactive metabolites formation and cytochrome P450 (unknown origin) inactivation rate-based reactive metabolites formation2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
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).
AID1677159Drug metabolism in human hepatocyte microsome fraction assessed as GSH conjugate formation by LC-MS/MS analysis
AID342774Binding affinity to human cloned muscarinic M1 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID738352Displacement of [3H]ketanserin from 5-HT2A receptor in human frontal cortex after 30 mins by scintillation counting2013Bioorganic & medicinal chemistry letters, Apr-01, Volume: 23, Issue:7
[11C]olanzapine, radiosynthesis and lipophilicity of a new potential PET 5-HT2 and D2 receptor radioligand.
AID114866Effective dose required to antagonize apomorphine-induced climbing in mice after administration of 0.18 mg/kg dose subcutaneously2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1570062Displacement of [3H]-raclopride from human D2 receptor expressed in HEK cells incubated for 1 hr by Cheng-Prusoff analysis based microbeta scintillation counting method2019European journal of medicinal chemistry, Oct-15, Volume: 180Synthesis of new 5,6,7,8-tetrahydropyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID29813Oral bioavailability in human2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID63866Inhibitory concentration against human Dopamine receptor D4.2 in CHO cells1996Journal of medicinal chemistry, Sep-27, Volume: 39, Issue:20
Structure-activity relationships of a series of novel (piperazinylbutyl)thiazolidinone antipsychotic agents related to 3-[4-[4-(6-fluorobenzo[b]thien-3-yl)-1-piperazinyl]butyl]-2,5,5- trimethyl-4-thiazolidinone maleate.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID386536Inhibition of human ERG potassium channel2008Bioorganic & medicinal chemistry, Apr-01, Volume: 16, Issue:7
A binary QSAR model for classification of hERG potassium channel blockers.
AID238882Inhibition of [3H]ketanserin binding to rat 5-hydroxytryptamine 2A receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID1185963Displacement of [3H]N-methylspiperone from human dopamine D2 receptor by liquid scintillation counting2014Bioorganic & medicinal chemistry letters, Sep-01, Volume: 24, Issue:17
Further evaluation of the tropane analogs of haloperidol.
AID1568825Displacement of [3H]-raclopride from human D2L receptor expressed in human HEK293 cells incubated for 1 hr by radioligand binding assay2019European journal of medicinal chemistry, Sep-15, Volume: 178Synthesis and computer-aided SAR studies for derivatives of phenoxyalkyl-1,3,5-triazine as the new potent ligands for serotonin receptors 5-HT
AID25468Area under curve (AUC) value of DOPAC level after total treatment in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1128460Inhibition of histamine H1 receptor (unknown origin)2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID185007Effect of compound on apomorphine induced locomotor hyperactivity (APO-induced LMA), from rat brain striatum at 10 umol/kg upon subcutaneous administration; LMA (locomotor activity)1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID1128454Displacement of [3H]-N-methylspiperone from rat recombinant dopamine D2 short receptor expressed in CHO cells2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID87529Half-maximal inhibition of [3H]7-OH-DPAT binding to Histamine H1 receptor in rat tissue homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID492640Displacement of [3H]ketanserin from 5HT2A receptor in CRL:CD(SD)BR-COBS rat cortex by scintillation spectrometry2010Journal of medicinal chemistry, Jun-24, Volume: 53, Issue:12
Discovery of bishomo(hetero)arylpiperazines as novel multifunctional ligands targeting dopamine D(3) and serotonin 5-HT(1A) and 5-HT(2A) receptors.
AID61808Binding affinity towards human dopamine-4.2 receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
AID63809Half-maximal inhibition of [3H]spiperone binding to Dopamine receptor D2 in rat striatal homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID87531In vitro binding affinity towards Histamine H1 receptor of rat frontal cortex homogenate by using radioligand [3H]pyrilamine2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID1128455Selectivity ratio of Ki for human recombinant full length 5HT2C receptor to Ki for human recombinant full length 5HT2A receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID232153Ratio of 5-HT2A receptor to that of dopamine 2 (D2) receptor in rat tissue homogenate2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID492643Displacement of [3H]SCH23390 from dopamine D1 receptor in CRL:CD(SD)BR-COBS rat striatum by scintillation spectrometry2010Journal of medicinal chemistry, Jun-24, Volume: 53, Issue:12
Discovery of bishomo(hetero)arylpiperazines as novel multifunctional ligands targeting dopamine D(3) and serotonin 5-HT(1A) and 5-HT(2A) receptors.
AID5090pKi value for 5-hydroxytryptamine 2 receptor binding site1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID1757456Agonist activity at muscarinic M1 receptor (unknown origin) expressed in CHO cells2021Bioorganic & medicinal chemistry letters, 05-15, Volume: 40Identification of 2-fluoro-8-methyl-11-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)-5H-dibenzo[b,e][1,4]diazepine with clozapine-like mixed activities at muscarinic acetylcholine, dopamine, and serotonin receptors.
AID141100Binding affinity towards human muscarinic receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
AID35276Inhibition of [3H]-prazosin binding to Alpha-1 adrenergic receptor in rat frontal cortex homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1570059Displacement of [3H]ketanserin from human 5HT2A receptor expressed in HEK293 cells incubated for 1.5 hrs by Cheng-Prusoff analysis based microbeta scintillation counting method2019European journal of medicinal chemistry, Oct-15, Volume: 180Synthesis of new 5,6,7,8-tetrahydropyrido[1,2-c]pyrimidine derivatives with rigidized tryptamine moiety as potential SSRI and 5-HT
AID63060Binding affinity towards human Dopamine receptor D22004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
AID678721Metabolic stability in human liver microsomes assessed as GSH adduct formation at 100 uM after 90 mins by HPLC-MS analysis2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID114871Effective dose required to induce catalepsy in mice after administration of 21.2 mg/kg dose through oral route2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID1172030Displacement of [3H]-ketanserin from 5-HT2AR in rat cortex2015Bioorganic & medicinal chemistry, Jan-01, Volume: 23, Issue:1
Antidepressant- and anxiolytic-like activity of 7-phenylpiperazinylalkyl-1,3-dimethyl-purine-2,6-dione derivatives with diversified 5-HT₁A receptor functional profile.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID141837Half-maximal inhibition of [3H]QNB binding to Muscarinic acetylcholine receptor M1 in rat frontal cortex homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
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).
AID1393472Antipsychotic activity in ip dosed Sprague-Dawley rat assessed as suppression of avoidance behavior by avoiding foot shock administered 60 mins prior to test by conditioned avoidance response test
AID1126945Displacement of [3H]-LSD from human recombinant 5-HT6 receptor expressed in HEK293 cell membrane after 1 hr by Microbeta scintillation counting analysis2014European journal of medicinal chemistry, May-06, Volume: 78SAR-studies on the importance of aromatic ring topologies in search for selective 5-HT(7) receptor ligands among phenylpiperazine hydantoin derivatives.
AID1393474Toxicity in ip dosed Sprague-Dawley rat assessed as induction of catalepsy measured every 30 mins up to 240 mins by bar test
AID238962Inhibition of [3H]nisoxetine binding to rat Norepinephrine transporter2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID180551The compound was tested in vivo for induction of catalepsy in rat after ip administration1999Journal of medicinal chemistry, Aug-26, Volume: 42, Issue:17
N-Substituted (2,3-dihydro-1,4-benzodioxin-2-yl)methylamine derivatives as D(2) antagonists/5-HT(1A) partial agonists with potential as atypical antipsychotic agents.
AID1128464Inhibition of rat adrenergic alpha1B receptor2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
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.
AID408340Inhibition of human ERG expressed in CHO cells by whole cell patch clamp technique2008Bioorganic & medicinal chemistry, Jun-01, Volume: 16, Issue:11
Support vector machines classification of hERG liabilities based on atom types.
AID715350Toxicity in rat assessed as decrease in total body fat at 4 mg/kg, po administered for 7 days relative to vehicle-treated control2012Bioorganic & medicinal chemistry letters, Sep-15, Volume: 22, Issue:18
Discovery of tetrahydropyridopyrimidine phosphodiesterase 10A inhibitors for the treatment of schizophrenia.
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).
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1217728Intrinsic clearance for reactive metabolites formation per mg of protein based on cytochrome P450 (unknown origin) inactivation rate by TDI assay2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID27167Delta logD (logD6.5 - logD7.4)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1217706Time dependent inhibition of CYP2C9 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID342787Binding affinity to human SERT2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID132467Antagonistic activity against apomorphine induced climbing in the mouse after po administration1999Journal of medicinal chemistry, Aug-26, Volume: 42, Issue:17
N-Substituted (2,3-dihydro-1,4-benzodioxin-2-yl)methylamine derivatives as D(2) antagonists/5-HT(1A) partial agonists with potential as atypical antipsychotic 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).
AID342786Binding affinity to rat NET2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID4782Binding affinity towards serotonin 5-HT2 receptor was determined in rat cortex using [3H]spiperone as ligand1996Journal of medicinal chemistry, Sep-27, Volume: 39, Issue:20
Structure-activity relationships of a series of novel (piperazinylbutyl)thiazolidinone antipsychotic agents related to 3-[4-[4-(6-fluorobenzo[b]thien-3-yl)-1-piperazinyl]butyl]-2,5,5- trimethyl-4-thiazolidinone maleate.
AID36113Binding affinity towards human alpha-1 adrenergic receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
AID37376In vitro binding affinity towards alpha-2 adrenergic receptor in rat frontal cortex homogenate using of [3H]clonidine as radioligand2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID246858In vivo effective dose of compound against 5-MeO-DMT induced head twitches in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID1823834Displacement of [3H]-prazosin from rat cortex membrane alpha1 adrenergic receptor expressed in human recombinant CHO-K1 cells at 1 uM after 30 mins by solid scintillation counting method relative to control
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID458632Displacement of [3H]spiperone from human dopamine D2 receptor at low affinity state expressed in HEK293 cells2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID1353520Displacement of [3H]-raclopride from human D2L receptor expressed in HEK293 cell membranes after 1 hr by Microbeta scintillation counting method2018European journal of medicinal chemistry, Mar-10, Volume: 147Computer-aided insights into receptor-ligand interaction for novel 5-arylhydantoin derivatives as serotonin 5-HT
AID342783Binding affinity to human cloned 5HT1A receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID1595144Displacement of [3H] ketanserin from human recombinant 5-HT2A receptor expressed in CHOK1 cells after 1 hr by microbeta scintillation counting method
AID1393365Displacement of [3H]-LSD from human 5-HT6R expressed in HEK293 cell membranes after 1 hr at 37 degC by microbeta counting method
AID28681Partition coefficient (logD6.5)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1217710Covalent binding in human liver microsomes measured per mg of protein using radiolabelled compound at 10 uM after 1 hr incubation by liquid scintillation counting2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID694796Displacement of [3H]-LSD from human 5-HT6 receptor expressed in HEK293 cells after 1 hr2012European journal of medicinal chemistry, Oct, Volume: 56The multiobjective based design, synthesis and evaluation of the arylsulfonamide/amide derivatives of aryloxyethyl- and arylthioethyl- piperidines and pyrrolidines as a novel class of potent 5-HT₇ receptor antagonists.
AID1393369Selectivity index, ratio of pKi for 5-HT2AR to pKi for human D2LR
AID1682829Binding affinity to adrenergic alpha1 receptor (unknown origin)
AID229410Selectivity ratio (5-HT2A/D2 )2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
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).
AID239052Inhibition of [3H]-spiperone binding to human Dopamine receptor D22005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID330537Increase in phospho-AMPK levels in H1RKO mouse hyphalamic slices at 500 nM after 30 mins by Western blotting2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID1393364Displacement of [3H]-ketanserin from human 5-HT2AR expressed in CHO-K1 cell membranes after 1.5 hrs by microbeta counting method
AID5171Inhibitory concentration against human 5-HT2A receptor in BEK cells1996Journal of medicinal chemistry, Sep-27, Volume: 39, Issue:20
Structure-activity relationships of a series of novel (piperazinylbutyl)thiazolidinone antipsychotic agents related to 3-[4-[4-(6-fluorobenzo[b]thien-3-yl)-1-piperazinyl]butyl]-2,5,5- trimethyl-4-thiazolidinone maleate.
AID246870In vivo effective dose against 5-MeO-DMT-induced head twitches in rats was determined2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID141838In vitro binding affinity towards M1 receptor of rat frontal cortex homogenate by using radioligand [3H]QNB2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID1677163In vivo receptor occupancy at human dopamine D1 receptor in schizophrenia patient brain at 10 mCi, iv by PET scanning
AID330556Binding affinity to leptin receptor at 100 nM2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID114872Effective dose required to induce catalepsy in mice after administration of 6.5 mg/kg dose subcutaneously2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID458635Activity at dopamine D2L receptor expressed in HEK293 cells coexpressing Galphaqi5 assessed as maximal efficacy relative to control2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID330559Binding affinity to neuropeptide Y receptor at 10 nM2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID330538Orexigenic activity in H1RKO mouse2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID1217709Time dependent inhibition of CYP3A4 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID458634Selectivity ratio of Ki for human dopamine D2 receptor at low affinity state to Ki for human dopamine D2 receptor at high affinity state2010Journal of medicinal chemistry, Mar-25, Volume: 53, Issue:6
Synthesis and evaluation of a set of 4-phenylpiperidines and 4-phenylpiperazines as D2 receptor ligands and the discovery of the dopaminergic stabilizer 4-[3-(methylsulfonyl)phenyl]-1-propylpiperidine (huntexil, pridopidine, ACR16).
AID342778Binding affinity to human cloned dopamine D3 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID1677160Selectivity ratio of Ki for human dopamine D1 receptor to human dopamine D2 receptor
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID36197Binding affinity towards human alpha-2 adrenergic receptor2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
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]
AID342773Binding affinity to human cloned 5HT6 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID1128462Inhibition of adrenergic alpha1A receptor (unknown origin)2014Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6
Discovery of a tetracyclic quinoxaline derivative as a potent and orally active multifunctional drug candidate for the treatment of neuropsychiatric and neurological disorders.
AID410331Displacement of [3H]SCH23390 from dopamine D1 receptor in CRL:CD(SD)BR-COBS rat striatum by scintillation spectrometry2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID410333Displacement of [3H]7OH-DPAT from dopamine D3 receptor expressed in Sf9 cells by scintillation spectrometry2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID63070Binding affinity towards human D2 dopamine receptor.2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID1823826Displacement of [3H]-methylspiperone from human D2 receptor transfected in CHO-K1 cells measured after 60 mins by scintillation counting method
AID1430532Binding affinity to 5HT2A receptor (unknown origin)
AID492641Displacement of [3H]8OH-DPAT from 5HT1A receptor in rat CRL:CD(SD)BR-COBS hippocampus by scintillation spectrometry2010Journal of medicinal chemistry, Jun-24, Volume: 53, Issue:12
Discovery of bishomo(hetero)arylpiperazines as novel multifunctional ligands targeting dopamine D(3) and serotonin 5-HT(1A) and 5-HT(2A) receptors.
AID692513Binding affinity to human histamine H1 receptor2011Journal of medicinal chemistry, Jan-13, Volume: 54, Issue:1
Histamine H3 receptor as a drug discovery target.
AID342777Binding affinity to human cloned dopamine D2 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID342779Binding affinity to human cloned dopamine D4 receptor2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Identification of a butyrophenone analog as a potential atypical antipsychotic agent: 4-[4-(4-chlorophenyl)-1,4-diazepan-1-yl]-1-(4-fluorophenyl)butan-1-one.
AID5616Binding affinity towards human 5-hydroxytryptamine 2C receptor2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID694797Binding affinity to human dopamine D2L receptor expressed in HEK293 cells after 1 hr2012European journal of medicinal chemistry, Oct, Volume: 56The multiobjective based design, synthesis and evaluation of the arylsulfonamide/amide derivatives of aryloxyethyl- and arylthioethyl- piperidines and pyrrolidines as a novel class of potent 5-HT₇ receptor antagonists.
AID114864Effective dose required to antagonize 5-MeO-DMT-induced head twitches in mice after administration of 1.45 mg/kg dose orally2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID239150Inhibition of [125I]iodosulpiride binding to human Dopamine receptor D32005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID5560Half-maximal inhibition of [3H]ketanserin binding to 5-hydroxytryptamine 2A receptor in rat cerebral cortex homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID4066Binding affinity towards 5-hydroxytryptamine 1A receptor from rat brain using [3H]-8-OH-DPAT as radioligand1999Journal of medicinal chemistry, Aug-26, Volume: 42, Issue:17
N-Substituted (2,3-dihydro-1,4-benzodioxin-2-yl)methylamine derivatives as D(2) antagonists/5-HT(1A) partial agonists with potential as atypical antipsychotic agents.
AID452390Antagonist activity at 5HT2A receptor2009Bioorganic & medicinal chemistry, Nov-15, Volume: 17, Issue:22
Dual acting norepinephrine reuptake inhibitors and 5-HT(2A) receptor antagonists: Identification, synthesis and activity of novel 4-aminoethyl-3-(phenylsulfonyl)-1H-indoles.
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]
AID678712Inhibition of human CYP1A2 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using ethoxyresorufin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID5569In vitro binding affinity towards 5-hydroxytryptamine 2A receptor in rat tissue homogenate using [3H]ketanserin as radioligand2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID330555Binding affinity to leptin receptor at 10 nM2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID37370Half-maximal inhibition of [3H]clonidine binding to Alpha-2 adrenergic receptor in rat frontal cortex homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID410336Displacement of [3H]mesulergine from 5HT2C receptor in CRL:(HA) BR albino guinea pig cortex by scintillation spectrometry2009Journal of medicinal chemistry, Jan-08, Volume: 52, Issue:1
Discovery of a new class of potential multifunctional atypical antipsychotic agents targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors: design, synthesis, and effects on behavior.
AID694794Displacement of [3H]-5-CT from human 5-HT7b receptor expressed in HEK293 cells after 1 hr2012European journal of medicinal chemistry, Oct, Volume: 56The multiobjective based design, synthesis and evaluation of the arylsulfonamide/amide derivatives of aryloxyethyl- and arylthioethyl- piperidines and pyrrolidines as a novel class of potent 5-HT₇ receptor antagonists.
AID599884Displacement of [3H]5-LSD from human 5HT6 receptor expressed in human HeLa cells2010Bioorganic & medicinal chemistry letters, Sep-15, Volume: 20, Issue:18
Novel 7-phenylsulfanyl-1,2,3,4,10,10a-hexahydro-pyrazino[1,2-a]indoles as dual serotonin 5-HT2C and 5-HT6 receptor ligands.
AID395327Dissociation constant, pKa by capillary electrophoresis2009Journal of medicinal chemistry, Mar-26, Volume: 52, Issue:6
Relationship between brain tissue partitioning and microemulsion retention factors of CNS drugs.
AID298489Displacement of [3H]paraxetine from human 5HT transporter expressed in HEK293 cells2007Journal of medicinal chemistry, Oct-18, Volume: 50, Issue:21
Principal component analysis differentiates the receptor binding profiles of three antipsychotic drug candidates from current antipsychotic drugs.
AID1757457Agonist activity at muscarinic M1 receptor (unknown origin) expressed in CHO cells at 10 uM relative to control2021Bioorganic & medicinal chemistry letters, 05-15, Volume: 40Identification of 2-fluoro-8-methyl-11-(1-methyl-1,2,3,6-tetrahydropyridin-4-yl)-5H-dibenzo[b,e][1,4]diazepine with clozapine-like mixed activities at muscarinic acetylcholine, dopamine, and serotonin receptors.
AID503306Antiproliferative activity against human PC3 cells at 2 uM 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.
AID330560Binding affinity to neuropeptide Y receptor at 100 nM2007Proceedings of the National Academy of Sciences of the United States of America, Feb-27, Volume: 104, Issue:9
From the Cover: Antipsychotic drug-induced weight gain mediated by histamine H1 receptor-linked activation of hypothalamic AMP-kinase.
AID185009Effect of compound on apomorphine induced locomotor hyperactivity (APO-induced LMA), from rat brain striatum at 3 umol/kg upon subcutaneous administration; LMA (locomotor activity) ND = not determined1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID246985Effective dose for antagonistic activity against m-chlorophenyl-piperazine induced anxiety in rats2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID1556425Displacement of [3H]ketanserin from human 5HT2A receptor expressed in CHOK1 cells incubated for 1 hr by liquid scintillation counter method2019European journal of medicinal chemistry, Oct-01, Volume: 1792-Aminoimidazole-based antagonists of the 5-HT
AID239010Inhibition of [125I]R91150 binding to human 5-hydroxytryptamine 2A receptor2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Discovery of new tetracyclic tetrahydrofuran derivatives as potential broad-spectrum psychotropic agents.
AID1677157In vivo receptor occupancy at dopamine D1 receptor in sc dosed rat brain by measuring free plasma concentration pretreated for 1 hr in presence of raclopride by LC-MS/MS analysis
AID1217704Time dependent inhibition of CYP1A2 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1242912Antagonist activity against 5-HT2A receptor (unknown origin) expressed in HEK293 cell membranes assessed as reduction in [35S]-GTPgammaS binding incubated for 30 mins by liquid scintillation counting method2015Bioorganic & medicinal chemistry letters, Sep-15, Volume: 25, Issue:18
Discovery of novel potent and selective ligands for 5-HT2A receptor with quinazoline scaffold.
AID25467Area under curve (AUC) value of DOPAC level after second treatment (24.8 uM/Kg) in dialysates collected from rat striatum.2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID65733In vitro binding affinity towards Dopamine receptor D2 in rat tissue homogenate using [3H]-spiperone as radioligand2004Journal of medicinal chemistry, Jan-01, Volume: 47, Issue:1
Pyrrolo[1,3]benzothiazepine-based serotonin and dopamine receptor antagonists. Molecular modeling, further structure-activity relationship studies, and identification of novel atypical antipsychotic agents.
AID603953In-vivo plasma to lung partition coefficients of the compound, logP(lung) in rat2008European journal of medicinal chemistry, Mar, Volume: 43, Issue:3
Air to lung partition coefficients for volatile organic compounds and blood to lung partition coefficients for volatile organic compounds and drugs.
AID36118Binding affinity towards Alpha-1 adrenergic receptor in human cortex membranes1999Journal of medicinal chemistry, Aug-26, Volume: 42, Issue:17
N-Substituted (2,3-dihydro-1,4-benzodioxin-2-yl)methylamine derivatives as D(2) antagonists/5-HT(1A) partial agonists with potential as atypical antipsychotic agents.
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.
AID1169863Binding affinity to 5HT2A receptor (unknown origin)2014Journal of medicinal chemistry, Nov-26, Volume: 57, Issue:22
Targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors for developing effective antipsychotics: synthesis, biological characterization, and behavioral studies.
AID678717Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-benzyloxyquinoline as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1217711Metabolic activation in human liver microsomes assessed as [3H]GSH adduct formation rate measured per mg of protein at 100 uM by [3H]GSH trapping assay2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID239151Inhibition of [3H]7-OH-DPAT binding to Dopamine D3 receptor expressed in Sf9 cells2005Journal of medicinal chemistry, Mar-24, Volume: 48, Issue:6
Novel atypical antipsychotic agents: rational design, an efficient palladium-catalyzed route, and pharmacological studies.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID492639Displacement of [3H]mesulergine from 5HT2C receptor in CRL:(HA) BR albino guinea pig cortex by scintillation spectrometry2010Journal of medicinal chemistry, Jun-24, Volume: 53, Issue:12
Discovery of bishomo(hetero)arylpiperazines as novel multifunctional ligands targeting dopamine D(3) and serotonin 5-HT(1A) and 5-HT(2A) receptors.
AID1172031Displacement of [3H]LSD from human cloned 5-HT6R expressed in HEK293 cells2015Bioorganic & medicinal chemistry, Jan-01, Volume: 23, Issue:1
Antidepressant- and anxiolytic-like activity of 7-phenylpiperazinylalkyl-1,3-dimethyl-purine-2,6-dione derivatives with diversified 5-HT₁A receptor functional profile.
AID1677156Inhibition of human ERG
AID1520006Displacement of [3H]-LSD from human 5-HT6R expressed in HEK293 cells after 1 hr by microbeta plate reader analysis
AID1393468Antipsychotic activity in ip dosed Sprague-Dawley rat assessed as reduction in PCP-induced hyper-locomotion pretreated for 60 mins followed by PCP addition measured for 30 mins starting 15 min after rat reintroduction to auto-tracks
AID141174Binding affinity towards human M1 receptor.2001Journal of medicinal chemistry, Feb-15, Volume: 44, Issue:4
Current and novel approaches to the drug treatment of schizophrenia.
AID61623Binding affinity to the dopamine receptor D2L in rat brain membranes1999Journal of medicinal chemistry, Aug-26, Volume: 42, Issue:17
N-Substituted (2,3-dihydro-1,4-benzodioxin-2-yl)methylamine derivatives as D(2) antagonists/5-HT(1A) partial agonists with potential as atypical antipsychotic agents.
AID1217708Time dependent inhibition of CYP2D6 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID65767Half-maximal inhibition of [3H]7-OH-DPAT binding to Dopamine receptor D3 in rat tissue homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID36199Binding affinity towards human alpha-2 adrenergic receptor2004Journal of medicinal chemistry, Mar-11, Volume: 47, Issue:6
Selective optimization of side activities: another way for drug discovery.
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.
AID65563Half-maximal inhibition of [3H]spiperone binding to Dopamine receptor D2 in rat striatal homogenate2002Journal of medicinal chemistry, Jan-17, Volume: 45, Issue:2
Pyrrolo[1,3]benzothiazepine-based atypical antipsychotic agents. Synthesis, structure-activity relationship, molecular modeling, and biological studies.
AID63824pKi value for Dopamine receptor D2 binding site1998Journal of medicinal chemistry, Sep-24, Volume: 41, Issue:20
New antipsychotic agents with serotonin and dopamine antagonist properties based on a pyrrolo[2,1-b][1,3]benzothiazepine structure.
AID1823847Anti-antidepressant like activity in Wistar rat assessed as reduction in locomotor activity by measuring total immobility time by Forced swim test
AID1169860Binding affinity to dopamine D2 receptor (unknown origin)2014Journal of medicinal chemistry, Nov-26, Volume: 57, Issue:22
Targeting dopamine D3 and serotonin 5-HT1A and 5-HT2A receptors for developing effective antipsychotics: synthesis, biological characterization, and behavioral studies.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
AID1346603Human 5-ht1e receptor (5-Hydroxytryptamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID624233Agonists at Human 5-Hydroxytryptamine receptor 5-HT1F1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1346893Human 5-HT2C receptor (5-Hydroxytryptamine receptors)2009Journal of psychopharmacology (Oxford, England), Jan, Volume: 23, Issue:1
Asenapine: a novel psychopharmacologic agent with a unique human receptor signature.
AID1345857Rat alpha1A-adrenoceptor (Adrenoceptors)2008Psychopharmacology, Jul, Volume: 199, Issue:1
Orthostatic hypotensive effect of antipsychotic drugs in Wistar rats by in vivo and in vitro studies of alpha1-adrenoceptor function.
AID624223Antagonists at Human 5-Hydroxytryptamine receptor 5-HT2A1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1346037Human H1 receptor (Histamine receptors)2003Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, Mar, Volume: 28, Issue:3
H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs.
AID1345235Rat 5-HT7 receptor (5-Hydroxytryptamine receptors)1996European journal of pharmacology, Dec-19, Volume: 317, Issue:2-3
Iloperidone binding to human and rat dopamine and 5-HT receptors.
AID1345170Human 5-HT6 receptor (5-Hydroxytryptamine receptors)2005Psychopharmacology, May, Volume: 179, Issue:2
Stable expression of constitutively activated mutant h5HT6 and h5HT7 serotonin receptors: inverse agonist activity of antipsychotic drugs.
AID1345615Human 5-HT1A receptor (5-Hydroxytryptamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID624210Agonists at Human 5-Hydroxytryptamine receptor 5-HT1A1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1345235Rat 5-HT7 receptor (5-Hydroxytryptamine receptors)1994The Journal of pharmacology and experimental therapeutics, Mar, Volume: 268, Issue:3
Binding of typical and atypical antipsychotic agents to 5-hydroxytryptamine-6 and 5-hydroxytryptamine-7 receptors.
AID1346893Human 5-HT2C receptor (5-Hydroxytryptamine receptors)2003Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, Mar, Volume: 28, Issue:3
H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs.
AID1346739Human 5-HT1F receptor (5-Hydroxytryptamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1345170Human 5-HT6 receptor (5-Hydroxytryptamine receptors)1996Journal of neurochemistry, Jan, Volume: 66, Issue:1
Cloning, characterization, and chromosomal localization of a human 5-HT6 serotonin receptor.
AID1345291Human 5-HT7 receptor (5-Hydroxytryptamine receptors)1998British journal of pharmacology, Jul, Volume: 124, Issue:6
Functional characterisation of the human cloned 5-HT7 receptor (long form); antagonist profile of SB-258719.
AID1259419Human 5-HT2A receptor (5-Hydroxytryptamine receptors)2003Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, Mar, Volume: 28, Issue:3
H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs.
AID1345788Human D2 receptor (Dopamine receptors)1998Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, Feb, Volume: 18, Issue:2
Do novel antipsychotics have similar pharmacological characteristics? A review of the evidence.
AID624223Antagonists at Human 5-Hydroxytryptamine receptor 5-HT2A2002European journal of pharmacology, Aug-16, Volume: 450, Issue:1
A comparison of the receptor binding and HERG channel affinities for a series of antipsychotic drugs.
AID1345920Rat alpha1D-adrenoceptor (Adrenoceptors)2008Psychopharmacology, Jul, Volume: 199, Issue:1
Orthostatic hypotensive effect of antipsychotic drugs in Wistar rats by in vivo and in vitro studies of alpha1-adrenoceptor function.
AID1345154Rat 5-HT6 receptor (5-Hydroxytryptamine receptors)1994The Journal of pharmacology and experimental therapeutics, Mar, Volume: 268, Issue:3
Binding of typical and atypical antipsychotic agents to 5-hydroxytryptamine-6 and 5-hydroxytryptamine-7 receptors.
AID1346037Human H1 receptor (Histamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1259419Human 5-HT2A receptor (5-Hydroxytryptamine receptors)2002European journal of pharmacology, Aug-16, Volume: 450, Issue:1
A comparison of the receptor binding and HERG channel affinities for a series of antipsychotic drugs.
AID624223Antagonists at Human 5-Hydroxytryptamine receptor 5-HT2A2003Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, Mar, Volume: 28, Issue:3
H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs.
AID624230Agonists at Human 5-Hydroxytryptamine receptor 5-ht1e1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1345615Human 5-HT1A receptor (5-Hydroxytryptamine receptors)1998European journal of pharmacology, Aug-21, Volume: 355, Issue:2-3
Agonist and antagonist actions of antipsychotic agents at 5-HT1A receptors: a [35S]GTPgammaS binding study.
AID1259419Human 5-HT2A receptor (5-Hydroxytryptamine receptors)2009Journal of psychopharmacology (Oxford, England), Jan, Volume: 23, Issue:1
Asenapine: a novel psychopharmacologic agent with a unique human receptor signature.
AID1346528Human 5-HT1D receptor (5-Hydroxytryptamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1346264Human 5-HT1B receptor (5-Hydroxytryptamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1346893Human 5-HT2C receptor (5-Hydroxytryptamine receptors)2000The Journal of pharmacology and experimental therapeutics, Oct, Volume: 295, Issue:1
Inverse agonist activity of atypical antipsychotic drugs at human 5-hydroxytryptamine2C receptors.
AID624210Agonists at Human 5-Hydroxytryptamine receptor 5-HT1A1998European journal of pharmacology, Aug-21, Volume: 355, Issue:2-3
Agonist and antagonist actions of antipsychotic agents at 5-HT1A receptors: a [35S]GTPgammaS binding study.
AID1259419Human 5-HT2A receptor (5-Hydroxytryptamine receptors)1996Psychopharmacology, Mar, Volume: 124, Issue:1-2
Risperidone compared with new and reference antipsychotic drugs: in vitro and in vivo receptor binding.
AID1345154Rat 5-HT6 receptor (5-Hydroxytryptamine receptors)1996European journal of pharmacology, Dec-19, Volume: 317, Issue:2-3
Iloperidone binding to human and rat dopamine and 5-HT receptors.
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.
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.
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.
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.
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.
AID1799301Radioligand Binding Assay (Ki) from Article 10.1016/j.bmc.2009.09.023: \\Dual acting norepinephrine reuptake inhibitors and 5-HT(2A) receptor antagonists: Identification, synthesis and activity of novel 4-aminoethyl-3-(phenylsulfonyl)-1H-indoles.\\2009Bioorganic & medicinal chemistry, Nov-15, Volume: 17, Issue:22
Dual acting norepinephrine reuptake inhibitors and 5-HT(2A) receptor antagonists: Identification, synthesis and activity of novel 4-aminoethyl-3-(phenylsulfonyl)-1H-indoles.
AID1347160Primary screen NINDS Rhodamine 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.
AID1347159Primary screen GU Rhodamine 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.
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.
AID1802951In Vitro Inhibition Assay from Article 10.3109/14756360903489581: \\Effects of some drugs on human erythrocyte glucose 6-phosphate dehydrogenase: an in vitro study.\\2010Journal of enzyme inhibition and medicinal chemistry, Dec, Volume: 25, Issue:6
Effects of some drugs on human erythrocyte glucose 6-phosphate dehydrogenase: an in vitro study.
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).
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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (5,880)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's437 (7.43)18.2507
2000's2795 (47.53)29.6817
2010's2015 (34.27)24.3611
2020's633 (10.77)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials1,340 (21.14%)5.53%
Reviews792 (12.49%)6.00%
Case Studies1,328 (20.95%)4.05%
Observational41 (0.65%)0.25%
Other2,838 (44.77%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (394)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Clinical Trial of Dipyridamole in Schizophrenia[NCT00349973]29 participants (Actual)Interventional2001-05-31Completed
A Randomized, Open-label Study Comparing the Effects of Olanzapine Pamoate Depot With Oral Olanzapine on Treatment Outcomes in Outpatients With Schizophrenia[NCT00320489]Phase 3524 participants (Actual)Interventional2006-04-30Completed
Risperidone Effects On Frontal And Temporal Cortical Function In Schizophrenia Patients Undergoing FMRI Cognitive Task Performance[NCT01234454]34 participants (Actual)Interventional2002-01-31Completed
Efficacy of Olanzapine in Break-through Emesis After Prophylaxis With Dexamethasone, 5-HT3 Receptor Antagonists and Aprepitant Compared to Metoclopramide[NCT01148264]Phase 223 participants (Actual)Interventional2010-07-31Terminated(stopped due to poor enrolment)
Randomized, Placebo-controlled Trial of Olanzapine Versus Aprepitant Plus Ondansetron and Dexamethasone as Antiemetic Prophylaxis in Patients Receiving High Emetic Chemotherapy[NCT03876938]Phase 3147 participants (Anticipated)Interventional2019-03-01Recruiting
A Randomised, Double-Blind, Placebo-Controlled Study to Evaluate the Effect of CORT118335 on Olanzapine-Induced Weight Gain in Healthy Subjects[NCT03877562]Phase 196 participants (Actual)Interventional2019-04-01Completed
A Multicenter, Double-Blind, Flexible-Dose, 6-Month Extension Trial Comparing the Safety and Efficacy of Asenapine With Olanzapine in Subjects Who Completed the Protocol 25543 (NCT 00212836; P05817)[NCT00265343]Phase 3306 participants (Actual)Interventional2005-12-31Completed
A Study Investigating the Relationship Between the Antipsychotic Response and Non-invasive Proxies of Neurochemistry in Schizophrenia[NCT06159322]40 participants (Anticipated)Observational2023-01-01Recruiting
Oral Rapidly Dissolving Olanzapine for Acute Primary Headache in the Emergency Department Setting: A Feasibility Trial[NCT03066622]Phase 4122 participants (Actual)Interventional2016-07-31Completed
Olanzapine With or Without Fosaprepitant for the Prevention of Chemotherapy Induced Nausea and Vomiting (CINV)in Patients Receiving Highly Emetogenic Chemotherapy (HEC): A Phase III Randomized, Double Blind, Placebo-Controlled Trial[NCT03578081]Phase 3690 participants (Actual)Interventional2018-10-15Completed
A Double Blind Pilot Trial to Evaluate Efficacy Trends and Safety of Risperidone and Olanzapine as add-on Therapy to Serotonin Type Antidepressants in Subjects With Treatment Resistant Depression (TRD)[NCT01282632]Phase 1/Phase 242 participants (Actual)Interventional2002-08-31Completed
A Twelve-Month, Prospective, Randomized, Active-Controlled, Open-Label, Flexible-Dose Study of Paliperidone Palmitate Compared With Oral Antipsychotic Treatment in Adults With Schizophrenia Who Have Been Recently Discharged From an Inpatient Psychiatric H[NCT01193166]Phase 40 participants (Actual)Interventional2010-08-31Withdrawn(stopped due to This study was stopped due to an internal reconsideration of priorities of the product portfolio.)
A Double-Blind, 9-Week Extension Study Evaluating the Safety and Maintenance of Effect of Asenapine vs. Olanzapine in the Treatment of Subjects With Acute Mania Clinical Trial Protocol A7501006 (Secondary Title: ARES)[NCT00143182]Phase 3504 participants (Actual)Interventional2005-01-07Completed
Phase1 Randomized, Double-Blind, Placebo/Active-Controlled, SAD, 2-Way, Incomplete Block, 2-Period Crossover, Safety, Tolerability, PK/PD Study of 3 Doses INP105 (Olanzapine Delivered by I231 POD® Device) Nasal Spray in Healthy Volunteers[NCT03624322]Phase 138 participants (Actual)Interventional2018-08-05Completed
A Multicentre, 8-week, Single-arm, Open-label, Pragmatic Trial to Explore Acceptance and Performance of Using a Digital Medicine System With Healthcare Professionals and Adult Subjects With Schizophrenia, Schizoaffective Disorder, or First Episode Psychos[NCT03568500]Phase 444 participants (Actual)Interventional2018-05-21Completed
A Single-Site, Double-Blind, Placebo-Controlled Cross-Over Trial Examining the Safety and Efficacy of Olanzapine Taken Daily for the Prevention of Episodic Migraine.[NCT00203307]3 participants (Actual)Interventional2004-05-31Terminated(stopped due to Study terminated by sponsor)
A Phase 1b, In-Patient Study to Evaluate the Safety, Tolerability, Pharmacodynamics, and Pharmacokinetics of the Co-Administration of Roluperidone and Olanzapine in Adult Subjects With Moderate to Severe Negative Symptoms of Schizophrenia[NCT06107803]Phase 118 participants (Anticipated)Interventional2023-10-13Recruiting
Blood Lactate Levels in Patients Treated With Typical or Atypical Antipsychotics[NCT01139463]60 participants (Actual)Observational2008-06-30Completed
Olanzapine as First Line Treatment for Prevention of Nausea and Vomiting Induced by Chemotherapy of Lung Cancer: a Multicenter, Double-blind and Randomized Trial[NCT03571126]Phase 4156 participants (Anticipated)Interventional2019-05-09Recruiting
Optimization of Treatment and Management of Schizophrenia in Europe[NCT01248195]Phase 4479 participants (Actual)Interventional2011-05-31Completed
Effectiveness of Antipsychotic Combination With Psychosocial Intervention on Outcome of Patients With Schizophrenia:One-Year Follow up.[NCT00654576]Phase 41,400 participants (Anticipated)Interventional2005-02-28Completed
Olanzapine for the Treatment of Chronic Nausea and/or Vomiting, Unrelated to Chemotherapy or Radiation, in Advanced Cancer Patient - A Pilot, Dose-Finding Trial[NCT03137121]Phase 2/Phase 330 participants (Actual)Interventional2017-07-12Completed
A Phase 3 Study to Evaluate Weight Gain of ALKS 3831 Compared to Olanzapine in Adults With Schizophrenia[NCT02694328]Phase 3561 participants (Actual)Interventional2016-03-02Completed
Olanzapine for the Treatment of Chronic Nausea and/or Vomiting, Unrelated to Chemotherapy or Radiation, in Advanced Cancer Patients - A Confirmatory Phase III MNCCTN Trial[NCT05403580]Phase 30 participants (Actual)Interventional2022-06-03Withdrawn(stopped due to Closed due to slow accrual)
A Randomized, Double-Blind, Active- and Placebo-controlled, Parallel-group, Multicenter Study to Evaluate the Efficacy and Safety of Extended-Release Paliperidone as Maintenance Treatment After an Acute Manic or Mixed Episode Associated With Bipolar I Dis[NCT00490971]Phase 3768 participants (Actual)Interventional2006-05-31Completed
Longitudinal Effect of Electroconvulsive Therapy on Schizophrenia and Bipolar Disorder: a MRI Study[NCT03651674]200 participants (Anticipated)Interventional2018-09-20Not yet recruiting
An Observational Drug Utilization Study of SYCREST^® (Asenapine) in the United Kingdom[NCT01498770]42 participants (Actual)Observational2013-04-01Completed
A Pilot Study on Efficacy and Safety of Olanzapine for the Treatment of Nausea and Vomiting in Palliative Cancer Care[NCT03679182]Phase 215 participants (Anticipated)Interventional2018-09-01Recruiting
Interventional, Randomized, Double-blind, Active-controlled Study of the Efficacy of Lu AF35700 in Patients With Early-in-disease or Late-in-disease Treatment-resistant Schizophrenia[NCT03230864]Phase 3119 participants (Actual)Interventional2017-07-20Terminated(stopped due to New data; the study was terminated based on new efficacy data from another study)
Effectiveness of Antipsychotic Drugs to Treat Psychosis Syndrome: an Open Label, Controlled Study[NCT02137616]300 participants (Anticipated)Interventional2012-06-30Recruiting
Olanzapine Augmentation of Buprenorphine-naloxone Treatment in OUD Patients With Comorbid Symptoms of Serious Mental Illness (SMI): A Prospective Open-label Single-arm 9-week Study[NCT05179772]Phase 20 participants (Actual)Interventional2022-07-28Withdrawn(stopped due to NIDA has advised us to terminate this protocol due to the difficulties in finding appropriate subjects.)
A Phase III, Randomized, Placebo-Controlled, Double-Blind Trial Evaluating the Safety and Efficacy of Sublingual Asenapine vs. Olanzapine and Placebo in In-Patients With an Acute Manic Episode Clinical Trial Protocol 7501005 (Secondary Title: ARES)[NCT00159796]Phase 3489 participants (Actual)Interventional2004-12-14Completed
HALO Trial: Haloperidol vs Olanzapine in Hyperactive Delirium in Palliative Care Patients; A Multi-Centre, Randomised-Controlled Trial[NCT04833023]Phase 372 participants (Anticipated)Interventional2022-05-18Recruiting
Olanzapine for the Prevention of Postoperative Nausea and Vomiting After Laparoscopic Surgery in High-risk Patients: A Randomized Controlled Trial[NCT04718727]Phase 1/Phase 2132 participants (Actual)Interventional2021-03-15Completed
Phase IIIb, Multicenter, Single-Arm Open-Label Study, Supporting the Development and the Validation of the MATHYS Scale (Multidimensional Assessment of THYmic States) in a Population of Bipolar Patients Treated With Olanzapine, Either in-Label (Manic and [NCT00259272]Phase 3141 participants (Actual)Interventional2005-11-30Completed
Prospective Observational Investigation of Olanzapine Versus Midazolam for the Treatment of Acute Undifferentiated Agitation in the Emergency Department[NCT03899506]206 participants (Actual)Observational2018-06-18Terminated(stopped due to Investigator Voluntary Pause)
Long-Term Efficacy and Safety Evaluation of Asenapine (10-20 mg/Day) in With Schizophrenia or Schizoaffective Disorder, in a Multicenter Trial Using (10-20 mg/Day) as a Control[NCT00212771]Phase 3440 participants (Actual)Interventional2004-09-30Completed
A Multicenter, Double-Blind, Flexible -Dose, 6-Month Trial Comparing the Efficacy and Safety of Asenapine With Olanzapine in Stable Subjects With Predominant, Persistent Negative Symptoms of Schizophrenia.[NCT00145496]Phase 3468 participants (Actual)Interventional2004-12-31Completed
Comparison of Single-Dose Plasma and Blood Concentrations of Aripiprazole, Olanzapine, Quetiapine, Paliperidone and Risperidone After Capillary and Venous Blood Sample Collection[NCT01607762]Phase 131 participants (Actual)Interventional2012-02-29Completed
Effects of the Serotonin 2A Receptor on Insulin Sensitivity and Secretion: a Double-blind Controlled Comparison of Olanzapine vs. Amisulpride:[NCT01160991]10 participants (Actual)Interventional2004-05-31Completed
A Phase 3, Randomized, Double-Blind, 52-Week Study of OLZ/SAM vs Olanzapine to Evaluate Weight Gain as Assessed by Change in BMI Z-Score in Pediatric Subjects With Schizophrenia or Bipolar I Disorder (ENLIGHTEN-Youth)[NCT05303064]Phase 3220 participants (Anticipated)Interventional2022-06-30Recruiting
A Phase II, Multi-center, Randomized, 4-week, Double-blind, Parallel Group, Placebo and Active-controlled Trial of the Safety and Efficacy of RO4917838 vs. Placebo in Patients With an Acute Exacerbation of Schizophrenia[NCT01234779]Phase 2301 participants (Actual)Interventional2011-02-28Completed
A Randomized, Multi-site, Parallel-group, Rater-blind Study Comparing Response With Aripiprazole Once Monthly and Standard of Care Oral Antipsychotics in Non-adherent Outpatients With Schizophrenia Identified Using the Brief Adherence Rating Scale[NCT02282085]Phase 4200 participants (Anticipated)Interventional2014-12-31Recruiting
The Switch Study - Efficacy of Early Antipsychotic Switch Versus Maintenance in Patients With Schizophrenia Poorly Responding to Two Weeks of Antipsychotic Treatment[NCT01029769]351 participants (Actual)Interventional2009-12-31Completed
A Multi-Center, Inpatient, Phase 2, Double-blind, Placebo-Controlled Dose Ranging Study of LY2140023 in Patients With DSM-IV Schizophrenia[NCT00520923]Phase 2654 participants (Actual)Interventional2007-09-30Completed
Effects of 5-HTR2A, DRD2,and COMT Genes Polymorphisms and Drug Plasma Concentration on Antipsychotic Response to Olanzapine in Treatment of Early-onset Schizophrenia[NCT02435654]Phase 4128 participants (Actual)Interventional2015-08-31Completed
Neuroendocrine, Metabolite Substrates, Clinical Symptoms and Cognitive Function in Schizophrenia[NCT02423096]200 participants (Anticipated)Observational [Patient Registry]2013-12-31Recruiting
[NCT02400866]Phase 258 participants (Anticipated)Interventional2015-05-31Not yet recruiting
The Effects of Antipsychotic Drugs on Brain Metabolism in Healthy Individuals[NCT02536846]Phase 435 participants (Actual)Interventional2017-11-17Completed
Phase II Randomized Trial to Evaluate Efficacy of Olanzapine With Short-acting 5HT3 Inhibitors in Chemotherapy-induced Nausea & Vomiting (CINV) Prophylaxis[NCT03478605]Phase 2130 participants (Anticipated)Interventional2018-05-25Recruiting
Intramuscular Olanzapine Versus Haloperidol or Midazolam for the Management of Acute Agitation in the Emergency Department - a Multicentre Randomised Clinical Trial[NCT02380118]Phase 4167 participants (Actual)Interventional2014-12-31Terminated(stopped due to Primary endpoint reached based on data projection from interim analysis.)
A Placebo-Controlled Double Blind Comparative Study of JNS007ER in Patients With Schizophrenia[NCT00396565]Phase 3394 participants (Actual)Interventional2006-07-31Completed
Effect of Antipsychotics on Central Insulin Action in Relation to Glucose Metabolism and Cognition in Healthy Volunteers[NCT03741478]Phase 164 participants (Anticipated)Interventional2019-10-22Recruiting
A Four-week, Multicentre, Double-blinded, Randomised, Active- and Placebo- Controlled, Parallel-group Trial Investigating Efficacy and Safety of Cannabidiol in Acute, Early-stage Schizophrenic Patients[NCT02088060]Phase 2150 participants (Anticipated)Interventional2014-03-31Active, not recruiting
A Randomised, Double-blind, Parallel-group, Active-controlled, Flexible Dose Study Exploring the Efficacy and Safety of 12 Weeks Treatment With Lu 31-130 in Patients With Schizophrenia[NCT00770744]Phase 293 participants (Actual)Interventional2008-09-30Completed
The Optimization of Antiemetic Regimen for Chemoradiotherapy-induced Nausea and Vomiting (C-RINV) in Locally Advanced Head and Neck Squamous Cell Carcinoma (LA-HNSCCs): A Prospective Phase Ⅱ Trial[NCT05202275]Phase 243 participants (Anticipated)Interventional2020-12-01Recruiting
Efficacy and Dosage of Olanzapine for Chemotherapy-induced Nausea and Vomiting Prophylaxis in Women With Gynecologic Cancers Receiving Carboplatin-based Regimen : a Double-blind, Placebo-controlled, Randomized Crossover Trial[NCT04232423]Phase 390 participants (Actual)Interventional2020-03-01Completed
Open-Label Comparative Study of Risperidone Versus Olanzapine for Mania in Preschool Children 4 to 6 Years of Age With Bipolar Spectrum Disorder[NCT00181935]Phase 440 participants Interventional2001-03-31Completed
Randomized, Placebo Controlled Study of FOND (Fosaprepitant, Ondansetron, Dexamethasone) Versus FOND+O (FOND Plus Olanzapine) for the Prevention of Chemotherapy Induced Nausea and Vomiting in Hematology Patients Receiving Highly Emetogenic Chemotherapy Re[NCT02635984]Phase 3108 participants (Actual)Interventional2015-11-30Completed
A Phase 3 Study to Determine the Antipsychotic Efficacy and Safety of ALKS 3831 in Adult Subjects With Acute Exacerbation of Schizophrenia[NCT02634346]Phase 3403 participants (Actual)Interventional2015-12-31Completed
Olanzapine for the Treatment of Post-Discharge Nausea and Vomiting After Ambulatory Surgery[NCT02755116]Phase 2180 participants (Actual)Interventional2016-04-30Completed
Olanzapine Improves the Chemotherapy Tolerance of Advanced Gastric Cancer: a Prospective Randomized Controlled Phase II Clinical Study[NCT03575637]Phase 2180 participants (Anticipated)Interventional2018-07-31Recruiting
A Long-Term, Open-Label, Multicenter Study of LY2140023 Compared to Atypical Antipsychotic Standard of Care in Patients With DSM-IV-TR Schizophrenia[NCT01129674]Phase 2/Phase 31,210 participants (Anticipated)Interventional2010-06-30Terminated(stopped due to The decision to stop the trial was based on efficacy results in the overall schizophrenia participant population.)
Clinical Comprehensive Intervention on Cognitive Impairment of Schizophrenia Patients With Metabolic Syndrome[NCT04518319]Phase 2120 participants (Anticipated)Interventional2020-10-01Suspended(stopped due to The COVID-19 affects the recruitment of patients.)
Olanzapine for the Prevention of Delayed Nausea and Vomiting in Patients With Gynecologic Cancers Receiving Carboplatin and Paclitaxel-based Chemotherapy and Guideline-directed Prophylactic Anti-emetics[NCT02290470]Phase 281 participants (Anticipated)Interventional2014-04-30Recruiting
Evaluation of the Necessity of Long-term Pharmacological Treatment With Antipsychotics for the Prevention of Relapse in Long-term Stabilized Schizophrenic Patients: a Randomized, Single-blind, Longitudinal Trial[NCT02307396]Phase 421 participants (Actual)Interventional2015-02-01Completed
Clozapine and Olanzapine in the Treatment of Violence in Schizophrenic Patients[NCT01123408]110 participants (Actual)Interventional1999-06-30Completed
A Long-Term, Phase 2, Multicenter, Randomized, Open-Label Comparative Safety Study of LY2140023 Versus Atypical Antipsychotic Standard of Care in Patients With DSM-IV-TR Schizophrenia[NCT00845026]Phase 2261 participants (Actual)Interventional2009-03-31Completed
A Phase IIa, Double-blind, Double-Dummy, Placebo-controlled, Randomized, Parallel-Group Study to Assess the Efficacy, Safety, Tolerability, and Pharmacokinetics of AZD2624 in Adult Schizophrenia Patients[NCT00686998]Phase 2106 participants (Actual)Interventional2008-05-31Completed
The Characteristics of Treatment Resistant Schizophrenia From the Illness Onset[NCT06128408]300 participants (Anticipated)Observational2023-12-01Not yet recruiting
A Prospective, Matched-Control, Randomized, Open-Label, Flexible-Dose, Study in Subjects With Recent-Onset Schizophrenia or Schizophreniform Disorder to Compare Disease Progression and Disease Modification Following Treatment With Paliperidone Palmitate L[NCT02431702]Phase 3337 participants (Actual)Interventional2015-07-08Completed
Pre-operative Olanzapine as Prophylactic Antiemetic in Oncologic Patients[NCT03631004]Phase 2/Phase 3100 participants (Actual)Interventional2018-10-01Completed
[NCT01149577]Phase 425 participants (Actual)Interventional2007-08-31Completed
Clozapine Versus Olanzapine as Treatment for Comorbid Psychotic Disorder and Substance Use Disorder[NCT03857581]Phase 4100 participants (Anticipated)Interventional2020-07-31Not yet recruiting
Evaluation of the Efficacy and Safety of Olanzapine as an Adjunctive Treatment for Anorexia Nervosa in Children and Adolescents: An Open-label Trial[NCT01184443]Phase 338 participants (Actual)Interventional2010-08-31Terminated(stopped due to Poor recruitment)
Clinical Effectiveness Of The Newer Antipsychotic Compounds Olanzapine, Quetiapine And Aripiprazole In Comparison With Low Dose Conventional Antipsychotics (Haloperidol And Flupentixol) In Patients With Schizophrenia[NCT01164059]Phase 4149 participants (Actual)Interventional2010-02-28Completed
Effect of Atypical Antipsychotics on Gene Expression in Soft Tissues of Healthy Subjects - A Placebo Controlled Randomised Pilot Study[NCT01185743]Phase 416 participants (Actual)Interventional2010-07-31Completed
Efficacy of Olanzapine Monotherapy for Treatment Bipolar Ⅰ Depression: a Randomized, Double-blind, Placebo Controlled Study[NCT01303601]Phase 468 participants (Actual)Interventional2009-01-31Completed
Continuation Electroconvulsive Therapy Associated With Pharmacotherapy Versus Pharmacotherapy Alone for Relapse Prevention in Major Depression. A Clinical, Controlled, Prospective and Randomized Trial[NCT01305707]Phase 4104 participants (Actual)Interventional2009-07-31Terminated(stopped due to Difficulties in recruiting)
Identification of Multi-modal Bio-markers for Early Diagnosis and Treatment Prediction in Schizophrenia Individuals[NCT03790085]Early Phase 12,700 participants (Anticipated)Interventional2018-09-01Recruiting
Proposal To Develop A Rapid And Cost-Effective Diagnostic Test For Schizophrenia[NCT03781115]Phase 124 participants (Anticipated)Interventional2017-11-20Recruiting
A Multicenter, Randomized, Double-blind, Parallel-controlled Injection of Olanzapine in the Treatment of Acute Agitation Associated With Schizophrenia and Bipolar I Disorder.[NCT05803642]Phase 3318 participants (Anticipated)Interventional2023-03-28Not yet recruiting
Analgesic Effect of Olanzapine in Cancer Pain: A Double-Blind Randomized Placebo-Controlled Parallel Group Pilot Study[NCT00737191]0 participants (Actual)Interventional2008-08-31Withdrawn(stopped due to No accrual; No patients enrolled)
Single-Dose Fasting In Vivo Bioequivalence Study of Olanzapine Tablets (5 mg; Mylan) and Zyprexa® Tablets (5 mg; Eli Lilly) in Healthy Volunteers[NCT00648921]Phase 130 participants (Actual)Interventional2003-06-30Completed
Comparison of Olanzapine and Lamotrigine in the Prevention of Recurrence of Depressive Episode in the Patients With Bipolar Disorders[NCT01864551]Phase 460 participants (Actual)Interventional2008-08-31Completed
A Study to Assess the Long-Term Efficacy and Safety of Olanzapine and Fluoxetine Combination Versus Fluoxetine Only in the Relapse Prevention of Stabilized Patients With Treatment-Resistant Depression[NCT00958568]Phase 3892 participants (Actual)Interventional2009-08-31Completed
An Exploratory Cognition Study Conducted as an add-on to Clinical Trial 11286, to Evaluate the Neurocognitive Effects of 12 Weeks Treatment With Sertindole and Olanzapine in Patients With Schizophrenia[NCT00759421]Phase 396 participants (Actual)Interventional2006-10-31Completed
Orally-Disintegrating vs. Regular Olanzapine Tablets: Effects on Weight and GI Hormones[NCT00384332]Phase 420 participants (Actual)Interventional2007-01-31Completed
Assessment of the Inter-patient Variability in Clinical Response and Correlated Genetic Variations in Substance Use Disorders[NCT05833399]200 participants (Anticipated)Observational2022-11-28Recruiting
Proof-of-Concept Trial of Palonosetron and Olanzapine Without Dexamethasone for the Prevention of Chemotherapy-Induced Nausea and Vomiting[NCT02970643]48 participants (Anticipated)Interventional2016-07-31Enrolling by invitation
Study to Assess the Efficacy and Safety of Olanzapine and Fluoxetine Combination Versus Placebo in Patients Ages 10-17 in the Treatment of Major Depressive Episodes Associated With Bipolar I Disorder[NCT00844857]Phase 4291 participants (Actual)Interventional2009-04-30Completed
A Randomized Comparison of the Acute Effects of Olanzapine and Ziprasidone on Whole Body Insulin Sensitivity in Healthy Volunteers[NCT00910988]46 participants (Actual)Interventional2009-02-28Completed
Effectiveness of 6 Antipsychotic Drugs in the Treatment of Acute Exacerbations of Chronic Inpatients With Schizophrenia: a Randomized Double-blind Study[NCT02192723]550 participants (Actual)Interventional2012-06-30Completed
Addition of Olanzapine to Standard CINV Prophylaxis in Hematopoietic Stem Cell Transplant[NCT04535141]Phase 391 participants (Actual)Interventional2020-08-18Completed
A Multicenter, Randomized, Double-Blind, Flexible-Dose, 6-Week Trial of the Efficacy and Safety of Asenapine Compared With Placebo Using Olanzapine Positive Control in Subjects With an Acute Exacerbation of Schizophrenia[NCT00151424]Phase 3277 participants (Actual)Interventional2005-02-15Completed
The Efficacy of Steroid-Sparing Anti-Emetic Therapy in Patients Treated With High or Moderate Emetogenic Chemotherapy; Single Center Non-Inferiority Open Label Randomized Controlled Trial[NCT05590923]Phase 4104 participants (Anticipated)Interventional2022-12-07Recruiting
A Multi-center, Randomized, Double Blind, Parallel, PhaseⅣ Trial to Evaluate the Efficacy and Safety of A-prexa Compared to Zyprexa in Patients With Schizophrenia, Schizophreniform Disorder and Schizoaffective Disorder[NCT02137993]Phase 464 participants (Actual)Interventional2012-03-31Completed
Cannabidiol as a Different Type of an Antipsychotic: Drug Delivery and Interaction Study With Approved Antipsychotics in Vivo[NCT02051387]Phase 174 participants (Actual)Interventional2013-01-31Completed
The Effect of Short Term Atypical Antipsychotic Administration Compared to Placebo on Hepatic Insulin Extraction and Muscarinic Mediation of B-Cell Function: A Small Mechanistic, Single-Site Study[NCT02447835]Phase 115 participants (Actual)Interventional2012-08-31Completed
Open-Label Pharmacokinetic Study to Evaluate the Steady-State Venous and Capillary Plasma Concentrations of Five Antipsychotics: Aripiprazole, Olanzapine, Paliperidone, Quetiapine and Risperidone[NCT02087579]Phase 1305 participants (Actual)Interventional2014-02-28Completed
A Double-Blind, Randomized, Multiple Dose Study of Weight Associated Parameters: SEP-363856 vs Prior Antipsychotic (PA) Standard of Care in Subjects With Schizophrenia Suffering From Metabolic Dysregulation[NCT05542264]Phase 160 participants (Anticipated)Interventional2022-11-15Recruiting
Molecular Mechanisms of Antipsychotic-induced Insulin Resistance in Healthy Volunteers[NCT02708394]Early Phase 131 participants (Actual)Interventional2017-02-01Completed
The Effectiveness of Supplementing Supported Employment With Behavioral Skills Training[NCT00183625]Phase 4107 participants (Actual)Interventional2000-06-30Completed
Interventions to Test the Alpha7 Nicotinic Receptor Model in Schizophrenia[NCT00509067]Phase 243 participants (Actual)Interventional2007-11-30Completed
A Randomized, Double-Blind, Placebo- and Active-Controlled, Parallel-Group Study to Evaluate the Efficacy and Safety of 3 Fixed Doses of JNJ-37822681 Administered Twice Daily in Subjects With Schizophrenia[NCT00728195]Phase 2498 participants (Actual)Interventional2008-11-30Completed
Metabolic Effects of Olanzapine in Patients With Newly Diagnosed Psychosis[NCT00446992]Phase 1/Phase 230 participants (Actual)Interventional2006-04-30Completed
A Randomized Controlled Trial to Evaluate the Effectiveness of Clozapine Versus Olanzapine, Quetiapine or Risperidone in Treatment Resistant Bipolar Disorder[NCT02562287]Phase 454 participants (Anticipated)Interventional2015-10-31Recruiting
A Multicenter, Randomized, Parallel-Group, Double-blind, Fixed-Dose, 28-Day Trial to Assess the Efficacy and Safety of SCH 900435 Compared With Placebo, Using Olanzapine as an Active Control in Subjects With an Acute Exacerbation of Schizophrenia (GUEST -[NCT00988728]Phase 20 participants (Actual)Interventional2011-02-28Withdrawn
A Randomized, Double Blind, Placebo and Active Controlled Parallel Group Study to Evaluate the Efficacy and Safety of Risperidone Long-acting Injectable (LAI) for the Prevention of Mood Episodes in the Treatment of Subjects With Bipolar I Disorder[NCT00391222]Phase 3585 participants (Actual)Interventional2006-11-30Completed
Efficacy and Safety of Olanzapine in the Extended Treatment for Manic or Mixed Episode of Bipolar I Disorder[NCT00266630]Phase 3139 participants (Actual)Interventional2005-11-30Completed
Tardive Dyskinesia and Cognitive Function[NCT00926965]Phase 480 participants (Actual)Interventional2003-01-31Completed
Assessment of Lipid Response to Acute Olanzapine in Healthy Adults[NCT04181385]Phase 2/Phase 315 participants (Anticipated)Interventional2019-01-01Recruiting
A Randomized, Double-blind, Comparison of the Efficacy and Safety of Olanzapine Versus Low-dose Olanzapine Plus Low-dose Trifluoperazine in the Treatment of Schizophrenia[NCT02704962]Phase 494 participants (Actual)Interventional2012-01-31Completed
A Comparison of the Effects of Modafinil on Olanzapine Associated Eating Behaviors in Normal Human Subjects[NCT00636896]50 participants (Actual)Interventional2006-07-31Completed
Neuroleptic and Huntington Disease. Comparison of : Olanzapine, la Tetrabenazine and Tiapride. A Multicentric, Randomised, Controlled Study.[NCT00632645]Phase 3180 participants (Actual)Interventional2009-04-30Completed
A Randomized Controlled Trial of Risperidone and Olanzapine for the Schizophrenic Patients With Neuroleptic-Induced Tardive Dyskinesia[NCT00621998]Phase 460 participants (Actual)Interventional2000-07-31Completed
Single-Dose Fasting In Vivo Bioequivalence Study of Olanzapine Tablets (20 mg; Mylan) and Zyprexa® Tablets (20 mg; Eli Lilly) in Healthy Volunteers[NCT00647972]Phase 132 participants (Actual)Interventional2003-05-31Terminated(stopped due to during Period 1 due to numerous orthostatic AEs that occurred. Subsequently, RLD was reduced to 5 mg due to safety concerns.)
An International, Multicenter, Large Simple Trial (LST) To Compare The Cardiovascular Safety Of Ziprasidone And Olanzapine[NCT00418171]Phase 418,239 participants (Actual)Interventional2002-02-28Completed
An Oral, Rising Single-Dose Tolerance, Pharmacokinetic, and Pharmacodynamic Study of Pf-00184562 Capsules In Healthy Volunteers[NCT00150215]Phase 118 participants Interventional2005-07-31Completed
Efficacy and Safety of Olanzapine in the Treatment of Patients With Bipolar I Disorder, Depressed: A Randomized, Double-Blind Comparison With Placebo[NCT00510146]Phase 3514 participants (Actual)Interventional2007-08-31Completed
The Assessment of the Safety, Efficacy, and Practicality of an Algorithm Including Amantadine, Metformin and Zonisamide for the Prevention of Olanzapine-Associated Weight Gain in Outpatients With Schizophrenia[NCT00401973]Phase 3199 participants (Actual)Interventional2006-11-30Completed
Therapeutic Drug Monitoring (TDM) in Child & Adolescent Psychiatry[NCT01057329]200 participants (Actual)Observational2010-01-31Completed
Early Predictors of Poor Treatment Response in Patients With Schizophrenia Treated With Atypical Antipsychotics[NCT03730857]Phase 1111 participants (Actual)Interventional2008-01-31Completed
A Phase 2a, Randomized, Double-Blind, Placebo-Controlled, Parallel-group Study to Assess the Safety and Efficacy of ASP4345 as Add-on Treatment for Cognitive Impairment in Subjects With Schizophrenia on Stable Doses of Antipsychotic Medication[NCT03557931]Phase 2233 participants (Actual)Interventional2018-07-13Completed
A Placebo-Controlled, Double-Blind Confirmatory Study of Rapid-Acting Intramuscular Olanzapine in Agitated Patients With Schizophrenia[NCT00640510]Phase 334 participants (Actual)Interventional2008-03-31Completed
Phase III Randomized Control Trial Investigating Olanzapine for the Prevention of Chemotherapy Induced Nausea and Vomiting in Patients With Gynecologic Malignancies Receiving Every 3-week Carboplatin and Paclitaxel Chemotherapy[NCT04503668]Phase 3170 participants (Anticipated)Interventional2020-12-28Recruiting
Single-Dose Food In Vivo Bioequivalence Study of Olanzapine Tablets (5 mg; Mylan) and Zyprexa® Tablets (5 mg; Eli Lilly) in Healthy Volunteers[NCT00647777]Phase 132 participants (Actual)Interventional2003-06-30Completed
Antipsychotic Polypharmacy in Schizophrenia[NCT00493233]100 participants (Anticipated)Interventional2006-11-30Completed
Joining Forces: Integrating Psychotropic Medication Into the Care of People With Mental Disorders in a Prayer Camp in Ghana[NCT02593734]Phase 4139 participants (Actual)Interventional2013-07-31Completed
An Exploratory Study Conducted as an add-on to Clinical Trial 11286, to Evaluate the Metabolic Effect of up to 12 Weeks Treatment With Sertindole and Olanzapine in Patients With Schizophrenia[NCT00759460]Phase 3250 participants (Actual)Interventional2007-03-31Completed
A Phase IIa, Randomized, Multicenter, Double-Blind, Active Comparator- and Placebo-Controlled, Clinical Trial to Study the Safety and Efficacy of MK8998 in Acutely Psychotic Patients With Schizophrenia[NCT00827918]Phase 2216 participants (Actual)Interventional2009-03-31Completed
Atypical Antipsychotics and Hyperglycemic Emergencies: Multicentre, Retrospective Cohort Study of Administrative Data[NCT02582736]725,489 participants (Actual)Observational2012-04-30Completed
Aprepitant- and Olanzapine- Containing Regimens for Prevention of Acute and Delayed Nausea and Vomiting Associated With High Dose Melphalan and BEAM in Autologous Stem Cell Transplant Patients[NCT02939287]Phase 3429 participants (Actual)Interventional2017-09-23Completed
A Randomized Open Label Study on the Efficacy, Tolerability, and Total Costs of Olanzapine Versus Conventional Antipsychotics in the Treatment of Acute Mania in Sweden[NCT00767715]Phase 411 participants (Actual)Interventional2004-10-31Terminated(stopped due to Trial discontinued due to low enrollment)
A Double-Blind Confirmatory Study Comparing Rapid-Acting Intramuscular Olanzapine and Rapid-Acting Intramuscular Placebo in Patients With an Exacerbation of Schizophrenia With Acute Psychotic Agitation[NCT00970281]Phase 391 participants (Actual)Interventional2009-09-30Completed
Metabolic Effects of Subchronic Dopamine D2 Receptor Blockade by Antipsychotic Drugs in Healthy Humans[NCT00625170]11 participants (Actual)Interventional2004-05-31Completed
Efficacy of Olanzapine, Netupitant and Palonosetron in Controlling Nausea and Vomiting Associated With Highly Emetogenic Chemotherapy in Patients With Breast Cancer[NCT04669132]Phase 250 participants (Actual)Interventional2020-12-17Completed
A Multicenter, Double-Blind, Randomized, Comparative Study of Aripiprazole and Olanzapine in the Treatment of Patients With Acute Schizophrenia[NCT00712686]Phase 3690 participants (Actual)Interventional2000-06-30Completed
Randomized, Placebo-controlled Parallel Group Study for the Evaluation of an Oral Dose of 10mg Olanzapine in Combination With Riluzole for the Treatment of Loss of Appetite in Patients With Amyotrophic Lateral Sclerosis (ALS)[NCT00876772]Phase 2/Phase 340 participants (Anticipated)Interventional2011-03-31Recruiting
A Multicenter, Double-Blind, Flexible -Dose, 6-Month Trial Comparing the Efficacy Safety of Asenapine With Olanzapine in Stable Subjects With Predominant, Persistent Negative Symptoms of Schizophrenia[NCT00212836]Phase 3481 participants (Actual)Interventional2005-04-21Completed
A Fifteen-month, Prospective, Randomized, Active-controlled, Open-label, Flexible Dose Study of Paliperidone Palmitate Compared With Oral Antipsychotic Treatment in Delaying Time to Treatment Failure in Adults With Schizophrenia Who Have Been Incarcerated[NCT01157351]Phase 4450 participants (Actual)Interventional2010-05-31Completed
Ondansetron With Olanzapine for the Treatment of Alcohol Dependence: A Preliminary Clinical Trial[NCT00678457]Phase 240 participants (Actual)Interventional2007-01-31Completed
A Randomised, Double-blind, Parallel-group, Flexible-dose Trial Evaluating the Efficacy and Safety of 12 Weeks of Treatment With Sertindole or Olanzapine in Patients With Schizophrenia in Asia[NCT00864045]Phase 3394 participants (Actual)Interventional2007-03-31Completed
Using a Visual Decision Aid (DA) to Facilitate Shared Decision Making (SDM) During Antipsychotic Treatment in Schizophrenia.[NCT01420575]8 participants (Actual)Interventional2010-10-31Terminated(stopped due to Low enrollment rate.)
FORESIGHT: Feasibility of Olanzapine at REduced doSe in hIGHly Emetogenic chemoTherapy: a Randomised Controlled Trial Against Aprepitant in Triple Therapy[NCT04075955]Phase 330 participants (Actual)Interventional2019-04-29Completed
GiSAS Trial: Aripiprazole, Olanzapine, and Haloperidol in the Long Term Treatment of Schizophrenia.[NCT01052389]Phase 4300 participants (Actual)Interventional2007-07-31Completed
A Double-Blind, Randomized Study Comparing Intramuscular Olanzapine Depot With Placebo in the Treatment of Patients With Schizophrenia[NCT00088478]Phase 3402 participants (Actual)Interventional2004-06-30Completed
A Double-Blind, Randomized, Placebo-Controlled Study of Perioperative Administration of Olanzapine to Prevent Postoperative Delirium in Joint Replacement Patients[NCT00699946]495 participants (Actual)Interventional2005-01-31Completed
Use, Effects and Side-effects of Second-generation Antipsychotics in a Naturalistic Setting.[NCT00932529]Phase 4226 participants (Actual)Interventional2003-02-28Completed
Atypical Antipsychotic Medication for Outpatients With Anorexia Nervosa[NCT00685334]Phase 422 participants (Actual)Interventional2003-11-30Completed
Sequenced Atypical Antipsychotics Therapy With Intensive or Basic Psychosocial Intervention for First-episode Schizophrenia: An Effectiveness Study[NCT01057849]600 participants (Anticipated)Interventional2008-09-30Recruiting
A Phase III, Double-Blind, Randomized, Active-Controlled, Two-Armed, Multicenter, Efficacy and Safety Assessment (ACTAMESA) of Org 5222 and Olanzapine in the Treatment of Patients With Schizophrenia or Schizoaffective Disorder[NCT00212784]Phase 31,225 participants (Actual)Interventional2003-09-04Completed
A New Pharmacotherapy for Alcohol Dependence: Olanzapine[NCT00746785]Phase 3304 participants (Actual)Interventional2002-09-30Completed
D-serine Antipsychotic Monotherapy for Treatment Refractory Schizophrenia[NCT00816894]Phase 218 participants (Actual)Interventional2009-01-31Completed
A 12-Month Randomized, Open-Label Study of Caregiver Psycho-education and Skills Training in Patients Recently Diagnosed With Schizophrenia, Schizoaffective Disorder, or Schizophreniform Disorder and Receiving Paliperidone Palmitate or Oral Antipsychotic [NCT02600741]296 participants (Actual)Observational2015-07-24Completed
An Exploratory Analysis of Immune and Inflammatory Response Associated With Clozapine Versus Non-Clozapine Antipsychotics in Individuals With Treatment-resistant Schizophrenia[NCT05741502]Phase 460 participants (Anticipated)Interventional2023-08-16Recruiting
Phase 4 Study of Efficacy and Safety of Tandospirone Combined With Atypical Antipsychotic Drugs to Improve Cognitive Function in Schizophrenia[NCT02040883]Phase 4100 participants (Anticipated)Interventional2014-02-28Not yet recruiting
Phase II Study of Rolapitant Plus Olanzapine, Palonosetron, and Dexamethasone in Patients With Germ Cell Tumors Undergoing 5-day Cisplatin-based Chemotherapy.[NCT03960151]Phase 20 participants (Actual)Interventional2018-05-31Withdrawn(stopped due to Compound was sold by funder and development ceased.)
The Effect of FOsamprenavir/Ritonavir on the Pharmacokinetics of a Single-dose of the Antipsychotic Agent olanZApine (FORZA)[NCT00977301]Phase 124 participants (Anticipated)Interventional2009-11-30Completed
An Investigation of the Sleep Architecture and Consequent Cognitive Changes in Olanzapine-Treated Depressed Patients[NCT00520507]Phase 427 participants (Actual)Interventional2007-10-31Completed
Clozapine vs. Olanzapine: An Effectiveness Study[NCT00169065]Phase 438 participants (Actual)Interventional1998-08-31Completed
A Multicentre Double-blinded Randomized Head-to-head Study[NCT00885690]11 participants (Actual)Interventional2009-04-30Terminated(stopped due to Due to recruitment problems)
[NCT00182013]Phase 4106 participants (Actual)Interventional2001-06-30Completed
A One-Year Multi-Centre Randomized, Double Blind, Controlled Effectiveness Study of Quetiapine and Olanzapine, Comparing Their Relative Potential in Improving Neuro-Cognitive Deficits, Functional Outcomes and Quality of Life in Schizophrenia[NCT00182442]Phase 480 participants Interventional2003-10-31Completed
Developmental Pharmacokinetics of Psychotropic Drugs: Olanzapine[NCT00183612]68 participants Interventional2000-05-31Terminated
Modulation of Regional Brain Activation in Schizophrenic Patients by Pharmacological Therapy With Amisulpride, Olanzapine or Haloperidol. A Study With Functional Magnetic Resonance Imaging (fMRI) and Diffusion Tensor Imaging (DTI)[NCT00419653]Phase 419 participants (Actual)Interventional2003-01-31Terminated(stopped due to Recruitment issues)
The Metabolic Syndrome in Patients With Schizophrenia[NCT00338949]Phase 477 participants (Actual)Interventional2006-06-30Completed
A Double-Blind Placebo Controlled Trial of Divalproex and Olanzapine in Bipolar I Disorder, Mixed Episode[NCT00402324]Phase 4202 participants (Actual)Interventional2006-12-31Completed
Brain Correlates of Olanzapine Treatment Response in BPD[NCT00275301]19 participants (Actual)Interventional2005-12-31Completed
Placebo- and Haloperidol-Controlled Double-Blind Trial of Olanzapine in Patients With Manic or Mixed Episode of Bipolar I Disorder[NCT00129220]Phase 3224 participants (Actual)Interventional2005-07-31Completed
Predicting Response to Risperidone Treatment Through Identification of Early-onset of Antipsychotic Drug Action in Schizophrenia.[NCT00337662]Phase 4628 participants (Actual)Interventional2006-05-31Completed
A 16-Week, Multicenter, Randomized, Open-label Study to Assess the Effects of Aripiprazole Versus Other Atypical Antipsychotics in the Treatment of Schizophrenic Patients With Metabolic Syndrome[NCT00508157]Phase 4125 participants (Actual)Interventional2007-11-30Terminated(stopped due to Slow Accrual)
A Multicenter, Randomized, Double-Blind, Parallel Group Study, Comparing The Efficacy And Tolerability Of Ziprasidone (Zeldox, Geodon) vs. Olanzapine (Zyprexa) In The Treatment And Maintenance Of Response In Patients With Acute Mania[NCT00329108]Phase 429 participants (Actual)Interventional2006-11-30Terminated(stopped due to Please see Brief Summary for Termination Reason.)
BMI Evaluation: Placebo and Active Comparator Trial of Olanzapine Zydis Pills Used Sublingually (PLATYPUS)[NCT00303602]Phase 4149 participants (Actual)Interventional2006-03-31Completed
A Comparative Study of New Medications for Psychosis in Adolescents[NCT00222495]30 participants Interventional2002-08-31Completed
Comparative Efficacy and Acceptability of Lithium, Valproate, Oxcarbazepine, Quetiapine, Olanzapine, and Ziprasidone in Bipolar I Disorder, Manic or Mixed Phase[NCT01893229]Phase 4120 participants (Anticipated)Interventional2013-09-30Recruiting
Efficacy of High Dose Olanzapine in a Controlled Fixed Dose-Response Trial for the Treatment of Schizophrenia and Schizoaffective Disorder[NCT00100776]Phase 4600 participants Interventional2003-09-30Completed
Olanzapine Versus Active Comparator in the Treatment of Bipolar I Disorder, Manic or Mixed[NCT00034580]Phase 4326 participants Interventional2001-08-31Completed
The Study of Olanzapine Plus Fluoxetine in Combination for Treatment-Resistant Depression Without Psychotic Features[NCT00035321]Phase 3600 participants Interventional2002-04-30Completed
Reduction of Body Weight in Olanzapine Treated Schizophrenia Patients by Adjunctive Supplementation of Antioxidants (Vitamins E + C) Plus Omega-3 Fatty Acids[NCT00211562]Phase 320 participants (Actual)Interventional2005-10-31Terminated
Ziprasidone Versus Olanzapine In The Treatment Of Schizophrenia: A Six Months, Double Blind Randomized, Parallel Group Study.[NCT00239109]Phase 4112 participants Interventional2003-04-30Completed
Atypical Antipsychotics for Continuation and Maintenance Treatment After an Acute Manic Episode[NCT01977300]Phase 3159 participants (Actual)Interventional2003-01-31Completed
Lack of Efficacy of Psychological and Pharmacological Treatments of Eating Disorders: Neurobiological Background[NCT01990755]112 participants (Actual)Interventional2010-05-31Completed
An Open Label, Randomised, 2-Period, 2-Treatment, 2-Sequence, Crossover, Single-Dose Bioequivalence Study of Olanzapine Orally Disintegrating 5mg Tablets (Test Formulation; Torrent Pharmaceuticals Ltd., India) Versus Zyprexa® Zydis® 5 mg Tablets (Referenc[NCT01996488]Phase 10 participants InterventionalCompleted
An Open Label, Randomised, 2-Period, 2-Treatment, 2-Sequence, Crossover, Single-Dose Bioequivalence Study of Olanzapine Orally Disintegrating 5mg Tablets (Test Formulation; Torrent Pharmaceuticals Ltd., India) Versus Zyprexa® Zydis® 5 mg Tablets (Referenc[NCT01996501]Phase 10 participants InterventionalCompleted
Assessment of Incidence of Adverse Events in a Naive Pediatric Population Treated With an (Typical and Atypical) Antipsychotic Drug Over 12 Months Follow-up[NCT02007928]200 participants (Actual)Interventional2013-04-30Completed
[NCT00006195]0 participants InterventionalRecruiting
CSP #451 - The Clinical and Economic Impact of Olanzapine in the Treatment of Schizophrenia[NCT00007774]Phase 4600 participants (Anticipated)Interventional1998-03-31Completed
Insulin Sensitivity in Patients With Schizophrenia or Schizoaffective Disorder Treated With Olanzapine and Risperidone[NCT00190749]Phase 4130 participants (Actual)Interventional2003-10-31Completed
A Random Assignment,Parallel Group, Open Label Comparison of Clinical Outcomes and Resource Utilization Among Bipolar Disorder Patients Receiving Either Long Acting Injectable Risperidone Microspheres (Risperdal Consta® ) or Other Second Generation Oral A[NCT00177164]Phase 350 participants (Actual)Interventional2003-11-30Completed
Olanzapine Plus Fosaprepitant Standard Antiemetic Therapy in the Prevention of Chemotherapy-induced Nausea and Vomiting in Patients Receiving High Emetic Risk Multi-day Chemotherapy: a Multicenter, Randomized, Double-blind, Placebo-controlled, Phase 3 Stu[NCT04536558]Phase 3352 participants (Anticipated)Interventional2020-10-01Not yet recruiting
A Randomized, Multicenter Clinical Trial to Assess the Efficacy and Safety of Clozapine vs Treatment as Usual for Treatment-resistant Psychosis in Adolescents and Young Adults With Intellectual Disability.[NCT04529226]Phase 2114 participants (Anticipated)Interventional2020-11-26Recruiting
The Danish Out-of-Hospital Cardiac Arrest Study - a Randomized, Placebo-controlled, Double-blind, Multi Center Trial[NCT05895838]Phase 31,000 participants (Anticipated)Interventional2023-06-16Recruiting
Cerebral Mechanism Involved in Appetite Increase in Schizophrenia Patients Treated With Atypical Antipsychotics (IIT)[NCT00290121]Phase 425 participants (Actual)Interventional2006-09-30Completed
Longitudinal Comparative Effectiveness of Bipolar Disorder Therapies[NCT02893371]1,037,352 participants (Actual)Observational2016-09-30Completed
Olanzapine Augmentation in Clozapine-resistant Schizophrenia: a Randomized Double-blind Study[NCT00918021]Phase 430 participants (Actual)Interventional2009-06-30Completed
Safety and Efficacy of Olanzapine (LY170053) in the Long-term Treatment for Patients With Bipolar I Disorder, Depressed[NCT00618748]Phase 3101 participants (Actual)Interventional2008-02-29Completed
A Prospective Randomized Open-label 6-Month Head-To-Head Trial to Compare Metabolic Effects of Paliperidone ER and Olanzapine in Subjects With Schizophrenia[NCT00645099]Phase 3462 participants (Actual)Interventional2007-10-31Completed
Haloperidol vs Olanzapine for the Management of ICU Delirium: A Randomized Clinical Trial[NCT00833300]200 participants (Anticipated)Interventional2008-06-30Terminated
Influence of Treatment With Olanzapine or Ziprasidone on Transcapillary Glucose Transport in Human Skeletal Muscle[NCT00297960]Phase 40 participants Interventional2005-04-30Completed
Combined Treatment of Cardiovascular Risk Factors In Newly Admitted Patients With Schizophrenia or Schizoaffective Disorder Who Are Receiving Olanzapine And Matched Controls[NCT00672464]Phase 40 participants (Actual)Interventional2008-04-30Withdrawn(stopped due to lack of funding)
A Randomized Trial of Individualised Care Versus Standard Care for Breast Cancer Patients at High Risk for Chemotherapy Induced Nausea and Vomiting. The ILIAD Study[NCT02861859]Phase 3221 participants (Actual)Interventional2016-12-31Completed
Whole Blood and Plasma Sample Collection for the Development of Antipsychotic Immunoassays From Participants Taking Aripiprazole, Olanzapine, Paliperidone, or Risperidone[NCT02634463]Phase 181 participants (Actual)Interventional2015-11-30Completed
The Role of miR-30 Family Dysregulation in Response to Antipsychotic Treatment[NCT02650102]Phase 1/Phase 2200 participants (Anticipated)Interventional2013-01-31Recruiting
Metabolic Effects of Antipsychotic Substitution in Children[NCT00910780]Phase 2/Phase 30 participants (Actual)Interventional2009-11-30Withdrawn(stopped due to Study was not funded.)
Effects of Integrated Treatment for Chinese Patients With Schizophrenia: 1-year Follow-up[NCT02850445]170 participants (Anticipated)Interventional2012-01-31Recruiting
A Multicenter, Randomized, Double-Blind, Flexible-Dose, Long-Term Extension Trial of the Safety and Maintenance of Effect of Asenapine Using Olanzapine Positive Control in Subjects Who Complete Protocols 041021 or 041022.[NCT00156091]Phase 3260 participants (Actual)Interventional2005-04-30Completed
[NCT01389908]2 participants (Anticipated)Interventional2011-06-30Recruiting
Acute Impact of IM Aripiprazole and Olanzapine on Insulin Resistance in High Risk Prediabetics[NCT01411930]Phase 415 participants (Actual)Interventional2009-03-31Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-sequence, Single Oral Dose, Crossover, Bioequivalence Study of Olanzapine Tablets 5 mg With Zyprexa® Tablets 5 mg in Healthy Subjects Under Fed Conditions[NCT01503424]Phase 148 participants (Actual)Interventional2011-08-31Completed
The Cognitive Effects of Risperidone and Olanzapine[NCT00108368]Phase 40 participants Interventional2003-10-31Completed
Pilot Study Evaluating the Safety and Efficacy of Open-Label Olanzapine Monotherapy in Treatment Refractory Bipolar Disorder Mania[NCT00194064]Phase 318 participants (Actual)Interventional2002-07-31Terminated(stopped due to Slow enrollment)
Treatment of Geriatric Bipolar Mood Disorders: A Pilot Study[NCT00177567]Phase 460 participants Interventional2001-07-31Completed
Efficacy and Safety of Olanzapine in Patients With Borderline Personality Disorder: A Randomized Double-Blind Comparison With Placebo[NCT00088036]Phase 3450 participants Interventional2004-02-29Completed
[NCT00089869]Phase 1/Phase 20 participants InterventionalCompleted
Olanzapine Versus Divalproex and Placebo in the Treatment of Mild to Moderate Mania Associated With Bipolar I Disorder[NCT00094549]Phase 4500 participants Interventional2004-10-31Completed
Comparison of Combination Olanzapine and Lithium and Combination Chlorpromazine and Lithium in the Treatment of a First Manic Episode With Psychotic Features.[NCT00202293]Phase 483 participants (Actual)Interventional2001-10-01Completed
Metabolic Effects of Antipsychotics in Children[NCT00205699]Phase 4144 participants (Actual)Interventional2006-04-30Completed
A Multicenter, Randomized, Double-Blind, Fixed-Dose, 6-Week Trial of the Efficacy and Safety of Asenapine Compared With Placebo Using Olanzapine Positive Control in Subjects With an Acute Exacerbation of Schizophrenia[NCT00156117]Phase 3417 participants (Actual)Interventional2005-05-12Completed
The Treatment Efficacy of Combination Atypical Antipsychotics With Sertraline in Patients With Schizophrenia[NCT04076371]1,640 participants (Actual)Interventional2012-01-31Completed
Glucose Regulation During Ziprasidone Treatment[NCT00205725]120 participants (Actual)Interventional2000-11-30Completed
[NCT00179231]80 participants Interventional2000-05-31Completed
A Randomized, Double-Blind Comparison of LY2140023, Olanzapine, and Placebo in the Treatment of Patients With Schizophrenia[NCT00149292]Phase 2195 participants (Actual)Interventional2005-08-23Completed
A 12-Week, Double-Blind Trial of Olanzapine and Placebo in the Treatment of Trichotillomania[NCT00182507]Phase 434 participants Interventional2000-06-30Completed
An Observational Study of Olanzapine Coated and Orodispersible Tablets Effectiveness in Schizophrenic and Bipolar Outpatients.[NCT00510211]1,131 participants (Actual)Observational2007-04-30Completed
Long-Term Olanzapine Treatment in Children With Autism[NCT00183404]Phase 2/Phase 332 participants (Actual)Interventional2004-09-30Completed
Neural Correlates of Emotional Processing in Depressed and Remitted Bipolar and Unipolar Depressed Subjects: An fMRI Investigation[NCT00188942]Phase 442 participants (Actual)Interventional2005-02-28Completed
Bipolar Depression Assessment Study on Tx Response[NCT00191399]Phase 4150 participants Interventional2004-05-31Completed
Double-Blind Long-term Study Comparing the Efficacy and Safety of Olanzapine Versus Haloperidol in Patients With Schizophrenia Previously Stabilized With Conventional Antipsychotic Treatment[NCT00191555]Phase 4360 participants Interventional2003-08-31Completed
An Evaluation of Divalproex vs. Olanzapine for Alcohol Abuse Relapse Prevention in Patients With Bipolar Disorder[NCT00221481]Phase 40 participants (Actual)InterventionalWithdrawn(stopped due to Lack of recruitment)
A Prospective/Parallel Study on Induced Weight Gain During Atypical Antipsychotic Treatment and Its Management With Psychoeducational Programme[NCT00191828]Phase 460 participants Interventional2003-03-31Completed
Phase 1 Study of Insulin Sensitivity, Adjusted β-Cell Function and Adiponectin Among Lean Drug-naïve Schizophrenic Subjects Treated With Atypical Antipsychotic Drugs[NCT00528359]36 participants (Actual)Observational2005-10-31Completed
"Re-examining Maintenance Antipsychotic Treatment in Schizophrenia: Extended Antipsychotic Dosing"[NCT04478838]Phase 4120 participants (Anticipated)Interventional2022-06-06Recruiting
An Open-label, Randomized Trial of Intramuscular (IM) Olanzapine Versus Intramuscular Combination of Haloperidol and Lorazepam in the Treatment of Acute Agitation in Schizophrenia[NCT00797277]Phase 367 participants (Actual)Interventional2006-07-31Completed
Safety and Efficacy of Four Intramuscular Interventions for the Management of Acute Psychomotor Agitation[NCT01485692]120 participants (Actual)Interventional2009-02-28Completed
Discontinuation of Antipsychotics and Antidepressants Among Patients With Dementia and BPSD Living in Nursing Homes - an Open Study.[NCT00433121]Phase 424 participants (Actual)Interventional2006-09-30Completed
[NCT00438776]Phase 342 participants (Actual)Interventional2007-02-28Completed
[NCT00036088]Phase 4530 participants Interventional2001-08-31Completed
Pilot Study of the Efficacy of Olanzapine in the Treatment of Anorexias Nervosa[NCT00592930]Phase 420 participants Interventional2000-06-30Completed
Managing Acute Schizophrenia, a Double Blind Comparison Between Two Atypical Antipsychotics - Olanzapine and Risperidone[NCT00485498]Phase 4122 participants (Actual)Interventional2003-04-30Completed
A Study Examining Clinical Therapeutic Dose of Rapid Acting Intra-Muscular Olanzapine in Japanese Agitated Patients With Schizophrenia[NCT00485810]Phase 1/Phase 231 participants (Actual)Interventional2004-06-30Completed
The Assessment of a Weight Management Program for Treatment-Emergent Weight Gain in Patients With Schizophrenia, Schizophreniform Disorder, and Schizoaffective Disorder During Olanzapine Therapy[NCT00485823]Phase 448 participants (Actual)Interventional2002-12-31Completed
A Double-Blind Randomized Comparison of the Efficacy and Safety of Intramuscular Olanzapine and Intramuscular Haloperidol in Acutely Agitated Patients With Schizophrenia[NCT00485901]Phase 350 participants (Actual)Interventional2004-07-31Completed
A Randomized, Double-Blind, Parallel-Group Study in Healthy Subjects to Characterize Insulin Sensitivity and Lipid Metabolism in Response to Treatment With ALKS 3831 and Olanzapine[NCT02922426]Phase 160 participants (Actual)Interventional2016-09-30Completed
A Randomized Trial to Compare the Efficiency and Side Effect Between Olanzapine and Long-acting Paliperidone Palmitate Injection in Schizophrenia[NCT02918825]100 participants (Actual)Interventional2016-09-01Completed
Metabolic Profile and Anthropometric Changes in Schizophrenia[NCT00534183]2,006 participants (Actual)Interventional2006-06-30Completed
Olanzapine in Cancer Cachexia-Associated Anorexia: A Double-Blind Placebo-Controlled Randomized Clinical Trial[NCT05243251]Phase 3164 participants (Anticipated)Interventional2021-12-25Recruiting
Severe Aberrant Behavior Among Persons With Mental Retardation. Project III: Behavioral Selectivity of Atypical Neuroleptic Drugs: Effects on Cognitive and Social Behaviors[NCT00065273]Phase 350 participants Interventional1998-07-31Completed
A Multicenter, Randomized, Naturalistic, Open-Label Study Between Aripiprazole and Standard of Care in the Management of Community-Treated Schizophrenic Patients (Schizophrenia Trial of Aripiprazole - STAR)[NCT00237913]Phase 3700 participants Interventional2004-07-31Completed
Metabolic Effects of Newer Antipsychotics in Older Patients[NCT00245206]Phase 4406 participants (Actual)Interventional2005-08-31Completed
A Multi Centre, Double-Blind, Double-Dummy, Placebo-Controlled, Randomised, Adaptive, Dose-Range Study To Evaluate the Safety and Efficacy of SB-773812 Administered Once Daily for 12 Weeks in Adults With Schizophrenia[NCT00259870]Phase 2338 participants (Actual)Interventional2005-09-30Completed
A Double-Blind, Randomized Study Comparing Intramuscular Olanzapine Depot to Oral Olanzapine and Low-Dose Depot in the Maintenance Therapy of Patients With Schizophrenia[NCT00088491]Phase 31,205 participants (Actual)Interventional2004-06-30Completed
The Comparison of Efficacy and Safety of Continuing Olanzapine to Switching to Quetiapine in Overweight or Obese Patients With Schizophrenia and Schizoaffective Disorder[NCT00090012]Phase 4340 participants Interventional2004-07-31Completed
Efficacy and Safety of Olanzapine in Patients With Borderline Personality Disorder: A Randomized Flexible Dose Double-Blind Comparison With Placebo[NCT00091650]Phase 3300 participants Interventional2004-03-31Completed
A Randomized Controlled Trial Study of Risperidone and Olanzapine for the Schizophrenic Patients With Neuroleptic-Induced Acute Dystonia or Parkinsonism[NCT00331825]Phase 470 participants Interventional2000-07-31Completed
A Randomized Double-Blind Study of Olanzapine Versus Aripiprazole in the Treatment of Schizophrenia[NCT00088049]Phase 4560 participants Interventional2003-10-31Completed
A Multicenter, Open-Label, Parallel-Group, Randomized, Flexible Dose Study To Evaluate the Safety and Tolerability of Switching From Existing Atypical Antipsychotics to Bifeprunox in Subjects With Schizophrenia or Schizoaffective Disorder[NCT00347425]Phase 3286 participants (Actual)Interventional2006-12-31Completed
[NCT00094640]Phase 10 participants InterventionalCompleted
Olanzapine Versus Aripiprazole in the Treatment of Acutely Ill Patients With Schizophrenia[NCT00103571]Phase 4600 participants Interventional2004-07-31Completed
A Randomized, 6-week Double-blind, Parallel Study to Evaluate the Efficacy and the Safety of Flexible Doses of Extended Release OROS Paliperidone Compared With Olanzapine in the Treatment of Patients With Schizophrenia[NCT00350467]Phase 3288 participants (Actual)Interventional2006-06-30Completed
Population Pharmacokinetic Study in Adolescent Patients With Schizophrenia or Bipolar I Disorder Treated With Olanzapine[NCT00113594]Phase 3100 participants Interventional2005-06-30Completed
A Randomized, Controlled ,Clinical Trial of a Herbal Combination of Aqueous Extracts of Bacopa Monnieri and Nardostachys Jatamansi in the Treatment of Schizophrenia, Compared to Standard Anti-Psychotic Drugs[NCT00483964]Phase 2200 participants (Actual)Interventional2005-09-30Completed
Olanzapine Versus Lithium Carbonate in the Treatment of Bipolar Disorder, Manic or Mixed Episodes[NCT00485680]Phase 3140 participants (Actual)Interventional2003-12-31Completed
Olanzapine for Prevention of Chemotherapy-induced Nausea and Vomiting in Children: A Multi-Centre Feasibility Study[NCT02129478]Phase 215 participants (Actual)Interventional2014-03-31Completed
ACTO: A Phase II, Randomized, Placebo-Controlled Study Evaluating Olanzapine in the Management of Cancer Cachexia[NCT05705492]Phase 244 participants (Anticipated)Interventional2024-01-31Suspended(stopped due to Pending protocol revisions)
Childhood Onset Psychotic Disorders: Characterization and Treatment With Atypical Neuroleptics[NCT00001656]Phase 425 participants (Actual)Interventional1997-06-30Completed
Tolerability, Safety, And Efficacy Of Ziprasidone (80 - 160 Mg/D) Versus Olanzapine (10 - 20 Mg/D), Risperidone (4 - 8 Mg/D) Or Quetiapine (300 - 750 Mg/D) In Pretreated Patients With Schizophrenia, Schizoaffective Disorder Or Schizophreniform Disorders -[NCT00159770]Phase 3290 participants Interventional2001-11-30Completed
Optimal Treatment Duration With Olanzapine Following Remission of Manic or Mixed Episode. An Open-Label, Randomized Trial Comparing Two Treatment Strategies.[NCT00191997]Phase 4180 participants Interventional2004-10-31Completed
Olanzapine Plus Carbamazepine Versus Carbamazepine Alone in the Treatment of Manic or Mixed Episodes Associated With Bipolar I Disorder[NCT00190892]Phase 4120 participants Interventional2004-09-30Completed
Effectiveness of Atypical Vs Conventional Antipsychotics[NCT00237861]Phase 40 participants InterventionalCompleted
A Randomized, Open-Label, Single Dose, Cross-over Study of Gastric Emptying Rate: SEP-363856 vs Prior Antipsychotic Standard of Care in Subjects With Schizophrenia[NCT05402111]Phase 131 participants (Actual)Interventional2022-06-13Completed
Efficacy of Olanzapine in Improving Task Engagement in Schizophrenia[NCT00440843]Phase 30 participants (Actual)Interventional2007-02-28Withdrawn
"Observational Study on the Effect of Switch to Lurasidone or Other Antipsychothics on Metabolic and Weight Changes in Subjects With Schizophrenia"[NCT04312503]95 participants (Actual)Observational2020-07-13Completed
Phase I Dose-Finding Pilot Study of the Safety and Tolerability of Olanzapine in Patients With Advanced Cancer and Weight Loss[NCT00489593]Phase 157 participants (Actual)Interventional2006-10-31Completed
Olanzapine/Fluoxetine Combination Versus Lamotrigine in the Treatment of Bipolar I Depression[NCT00485771]Phase 4403 participants (Actual)Interventional2003-11-30Completed
Weight Gain Management in Patients With Schizophrenia During Treatment With Olanzapine in Association With Nizatidine[NCT00486005]Phase 474 participants (Actual)Interventional2003-02-28Completed
Study of Subcutaneous Olanzapine for Hyperactive or Mixed Delirium[NCT00512291]25 participants (Actual)Interventional2005-06-30Completed
Olanzapine vs Placebo for Outpatients With Anorexia Nervosa[NCT01170117]152 participants (Actual)Interventional2010-08-31Completed
Early Recognition and Optimal Treatment of Delirium in Patients With Advanced Cancer[NCT01539733]101 participants (Actual)Interventional2010-03-31Completed
Comparative Effectiveness of Antipsychotic Medications in Patients With Schizophrenia (CATIE Schizophrenia Trial)[NCT00014001]Phase 41,600 participants Interventional2000-12-31Completed
A Controlled Trial of Olanzapine Versus Active Comparator in the Treatment of Schizophrenic and Schizoaffective Subjects With Comorbid Depression[NCT00034801]Phase 4378 participants Interventional2001-09-30Completed
Treatment and Outcome of Early Onset Bipolar Disorder[NCT00048802]Phase 440 participants Interventional2002-08-31Completed
Olanzapine Versus Placebo in the Treatment of Mania in Adolescents With Bipolar I Disorder[NCT00050206]Phase 4130 participants Interventional2002-11-30Completed
Olanzapine Versus Placebo in the Treatment of Adolescents With Schizophrenia[NCT00051298]Phase 3107 participants (Actual)Interventional2002-11-30Completed
Comparative Effectiveness of Antipsychotic Medications in Patients With Alzheimer's Disease (CATIE Alzheimer's Disease Trial)[NCT00015548]450 participants Interventional2001-03-31Completed
The Minimal Effective Dose of Antipsychotic Medication in Older Patients With Schizophrenia: a PET Study.[NCT00716755]45 participants (Actual)Interventional2009-10-31Completed
Psychopharmacologic Aspects of Motor Slowing in Schizophrenia[NCT00018668]Phase 40 participants Interventional2000-10-31Completed
A Controlled Study of Olanzapine in Children With Autism[NCT00057408]Phase 278 participants (Anticipated)Interventional2003-05-31Completed
Efficacy and Tolerability of Olanzapine, Quetiapine and Risperidone in the Treatment of First Episode Psychosis: A Randomized Double Blind 52-Week Comparison[NCT00034892]Phase 30 participants Interventional2002-03-31Completed
A Randomized, Double-Blind Study of Depakote Monotherapy, Olanzapine Monotherapy, and Combination Therapy of Depakote Plus Olanzapine in Stable Subjects During the Maintenance Phase of Bipolar Illness[NCT00071253]Phase 4180 participants Interventional2003-07-31Terminated
Glucose Regulation During Risperidone and Olanzapine Treatment[NCT00205738]120 participants (Actual)Interventional2000-07-31Completed
Randomized Comparison of Monotherapy (Risperidone, Quetiapine, or Olanzapine) Versus Combination Therapy (Risperidone, Quetiapine, or Olanzapine + Divalproex)in the Management of Dementia With Agitation: A Pilot Comparison of Two Standard Therapies[NCT00208819]Phase 450 participants (Anticipated)Interventional2003-09-30Completed
A Study of the Safety and Efficacy of Depakote ER Plus an Atypical Antipsychotic Vs. an Atypical Antipsychotic Alone in the Treatment of Schizophrenia[NCT00073164]Phase 2400 participants Interventional2003-07-31Completed
A Randomized Double-blind, Parallel Group Study Comparing Olanzapine (Zyprexa) With Haloperidol (Novo-peridol) for the Relief of Nausea and Vomiting in Patients With Advanced Cancer[NCT00124930]Phase 380 participants (Anticipated)Interventional2005-05-31Terminated(stopped due to Study suspended due to low enrollment)
Effect of Lurasidone Vs Olanzapine on Neurotrophic Biomarkers and Cardiometabolic Parameters in First Episode Untreated Schizophrenia: A Randomized, Open Label, Active Controlled Study[NCT03304457]Phase 4100 participants (Actual)Interventional2017-08-25Completed
A Multicenter, Double-Blind, Randomized Trial Of Ziprasidone (80 - 160 Mg) Versus Olanzapine (10 - 20 Mg) In Patients With Recent-Onset Schizophrenia, Schizoaffective And Schizophreniform Disorder.[NCT00145444]Phase 3100 participants Interventional2003-03-31Completed
Energy Homeostasis and Metabolism in Patients With Schizophrenic Disorders Under Treatment With Atypical Antipsychotics[NCT00148564]Phase 440 participants (Actual)Interventional2004-03-31Completed
An Open-Label Study of Intramuscular Olanzapine Depot in Patients With Schizophrenia or Schizoaffective Disorder[NCT00088465]Phase 3931 participants (Actual)Interventional2004-08-31Completed
Effects of Risperidone and Olanzapine on Weight Gain, Physical Health, and Outcome in a Community Sample of Severity and Persistently Ill Patients[NCT00179062]300 participants (Actual)Interventional2000-02-29Completed
Treating Refractory Childhood Schizophrenia[NCT00048828]Phase 441 participants (Actual)Interventional2001-10-31Completed
Preventing Relapse: Oral Antipsychotics Compared To Injectables: Evaluating Efficacy (PROACTIVE)[NCT00330863]Phase 4357 participants (Actual)Interventional2006-05-31Completed
A Phase 3 Randomized, Placebo-and Active Comparator Controlled, Clinical Trial to Study the Safety and Efficacy of Two Doses of Lurasidone HCl in Acutely Psychotic Patients With Schizophrenia.[NCT00615433]Phase 3478 participants (Actual)Interventional2008-01-31Completed
Glucose and Lipid Metabolism on Antipsychotic Medication[NCT00515723]96 participants (Actual)Interventional2001-09-30Completed
A Proof of Concept, Multi-Center, Randomized, Double-Blind, Parallel, Placebo-Controlled, Study of Zonisamide Sustained Release (SR) 360 mg Versus Placebo in the Prevention of Weight Gain Associated With Olanzapine Therapy for Psychosis[NCT00734435]Phase 226 participants (Actual)Interventional2008-09-30Terminated(stopped due to Sponsor Decision- Financial Considerations)
Acute Impact of Antipsychotics on Insulin Sensitivity: A Novel Human Model[NCT00895921]Phase 430 participants (Actual)Interventional2008-11-30Completed
Prospective Observational Investigation of Olanzapine Versus Haloperidol Versus Ziprasidone Versus Midazolam for the Treatment of Acute Undifferentiated Agitation in the Emergency Department[NCT03211897]737 participants (Actual)Observational2017-06-15Completed
Atypical Antipsychotic Medication in Anorexia Nervosa[NCT00692185]Phase 223 participants (Actual)Interventional2005-10-31Completed
Treatment of Refractory Nausea[NCT03367572]Phase 31,600 participants (Anticipated)Interventional2018-04-19Recruiting
Neuroleptic Induced Movement Disorders in Older Patients[NCT00255879]Phase 1250 participants Interventional1999-01-31Completed
A Six-month, Double-blind, Randomized, International, Multicenter Trial to Evaluate the Glucoregulatory Effects of Risperidone and Olanzapine in Subjects With Schizophrenia or Schizoaffective Disorder[NCT00236379]Phase 459 participants (Actual)InterventionalCompleted
A Multicenter, Double-Blind, Flexible-Dose, 6-Month Extension Trial Comparing the Safety and Efficacy of Asenapine With Olanzapine in Subjects Who Completed Protocol A7501013[NCT00174265]Phase 3196 participants (Actual)Interventional2005-07-31Completed
A Randomized, Double-Blind, Placebo-Controlled, Olanzapine-Referenced, Parallel Group Safety, Efficacy, and Tolerability Study of SCA-136 in Subjects With Acute Exacerbations of Schizophrenia[NCT00265551]Phase 2300 participants Interventional2006-01-31Completed
Double Blind Placebo Controlled Investigation of Amantadine for Retarding Weight Gain in First Episode Adlt Psychotic Subjects Beginning Therapy With Olanzapine.[NCT00287352]Phase 140 participants (Actual)Interventional2005-05-31Completed
Independent Investigator Grant Study-Comparative Effects of Chronic Treatment With Olanzapine and Risperidone on Glucose and Lipid Metabolism[NCT00287820]Phase 446 participants (Anticipated)Interventional2004-02-29Completed
Bergen Psychosis Project 2 - The Bergen-Stavanger-Innsbruck-Trondheim Study[NCT01446328]Phase 4151 participants (Actual)Interventional2011-10-31Completed
PREFERENCE: 12-Week Open Label Trial On Olanzapine Orodispersible Tablet Vs. Oral Olanzapine Preference Study[NCT00324051]Phase 4284 participants (Actual)Interventional2006-05-31Completed
A Multi-center, Randomized, Open, Treatment-switching Study From Orally Administered Antipsychotic Monotherapy in the Treatment of Chronic Schizophrenic and Schizoaffective Patients[NCT00304616]Phase 4500 participants Interventional2004-10-31Completed
The Impact of Pre-operative Olanzapine on Quality of Recovery-40 Scores After Discharge From Ambulatory Surgery[NCT05676294]Phase 2455 participants (Anticipated)Interventional2023-06-26Recruiting
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-sequence, Single Oral Dose, Crossover, Bioequivalence Study of Olanzapine Tablets 5 mg With Zyprexa® Tablets 5 mg in Healthy Subjects Under Fasting Conditions[NCT01503398]Phase 148 participants (Actual)Interventional2011-08-31Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-sequence, Two-period, Single-dose, Crossover Bioequivalence Study of Olanzapine 5 mg OD Tablets With Zyprexa Zydis 5 mg Tablets in Healthy Subjects Under Fasting Conditions[NCT01503437]Phase 122 participants (Actual)Interventional2006-11-30Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-sequence, Two-period, Single-dose, Crossover Bioequivalence Study of Olanzapine 5 mg OD Tablets With Zyprexa Zydis 5 mg Tablets in Healthy Subjects Under Fed Conditions[NCT01503450]Phase 126 participants (Actual)Interventional2006-11-30Completed
Oro-dispersible Olanzapine (Wafer) Versus Conventional Oral Haloperidol or Diazepam Tablets for the Management of Acute Agitation in the Accident and Emergency Department - a Multicentre Randomised Clinical Trial[NCT03246620]Phase 412 participants (Actual)Interventional2017-09-01Terminated(stopped due to The study was terminated prematurely due to difficulties in patient recruitment and associated potential for selection bias.)
[NCT03007303]30 participants (Anticipated)Observational [Patient Registry]2016-06-30Recruiting
Interventional, Randomised, Double-blind, Active-controlled, Fixed-dose Study of Lu AF35700 in Patients With Treatment-resistant Schizophrenia[NCT02717195]Phase 31,098 participants (Actual)Interventional2016-04-30Completed
Randomized Multicentric Open-label Phase III Clinical Trial to Evaluate the Efficacy of Continual Treatment Versus Discontinuation Based in the Presence of Prodromes in a First Episode of Non-affective Psychosis.[NCT01765829]Phase 3104 participants (Anticipated)Interventional2012-11-30Recruiting
A Randomized, Open Label Trial of Olanzapine Versus Lithium in the Treatment of Acute Depression in Patients With Bipolar II or Bipolar Not Otherwise Specified.[NCT02287259]Phase 450 participants (Actual)Interventional2014-11-30Completed
Olanzapine Augmentation Therapy in Treatment-resistant Depression: a Double-blind Placebo-controlled Trial[NCT00273624]Phase 30 participants (Actual)Interventional2005-06-30Withdrawn(stopped due to Study withdrawn before inclusion of first participant for administrative reasons)
Correlation Between Cognitive Function and Relapse of Schizophrenia Regarding Dose Reduction in Patients Undergoing High-dose Antipsychotic Therapy[NCT03019887]139 participants (Actual)Interventional2011-04-30Completed
Sequenced Treatment Alternatives to Relieve Adolescent Depression (STAR-AD) a Multicentre Open-label Randomized Controlled Trial Protocol[NCT05814640]Phase 1/Phase 2520 participants (Anticipated)Interventional2023-02-20Recruiting
A Pilot Study on the Efficacy and Safety of Olanzapine in Improving Symptoms and Gastric Motility in Gastroparesis[NCT01625923]3 participants (Actual)Interventional2013-01-31Terminated(stopped due to Inadequate recruitment numbers)
Open-label Randomized Controlled Trial of Oral Transmucosal Haloperidol and Olanzapine in the Treatment of Terminal Delirium[NCT04750395]Phase 280 participants (Anticipated)Interventional2021-09-01Recruiting
Optimal Duration of Olanzapine Add-on Therapy in Major Depression: a Placebo-controlled, Randomized, Phase III, Pilot Study in Parallel Group Design[NCT00568672]Phase 30 participants (Actual)Interventional2007-10-31Withdrawn(stopped due to Withdrawn because of personal ressources before inclusion of the first patient)
A Multicenter, Randomized, Double-Blind, Parallel-Group Fixed-Dose Study of the Effect on Weight of Befeprunox Versus Olanzapine in the Treatment of Outpatients With Schizophrenia.[NCT00380224]Phase 3120 participants (Anticipated)Interventional2006-07-31Completed
A Phase III, Randomized, Placebo-Controlled, Double-Blind Trial Evaluating the Safety and Efficacy of Sublingual Asenapine vs. Olanzapine and Placebo in In-Patients With an Acute Manic Episode Clinical Trial Protocol 7501004 (Secondary Title: ARES)[NCT00159744]Phase 3488 participants (Actual)Interventional2004-11-30Completed
Tocilizumab, Dexamethasone, Olanzapine, Flow-targeted Versus Pressure-targeted Hemodynamic Management, and Low Tidal Volume Ventilation in Patients Undergoing On-pump Cardiac Surgery - a Multifactorial Design Randomized Trial[NCT05635227]1,200 participants (Anticipated)Interventional2022-11-10Recruiting
Evaluating the Safety and Efficacy of Empagliflozin Addition in Modulating Metabolic Disturbances Associated With Olanzapine in Schizophrenia Patients.A Double-Blind, Randomized, Placebo-Controlled Trial[NCT05669742]Phase 340 participants (Anticipated)Interventional2023-01-31Not yet recruiting
Double-Blind Placebo-Controlled Olanzapine Add-on Therapy in the Treatment of Acute Syndromal and Subsyndromal Exacerbations in Bipolar Disorders[NCT00186017]Phase 450 participants (Actual)Interventional2005-07-31Completed
Treatment of Schizophrenia and Related Disorders in Children and Adolescents[NCT00053703]Phase 4116 participants (Actual)Interventional2002-02-28Completed
Prospective Randomised Double Blind Trial of Ketiapine and Olanzapine Comparative Efficacy for Fast Sedation of Severely Agitated Patients in Emergency Psychiatric Ward[NCT03216941]Phase 4500 participants (Actual)Interventional2015-01-01Completed
Neurocognitive Effects of Ziprasidone: Relationship to Working Memory and Dopamine Blockade[NCT00225498]35 participants (Actual)Interventional2002-06-30Completed
An Open-label, Prospective, Randomized and Comparative Study of Patient Satisfaction Between Continued Administration of Previous Antipsychotics Versus Switched Administration to Paliperidone ER in Non-satisfied Patients With Previous Antipsychotic Drug[NCT01592201]Phase 413 participants (Actual)Interventional2012-07-31Terminated(stopped due to This study was early terminated due to insufficient enrollment required for hypothesis testing.)
A Study to Evaluate the Effect of ALKS 3831 Compared to Olanzapine on Body Weight in Young Adults With Schizophrenia, Schizophreniform, or Bipolar I Disorder Who Are Early in Their Illness[NCT03187769]Phase 3426 participants (Actual)Interventional2017-06-08Completed
A Randomized Double-blind Controlled Trial to Assess the Benefits of Olanzapine and Amisulpride Combination Treatment in Acutely Ill Schizophrenia Patients. - COMBINE[NCT01609153]Phase 4328 participants (Actual)Interventional2012-06-30Completed
A Multicenter, Double-Blind, Fixed-Dose, Long-Term Extension Trial of the Safety of Asenapine Using Olanzapine as an Active Control in Subjects Diagnosed With Schizophrenia Who Completed Protocol P05688[NCT01617200]Phase 3105 participants (Actual)Interventional2012-12-31Completed
A Long-Term, Open-Label, Safety Study of Oral Olanzapine in Adolescents With Bipolar I Disorder (Manic or Mixed Episodes) or Schizophrenia[NCT00982020]Phase 4203 participants (Actual)Interventional2009-09-30Completed
Effectiveness of Selective Serotonin Reuptake Inhibitors Combined With Antipsychotic Medication for the Treatment of Psychotic Depression[NCT00056472]Phase 3259 participants (Actual)Interventional2003-01-31Completed
Developing a Single Patient Open-label Trial Tapering Algorithm for Antipsychotics in Long-Term Care - A Pilot Study[NCT02958800]20 participants (Anticipated)Interventional2016-12-31Recruiting
A Double-Blind Dose-Response Study Comparing Rapid Acting Intramuscular Olanzapine and Intramuscular Placebo in Agitated Patients With Schizophrenia[NCT00316238]Phase 2160 participants (Anticipated)Interventional2006-04-30Completed
Neurobiology/Treatment of Obsessive-Compulsive Disorder[NCT00000373]Phase 474 participants (Actual)Interventional1992-09-30Completed
A Sequential and Parallel Cohort Design to Test the Clinical Utility of Antipsychotic Medication Levels in Plasma as Determined by Liquid Chromatography-Tandem Mass Spectrometry[NCT02462473]Phase 29 participants (Actual)Interventional2015-05-31Terminated(stopped due to Due to poor enrollment sponsor terminated early after enrolling 9 in Cohort 1 and no enrollment in Cohorts 2 and 3.)
Efficacy and Safety Addition of Low Dose Olanzapine to the Standard Prophylaxis of Nausea and Vomiting Induced by Highly-emetogenic Chemotherapy in Children and Adolescents (OZONE-V)[NCT05346731]Phase 3210 participants (Anticipated)Interventional2022-04-01Recruiting
Olanzapine for the Prevention of Chemotherapy Induced Nausea and Vomiting (CINV) in Patients Receiving Highly Emetogenic Chemotherapy (HEC): A Randomized, Double-Blind, Placebo-Controlled Trial[NCT02116530]Phase 3401 participants (Actual)Interventional2014-08-31Completed
Fosaprepitant , Tropisetron and Olanzapine for the Prevention of Nausea and Vomiting in Patients With Breast Cancer Receiving Anthracycline/Cyclophosphamide-containing Chemotherapy[NCT05242874]Phase 3403 participants (Anticipated)Interventional2022-01-01Recruiting
Quantitative Assessment and Comparison of Metabolic Changes in Non-psychotic Adults Taking the Antipsychotic Medications Fanapt (Iloperidone) or Zyprexa (Olanzapine) or Placebo[NCT01920802]Phase 431 participants (Actual)Interventional2012-11-30Completed
[NCT02977741]0 participants (Actual)Observational2016-11-30Withdrawn(stopped due to Inability to recruit patients)
Melatonin Metabolism Abnormality in Patients With Schizophrenia or Schizoaffective Disorder Treated With Olanzapine and Melatonin Dose Finding for the Correction of the Metabolic Abnormality[NCT00512070]20 participants (Anticipated)Interventional2007-07-31Active, not recruiting
Metabolic Effects of Olanzapine in Healthy Males[NCT01496183]24 participants (Actual)Interventional2007-10-31Completed
A Study to Assess the Short-Term Efficacy and Safety of Olanzapine and Fluoxetine Compared to Placebo and Fluoxetine for Nonpsychotic Treatment-Resistant Depression[NCT01687478]Phase 3176 participants (Actual)Interventional2012-09-30Terminated(stopped due to Interim assessment: Lack of efficacy)
Preventing Morbidity in First-Episode Schizophrenia[NCT00000374]Phase 4125 participants (Actual)Interventional1998-09-30Completed
Comparative Efficacy and Safety of Low Dose Amisulpride Vs Olanzapine-Fluoxetine Combination in the Treatment of Post Schizophrenic Depression: A Randomized Controlled Trial[NCT04876521]Phase 460 participants (Anticipated)Interventional2021-05-04Recruiting
Efficacy of Hydroxyzine Versus Treatment as Usual for Panic Disorder: An Eight-Week, Open Label, Pilot, Randomized Controlled Trial.[NCT05737511]Phase 480 participants (Anticipated)Interventional2023-12-30Not yet recruiting
Pharmacovigilance in Gerontopsychiatric Patients[NCT02374567]Phase 3407 participants (Actual)Interventional2015-01-31Terminated
Effect of Ketanserin, Olanzapine, and Lorazepam After LSD Administration on the Acute Response to LSD in Healthy Subjects[NCT05964647]Phase 120 participants (Anticipated)Interventional2023-12-01Not yet recruiting
"Olanzapine for Prevention of Nausea and Vomiting in Children and Adolescents Receiving Highly Emetogenic Chemotherapy (HEC): An Investigator Initiated, Randomized, Open-label Trial (PRaCTiCE Trial: PRevention of ChemoTherapy Induced Emesis in Children)"[NCT03219710]Phase 3240 participants (Actual)Interventional2017-07-01Completed
A Phase 2, Efficacy, Safety and Tolerability Study of ALKS 3831 in Schizophrenia With Alcohol Use Disorder[NCT02161718]Phase 2300 participants (Actual)Interventional2014-05-31Completed
Randomized Controlled Trial of Olanzapine for the Control of Chemotherapy-induced Vomiting in Children Receiving Highly Emetogenic Chemotherapy[NCT03118986]Phase 2200 participants (Anticipated)Interventional2017-08-10Recruiting
A Phase 2, Randomized, Multicenter, Safety, Tolerability, and Dose-Ranging Study of Samidorphan, a Component of ALKS 3831, in Adults With Schizophrenia Treated With Olanzapine[NCT01903837]Phase 2347 participants (Actual)Interventional2013-06-30Completed
Telmisartan as an Adjunctive Treatment for Metabolic Problems in Patients With Schizophrenia[NCT00981526]Phase 466 participants (Actual)Interventional2009-03-31Completed
Olanzapine in the Treatment of Low Weight and Obsessional Thinking Among Those With Anorexia Nervosa: A Double Blind Placebo Controlled Study[NCT00260962]Phase 234 participants (Actual)Interventional2000-09-30Completed
Olanzapine or Dexamethasone, With 5-HT3 RA and NK-1 RA, to Prevent Nausea and Vomiting Induced by Cisplatin-Based Doublet Chemotherapy: A Non-inferiority, Prospective, Multi-Centered, Randomized, Controlled, Phase III Clinical Trial[NCT04437017]Phase 3557 participants (Actual)Interventional2020-02-03Completed
Amisulpride Versus Olanzapine Treatment for Behavioral and Psychological Symptoms in Patients With Dementia of the Alzheimer Type:A Randomized, Open-label, Prospective Study[NCT04341467]76 participants (Anticipated)Interventional2019-12-01Recruiting
Utility of Olanzapine in the Treatment of Opioid Withdrawal in the Emergency Department[NCT02643355]70 participants (Actual)Interventional2015-11-30Completed
A Randomized Study to Determine the Efficacy and Tolerability of Olanzapine for the Prevention of Chemotherapy-Induced Nausea and Vomiting in Chinese Breast Cancer Patients[NCT03079219]Phase 3120 participants (Actual)Interventional2017-03-23Completed
A Phase 1, Open-Label Study of the Breast Milk Pharmacokinetics of Olanzapine and Samidorphan in Healthy Lactating Women[NCT05547100]Phase 112 participants (Actual)Interventional2022-09-14Completed
Effectiveness of Switching Antipsychotic Medications[NCT00044655]Phase 4219 participants (Actual)Interventional2001-07-31Completed
An Efficacy Study Comparing Olanzapine and Mirtazapine in the Improvement of Unintentional Weight Loss for Patients With Advanced Stage Cancer[NCT05170919]Phase 2170 participants (Anticipated)Interventional2022-01-20Enrolling by invitation
Clinical Management of Metabolic Problems in Patients With Schizophrenia[NCT00423878]Phase 4215 participants (Actual)Interventional2007-01-31Completed
A Double-blind, Placebo-controlled, Crossover Study Examining the Acute Effects of Olanzapine on Plasma Leptin, Glucose Tolerance and Free Fatty Acids in Healthy Volunteers[NCT00741026]15 participants (Actual)Interventional2008-08-31Completed
Comparison of Optimal Antipsychotic Treatments for Schizophrenia Pilot Study[NCT00802100]Phase 421 participants (Actual)Interventional2008-12-31Completed
Improving Metabolic Parameters of Antipsychotic Child Treatment (IMPACT)[NCT00806234]Phase 4127 participants (Actual)Interventional2009-01-31Completed
A Multicenter, Randomized, Double-Blind, Fixed-Dose, 6-Week Trial of the Efficacy and Safety of Asenapine Compared With Placebo Using Olanzapine as an Active Control in Subjects With an Acute Exacerbation of Schizophrenia[NCT01617187]Phase 3360 participants (Actual)Interventional2012-12-04Completed
Sustaining Remission of Psychotic Depression[NCT01427608]Phase 4269 participants (Actual)Interventional2011-10-31Completed
A Randomized Phase III Trial of Olanzapine Versus Megestrol Acetate for Cancer-Associated Anorexia[NCT04939090]Phase 3360 participants (Anticipated)Interventional2021-10-15Recruiting
Estimating the Optimal Dynamic Antipsychotic Treatment Regime: Sequential Multiple-assignment Randomized Clinical Antipsychotic Trials in Chinese Patients With First-episode Psychosis.[NCT03510325]Phase 41,260 participants (Anticipated)Interventional2018-10-01Not yet recruiting
A Double-Blind, 40-Week Continuation Study Evaluating the Safety of Asenapine and Olanzapine in the Treatment of Subjects With Acute Mania Clinical Trial Protocol A7501007 (Secondary Title: ARES)[NCT00159783]Phase 3218 participants (Actual)Interventional2005-07-31Completed
Olanzapine and 5-HT3 With or Without Dexamethasone to Prevent Nausea and Vomiting Induced by Chemotherapy::A Non-inferiority, Prospective, Multi-Centered, Randomized, Controlled, Phase III Clinical Trial[NCT05805800]Phase 3238 participants (Anticipated)Interventional2023-03-15Recruiting
A Comparative, Open-label, Randomized, Two-period Bioequivalence Study of Olanzapine Film-coated Tablets 5 mg (JSC Farmak, Ukraine) vs Zyprexa® Coated Tablets 5 mg (Eli Lilly, Nederland B V) in Healthy Subjects Under Fasted Conditions.[NCT05123976]Phase 132 participants (Actual)Interventional2020-10-21Completed
NMDA Antagonists in Bipolar Depression[NCT01833897]Phase 48 participants (Actual)Interventional2013-03-31Completed
A Pilot Study Comparing Olanzapine and Aprepitant for the Prevention of Chemotherapy Induced Nausea and Vomiting in Pediatric Patients Receiving Highly Emetogenic Chemotherapy[NCT02097823]Phase 215 participants (Actual)Interventional2014-02-28Completed
Psychopharmacological Treatment of Emotional Distress: A Randomized Controlled Trial[NCT06133114]Phase 480 participants (Anticipated)Interventional2023-12-31Not yet recruiting
A Phase III Randomized, Double-blind, Placebo-controlled, Cross-over Study to Evaluate Olanzapine Combined With Fosaprepitant, Ondansetron, and Dexamethasone for Preventing Nausea and Vomiting in Patients With Testicular Cancer Receiving 5-day Cisplatin C[NCT05244577]Phase 375 participants (Anticipated)Interventional2022-01-18Recruiting
Akynzeo or Olanzapine for Patients Who Experience Breakthrough CINV in Patient Receiving Moderately or Highly Emetogenic Chemotherapy After First Cycle of Chemotherapy[NCT06065722]Phase 2100 participants (Anticipated)Interventional2023-09-09Recruiting
A Double-Blind, Placebo-Controlled Study of Zonisamide to Prevent Olanzapine-Associated Weight Gain[NCT00363376]Phase 342 participants (Actual)Interventional2008-01-31Completed
Aprepitant ,Olanzapine,Palonosetron and Dexamethasone for the Prevention of Chemotherapy-induced Nausea and Vomiting---A Randomized Single Center Phase III Trial[NCT02484911]Phase 3120 participants (Actual)Interventional2015-05-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00001656 (12) [back to overview]Change in the Bunney-Hamburg Rating Scale for Anxiety
NCT00001656 (12) [back to overview]Change in the Brief Psychiatric Rating Scale-24
NCT00001656 (12) [back to overview]Change in Bunney-Hamburg Rating Scale for Mania
NCT00001656 (12) [back to overview]Change in Bunney-Hamburg Rating Scale for Depression
NCT00001656 (12) [back to overview]Change in Body Mass Index (BMI)
NCT00001656 (12) [back to overview]Change in the Scale for the Assessment of Positive Symptoms
NCT00001656 (12) [back to overview]Change in Extrapyramidal Movements as Measured by the Simpson Angus Scale Score
NCT00001656 (12) [back to overview]Change in Extrapyramidal Movements as Measured by the Abnormal Involuntary Movements Scale (AIMS)
NCT00001656 (12) [back to overview]Change in the Scale for the Assessment of Negative Symptoms
NCT00001656 (12) [back to overview]Change in Weight
NCT00001656 (12) [back to overview]Change in the Clinical Global Impression Severity of Symptoms Scale
NCT00001656 (12) [back to overview]Change in the Bunney-Hamburg Rating Scale for Psychosis
NCT00044655 (1) [back to overview]Number Who Discontinued Medication Within First 6 Study Months
NCT00053703 (6) [back to overview]Change From Baseline in Weight at Week 8
NCT00053703 (6) [back to overview]Change From Baseline in Barnes Akathisia Scale at Week 8
NCT00053703 (6) [back to overview]Change From Baseline in Body Mass Index Change, kg/m2, at Week 8
NCT00053703 (6) [back to overview]Change From Baseline in PANSS Negative Symptom Subscale at Week 8
NCT00053703 (6) [back to overview]Change From Baseline in PANSS Positive Symptom Subscale Score at 8 Weeks.
NCT00053703 (6) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total Score at 8 Weeks
NCT00056472 (3) [back to overview]Scores on CGI-S Compared to Baseline Over the Course of the Trial
NCT00056472 (3) [back to overview]Mean Score Hamilton Depression Rating Scale (Ham-D) Over the Course of the Trial From Week to Week.
NCT00056472 (3) [back to overview]Remission of Depression Hamilton Depression Scale (Ham-D) and Psychosis Schedule for Affective Disorders in Schizophrenia - Delusional Item (SADS) During the Course of the Trial
NCT00088465 (20) [back to overview]Change From Baseline in Weight at Month 76 Endpoint
NCT00088465 (20) [back to overview]Number of Participants Having Normal Fasting Baseline Glucose Value With Treatment-Emergent High Fasting Glucose at Any Time Post Baseline
NCT00088465 (20) [back to overview]Number of Participants With Potentially Clinically Significant (PCS) Weight Gain at Month 76 Endpoint
NCT00088465 (20) [back to overview]Change From Baseline in Clinical Global Impression-Severity of Illness (CGI-S) Scores at Month 72 Endpoint
NCT00088465 (20) [back to overview]Number of Psychiatric Visits
NCT00088465 (20) [back to overview]Change From Baseline in PANSS General Psychopathology Subscales at Month 76 Endpoint
NCT00088465 (20) [back to overview]Number of Participants With Treatment-Emergent Abnormal High Prolactin at Any Time Post Baseline
NCT00088465 (20) [back to overview]Patient Satisfaction With Medication Questionnaire-Modified (PSMQ) at Month 76 Endpoint
NCT00088465 (20) [back to overview]Number of Participants With Treatment-Emergent Abnormal High Alanine Transaminase (ALT), High Aspartate Transaminase (AST), High Total Bilirubin at Any Time Post Baseline
NCT00088465 (20) [back to overview]Number of Participants With Extrapyramidal Symptoms at Any Time
NCT00088465 (20) [back to overview]Number of Participants With Adverse Events (AE)
NCT00088465 (20) [back to overview]Number of Participants Having Normal Fasting Baseline Lipid Value With Treatment-Emergent High Fasting Lipid at Any Time Post Baseline
NCT00088465 (20) [back to overview]Change From Baseline in 36-Item Short Form Health Survey (SF-36) at Month 76 Endpoint
NCT00088465 (20) [back to overview]Change From Baseline in PANSS Positive Scores at Month 76 Endpoint
NCT00088465 (20) [back to overview]Plasma Olanzapine Concentrations in Participants During Long-Term Treatment by Year
NCT00088465 (20) [back to overview]Change From Baseline in PANSS Negative Scores at Month 76 Endpoint
NCT00088465 (20) [back to overview]Days of Hospitalization
NCT00088465 (20) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total Scores at Month 76 Endpoint
NCT00088465 (20) [back to overview]Change From Baseline in the Heinrichs-Carpenter Quality of Life Scale (QLS) Total Score at Month 76 Endpoint
NCT00088465 (20) [back to overview]Change From Baseline in the Subjective Well-Being Under Neuroleptic Treatment-Short Form (SWN-S) at Month 76 Endpoint
NCT00129220 (11) [back to overview]Percentage of Participants Who Switched to Symptomatic Depression
NCT00129220 (11) [back to overview]Change From Baseline to 3 Week and 6 Week Endpoints in the Positive Subscore of Positive and Negative Syndrome Scale (PANSS)
NCT00129220 (11) [back to overview]Change From Baseline to 3 Week Endpoint in Young Mania Rating Scale (YMRS) Total Score
NCT00129220 (11) [back to overview]Change From Baseline to 3 Week and 6 Week Endpoints in Clinical Global Impression - Bipolar Version (CGI-BP) Mania Subscale
NCT00129220 (11) [back to overview]Remission Rate of Bipolar Disorder (Olanzapine Versus Haloperidol)
NCT00129220 (11) [back to overview]Change From Baseline to 6 Week Endpoint in Young Mania Rating Scale (YMRS)
NCT00129220 (11) [back to overview]Change From Baseline to 6 Week Endpoint in Clinical Global Impressions - Bipolar Version (CGI-BP), Overall Severity of Illness
NCT00129220 (11) [back to overview]Response Rate of Manic Symptoms at 3 Weeks and 6 Weeks
NCT00129220 (11) [back to overview]Remission Rate of Manic Symptoms at 3 Weeks and 6 Weeks
NCT00129220 (11) [back to overview]Percentage of Participants Who Switched to Syndromic Depression
NCT00129220 (11) [back to overview]Maximum Change From Baseline During 6-Week Period in Drug-Induced Extrapyramidal Symptoms Scale (DIEPSS) Total Score
NCT00145496 (3) [back to overview]Change From Baseline in Negative Symptoms of Schizophrenia Measured by the Negative Symptom Assessment (NSA) Scale Total Score
NCT00145496 (3) [back to overview]Change From Baseline in Quality of Life Measured by the Quality of Life Scale (QLS) Total Score
NCT00145496 (3) [back to overview]Change From Baseline in Body Weight
NCT00159783 (9) [back to overview]Concomitant Medications
NCT00159783 (9) [back to overview]Extrapyramidal Symptoms [EPS]
NCT00159783 (9) [back to overview]Number of Participants With Markedly Abnormal Vital Sign Changes
NCT00159783 (9) [back to overview]Number of Participants With Abnormal Physical Examination Findings
NCT00159783 (9) [back to overview]Number of Participants With Laboratory Values Outside Normal Range
NCT00159783 (9) [back to overview]Body Weight
NCT00159783 (9) [back to overview]Abdominal Girth
NCT00159783 (9) [back to overview]Participants Who Experienced Adverse Event(s)
NCT00159783 (9) [back to overview]Number of Participants With Abnormal Electrocardiogram
NCT00174265 (2) [back to overview]Change From Baseline in Negative Symptoms of Schizophrenia Measured by the Negative Symptom Assessment (NSA) Scale Total Score
NCT00174265 (2) [back to overview]Change From Baseline in Quality of Life Measured by the Quality of Life Scale (QLS) Total Score
NCT00177164 (4) [back to overview]BMI
NCT00177164 (4) [back to overview]Number of Participants With Treatment Emergent Hyperlipidemia
NCT00177164 (4) [back to overview]Number of Participants With Treatment - Emergent Hyperglycemia
NCT00177164 (4) [back to overview]Evaluate the Number of Clinical Events (Pooled) Occurring Between 3-15 Months Following a Switch/Stabilization of the Antipsychotic Agents Among Patients Who Receive Either Risperidal Consta or One of the 4 Marketed 2nd Generation Antipsychotic Agents.
NCT00183625 (2) [back to overview]Total Weeks Worked
NCT00183625 (2) [back to overview]Body Mass Index
NCT00186017 (4) [back to overview]Mean Change in Hamilton Anxiety Rating Scales (HAM-A)
NCT00186017 (4) [back to overview]Mean Change in MADRS After 1 Week of Treatment.
NCT00186017 (4) [back to overview]Mean Change in CGI-BP-OS After 1 Week of Treatment
NCT00186017 (4) [back to overview]Mean Change in YMRS After 1 Week of Treatment
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Brief Psychiatric Rating Scale Scores.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Body Mass Index (BMI)
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Abnormal Involuntary Movement Scale Scores.
NCT00190749 (30) [back to overview]Pairwise Correlation Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Barnes Akathisia Scale Scores.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Visceral Fat Area.
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Abnormal Involuntary Movement Scale Scores
NCT00190749 (30) [back to overview]Pairwise Correlations Between Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Eating Behavior Assessment Scale Scores.
NCT00190749 (30) [back to overview]Change in Baseline to Last Observation In Normalized Insulin Sensitivity Index at Low Insulin Phase Using Change in Weight as a Covariate
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Weight
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Waist Circumference
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Visceral Fat Area
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in the Ratio of the Visceral Fat Area to the Subcutaneous Fat Area
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Subcutaneous Fat Area
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Simpson Angus Scale Scores
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Triglycerides
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Total Cholesterol
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Lipoprotein Subclasses
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including High Density Lipoprotein (HDL)
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Direct Low Density Lipoprotein (LDL)
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Eating Behavior Assessment Scale Scores
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Clinical Global Impression - Severity of Illness Scores
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Brief Psychiatric Rating Scale (BPRS) Scores
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Body Mass Index
NCT00190749 (30) [back to overview]Change From Baseline to 12 Week Endpoint in Barnes Akathisia Rating Scale (BARS) Scores
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Weight.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Waist Circumference.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in the Simpson Angus Scale Scores.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Subcutaneous Fat Area.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Ratio of Visceral Fat Area to the Subcutaneous Fat Area.
NCT00190749 (30) [back to overview]Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Clinical Global Impression - Severity of Illness Scale Scores.
NCT00203307 (1) [back to overview]Difference in Migraine Headache Periods During the Active Treatment Period as Compared to the Placebo Treatment Period, Per Subject.
NCT00205699 (6) [back to overview]Change in DEXA % Body Fat
NCT00205699 (6) [back to overview]Change in Insulin-stimulated Glucose Rate of Appearance (Glucose Ra)
NCT00205699 (6) [back to overview]Change in Insulin-stimulated Glucose Rate of Disappearance (Glucose Rd)
NCT00205699 (6) [back to overview]Change in Insulin-stimulated Glycerol Rate of Appearance (Glycerol Ra)
NCT00205699 (6) [back to overview]Change in MRI-measured Visceral Abdominal Fat
NCT00205699 (6) [back to overview]Change in MRI-measured Subcutaneous Abdominal Fat
NCT00225498 (1) [back to overview]Working Memory
NCT00259272 (16) [back to overview]Baseline MATHYS Assessment - Principal Component Analysis and Orthogonal Transformation Matrix
NCT00259272 (16) [back to overview]Change From Baseline to 6 Week and 24 Week Endpoints in HAMA Total Scores - According to Thymic Reactivity Assessment
NCT00259272 (16) [back to overview]Mean Change From Baseline to 6 Week and 24 Week Endpoints in the Hamilton Anxiety Scale (HAMA) Total Score
NCT00259272 (16) [back to overview]Increases and Decreases in Fasting Glucose Levels
NCT00259272 (16) [back to overview]Increases and Decreases in Lipid Levels
NCT00259272 (16) [back to overview]Mean Change From Baseline to 24 Week Endpoint in Glycaemia Levels (Glucose Fasting Levels)
NCT00259272 (16) [back to overview]Mean Change From Baseline to 6 Week and 24 Week Endpoints in the Hamilton 17-Items Depression Scale (HAMD-17) Total Score
NCT00259272 (16) [back to overview]Mean Changes From Baseline to 6 Week and 24 Week Endpoints in the Multidimensional Assessment of THYmic States Scale (MATHYS) Total Score
NCT00259272 (16) [back to overview]Change From Baseline to 6 Week and 24 Week Endpoints in HAMD-17 Total Scores - According to Thymic Reactivity Assessment
NCT00259272 (16) [back to overview]Mean Change From Baseline to 24 Week Endpoint in Lipids
NCT00259272 (16) [back to overview]Change From Baseline to 6 Week and 24 Week Endpoints in YMRS Total Scores - According to Thymic Reactivity Assessment
NCT00259272 (16) [back to overview]Mean Change From Baseline to 6 Week and 24 Week Endpoints in the Young Mania Rating Scale (YMRS) Total Score
NCT00259272 (16) [back to overview]Weight Gain Compared to Baseline
NCT00259272 (16) [back to overview]Wellness Interventional Program for Weight Gain Management in Patients (for Those Who Gain at Anytime More Than 7% of Body Weight, Compared to Baseline)
NCT00259272 (16) [back to overview]MATHYS Total Score at Baseline - According to Thymic Reactivity Assessment
NCT00259272 (16) [back to overview]Mean Change From Baseline to 24 Week Endpoint in Weight
NCT00260962 (2) [back to overview]Obsessions
NCT00260962 (2) [back to overview]Body Mass Index (BMI) (kg/m^2)
NCT00265343 (2) [back to overview]Long-term Change in Negative Symptoms of Schizophrenia Measured by the Negative Symptom Assessment (NSA) Scale
NCT00265343 (2) [back to overview]Change in Quality of Life Measured by Quality of Life Scale (QLS)
NCT00266630 (20) [back to overview]Number of Participants With Response of Manic Symptoms - Olanzapine Monotherapy Arm Only
NCT00266630 (20) [back to overview]Number of Participants With Treatment-Emergent Dyskenisia Based on DIEPSS Scores
NCT00266630 (20) [back to overview]Number of Participants With Treatment-Emergent Dystonia Based on DIEPSS Scores
NCT00266630 (20) [back to overview]Number of Participants With Treatment-Emergent Parkinsonism Based on DIEPSS Scores
NCT00266630 (20) [back to overview]Clinical Global Impressions - Bipolar Version, Severity of Illness (CGI-BP) Overall, Visit Data
NCT00266630 (20) [back to overview]Number of Participants With Treatment-emergent Abnormal, High, or Low Laboratory Values
NCT00266630 (20) [back to overview]Change From Baseline to Endpoint on the YMRS Total Score - Olanzapine + Mood Stabilizer Only
NCT00266630 (20) [back to overview]Positive and Negative Syndrome Scale Positive Scores - Visit Data
NCT00266630 (20) [back to overview]Number of Participants With Potentially Clinically Significant Changes in Vital Signs and Weight
NCT00266630 (20) [back to overview]Number of Participants With Potentially Clinically Significant Changes in Laboratory Analytes
NCT00266630 (20) [back to overview]Maximum Change From Baseline to Endpoint on the Drug Induced Extra-Pyramidal Symptoms Scale (DIEPSS) - Total Score
NCT00266630 (20) [back to overview]Number of Participants With Relapse of Depressive Symptoms
NCT00266630 (20) [back to overview]Number of Participants With Potentially Clinically Significant Changes in Electrocardiograms - High Fridericia Corrected QT Interval (QTcF)
NCT00266630 (20) [back to overview]Number of Participants Who Switched to Syndromic Depression
NCT00266630 (20) [back to overview]Number of Participants Who Experienced Switch to Symptomatic Depression as Measured by the Hamilton Depression Scale - 17 Item Version (HAMD-17)
NCT00266630 (20) [back to overview]Change From Baseline to Endpoint in Young Mania Rating Scale (YMRS) Total Scores - Olanzapine Monotherapy Arm Only
NCT00266630 (20) [back to overview]Number of Participants With Treatment-Emergent Akathisia Based on DIEPSS Scores
NCT00266630 (20) [back to overview]Number of Participants With Relapse of Manic Symptoms - Olanzapine Monotherapy Arm Only
NCT00266630 (20) [back to overview]Number of Participants With Remission of Mania - Olanzapine Monotherapy Arm Only
NCT00266630 (20) [back to overview]Number of Participants Who Experienced Remission of Bipolar Disorder
NCT00275301 (1) [back to overview]Change in Brain Metabolism From Baseline to Eight Weeks as Seen in PET Scan
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in the Clinical Global Impression-Severity (CGI-S) Scale
NCT00303602 (18) [back to overview]Number of Participants Discontinuing the Trial by Visit (Week)
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Glycosylated Hemoglobin
NCT00303602 (18) [back to overview]Number of Participants Meeting a Definition for the Presence of Metabolic Syndrome as Defined by Adult Treatment Panel III (ATP III) Criteria at Baseline and 16 Week Endpoint
NCT00303602 (18) [back to overview]Number of Patients Achieving at Least 5% Loss of Body Weight in Any Post-Baseline Period
NCT00303602 (18) [back to overview]Time Course of Change From Baseline in Body Mass Index (BMI)
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Blood Pressure
NCT00303602 (18) [back to overview]Change From Baseline to 16 Week Endpoint in Fasting Plasma Glucose
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Fasting Lipoproteins (Total Cholesterol, High-Density Lipoprotein Cholesterol [HDL-Cholesterol], Low-Density Lipoprotein Cholesterol [LDL-Cholesterol] [Calculated], and Triglycerides)
NCT00303602 (18) [back to overview]Mean Changes From Baseline to 16 Week Endpoint Homeostasis Model Assessments of Insulin Sensitivity HOMA-S (Calculated)
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Waist Circumference
NCT00303602 (18) [back to overview]Change From Baseline to 16 Week Endpoint in Subjective Appetite Using a Visual Analog Scale
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Weight
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Body Mass Index (BMI) for the Treatment Completers
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Body Mass Index (BMI)
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in Fasting Serum Insulin
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in the Subjective Well-Being Under Neuroleptics (SWN) Scale
NCT00303602 (18) [back to overview]Mean Change From Baseline to 16 Week Endpoint in the Global Assessment of Functioning (GAF) Scale
NCT00320489 (26) [back to overview]Change From Baseline in Clinical Global Impression - Severity of Illness (CGI-S) Scale Scores at 104 Weeks
NCT00320489 (26) [back to overview]Median Time to Discontinuation for Any Reason (Excluding Sponsor Decision)
NCT00320489 (26) [back to overview]Median Time to Relapse
NCT00320489 (26) [back to overview]Resource Utilization: Days of Unpaid Care, Days of Workdays Missed, Days of Paid Care Per Week During the Study
NCT00320489 (26) [back to overview]Participants With Treatment-Emergent High Alanine Transaminase (ALT), Aspartate Transaminase (AST), and Total Bilirubin
NCT00320489 (26) [back to overview]Participants With Normal to High Fasting Glucose, Fasting Total Cholesterol, and Fasting Triglycerides
NCT00320489 (26) [back to overview]Change From Baseline in Working Alliance Inventory (WAI) Total Score at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Weight at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Schizophrenia Objective Functioning Instrument (SOFI) Global Score at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Scale to Assess Unawareness of Mental Disorder (SUMD) Total Score at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Overall Health Status Assessment Using the EuroQol: 5 Dimensions Questionnaire (EQ-5D) at 104 Weeks
NCT00320489 (26) [back to overview]Patient Satisfaction With Medication Questionnaire-Modified (PSMQ) at 104 Weeks (All Items)
NCT00320489 (26) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total and Subscale Scores at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Brief Psychiatric Rating Scale (BPRS) Total Score at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Heinrich-Carpenter Quality of Life in Schizophrenia Scale (QLS) Total Score at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in Burden Assessment Scale (BAS) Total Score at 104 Weeks
NCT00320489 (26) [back to overview]Change From Baseline in 36-Item Short Form Health Survey (SF-36) at 104 Weeks, All Domains and Summary Scores
NCT00320489 (26) [back to overview]Resource Utilization: Number of Outpatient Surgeries During the Study, 24 Months After Randomization
NCT00320489 (26) [back to overview]Resource Utilization: Number of Outpatient Physician Visits During the Study
NCT00320489 (26) [back to overview]Patient Attitude Toward Treatment Using the Drug Attitude Inventory (DAI) Scale Total Score at 104 Weeks
NCT00320489 (26) [back to overview]Participants With Treatment-Emergent Abnormal High Prolactin at 104 Weeks
NCT00320489 (26) [back to overview]Participants With Potentially Clinically Significant (PCS) Weight Gain at 104 Weeks
NCT00320489 (26) [back to overview]Participants Discontinuing Because of an Adverse Event (AE) or Death
NCT00320489 (26) [back to overview]Number of Participants With All-Cause Discontinuations (Excluding Sponsor Decision)
NCT00320489 (26) [back to overview]Number of Participants Experiencing Relapse
NCT00320489 (26) [back to overview]Number of Hospitalization Days
NCT00330863 (3) [back to overview]Number of Patients Discontinuing From the Study
NCT00330863 (3) [back to overview]Substantial Clinical Deterioration Measured by Psychotic Symptoms
NCT00330863 (3) [back to overview]Side Effects and Metabolic Measures
NCT00337662 (18) [back to overview]Vital Signs - Change From Baseline to 10 Week Endpoint in Standing Diastolic Blood Pressure
NCT00337662 (18) [back to overview]Vital Signs - Change From Baseline to 10 Week Endpoint in Standing Mean Arterial Pressure
NCT00337662 (18) [back to overview]Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Body Mass Index
NCT00337662 (18) [back to overview]Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Body Weight
NCT00337662 (18) [back to overview]Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Sitting Pulse Rate
NCT00337662 (18) [back to overview]Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Standing Systolic Blood Pressure
NCT00337662 (18) [back to overview]Mean Change From Baseline to 10 Week Endpoint in Extrapyramidal Symptoms as Measured by the Barnes Akathisia Rating Scale - Total Score
NCT00337662 (18) [back to overview]Mean Change From Baseline to 10 Week Endpoint in Extrapyramidal Symptoms as Measured by the Modified Simpson-Angus Scale
NCT00337662 (18) [back to overview]Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Standing Pulse Rate
NCT00337662 (18) [back to overview]Changes From Study Period II Baseline (Week 0) to Weeks 3, 4, 6, 8, and 12 in Positive and Negative Syndrome Scale (PANSS) Total Score in Early Onset Response and Not Early Onset Response-Risperidone Patients
NCT00337662 (18) [back to overview]Changes From Study Period III Baseline (Week 2) to Weeks 3, 4, 6, 8, and 12 in Positive and Negative Syndrome Scale Total Score in Not Early Onset Response-Risperidone and Not Early Onset Response-Olanzapine Patients
NCT00337662 (18) [back to overview]Number of Participants in the Early Onset and Not Early Onset-Risperidone Groups Who Show a 50% or Greater Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Baseline or Meet 'a Priori' Specified Criteria for Remission
NCT00337662 (18) [back to overview]Number of Participants in the Not Early Onset-Risperidone and Not Early Onset-Olanzapine Groups Who Show a 50% or Greater Reduction in Positive and Negative Syndrome Scale Total Score From Baseline or Meet 'a Priori' Specified Criteria for Remission
NCT00337662 (18) [back to overview]Number of Participants With Psychiatric Hospitalizations in the Early Onset and Not Early Onset-Risperidone Groups
NCT00337662 (18) [back to overview]Mean Change From Baseline to 10 Week Endpoint in Extrapyramidal Symptoms as Measured by the Abnormal Involuntary Movement Scale (AIMS)- Non-Global Total Score
NCT00337662 (18) [back to overview]Number of Participants With Treatment-Emergent Abnormal Fasting Laboratory Analytes Reported in >=2% of All Participants
NCT00337662 (18) [back to overview]The Number of Participants in the Early Onset (EO) and Not Early Onset-Risperidone (NEO-RIS) Groups Who Show a 20% or Greater Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score
NCT00337662 (18) [back to overview]The Number of Participants in the Not Early Onset-Risperidone (NEO-RIS) and Not Early Onset-Olanzapine (NEO-OLZ) Groups Who Show a 20% or Greater Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score
NCT00338949 (2) [back to overview]Change in Visceral Fat Mass From Baseline to Week 26
NCT00338949 (2) [back to overview]Change in Insulin Sensitivity Index From Baseline to Week 26 ((1/mU/L) x 1/Min)
NCT00349973 (3) [back to overview]Change in Positive Symptoms by Treatment Assignment
NCT00349973 (3) [back to overview]The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)
NCT00349973 (3) [back to overview]Change in Negative Symptoms by Treatment Assignment
NCT00384332 (2) [back to overview]Weight in Kilograms at Baseline, Weeks 1, 4, 6, and 8
NCT00384332 (2) [back to overview]Change From Baseline Montgomery Asberg Depression Rating Scale
NCT00391222 (7) [back to overview]Change From Double-blind Baseline to Endpoint in Montgomery Åsberg Depression Rating Scale (MADRS)
NCT00391222 (7) [back to overview]Change From Double-blind Baseline to Endpoint in Young Mania Rating Scale (YMRS)
NCT00391222 (7) [back to overview]Time to Early Study Discontinuation for Any Reason
NCT00391222 (7) [back to overview]Time to Recurrence of a Mood Episode (Exploratory/Olanzapine)
NCT00391222 (7) [back to overview]Time to Recurrence of an Elevated Mood (Hypomanic, Manic, or Mixed) Episode
NCT00391222 (7) [back to overview]Time to Recurrence of a Mood Episode (Risperidone LAI Versus Placebo)
NCT00391222 (7) [back to overview]Time to Recurrence of a Depressive Episode
NCT00396565 (6) [back to overview]Change From Baseline in the Total Positive and Negative Syndrome Scale (PANSS).
NCT00396565 (6) [back to overview]Change From Baseline in Clinical Global Impression Scale (CGI-S)
NCT00396565 (6) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) - General Psychopathology Subscale Score
NCT00396565 (6) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) - Negative Subscale Score
NCT00396565 (6) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) - Positive Subscale Score
NCT00396565 (6) [back to overview]Proportion of Responders (≥30% Decrease in Total Positive and Negative Syndrome Scale [PANSS])
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Triglycerides
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Hemoglobin A1c
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Low Density Lipoprotein (LDL) Cholesterol
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Weight
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Brief Psychiatric Rating Scale (BPRS) Total Score
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Clinical Global Impression - Severity Scale (CGI-S)
NCT00401973 (11) [back to overview]Change From Baseline to Endpoint in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score
NCT00401973 (11) [back to overview]Correlations Between Weight Changes and Changes in Eating Inventory (EI) and Food Craving Inventory (FCI) at 2 Weeks and 22 Weeks
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Glucose
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting High Density Lipoprotein (HDL) Cholesterol
NCT00401973 (11) [back to overview]Mean Change From Baseline to Endpoint in Fasting Total Cholesterol
NCT00402324 (13) [back to overview]Mean Change in Hamilton Depression Rating Scale-21 (HAMD) Scores From Baseline to Endpoint.
NCT00402324 (13) [back to overview]Mean Change in Clinical Global Impression for Bipolar Illness Severity (CGI-BP) From Baseline to Endpoint
NCT00402324 (13) [back to overview]Clinically Significant Vital Signs - Percentage of Participants With Baseline-to-Endpoint Weight Increase of at Least Seven Percent (7%)
NCT00402324 (13) [back to overview]Clinically Significant Vital Signs - Body Mass Index Change From Baseline
NCT00402324 (13) [back to overview]Clinically Significant Vital Signs - Weight Change From Baseline
NCT00402324 (13) [back to overview]Clinically Significant Laboratory Values - Bilirubin Total Change From Baseline
NCT00402324 (13) [back to overview]Clinically Significant Laboratory Values - Fasting Triglycerides Change From Baseline
NCT00402324 (13) [back to overview]Clinically Significant Laboratory Values - Fasting Cholesterol Change From Baseline
NCT00402324 (13) [back to overview]Clinically Significant Laboratory Values - Fasting Blood Glucose Change From Baseline
NCT00402324 (13) [back to overview]Number of Patients Hospitalized Due to Relapse of Mania or Depression.
NCT00402324 (13) [back to overview]Number of Participants Meeting the Criteria for Mixed Response
NCT00402324 (13) [back to overview]Number of Participants Meeting the Criteria for Mixed Onset of Action
NCT00402324 (13) [back to overview]Mean Change in Young Mania Rating Scale (YMRS) Scores From Baseline to Endpoint.
NCT00423878 (2) [back to overview]Change in Non-HDL Cholesterol Level for Patients Assigned to Stay and Patients Assigned to Switch Over 24 Weeks
NCT00423878 (2) [back to overview]Efficacy Failure, Defined as Psychiatric Hospitalization, a 25 Percent Increase From Baseline on the Positive and Negative Syndrome Scale or Substantial Clinical Deterioration on the Clinical Global Impressions-Change (CGI-C)
NCT00446992 (9) [back to overview]Triglycerides
NCT00446992 (9) [back to overview]Body Mass Index
NCT00446992 (9) [back to overview]Cholesterol Total
NCT00446992 (9) [back to overview]LDL
NCT00446992 (9) [back to overview]Fasting Glucose
NCT00446992 (9) [back to overview]HDL
NCT00446992 (9) [back to overview]Hemoglobin A1c
NCT00446992 (9) [back to overview]IL-6
NCT00446992 (9) [back to overview]Fasting Insulin
NCT00490971 (7) [back to overview]Clinical Global Impression - Bipolar Disorder - Severity of Illness (CGI-BP-S): Change From Baseline
NCT00490971 (7) [back to overview]Global Assessment of Functioning (GAF): Change From Baseline
NCT00490971 (7) [back to overview]Montgomery-Asberg Depression Rating Scale (MADRS)
NCT00490971 (7) [back to overview]Time to Recurrence of Depressive Symptoms Associated With Bipolar I Disorder
NCT00490971 (7) [back to overview]Young Mania Rating Scale (YMRS): Change From Baseline
NCT00490971 (7) [back to overview]Time to Recurrence of Manic Symptoms Associated With Bipolar I Disorder
NCT00490971 (7) [back to overview]Time to Recurrence of Any Mood Symptoms (Manic or Depressive) Associated With Bipolar I Disorder
NCT00508157 (2) [back to overview]Number of Participants Remaining on Metabolic Syndrome at Week 16
NCT00508157 (2) [back to overview]Mean Percent Change From Baseline in Fasting Non-high Density Lipoprotein (HDL) Cholesterol at Week 16
NCT00509067 (3) [back to overview]Clinical Global Impression
NCT00509067 (3) [back to overview]MATRICS Verbal Learning and Memory
NCT00509067 (3) [back to overview]Negative Symptoms Measured on Positive and Negative Syndrome Scale (PANSS)
NCT00510146 (52) [back to overview]Percentage of Participants With Psychotic Disorders and Mood Disorders With Psychotic Features at Endpoint on MINI Psychotic Disorders Module (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Extra-Pyramidal Symptoms (EPS) At Endpoint As Measured by Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS) (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Extra-Pyramidal Symptoms (EPS) at Endpoint As Measured by Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS) (Open-Label Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Major Depressive Episode at Endpoint on Mini International Neuropsychiatric Interview (MINI), Depressive Episode Module (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Non-Alcohol Psychoactive Substance Use Disorder at Endpoint on MINI Substance Dependence/Abuse Module (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With High Suicidality at Endpoint (Open-Label Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Current Hypomanic Episode at Endpoint on MINI Manic Episode Module (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Emergence of Mania During the Study (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Emergence of Mania During the Study (Open-Label Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Recovery (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Recovery (Open-Label Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Symptomatic Remission At Any Time (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Symptomatic Remission in the MADRS Total Score (Open-Label Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Symptomatic Response at Endpoint (Acute Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Symptomatic Response in Montgomery-Asberg Depression Rating (MADRS) Depression Rating (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Alanine Amino Transferase/Serum Glutamate Pyruvate Transaminase (ALT/SGPT), Aspartate Aminotransferase/Serum Glutamic Oxaloacetic Transaminase (AST/SGOT), Gamma Glutamyl Transferase (GGT)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Albumin (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Albumin and Total Protein (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Alkaline Phosphatase, Creatinine Phosphokinase (CPK), GGT (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Blood Pressure (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Blood Pressure (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Chloride (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Clinical Global Improvement- Bipolar (CGI-BP) Severity of Illness Scores-Mania, Depression, Overall Bipolar Illness Scores (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Creatinine (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Direct Bilirubin, Total Bilirubin, Uric Acid (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in ECG (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Erythrocyte Count (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Erythrocyte Count (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Glucose and Lipids (Cholesterol, Triglycerides, HDL Cholesterol, LDL Cholesterol)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Glucose and Lipids (Cholesterol, Triglycerides, HDL Cholesterol, LDL Cholesterol) (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Hamilton Depression Rating Scale-17 (HAMD-17) Total Score (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Heart Rate (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Heart Rate (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Hematocrit (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Hemoglobin (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Hemoglobin (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Hemoglobin A1c (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in MINI Suicidality Total Scores (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Platelet Count (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Prolactin (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Prolactin (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Uric Acid (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Urinalysis (UA)- Specific Gravity (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Weight (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Weight (Open-Label Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Young Mania Rating Scale (YMRS) Total Score (Acute Phase)
NCT00510146 (52) [back to overview]Change From Baseline to Endpoint in Young Mania Rating Scale (YMRS) Total Score (Open-Label Phase)
NCT00510146 (52) [back to overview]Change in Electrocardiogram (ECG) From Baseline to Endpoint (Acute Phase)
NCT00510146 (52) [back to overview]Number of Participants With Adverse Events (Acute Phase)
NCT00510146 (52) [back to overview]Number of Participants With Adverse Events (Open-Label Phase)
NCT00510146 (52) [back to overview]Percentage of Participants With Alcohol Dependence and Abuse at Endpoint on MINI Alcohol Dependence/Abuse Module (Acute Phase)
NCT00515723 (2) [back to overview]DEXA Total Fat
NCT00515723 (2) [back to overview]Clamp Derived Insulin Sensitivity (mg/kg/Min)
NCT00615433 (2) [back to overview]Change in Total PANSS (Positive and Negative Syndrome Scale)Score From Baseline to the End of the Double Blind Treatment Period.
NCT00615433 (2) [back to overview]CGI-S (Clinical Global Impression - Severity) Change From Baseline to the End of the Double-blind Treatment.
NCT00618748 (12) [back to overview]Change From Baseline in Prolactin at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Change From Baseline in Glucose and Lipid Panel at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Change From Baseline in Hemoglobin (HbA1c) at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Change From Baseline in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Change From Baseline to in QTcF at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Percentage of Participants With Adverse Events Leading to Discontinuation
NCT00618748 (12) [back to overview]Percentage of Participants With Emergence of Mania at Week 24 or Week 48
NCT00618748 (12) [back to overview]Percentage of Participants With High Suicidality at Week 24 or Week 48
NCT00618748 (12) [back to overview]Percentage of Participants With Extra-Pyramidal Symptoms (EPS) at Week 24 or Week 48
NCT00618748 (12) [back to overview]Change From Baseline in Clinical Global Improvement- Bipolar (CGI-BP) at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Change From Baseline in Young Mania Rating Scale (YMRS) Total Score at Week 24 or Week 48 Endpoint
NCT00618748 (12) [back to overview]Change From Baseline in Weight at Week 24 or Week 48 Endpoint
NCT00640510 (4) [back to overview]Number of Participants With Scores of 4 to 7 in the Agitation-Calmness Evaluation Scale (ACES) at Each Timepoint
NCT00640510 (4) [back to overview]Change From Baseline to Each Timepoint in Positive and Negative Syndrome Scale-Excited Component (PANSS-EC)
NCT00640510 (4) [back to overview]Number of Responders at 2 Hours After First Intramuscular (IM) Injection
NCT00640510 (4) [back to overview]Change From Baseline to 2 Hours Post the First Intramuscular (IM) Injection in Positive and Negative Syndrome Scale-Excited Component (PANSS-EC)
NCT00645099 (19) [back to overview]Change From Baseline at End Point in Body Weight
NCT00645099 (19) [back to overview]Change From Baseline at End Point in Waist Circumference
NCT00645099 (19) [back to overview]Change From Baseline at End Point of Mari-Type Analysis of Glucose Sensitivity for Insulin
NCT00645099 (19) [back to overview]Change From Baseline at End Point of the Insulinogenic Index
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Converted Insulin
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Fasting Glucose
NCT00645099 (19) [back to overview]Change From Baseline to End Point in High Density Lipoprotein
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Homeastatic Model Assessment of Insulin Resistance (HOMA-IR)
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Homeostatic Model Assessment of Beta-cell Function (HOMA-%B)
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Low Density Lipoprotein Cholesterol (Friedwald QT)
NCT00645099 (19) [back to overview]Change From Baseline to End Point in the Triglycerides (TG) to High Density Lipoprotein (HDL) Ratio (TG:HDL Ratio)
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Total Cholesterol
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Total Positive and Negative Syndrome Scale Score (PANSS)
NCT00645099 (19) [back to overview]Change From Baseline to End Point in Triglycerides
NCT00645099 (19) [back to overview]Number of Patients First Meeting the NCEP/ATP III Criteria for Metabolic Syndrome During Follow-up
NCT00645099 (19) [back to overview]Number of Patients Meeting the Criteria for Type 2 Diabetes Mellitus During Follow-up
NCT00645099 (19) [back to overview]Number of Patients With Impaired Fasting Glucose
NCT00645099 (19) [back to overview]Number of Patients With Onset of Impaired Glucose Tolerance
NCT00645099 (19) [back to overview]Change From Baseline at End Point in Body Mass Index (BMI)
NCT00685334 (2) [back to overview]Change From Baseline in Weight (Lbs.) at 12 Weeks
NCT00685334 (2) [back to overview]Tolerability
NCT00686998 (1) [back to overview]Positive and Negative Syndrome Scale (PANSS) Total Score Change From Baseline
NCT00692185 (2) [back to overview]Symptom Severity Assessed by Yale Brown Cornell-Eating Disorders Scale
NCT00692185 (2) [back to overview]Weight Gain
NCT00741026 (12) [back to overview]Systolic Blood Pressure
NCT00741026 (12) [back to overview]Plasma Leptin
NCT00741026 (12) [back to overview]Plasma Free Fatty Acid
NCT00741026 (12) [back to overview]Diastolic Blood Pressure
NCT00741026 (12) [back to overview]Oral Glucose Tolerance
NCT00741026 (12) [back to overview]LDL Cholesterol
NCT00741026 (12) [back to overview]Heart Rate
NCT00741026 (12) [back to overview]Body Weight
NCT00741026 (12) [back to overview]BMI
NCT00741026 (12) [back to overview]HDL Cholesterol
NCT00741026 (12) [back to overview]Triglycerides
NCT00741026 (12) [back to overview]Total Cholesterol
NCT00746785 (1) [back to overview]Drinks Per Drinking Day
NCT00797277 (2) [back to overview]Change of the Agitation-Calmness Evaluation Scale (ACES) Score From Baseline to 120 Minutes After 1st Injection
NCT00797277 (2) [back to overview]The Change of the Positive and Negative Symptom Scale Excited Component (PANSS-EC) Score From Baseline to 120 Minutes After First Injection
NCT00802100 (2) [back to overview]Feasibility of Randomizing a Cohort of Participants Meeting the Inclusion and Exclusion Criteria of the Study
NCT00802100 (2) [back to overview]Antipsychotic Efficacy, Defined as Completion of the Trial Without Psychiatric Hospitalization, Clinician Decision to Discontinue Treatment, or Patient Decision to Discontinue Treatment
NCT00806234 (4) [back to overview]Triglyceride Levels
NCT00806234 (4) [back to overview]Change in Whole Body Insulin Sensitivity Index
NCT00806234 (4) [back to overview]Body Mass Index (BMI) Z-score Change
NCT00806234 (4) [back to overview]Change in Low Density Lipoprotein (LDL) Cholesterol Level
NCT00827918 (7) [back to overview]Mean Change From Baseline in Clinical Global Impression - Severity of Illness Scale (CGI-S) at Week 4
NCT00827918 (7) [back to overview]Mean Change From Baseline in PANSS Negative Subscale at Week 4
NCT00827918 (7) [back to overview]Mean Change From Baseline in the Positive and Negative Syndrome Scale (PANSS) at Week 4
NCT00827918 (7) [back to overview]Percentage of Participants With Response at Week 4
NCT00827918 (7) [back to overview]Number of Participants Who Experienced at Least One Adverse Event
NCT00827918 (7) [back to overview]Number of Participants Who Discontinued Study Drug Due to an Adverse Event
NCT00827918 (7) [back to overview]Mean Change From Baseline in PANSS Positive Subscale at Week 4
NCT00844857 (20) [back to overview]Change From Baseline in Weight Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in the YMRS Total Score at Week 8
NCT00844857 (20) [back to overview]Change From Baseline in the Quality of Life Questionnaire for Children and Adolescents (KINDL) Parent Scale Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in the Quality of Life Questionnaire for Children and Adolescents (KINDL) Kid and Kiddo Combined Scale Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in the Clinical Global Impression Scale - Bipolar Version (CGI-BP) Score at Week 8
NCT00844857 (20) [back to overview]Change From Baseline in the Children's Depression Rating Scale Revised (CDRS-R) Total Score at Week 8
NCT00844857 (20) [back to overview]Change From Baseline in Symptoms of Attention-Deficit/Hyperactivity Disorder Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in Prolactin Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in Electrocardiogram (ECG) QTcF Interval Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in Alanine Aminotransferase/Serum Glutamic-Pyruvic Transaminase (ALT/SGPT) Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in the CDRS-R Total Score Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With Treatment Emergent Suicidal Ideation or Behavior Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants in Each Improvement Category Up to Week 8
NCT00844857 (20) [back to overview]Change From Baseline in Fasting Metabolic Parameters Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With Response Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With Remission Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With at Least One Treatment-Emergent Incident of Parkinsonism Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With at Least One Treatment-Emergent Incident of Dyskinesia Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With at Least One Treatment-Emergent Incident of Akathisia Up to Week 8
NCT00844857 (20) [back to overview]Percentage of Participants With at Least One Incident of Worsening of Mania Up to Week 8
NCT00845026 (26) [back to overview]Change From Baseline in 16-Item Negative Symptoms Assessment (NSA-16) Total Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Abnormal Involuntary Movement Scale (AIMS) Total Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Barnes Akathisia Scale (BAS) Global Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Clinical Global Impression Severity Scale (CGI-S) at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Measurement and Treatment Research to Improve Cognition in Schizophrenia Consensus Cognitive Battery (MCCB): Overall Composite T-Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Number of Psychiatric Visits at 24 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Personal and Social Performance (PSP) at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Subjective Well-Being Under Neuroleptic Treatment-Short Form (SWN-S) Total Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Percentage of Participants With Response (Rate of Response) at 6 and 24 Weeks Endpoints
NCT00845026 (26) [back to overview]Number of Participants With Treatment-Emergent Change in Neurological Examination
NCT00845026 (26) [back to overview]Number of Participants With Suicidal Behaviors and Ideations Baseline Through 52 Weeks
NCT00845026 (26) [back to overview]Change From Baseline in Pulse Rate at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Number of Participants With Potentially Clinical Significant Change in Lipids Level
NCT00845026 (26) [back to overview]Number of Participants With Shift From Baseline to Maximum Post-Baseline Grading in Electroencephalograms (EEGs)
NCT00845026 (26) [back to overview]Change From Baseline in EuroQoL Questionnaire-5 Dimension (EQ-5D) at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Blood Pressure (BP) at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in Simpson-Angus Scale (SAS) Total Score at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Time to Discontinuation Due to Adverse Event (AE)
NCT00845026 (26) [back to overview]Percentage of Participants With Remission (Rate of Remission) at Week 24 Endpoint
NCT00845026 (26) [back to overview]Percentage of Participants With Relapse (Rate of Relapse)
NCT00845026 (26) [back to overview]Number of Participants With Potentially Clinically Significant Changes in QT Intervals Electrocardiograms (ECGs)
NCT00845026 (26) [back to overview]Number of Participants With Potentially Clinical Significant Change in Fasting Glucose Level
NCT00845026 (26) [back to overview]Change From Baseline in Weight at 52 Weeks Endpoint
NCT00845026 (26) [back to overview]Change From Baseline in University of California-San Diego (UCSD) Performance-Based Skills Assessment-B (UPSA-B) Total Score at 52 Weeks Endpoint
NCT00895921 (3) [back to overview]Change in Glucose Disposition
NCT00895921 (3) [back to overview]Change in Percent of Insulin Suppression of Endogenous Glucose Production
NCT00895921 (3) [back to overview]Akathisia
NCT00910988 (4) [back to overview]Adipose Tissue Insulin Sensitivity
NCT00910988 (4) [back to overview]Hepatic Insulin Sensitivity
NCT00910988 (4) [back to overview]Peripheral Insulin Sensitivity
NCT00910988 (4) [back to overview]Whole Body Insulin Sensitivity
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent High Fasting Low-Density Lipoprotein (LDL) Cholesterol
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent High Fasting Glucose
NCT00958568 (39) [back to overview]Percent of Participants With Suicide-Related Thoughts and Behaviors
NCT00958568 (39) [back to overview]Kaplan-Meier Estimate of Percentage of Subjects Not Relapsing at Week 27 (Day 189)
NCT00958568 (39) [back to overview]Time to Relapse by Any Criteria
NCT00958568 (39) [back to overview]Time to Relapse Based on the Montgomery-Åsberg Depression Rating Scale (MADRS) Score With Concomitant Clinical Global Impressions-Severity (CGI-S) of Depression Score
NCT00958568 (39) [back to overview]Time to Relapse as Measured by Hospitalization for Depression or Suicidality
NCT00958568 (39) [back to overview]Time to Relapse as Measured by Discontinuation Due to Lack of Efficacy/Worsening of Depression/Suicidality
NCT00958568 (39) [back to overview]Resource Utilization - Average Number of Hours Worked for Pay Per Week at Week 47
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent Dyskinesia
NCT00958568 (39) [back to overview]Percentage of Participants Who Relapse by Any Criteria
NCT00958568 (39) [back to overview]Percentage of Participants Who Relapse Based on Montgomery-Åsberg Depression Rating Scale (MADRS) Score With Concomitant Clinical Global Impressions-Severity (CGI-S) of Depression Score
NCT00958568 (39) [back to overview]Percentage of Participants Who Relapse as Measured by Hospitalization for Depression or Suicidality
NCT00958568 (39) [back to overview]Percentage of Participants Who Relapse as Measured by Discontinuation Due to Lack of Efficacy/Worsening of Depression/Suicidality
NCT00958568 (39) [back to overview]Percentage of Participants Responding to Treatment During Open-Label Acute Treatment Phase
NCT00958568 (39) [back to overview]Percentage of Participants Achieving Remission at Any Point During Stabilization Treatment Phase
NCT00958568 (39) [back to overview]Percent of Participants With Week 20-to-Week 47 Endpoint Increase in Weight of at Least 7%
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent Parkinsonism
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent Low Fasting High-Density Lipoprotein (HDL) Cholesterol
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent Hepatic Events
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent Corrected (for Rate) Cardiac QT Interval Using Fridericia's Formula (QTcF) on Electrocardiogram ≥500 Milliseconds (Msec)
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent Akathisia
NCT00958568 (39) [back to overview]Percent of Participants With a 60 Milliseconds (Msec) Increase in Fridericia-Corrected (for Rate) Cardiac QT Interval (QTcF) on Electrocardiogram
NCT00958568 (39) [back to overview]Percentage of Participants Maintaining Remission
NCT00958568 (39) [back to overview]Change From Week 20 to Week 47 Endpoint in the Sheehan Disability Scale (SDS)
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Clinical Global Impressions - Severity (CGI-S) of Depression Using Mixed-Effects Model Repeated Measures (MMRM) Analysis
NCT00958568 (39) [back to overview]Percentage of Participants Maintaining Response at Any Point During Stabilization Treatment Phase
NCT00958568 (39) [back to overview]Resource Utilization (Number of Psychiatric Visits, Number of Emergency Room or Equivalent Facility Visits for Psychiatric Illness)
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent High Fasting Triglycerides
NCT00958568 (39) [back to overview]Percent of Participants With Treatment-Emergent High Fasting Total Cholesterol
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Fasting Glucose
NCT00958568 (39) [back to overview]Mean Change in Corrected (for Rate) Cardiac QT Interval Using Fridericia's Formula (QTcF) on Electrocardiogram
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Weight
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Montgomery-Asberg Depression Rating Scale (MADRS) Using Mixed-Effects Model Repeated Measures (MMRM) Analysis
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Montgomery-Asberg Depression Rating Scale (MADRS) Using Last Observation Carried Forward (LOCF) Analysis
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Fasting Triglycerides
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Fasting Total Cholesterol
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Fasting Low-Density Lipoprotein (LDL) Cholesterol
NCT00958568 (39) [back to overview]Mean Change From Week 20 to Week 47 in Fasting High-Density Lipoprotein (HDL) Cholesterol
NCT00970281 (6) [back to overview]Percentage of Participants With Treatment-Emergent Extrapyramidal Symptoms Based on the Drug Induced Extrapyramidal Symptoms Scale (DIEPSS) Score up to 24 Hours After the First Intramuscular (IM) Injection
NCT00970281 (6) [back to overview]Percentage of Participants With Scores of 4 to 7 in the Agitation-Calmness Evaluation Scale (ACES) Score up to 24 Hours After the First Intramuscular (IM) Injection
NCT00970281 (6) [back to overview]Change From Baseline in the Positive and Negative Syndrome Scale - Excited Component (PANSS-EC) Total Score up to 24 Hours After the First Intramuscular (IM) Injection
NCT00970281 (6) [back to overview]Percentage of Participants With 40% or Greater Percent Decrease in the Positive and Negative Syndrome Scale - Excited Component (PANSS-EC) Total Score up to 2 Hours After the First Intramuscular (IM) Injection
NCT00970281 (6) [back to overview]Change From Baseline in PANSS-EC Total Score up to 90 Minutes After the First Intramuscular (IM) Injection
NCT00970281 (6) [back to overview]Change From Baseline in the Positive and Negative Syndrome Scale-Excited Component (PANSS-EC) Total Score up to 2 Hours After the First Intramuscular (IM) Injection
NCT00981526 (6) [back to overview]Body Composition: Percent Total Body Fat
NCT00981526 (6) [back to overview]Body Composition: Waist to Hip Ratio
NCT00981526 (6) [back to overview]Insulin Resistance
NCT00981526 (6) [back to overview]Triglycerides
NCT00981526 (6) [back to overview]Lipid Metabolism - LDL-cholesterol and HDL-cholesterol
NCT00981526 (6) [back to overview]Psychopathology - PANSS Total, PANSS - Negative Score, PANNS - Positive Score and SANS - Total Scores.
NCT00982020 (8) [back to overview]Mean Change From Baseline to 52 Weeks in Anchored Version of the Brief Psychiatric Rating Scale for Children (BPRS-C) for Participants With Schizophrenia
NCT00982020 (8) [back to overview]Mean Change From Baseline to 52 Weeks in Body Mass Index (BMI) for All Participants
NCT00982020 (8) [back to overview]Mean Clinical Global Impression of Improvement (CGI-I) at 52 Weeks for All Participants
NCT00982020 (8) [back to overview]Mean Change From Baseline to Endpoint in Body Mass Index (BMI) for Participants With Duration of Treatment of at Least 6 Months
NCT00982020 (8) [back to overview]Mean Change From Baseline to 52 Weeks in Waist Circumference for All Participants
NCT00982020 (8) [back to overview]Mean Change From Baseline to 52 Weeks in Adolescent Structured Young Mania Rating Scale (YMRS) for Participants With Bipolar I Disorder
NCT00982020 (8) [back to overview]Mean Change From Baseline to 52 Weeks in Clinical Global Impression - Severity (CGI-S) for All Participants
NCT00982020 (8) [back to overview]Time to Event for 7%, 15%, and 25% Weight Gain for All Participants
NCT01157351 (6) [back to overview]Time to First Psychiatric Hospitalization
NCT01157351 (6) [back to overview]Change From Baseline in Personal and Social Performance (PSP) Total Score During Overall Treatment Duration
NCT01157351 (6) [back to overview]Change From Baseline in Clinical Global Impression - Severity (CGI-S) Score During Overall Treatment Duration
NCT01157351 (6) [back to overview]Time to First Psychiatric Hospitalization or Arrest/Incarceration
NCT01157351 (6) [back to overview]Percentage of Participants in Each Event Category of First Treatment Failure
NCT01157351 (6) [back to overview]Time to First Treatment Failure
NCT01170117 (2) [back to overview]Rate of Weight Change
NCT01170117 (2) [back to overview]Psychological Change
NCT01427608 (4) [back to overview]Changes in Metabolic Measure: Cholesterol
NCT01427608 (4) [back to overview]Changes in Metabolic Measures: Triglycerides
NCT01427608 (4) [back to overview]Changes in Metabolic Measures: Weight
NCT01427608 (4) [back to overview]Number of Subjects at Risk of Relapse During the Randomized Phase.
NCT01496183 (13) [back to overview]Physical Activity as Measured Using a Physical Activity Monitor
NCT01496183 (13) [back to overview]Change From Baseline in Leptin
NCT01496183 (13) [back to overview]Change From Baseline in Resting Metabolic Rate
NCT01496183 (13) [back to overview]Change From Baseline Total Cholesterol
NCT01496183 (13) [back to overview]Change From Baseline Triglycerides
NCT01496183 (13) [back to overview]HDL
NCT01496183 (13) [back to overview]Laboratory Breakfast Intake
NCT01496183 (13) [back to overview]LDL
NCT01496183 (13) [back to overview]Change From Baseline in Weight
NCT01496183 (13) [back to overview]Change From Baseline in 24-Hour Dietary Recall
NCT01496183 (13) [back to overview]Change From Baseline in Body Composition
NCT01496183 (13) [back to overview]Change From Baseline in Glucose
NCT01496183 (13) [back to overview]Change From Baseline in Insulin
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Marder Factor Hostility/Excitement Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Marder Factor Negative Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Marder Factor Positive Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Negative Subscale Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Positive Subscale Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Total Score at Days 4, 7, 14, 21, 28 and 35
NCT01617187 (16) [back to overview]Percentage of Participants Who Are Clinical Global Impression Scale-Improvement (CGI-I) Responders at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Percentage of Participants Who Are PANSS Responders (≥30% Reduction From Baseline in PANSS Total Score) at Days 4, 7, 14, 21, 28 and 35
NCT01617187 (16) [back to overview]Change From Baseline in Body Weight at Day 42
NCT01617187 (16) [back to overview]Change From Baseline in CGI-S Score at Day 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS General Psychopathology Subscale Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Total Score at Day 42
NCT01617187 (16) [back to overview]Percentage of Participants Who Are PANSS Responders (≥30% Reduction From Baseline in PANSS Total Score) at Day 42
NCT01617187 (16) [back to overview]Change From Baseline in CGI-S Score at Days 4, 7, 14, 21, 28 and 35
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Marder Factor Anxiety/Depression Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01617187 (16) [back to overview]Change From Baseline in PANSS Marder Factor Disorganized Thought Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42
NCT01625923 (5) [back to overview]Change in Mean Gastric Emptying Time
NCT01625923 (5) [back to overview]Change in Mean Serum Glucose
NCT01625923 (5) [back to overview]Change in Mean Ghrelin Levels Over Time
NCT01625923 (5) [back to overview]Change in Mean BMI
NCT01625923 (5) [back to overview]Mean GCSI-DD Before/After Treatment With Olanzapine
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in the Barnes Akathisia Scale (BAS)
NCT01687478 (9) [back to overview]Percentage of Participants Who Achieve a Response Based on a ≥50% Reduction From Baseline in MADRS Total Score
NCT01687478 (9) [back to overview]Percentage of Participants Who Achieve Remission Based on MADRS Total Score ≤10 at 8 Weeks
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in the Sheehan Disability Scale (SDS)
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in the Short-Form 36 Health Survey (SF-36)
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in the Simpson-Angus Scale (SAS)
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in Clinical Global Impressions-Severity of Depression (CGI-S) Scale
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in Montgomery-Äsberg Depression Rating Scale (MADRS)
NCT01687478 (9) [back to overview]Mean Change From Baseline to 8 Week Endpoint in the Abnormal Involuntary Movement Scale (AIMS)
NCT01833897 (5) [back to overview]Hamilton Depression Rating Scale (HAM-D)
NCT01833897 (5) [back to overview]Beck's Depression Inventory
NCT01833897 (5) [back to overview]Hamilton Anxiety Scale
NCT01833897 (5) [back to overview]HAM-D Suicide Item
NCT01833897 (5) [back to overview]Loss of Motivated Behavior HAM-D Factor
NCT01903837 (5) [back to overview]Change in Clinical Global Impressions - Severity (CGI-S) From Baseline to Day 92
NCT01903837 (5) [back to overview]Absolute Change in Total Positive and Negative Syndrome Scale (PANSS) Score
NCT01903837 (5) [back to overview]Absolute Change in Body Weight (kg) From Baseline to Day 92
NCT01903837 (5) [back to overview]Percentage of Subjects Exhibiting Significant Weight Gain at Day 92
NCT01903837 (5) [back to overview]Percent Change in Body Weight (Kilogram) From Baseline to Day 92
NCT01920802 (8) [back to overview]Change in Adiposity
NCT01920802 (8) [back to overview]Change in Food Intake
NCT01920802 (8) [back to overview]Change in Insulin
NCT01920802 (8) [back to overview]Change in Lipid Metabolism
NCT01920802 (8) [back to overview]Insulin Resistance
NCT01920802 (8) [back to overview]Change Glucose in People Taking Olanzapine or Iloperidone
NCT01920802 (8) [back to overview]Change in Leptin
NCT01920802 (8) [back to overview]Change in Body Weight
NCT02097823 (6) [back to overview]Number of Participants With Adverse Events.
NCT02097823 (6) [back to overview]Feasibility of Recruitment and Data Collection.
NCT02097823 (6) [back to overview]Complete Response in Overall Phase
NCT02097823 (6) [back to overview]Complete Response in Delayed Phase
NCT02097823 (6) [back to overview]Complete Response in Acute Phase
NCT02097823 (6) [back to overview]Good Control of Nausea
NCT02116530 (5) [back to overview]Mean Scores of Potential Toxicities Related to Olanzapine as Measured by the Nausea and Vomiting Daily Diary/Questionnaire
NCT02116530 (5) [back to overview]Median Nausea Scores
NCT02116530 (5) [back to overview]Proportion of Patients With Complete Response
NCT02116530 (5) [back to overview]Proportion of Patients With no Nausea
NCT02116530 (5) [back to overview]Frequency of Rescue Medication
NCT02129478 (3) [back to overview]Patient Outcomes
NCT02129478 (3) [back to overview]Number of Participants With Adverse Events as a Measure of Safety and Tolerability
NCT02129478 (3) [back to overview]Proportion of Patients With Complete CINV Control
NCT02161718 (2) [back to overview]Number of Participants With Independent Adjudication Committee (IAC) Adjudicated Event of Exacerbation of Disease (EEDS)
NCT02161718 (2) [back to overview]Number of Events of Exacerbation of Disease (EEDS)
NCT02431702 (31) [back to overview]Part 3 (EDP): Number of Participants With Change From Baseline in Severity of Psychotic Symptoms, as Measured by CRDPSS
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Adjusted Intracortical Myelin (ICM) Fraction Score as Measured by Inversion Recovery (IR) and Spin Echo Magnetic Resonance Imaging (MRI)
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Attention/Vigilance Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Clinical Global Impression Severity (CGI-S) Score
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Cognition as Measured by the MATRICS Consensus Cognitive Battery (MCCB) Composite Score
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Functioning as Measured by the Personal and Social Performance (PSP) Total Score
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Medication Satisfaction Questionnaire (MSQ) Total Score
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Reasoning and Problem Solving: MCCB Domain
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Social Cognition Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Speed of Processing Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Verbal Learning Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Visual Learning Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Reasoning and Problem Solving: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Social Cognition Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Speed of Processing Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Change From Baseline in Working Memory Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (Disease Modification): Change From Baseline in Adjusted Intracortical Myelin Fraction Score as Measured by Inversion Recovery (IR) and Spin Echo Magnetic Resonance Imaging (SE MRI)
NCT02431702 (31) [back to overview]Part 3 (Disease Modification): Change From Baseline in Cognition as Measured by the MATRICS Consensus Cognitive Battery (MCCB) Composite Score
NCT02431702 (31) [back to overview]Part 3 (Disease Modification): Personal and Social Performance (PSP) Total Observed Score
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Adjusted Intracortical Myelin Fraction Score as Measured by Inversion Recovery (IR) and Spin Echo Magnetic Resonance Imaging (MRI)
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Visual Learning Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Clinical Global Impression Severity (CGI-S) Score
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Functioning as Measured by the Personal and Social Performance (PSP) Total Score
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Medication Satisfaction Questionnaire (MSQ) Score
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Attention/Vigilance Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Working Memory Score: MCCB Domain
NCT02431702 (31) [back to overview]Part 3 (EDP): Time to First Treatment Failure
NCT02431702 (31) [back to overview]Part 3 (Extended Disease Progression [EDP]): Change From Baseline in Cognition as Measured by the MATRICS Consensus Cognitive Battery (MCCB) Composite Score
NCT02431702 (31) [back to overview]Part-2 (Disease Progression): Time to First Treatment Failure
NCT02431702 (31) [back to overview]Part 2 (Disease Progression): Number of Participants With Change From Baseline in Severity of Psychotic Symptoms, as Measured by Clinician-Rated Dimensions of Psychosis Symptom Severity Scale (CRDPSS)
NCT02431702 (31) [back to overview]Part 3 (EDP): Change From Baseline in Verbal Learning Score: MCCB Domain
NCT02462473 (8) [back to overview]Patient Satisfaction Survey (PSS) Total Score at Week 0 and 12
NCT02462473 (8) [back to overview]Adherence to Antipsychotic Medication as Assessed by Brief Adherence Rating Scale (BARS) at Week 0 and 12
NCT02462473 (8) [back to overview]Antipsychotic Medication Plasma Levels (AMPL) During the Active Assessment Phase at Week 12
NCT02462473 (8) [back to overview]Clinical Global Impression-Severity (CGI-S) Score at Week 0 and 12
NCT02462473 (8) [back to overview]Clinician's Rating Scale of Adherence (CRS) Score at Week 0 and 12
NCT02462473 (8) [back to overview]Number of Participants With Medication Treatment Modifications (MTM)
NCT02462473 (8) [back to overview]Number of Participants With Factors Considered in Clinical Decision as Assessed by Clinical Assessment of the Schizophrenia Patient (CASP)
NCT02462473 (8) [back to overview]Dimensions of Psychosis Symptom Severity Scale (DPSS) Total Score at Week 0 and 12
NCT02484911 (12) [back to overview]Proportion of Participants Receiving HEC With Complete Response in Overall Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving HEC With Complete Response in the Acute Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving HEC With Complete Response in the Delayed Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving HEC With No Vomiting in the Acute Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving HEC With No Vomiting in the Delayed Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving HEC With No Vomiting in the Overall Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving MEC With Complete Response in Overall Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving MEC With Complete Response in the Acute Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving MEC With Complete Response in the Delayed Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving MEC With No Vomiting in the Acute Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving MEC With No Vomiting in the Delayed Phase
NCT02484911 (12) [back to overview]Proportion of Participants Receiving MEC With No Vomiting in the Overall Phase
NCT02536846 (33) [back to overview]Change in The Columbia Suicide Severity Rating Scale Score
NCT02536846 (33) [back to overview]Change in Surface Area of the Frontal, Parietal and Temporal Regions
NCT02536846 (33) [back to overview]Change in LUNSERS (Liverpool University Neuroleptic Side Effect Rating Scale) Score
NCT02536846 (33) [back to overview]Change in Hip Circumference
NCT02536846 (33) [back to overview]Change in Fractional Anisotropy (FA) Measured by Diffusion Tensor Imaging (DTI)
NCT02536846 (33) [back to overview]Change in fMRI Resting State Functional Connectivity
NCT02536846 (33) [back to overview]Change in Body Weight
NCT02536846 (33) [back to overview]Change in Young Mania Rating Scale (YMRS) Score
NCT02536846 (33) [back to overview]Change in Total Caloric Intake
NCT02536846 (33) [back to overview]Change in the Symptoms Checklist - 90 - Revised Global Severity Score
NCT02536846 (33) [back to overview]Change in the Prodromal Questionnaire, Brief Version Total Score
NCT02536846 (33) [back to overview]Change in Serum Insulin Levels
NCT02536846 (33) [back to overview]Change in Prolactin Levels
NCT02536846 (33) [back to overview]Change in Pittsburgh Sleep Quality Index Score
NCT02536846 (33) [back to overview]Change in Montgomery-Asberg Depression Rating Scale (MADRS) Score
NCT02536846 (33) [back to overview]Change in MATRICS Cognitive Consensus Battery (MCCB) Total Composite Score
NCT02536846 (33) [back to overview]Change in Brain Phosphocreatine (PCr)
NCT02536846 (33) [back to overview]Change in Fasting Total Cholesterol Level
NCT02536846 (33) [back to overview]Change in GABA Concentration
NCT02536846 (33) [back to overview]Change in Glutamate Metabolite Concentration
NCT02536846 (33) [back to overview]Change in The Wisconsin Schizotypy Scales - Short Form Scores
NCT02536846 (33) [back to overview]Change in Hemoglobin A1c Level
NCT02536846 (33) [back to overview]Change in Beck Anxiety Inventory (BAI) Score
NCT02536846 (33) [back to overview]Change in Waist Circumference
NCT02536846 (33) [back to overview]Change in Volumes of the Frontal, Parietal and Temporal Lobe Regions
NCT02536846 (33) [back to overview]Change in the World Health Organization Quality of Life Questionnaire Score
NCT02536846 (33) [back to overview]Change in the Early Psychosis Social Scale Survey Score
NCT02536846 (33) [back to overview]Change in the State-Trait Anxiety Inventory for Adults Scores
NCT02536846 (33) [back to overview]Change in Beck Depression Inventory (BDI) Score
NCT02536846 (33) [back to overview]Change in Blood Glucose Levels
NCT02536846 (33) [back to overview]Change in Brain Creatine Kinase (CK) Forward Reaction Rate
NCT02536846 (33) [back to overview]Change in Brain Nicotinamide Adenine Dinucleotide Metabolites NAD+/NADH
NCT02536846 (33) [back to overview]Change in Brain Parenchymal pH
NCT02634346 (3) [back to overview]Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total Score at Week 4
NCT02634346 (3) [back to overview]Incidence of Adverse Events
NCT02634346 (3) [back to overview]Change From Baseline in Clinical Global Impressions-Severity (CGIS) Score at Week 4
NCT02635984 (8) [back to overview]Percent of Patients Achieving Complete Protection in Overall Assessment Phase
NCT02635984 (8) [back to overview]Overall Percentage of Patients Who Had a Complete Response
NCT02635984 (8) [back to overview]Percent of Patients With Complete Response in Acute Phase
NCT02635984 (8) [back to overview]Percent of Patients With Complete Response in Delayed Phase
NCT02635984 (8) [back to overview]Percent of Patients With no Nausea in Overall Assessment Period
NCT02635984 (8) [back to overview]Percent of Patients With no Significant Nausea in Overall Assessment Period
NCT02635984 (8) [back to overview]Percent of Participants With no Significant Nausea in Acute Phase
NCT02635984 (8) [back to overview]Percent of Participants With no Significant Nausea in Delayed Phase
NCT02643355 (4) [back to overview]Clinical Opiate Withdrawal Scale Score at 1 Hour Post Medication
NCT02643355 (4) [back to overview]Clinical Opiate Withdrawal Scale Score at 2 Hours Post Medication
NCT02643355 (4) [back to overview]Clinical Opiate Withdrawal Scale Score at the Time of Disposition
NCT02643355 (4) [back to overview]Number of Participants That Received Rescue Medication for Withdrawal Symptoms Within 1 Hour
NCT02694328 (4) [back to overview]Number of Participants Experiencing of Adverse Events (AEs)
NCT02694328 (4) [back to overview]Percent Change From Baseline in Body Weight at Week 24
NCT02694328 (4) [back to overview]Percentage of Participants With >/= 7% Weight Gain at Week 24
NCT02694328 (4) [back to overview]Percentage of Participants With >/= 10% Weight Gain at Week 24
NCT02717195 (8) [back to overview]Change From Randomization to Week 10 in Global Clinical Impression - Severity of Illness (CGI-S) Score
NCT02717195 (8) [back to overview]Change From Randomization to Week 10 in Positive and Negative Syndrome Scale (PANSS) Total Score
NCT02717195 (8) [back to overview]Change From Randomization to Week 10 in PSP Total Personal and Social Performance (PSP) Total Score
NCT02717195 (8) [back to overview]Response at Week 10, Defined as ≥20% Reduction in PANSS Total Score, PANSS (Positive and Negative Syndrome Scale) Total Score ≤70, CGI-S (Clinical Global Impression Scale - Severity of Illness) Score <4
NCT02717195 (8) [back to overview]Response at Week 10, Defined as ≥20% Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Randomization
NCT02717195 (8) [back to overview]Response at Week 10, Defined as ≥30% Reduction in PANSS Total Score From Randomization
NCT02717195 (8) [back to overview]Response at Week 10, Defined as ≥40% Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Randomization
NCT02717195 (8) [back to overview]Response at Week 10, Defined as ≥50% Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Randomization
NCT02755116 (5) [back to overview]Number of Participants With Severe PONV
NCT02755116 (5) [back to overview]Number of Participants With Severe Nausea
NCT02755116 (5) [back to overview]Number of Participants With Postdischarge Vomiting
NCT02755116 (5) [back to overview]Number of Participants With Nausea and/or Vomiting
NCT02755116 (5) [back to overview]Number of Participants With PONV
NCT03019887 (1) [back to overview]Number of Participants With Relapse
NCT03066622 (3) [back to overview]Comparison of Duration of ED Length of Stay
NCT03066622 (3) [back to overview]Number of Participants That Receive Peripheral Intravenous Catheterization
NCT03066622 (3) [back to overview]Change in Pain Scores Based on Patient Questionnaire
NCT03137121 (3) [back to overview]Mean Nausea Scores
NCT03137121 (3) [back to overview]Number of Emetic Episodes
NCT03137121 (3) [back to overview]"Number of Treatment-related Adverse Events as Assessed by CTCAE v4.0."
NCT03187769 (6) [back to overview]Percentage of Subjects With ≥7% Weight Gain at Week 12
NCT03187769 (6) [back to overview]Percent Change From Baseline in Body Weight at Week 12
NCT03187769 (6) [back to overview]Percentage of Subjects With ≥10% Weight Gain at Week 12
NCT03187769 (6) [back to overview]Number of Participants Experiencing of Adverse Events (AEs)
NCT03187769 (6) [back to overview]Change From Baseline in Waist Circumference at Week 12
NCT03187769 (6) [back to overview]Change From Baseline in Clinical Global Impression-Severity (CGI-S) Score Within the ALKS 3831 Group at Week 12
NCT03230864 (5) [back to overview]Response
NCT03230864 (5) [back to overview]Change From Randomization to Week 8 in Global Clinical Impression - Severity of Illness (CGI-S) Score
NCT03230864 (5) [back to overview]Change From Randomization to Week 8 in PANSS Marder Negative Factor Score
NCT03230864 (5) [back to overview]Change From Randomization to Week 8 in Positive and Negative Syndrome Scale (PANSS) Total Score
NCT03230864 (5) [back to overview]Change From Randomization to Week 8 in 16-item Negative Symptom Assessment (NSA-16 Total) Score
NCT03557931 (8) [back to overview]Number of Participants With Adverse Event (AE)
NCT03557931 (8) [back to overview]Number of Participants With Clinically Significant Differences in Abnormal Involuntary Movement Scale (AIMS) Values
NCT03557931 (8) [back to overview]Number of Participants With Clinically Significant Differences in Barnes Akathisia Rating Scale (BARS) Values
NCT03557931 (8) [back to overview]Number of Participants With Clinically Significant Differences in Simpson Angus Scale (SAS) Values
NCT03557931 (8) [back to overview]Change From Baseline to Week 12/End of Treatment (EoT) in Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) Neurocognitive Composite Score
NCT03557931 (8) [back to overview]Change From Baseline to Week 12/EoT in University of California San Diego Performance-based Skills Assessment-2 Extended Range (UPSA-2-ER) Total Score
NCT03557931 (8) [back to overview]Number of Participants With Clinically Significant Differences in Columbia-Suicide Severity Rating Scale (C-SSRS) Values
NCT03557931 (8) [back to overview]Concentration at Trough Level (Ctrough) for ASP4345
NCT03568500 (2) [back to overview]Percentage Of Days With Good Patch Coverage
NCT03568500 (2) [back to overview]Participant Adherence
NCT03578081 (5) [back to overview]Potential Toxicities as Ascribed to Olanzapine as Measured by the Nausea and Vomiting Daily Diary/Questionnaire
NCT03578081 (5) [back to overview]Average Nausea Scores (0-10) Repeatedly Measured by the Nausea and Vomiting Daily Diary/Questionnaire
NCT03578081 (5) [back to overview]No Nausea Rate Defined as a Response of 0 in the Nausea Item of Nausea and Vomiting Daily Diary/Questionnaire in the Overall (0-120 Hours), Acute (0-24 Hours), and Delayed (24-120 Hours) Periods
NCT03578081 (5) [back to overview]Total Frequency of Rescue Medication as Measured by the Nausea and Vomiting Daily Diary/Questionnaire
NCT03578081 (5) [back to overview]Complete Response (CR) (no Emetic Episodes and no Use of Rescue Medication) During the Acute, Delayed and the Overall Periods as Measured by the Nausea and Vomiting Daily Diary/Questionnaire
NCT04535141 (10) [back to overview]Frequency of Nausea in the Acute Phase
NCT04535141 (10) [back to overview]Total Number of Rescue Medications Needed -Delayed
NCT04535141 (10) [back to overview]Number of Subjects Achieved Nausea Endpoint in the Delayed Phase.
NCT04535141 (10) [back to overview]Number of Subjects Achieved Emesis Endpoint in Acute Phase.
NCT04535141 (10) [back to overview]Total Number of Rescue Medications Needed Acute
NCT04535141 (10) [back to overview]Frequency of Somnolence
NCT04535141 (10) [back to overview]Number of Subjects Achieving Minimal Nausea
NCT04535141 (10) [back to overview]Safety Endpoint: Qtc Prolongation
NCT04535141 (10) [back to overview]Severity of Nausea in Delayed Phase
NCT04535141 (10) [back to overview]Number of Emesis Episodes in Delayed Phase

Change in the Bunney-Hamburg Rating Scale for Anxiety

Measures change in the severity of anxiety; Minimum score = 0; maximum score = 7; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-0.5
Clozapine Group0.6

[back to top]

Change in the Brief Psychiatric Rating Scale-24

A 24-item scale measuring change in interpersonal behaviors, mood, psychosis, anxiety, speech, sleep, orientation and physical activity. Lowest score = 24; highest score = 168; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-13
Clozapine Group-19

[back to top]

Change in Bunney-Hamburg Rating Scale for Mania

Measures change in the severity of mania; Minimum score = 0; maximum score = 7; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-0.4
Clozapine Group-0.8

[back to top]

Change in Bunney-Hamburg Rating Scale for Depression

Measures change in severity of depression; Minimum score = 0; maximum score = 7; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group0.4
Clozapine Group0.2

[back to top]

Change in Body Mass Index (BMI)

BMI is calculated by the following formula: weight (in kilograms) divided by the square of the height (in meters) (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

Interventionkg/m² (Mean)
Olanzapine Group1.4
Clozapine Group1.6

[back to top]

Change in the Scale for the Assessment of Positive Symptoms

Measures change in hallucinations, delusions, bizarre behavior, and thought organization. Minimum score = 0; maximum score = 170; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-7
Clozapine Group-21

[back to top]

Change in Extrapyramidal Movements as Measured by the Simpson Angus Scale Score

minimum score = 10; maximum score = 90; lower score considered a more favorable outcome (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

Interventionscores on a scale (Median)
Olanzapine Group0
Clozapine Group0

[back to top]

Change in Extrapyramidal Movements as Measured by the Abnormal Involuntary Movements Scale (AIMS)

minimum score = 10; maximum score = 50; lower score is considered a more favorable outcome (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

Interventionscores on a scale (Median)
Olanzapine Group0
Clozapine Group0

[back to top]

Change in the Scale for the Assessment of Negative Symptoms

Measures change in affective flattening or blunting, alogia, avolition/apathy, anhedonia/asociality, attention; minimum score = 0; maximum score = 125; lower values are considered a better outcome (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-14
Clozapine Group-25

[back to top]

Change in Weight

(NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

Interventionkilograms (Mean)
Olanzapine Group3.6
Clozapine Group3.8

[back to top]

Change in the Clinical Global Impression Severity of Symptoms Scale

Measures change in the severity of symptoms; Minimum score = 1; maximum score = 7; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-0.6
Clozapine Group-1.6

[back to top]

Change in the Bunney-Hamburg Rating Scale for Psychosis

Measures change in psychosis severity; Minimum score = 0; maximum score = 7; lower score is considered a better outcome. (NCT00001656)
Timeframe: 8 week double-blind study period; baseline and 8 weeks

InterventionScores on a scale (Mean)
Olanzapine Group-3.1
Clozapine Group-4

[back to top]

Number Who Discontinued Medication Within First 6 Study Months

(NCT00044655)
Timeframe: Measured at Six Months

Interventionparticipants (Number)
Stay11
Switch23

[back to top]

Change From Baseline in Weight at Week 8

change in weight from baseline to week 8 in kg (NCT00053703)
Timeframe: 8 weeks

InterventionKg (Mean)
Olanzapine6.12
Risperidone3.64
Molindone0.34

[back to top]

Change From Baseline in Barnes Akathisia Scale at Week 8

Barnes Akathisia Scale is a clinician rated scale which considers information based on observation of the participant as well as participant report. The scale includes 3 items rated between 0- none to 3 severe and 1 summary item rated between 0 none to 5 severe. All items are summed to obtain the total score. The minimal total score is 0 and the maximal score is 14 with higher scores reflecting more severe akathisia. A score of 4 or more is clinically significant. (NCT00053703)
Timeframe: 8 weeks

Interventionunits on a scale (Mean)
Olanzapine0.19
Risperidone0.41
Molindone1.23

[back to top]

Change From Baseline in Body Mass Index Change, kg/m2, at Week 8

Change from baseline in Body Mass Index Change, kg/m2, at week 8, last observation was carried forward for individuals who withdrew from treatment early. (NCT00053703)
Timeframe: 8 weeks

Interventionkg/m2 (Mean)
Olanzapine1.27
Risperidone2.20
Molindone0.15

[back to top]

Change From Baseline in PANSS Negative Symptom Subscale at Week 8

The PANSS (described above) includes 7 items that reflect negative psychotic symptoms such as amotivation and social withdrawal. As are all items within the PANSS, items are categorically rated by the clinician between 0 - no symptoms to 7 extreme symptoms. The minimal score is 0 reflecting no positive symptoms to 49 reflecting that all items were extreme. Higher scores reflect more severe symptoms. Scores above 18 are usually clinically significant. (NCT00053703)
Timeframe: 8 weeks

Interventionunits on a scale (Mean)
Olanzapine-5.3
Risperidone-5.1
Molindone-5.8

[back to top]

Change From Baseline in PANSS Positive Symptom Subscale Score at 8 Weeks.

The PANSS (described above) includes 7 items that reflect positive psychotic symptoms such as hallucinations and delusions. As are all items within the PANSS, items are categorically rated by the clinician between 0 - no symptoms to 7 extreme symptoms. The minimal score is 0 reflecting no positive symptoms to 49 reflecting that all items were extreme. Higher scores reflect more severe symptoms. Scores above 18 are usually clinically significant. (NCT00053703)
Timeframe: 8 weeks

Interventionunits on a scale (Mean)
Olanzapine-8.9
Risperidone-8.4
Molindone-8.8

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total Score at 8 Weeks

Assessed with the Positive and Negative Syndrome Scale in which a clinician rates various psychotic symptoms on the basis of observation of the participant, interview with the participant, and review of all other available information including informant reports. The scale consists of 30 items which are rated categorically between 1 - no symptoms to 7 - extreme symptoms. The minimal score is 0 and the maximal score is 210, with higher scores reflecting more symptoms. Typically scores > that 60 are considered clinically significant. (NCT00053703)
Timeframe: 8 weeks

Interventionunits on a scale (Mean)
Olanzapine-26.6
Risperidone-23.7
Molindone-27.0

[back to top]

Scores on CGI-S Compared to Baseline Over the Course of the Trial

A measure of overall symptom severity, the Clinical Global Impressions, Severity of Illness Scale (CGI-S). It is a seven point scale with a one indicating not at all ill, and seven indicating the most extremely ill. This rating was done each week after baseline by the PI at each site after visiting with the patient. (NCT00056472)
Timeframe: Weeks 1 to 12

Interventionunits on CGI scale (Mean)
Pharmacotherapy2.24
Monotherapy2.48

[back to top]

Mean Score Hamilton Depression Rating Scale (Ham-D) Over the Course of the Trial From Week to Week.

The Ham-D measures depression severity. Scores on Ham-D range from 0 to 52 with higher scores indicating more severe depression. (NCT00056472)
Timeframe: Weeks 1 to 12

InterventionScores on Ham-D (Mean)
Pharmacotherapy13.27
Monotherapy16.63

[back to top]

Remission of Depression Hamilton Depression Scale (Ham-D) and Psychosis Schedule for Affective Disorders in Schizophrenia - Delusional Item (SADS) During the Course of the Trial

"Remission was defined as scores on Ham-D of less than 10 at two consecutive assessments and the absence of delusions (measured as SADS delusional item scores of 1) at the second assessment of the two-assessment remission of depression interval.~Scores on Ham-D range from 0 to 52 with higher scores indicating more severe depression. Scores on SADS range from 1 to 7 with higher scores indicating the delusions(s) more adversely effect the subject's behavior." (NCT00056472)
Timeframe: Weeks 1 to 12

Interventionparticipants (Number)
Pharmacotherapy54
Monotherapy31

[back to top]

Change From Baseline in Weight at Month 76 Endpoint

Mean change in weight from baseline to last observation carried forward (LOCF) endpoint. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionkilogram (kg) (Mean)
Intramuscular Olanzapine Depot2.10

[back to top]

Number of Participants Having Normal Fasting Baseline Glucose Value With Treatment-Emergent High Fasting Glucose at Any Time Post Baseline

Normal to high fasting glucose ≤100 milligrams per deciliter (mg/dL) at baseline to ≥126 mg/dL any time post baseline. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
Intramuscular Olanzapine Depot20

[back to top]

Number of Participants With Potentially Clinically Significant (PCS) Weight Gain at Month 76 Endpoint

PCS weight gain is defined as a ≥7% increase in weight from baseline. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
Intramuscular Olanzapine Depot373

[back to top]

Change From Baseline in Clinical Global Impression-Severity of Illness (CGI-S) Scores at Month 72 Endpoint

Measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00088465)
Timeframe: Baseline, up to 72 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot-0.17

[back to top]

Number of Psychiatric Visits

Psychiatric visits were outpatient visits to a psychiatrist or psychiatric nurse. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionvisits (Number)
Intramuscular Olanzapine Depot14102

[back to top]

Change From Baseline in PANSS General Psychopathology Subscales at Month 76 Endpoint

PANSS General Psychopathology Subscale is the Remaining 16 PANSS questions or PANSS Question15 through Question 30. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). The sum of the 16 items is defined as the PANSS General Psychopathology Subscales. Possible score ranges from 16 to 112. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot0.19

[back to top]

Number of Participants With Treatment-Emergent Abnormal High Prolactin at Any Time Post Baseline

Prolactin normal reference ranges for female: 2.0 - 29.0 nanograms per milliliter (ng/mL); male: 2.0 - 20.0 ng/mL. High value is defined as a change from a value less than or equal to the high limit at all baseline visits to a value greater than the high limit at any time after baseline. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
Intramuscular Olanzapine Depot100

[back to top]

Patient Satisfaction With Medication Questionnaire-Modified (PSMQ) at Month 76 Endpoint

Self-rated scale that measures patient's level of satisfaction with current antipsychotic medication. Consists of 3 items assessing satisfaction with current study medication (scored from 1='very dissatisfied' to 5='very satisfied'), preference comparing current study medication versus previous medications (scored from 1='much prefer previous medication' to 5='much prefer study medication'), and side effects of current study medication compared with previous medications (scored from 1='much less side effects' to 5='much more side effects'). Range of possible scores is 3-15. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionpercent of participants (Number)
Depot, somewhat or very satisfiedDepot vs. oral, prefer or much preferDepot vs. oral, less or much less side effects
Intramuscular Olanzapine Depot73.266.873.3

[back to top]

Number of Participants With Treatment-Emergent Abnormal High Alanine Transaminase (ALT), High Aspartate Transaminase (AST), High Total Bilirubin at Any Time Post Baseline

High ALT is defined as a baseline value of <3 times the upper limit of normal (ULN) to ≥3 times the ULN at any time post baseline. High AST is defined as a baseline value of <5 times the ULN to ≥5 times the ULN at any time post baseline. High total bilirubin is defined as a baseline value of <2 times the ULN to ≥2 times the ULN at any time post baseline. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
ALT (n=901)AST (n=909)Total Bilirubin (n=912)
Intramuscular Olanzapine Depot615524

[back to top]

Number of Participants With Extrapyramidal Symptoms at Any Time

Extrapyramidal symptoms are defined as Simpson-Angus total score (SAS) >3 at any post-baseline visit; Barnes Akathisia Scale (BAS) global score ≥2 at any post-baseline visit; A score ≥3 for any of Abnormal Involuntary Movement Scale (AIMS) for items 1-7 or a score ≥2 for any two of these items. Score for SAS is 0-4 for each of the 10 questions, with 0=normal and 4=extreme. The possible total score for SAS is 0-40. Possible score for BAS is 0-5, with 0=absent and 5=sever. Score 0-4 for each item of AIMS, with 0 =none and 4= sever. Possible total score for items 1-7 is 0-28. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
SAS (n=819)BAS (n=856)AIMS (n=860)
Intramuscular Olanzapine Depot663428

[back to top]

Number of Participants With Adverse Events (AE)

The list of serious adverse events (SAE) and other non-serious adverse events (AE) are in Adverse Events Section. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
AESAE
Intramuscular Olanzapine Depot501170

[back to top]

Number of Participants Having Normal Fasting Baseline Lipid Value With Treatment-Emergent High Fasting Lipid at Any Time Post Baseline

Normal to high fasting total cholesterol ≤200 mg/dL at baseline to ≥240 mg/dL any time post baseline. Fasting triglycerides <150 mg/dL at baseline to ≥200 mg/dL and <500 mg/dL any time post baseline. (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventionparticipants (Number)
Cholesterol (n=873)Triglycerides (n=879)
Intramuscular Olanzapine Depot2841

[back to top]

Change From Baseline in 36-Item Short Form Health Survey (SF-36) at Month 76 Endpoint

A self-reported questionnaire that consists of 36 questions covering 8 health domains (physical functioning, social functioning, bodily pain, vitality, mental health, role-physical, role-emotional and general health). Each domain is scored by summing the individual items and transforming the scores into a 0 to 100 scale, with higher scores indicating better health status or functioning. The mental component summary (MCS) and the physical component summary (PCS) have been constructed based on the 8 SF-36 domains. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Mental component summaryPhysical component summary
Intramuscular Olanzapine Depot0.94-0.36

[back to top]

Change From Baseline in PANSS Positive Scores at Month 76 Endpoint

PANSS questions 1-7. Assesses positive symptoms associated with schizophrenia. 7 items make up the positive scale (ex. delusions, conceptual disorganization, and hallucinatory behavior). Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). Total positive subscale scores range from 7 to 49. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot0.21

[back to top]

Plasma Olanzapine Concentrations in Participants During Long-Term Treatment by Year

Plasma olanzapine concentrations are expressed as (nanogram/milliliter)/(milligram/day) ([ng/mL]/[mg/day]). (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Intervention(ng/mL)/(mg/day) (Mean)
0.25 year (n= 130)1 year (n= 189)2 years (n= 166)3 years (n= 148)4 years (n= 109)5 years (n= 87)6 years (n= 28)
Intramuscular Olanzapine Depot2.232.512.452.652.572.592.73

[back to top]

Change From Baseline in PANSS Negative Scores at Month 76 Endpoint

PANSS questions 8-14. Assesses negative symptoms associated with schizophrenia. 7 items make up the negative scale (e.g. blunted affect, emotional withdrawal, poor rapport, and passive/apathetic social withdrawal). Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). Total negative subscale scores range from 7 to 49. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot-0.08

[back to top]

Days of Hospitalization

This is the total number of days for all hospitalized patients that were admitted to General, Psychiatric Ward as well as Intensive Care Unit (ICU). (NCT00088465)
Timeframe: Randomization to end of study up to 76 months

Interventiondays (Number)
Regular hospitalPsychiatric hospitalICU
Intramuscular Olanzapine Depot238635587134

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total Scores at Month 76 Endpoint

Assesses the positive symptoms, negative symptoms, and general psychopathology specifically associated with schizophrenia. The scale consists of 30 items. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). The sum of the 30 items is defined as the PANSS total score and ranges from 30 to 210. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot0.30

[back to top]

Change From Baseline in the Heinrichs-Carpenter Quality of Life Scale (QLS) Total Score at Month 76 Endpoint

Heinrich-Carpenter QLS is an interviewer-rated scale which measures the impact of negative symptoms on occupational, social, and psychological functioning in patients with schizophrenia or schizoaffective disorder. Each of 21 items is rated on a scale from 0 (severely impaired functioning) to 6 (normal or adequate functioning), for a total score range of 0-126. Results are presented as change in Total score. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot6.75

[back to top]

Change From Baseline in the Subjective Well-Being Under Neuroleptic Treatment-Short Form (SWN-S) at Month 76 Endpoint

The Subjective Well-Being under Neuroleptic Treatment-Short Form (SWN-S) is a patient self-rated scale developed to measure the subjective well-being for the previous 7 days of a patient under neuroleptic treatment. The SWN-S consists of 20 items (each item is rated from 1=not at all to 6=very much). Possible total score ranges from 20-120. (NCT00088465)
Timeframe: Baseline, up to 76 months

Interventionunits on a scale (Mean)
Intramuscular Olanzapine Depot0.86

[back to top]

Percentage of Participants Who Switched to Symptomatic Depression

Switch to symptomatic depression was defined as HAMD-17 total score ≥13 at any time in the participants with HAMD-17 total scores ≤7 at baseline. The 17-item HAMD measures depression severity. Each item was evaluated and scored using either a 5-point scale (e.g. absent, mild, moderate, severe, very severe) or a 3-point scale (e.g. absent, mild, marked). The total score of HAMD-17 may range from 0 (normal) to 52 (severe). (NCT00129220)
Timeframe: 3 weeks, 6 weeks

,,
Interventionpercentage of participants (Number)
3-Week Symptomatic Depression Rate6-Week Symptomatic Depression Rate
Haloperidol16.716.7
Olanzapine2.42.4
Placebo1.32.7

[back to top]

Change From Baseline to 3 Week and 6 Week Endpoints in the Positive Subscore of Positive and Negative Syndrome Scale (PANSS)

Assesses positive symptoms associated with schizophrenia. 7 items make up the Positive scale (ex. delusions, conceptual disorganization, and hallucinatory behavior). Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). Total Positive Subscale scores range from 7 to 49. For this study, the score was converted to 0 to 6 for each item range; hence, the total positive subscale score ranges from 0 to 42. (NCT00129220)
Timeframe: Baseline, 3 weeks, 6 weeks

,,
Interventionunits on a scale (Mean)
3-Week Change6-Week Change
Haloperidol-1.8-1.6
Olanzapine-1.8-2.2
Placebo-0.0-0.3

[back to top]

Change From Baseline to 3 Week Endpoint in Young Mania Rating Scale (YMRS) Total Score

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00129220)
Timeframe: Baseline, 3 weeks

Interventionunits on a scale (Mean)
Olanzapine-12.6
Haloperidol-14.3
Placebo-6.8

[back to top]

Change From Baseline to 3 Week and 6 Week Endpoints in Clinical Global Impression - Bipolar Version (CGI-BP) Mania Subscale

A global rating scale for severity of patients adapted to bipolar disorder. Measures severity of the patient's overall severity of manic symptoms on a scale of 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00129220)
Timeframe: Baseline, 3 weeks, 6 weeks

,,
Interventionunits on a scale (Mean)
3-Week Change6-Week Change
Haloperidol-1.7-1.9
Olanzapine-1.2-1.7
Placebo-0.6-1.0

[back to top]

Remission Rate of Bipolar Disorder (Olanzapine Versus Haloperidol)

Remission of bipolar disorder was defined as completing the 6-week period with meeting the criteria for Young Mania Rating Scale (YMRS) total score of 12 or less and 17-Item Hamilton Depression Rating Scale (HAMD-17) total scores of 7 or less at Week 6. YMRS is an 11-item scale measuring severity of manic episodes; total score ranges = 0 (normal) to 60 (severe). The 17-item HAMD measures depression severity; total score ranges = 0 (normal) to 52 (severe). Remission Rate (percent) = number of patients meeting remission criteria divided by number of patients in treatment arm, multiplied by 100. (NCT00129220)
Timeframe: 6 weeks

Interventionpercentage of participants (Number)
Olanzapine44.2
Haloperidol20.0

[back to top]

Change From Baseline to 6 Week Endpoint in Young Mania Rating Scale (YMRS)

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00129220)
Timeframe: Baseline, 6 weeks

Interventionunits on a scale (Mean)
Olanzapine-16.0
Haloperidol-14.7
Placebo-10.1

[back to top]

Change From Baseline to 6 Week Endpoint in Clinical Global Impressions - Bipolar Version (CGI-BP), Overall Severity of Illness

A global rating scale for severity of patients adapted to bipolar disorder. Measures severity of the patient's overall severity of overall mood symptoms on a scale of 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00129220)
Timeframe: Baseline, 6 weeks

Interventionunits on a scale (Mean)
Olanzapine-1.6
Haloperidol-1.3
Placebo-0.9

[back to top]

Response Rate of Manic Symptoms at 3 Weeks and 6 Weeks

Participants who had 50 percent or more decrease from the baseline in YMRS total scores were defined as a responder. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. Response Rate (percent) = number of patients meeting response criterion for manic symptom divided by number of patients in treatment arm, multiplied by 100. (NCT00129220)
Timeframe: Baseline, 3 weeks, 6 weeks

,,
Interventionpercentage of participants (Number)
3 Week Response Rate6 Week Response Rate
Haloperidol65.065.0
Olanzapine51.067.3
Placebo44.355.7

[back to top]

Remission Rate of Manic Symptoms at 3 Weeks and 6 Weeks

Participants who had a YMRS total score of 12 or less were considered to be in remission of manic symptoms. YMRS is an 11-item scale that measures severity of manic episodes; total score ranges from 0 (normal) to 60 (severe). Remission Rate (percent) = number of patients meeting remission criteria divided by number of patients in treatment arm, multiplied by 100. (NCT00129220)
Timeframe: 3 weeks, 6 weeks

,,
Interventionpercentage of participants (Number)
3-Week Remission Rate6-Week Remission Rate
Haloperidol65.060.0
Olanzapine47.163.5
Placebo41.252.6

[back to top]

Percentage of Participants Who Switched to Syndromic Depression

Switch to syndromic depression was operationally defined by meeting both of the following criteria: At baseline, the symptoms did not meet the criteria for a mixed episode based on the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition, Text Revision (DSM-IV-TR). The critiera were met for a Major Depressive Episode (MDE), at any point after randomization, based on DSM-IV-TR. Rather than the 2-week period required for an MDE in the DSM-IV-TR, the patient had to meet the criteria of an MDE for at least 7 consecutive days (during Weeks 1 through 6). (NCT00129220)
Timeframe: 3 weeks, 6 weeks

,,
Interventionpercentage of participants (Number)
3-Week Syndromic Depression Rate6-Week Syndromic Depression Rate
Haloperidol5.35.3
Olanzapine0.01.1
Placebo0.00.0

[back to top]

Maximum Change From Baseline During 6-Week Period in Drug-Induced Extrapyramidal Symptoms Scale (DIEPSS) Total Score

Drug Induced Extra-Pyramidal Symptoms Scale (DIEPSS) is a scale used to evaluate the severity of drug induced extra-pyramidal symptoms occurring during antipsychotic drug treatment. Scale consists of 8 individual symptom scales with scores ranging from 0 (none/normal) to 4 (severe). The total score is the sum of the 8 item scores, for a total range of 0 (normal) to 32 (severe). (NCT00129220)
Timeframe: Baseline to 6 weeks

,,
Interventionunits on a scale (Mean)
BaselineMaximum Change from Baseline
Haloperidol0.502.70
Olanzapine0.200.70
Placebo0.300.09

[back to top]

Change From Baseline in Negative Symptoms of Schizophrenia Measured by the Negative Symptom Assessment (NSA) Scale Total Score

The NSA Scale is a 16-item clinician-rated instrument for rating the negative symptomatology of schizophrenia. Total score ranges from 16 to 96, with greater scores indicating greater severity of symptoms. (NCT00145496)
Timeframe: Day 182

,
InterventionUnits on a Scale (Mean)
BaselineChange From Baseline at Day 182
Asenapine60.4-9.7
Olanzapine61.3-9.2

[back to top]

Change From Baseline in Quality of Life Measured by the Quality of Life Scale (QLS) Total Score

The Quality of Life Scale is a 21-item clinician-rated scale for rating psychosocial functioning (Interpersonal Relations, Instrumental Role, Intrapsychic Foundations, and Common Objects and Activities). The score ranges from 0 to 126, with greater values indicating better quality of life. (NCT00145496)
Timeframe: Day 182

,
InterventionUnits on a Scale (Mean)
BaselineChange From Baseline at Day 182
Asenapine46.311.1
Olanzapine44.27.1

[back to top]

Change From Baseline in Body Weight

(NCT00145496)
Timeframe: Day 182

,
Interventionkg (Mean)
BaselineChange From Baseline at Day 182
Asenapine84.20.0
Olanzapine84.72.6

[back to top]

Concomitant Medications

"Concomitant medications are any medications taken on or after the date of first dose of double-blind study drug through the date of~last dose of double-blind study drug." (NCT00159783)
Timeframe: Up to 40 weeks

,,
InterventionParticipants (Number)
Participants with no concomitant medicationsParticipants with >=1 concomitant medication
Asenapine2158
Olanzapine3176
Placebo/Asenapine1022

[back to top]

Extrapyramidal Symptoms [EPS]

"EPS was assessed using the (1) involuntary movement scale [AIMS], (2) Barnes Akathisia Rating Scale [BARS], and (3) Simpson Angus Rating Scale SARS.~AIMS score range 0-4; higher scores indicate greater symptom severity.~BARS score rang 0-9; higher scores indicate greater severity of akathisia.~SARS score range 0-40; higher scores indicate greater degree of Parkinsonism." (NCT00159783)
Timeframe: Week 40 or endpoint

,,
InterventionUnits on a scale (Mean)
AIMSBARSSARS
Asenapine0.10.20.2
Olanzapine0.00.10.3
Placebo/Asenapine0.40.40.6

[back to top]

Number of Participants With Markedly Abnormal Vital Sign Changes

"Vital signs measured: sitting blood pressure, heart rate.~Definitions:~Markedly abnormal decreases: heart rate (HR) - if ≤50 bpm and decrease from baseline of ≥15 beats per minute (bpm); systolic blood pressure (SBP) - if ≤90 mm Hg and decrease from baseline of ≥20 mm Hg; diastolic blood pressure (DBP) - if ≤50 mm Hg and decrease from baseline of ≥15 mm Hg.~Markedly abnormal increases: HR - if ≥110 bpm and increase from baseline of ≥15 bpm; SBP - if ≥180 mm Hg and increase from baseline of ≥20 mm Hg; DBP - if ≥105 mm Hg and increase from baseline of ≥15 mm Hg." (NCT00159783)
Timeframe: Post-baseline (at Week 4, 12, 20, 28, and 40 or endpoint)

InterventionParticipants (Number)
Placebo/Asenapine2
Asenapine12
Olanzapine11

[back to top]

Number of Participants With Abnormal Physical Examination Findings

Physical exam (PE) included assessment of general appearance, skin, head, eyes, ears, nose, throat, lungs, blood pressure, cardiac rhythm & rate, neurologic status, and abdomen. The findings were deemed to be normal/abnormal based on the clinical judgment of the investigator. (NCT00159783)
Timeframe: Week 40 or endpoint

InterventionParticipants (Number)
All Treatment Groups32

[back to top]

Number of Participants With Laboratory Values Outside Normal Range

"Normal ranges were provided by the central laboratory.~Biochemistry = electrolytes, creatine kinase, liver enzymes, blood urea nitrogen, creatinine, alkaline phosphatase, protein, albumin~Metabolic chemistry = cholesterol, glucose, triglycerides, glycosylated hemoglobin~Endocrinology/miscellaneous = insulin, prolactin~Hematology = hemoglobin, red blood cell count, white blood cell count, platelets, hematocrit, neutrophils, lymphocytes, monocytes, eosinophils, basophils" (NCT00159783)
Timeframe: Week 40 or endpoint

,,
InterventionParticipants (Number)
BiochemistryMetabolic chemistryEndocrinology/miscellaneousHematology
Asenapine76323590
Olanzapine115963983
Placebo/Asenapine2517722

[back to top]

Body Weight

Weight change from baseline (NCT00159783)
Timeframe: Baseline to Week 40 or endpoint

,,
InterventionKilograms (Mean)
BaselineChange from baseline to Week 40 or endpoint
Asenapine68.13.5
Olanzapine72.06.0
Placebo/Asenapine81.41.7

[back to top]

Abdominal Girth

Change in abdominal girth from baseline (NCT00159783)
Timeframe: Baseline to Week 40 or endpoint

,,
InterventionCentimeters (cm) (Mean)
BaselineChange from baseline to Week 40 or endpoint
Asenapine86.82.6
Olanzapine89.45.0
Placebo/Asenapine91.13.0

[back to top]

Participants Who Experienced Adverse Event(s)

"Adverse event (AE) data, both serious and non-serious, were collected. Serious AEs were also collected up to 30 days post last dose of study drug.~An AE is defined as any untoward medical occurrence in a participant administered a pharmaceutical product. It does not necessarily have to have a causal relationship with this treatment.~An AE is defined as serious if it results in death, is life-threatening, requires in-patient hospitalization or prolongs existing hospitalization, results in persistent or significant disability/incapacity, or is a congenital anomaly/birth defect." (NCT00159783)
Timeframe: Up to 40 weeks

InterventionParticipants (Number)
Placebo/Asenapine23
Asenapine68
Olanzapine85

[back to top]

Number of Participants With Abnormal Electrocardiogram

This is the number of participants with electrocardiogram (ECG) adverse events. (NCT00159783)
Timeframe: Week 40 or endpoint

,,
InterventionParticipants (Number)
Sinus bradycardiaBundle branch block rightECG QRS complex prolongedECG ST segment depressionECG T wave inversionSupraventricular extrasystolesVentricular extrasystoles
Asenapine2100000
Olanzapine0011111
Placebo/Asenapine0000000

[back to top]

Change From Baseline in Negative Symptoms of Schizophrenia Measured by the Negative Symptom Assessment (NSA) Scale Total Score

The NSA Scale is a 16-item clinician-rated instrument for rating the negative symptomatology of schizophrenia. Total score ranges from 16 (best) to 96 (worst), with greater scores indicating greater severity of symptoms. (NCT00174265)
Timeframe: Baseline of A7501013 to Day 365

,
InterventionUnits on a Scale (Least Squares Mean)
BaselineChange from Baseline at Day 365
Asenapine61.5-15.8
Olanzapine60.3-11.0

[back to top]

Change From Baseline in Quality of Life Measured by the Quality of Life Scale (QLS) Total Score

The QLS is a 21-item clinician-rated scale for rating psychosocial functioning (Interpersonal Relations, Instrumental Role, Intrapsychic Foundations, and Common Objects and Activities). The score ranges from 0 (worst) to 126 (best), with greater values indicating better quality of life. (NCT00174265)
Timeframe: Baseline of A7501013 to Day 365

,
InterventionUnits on a Scale (Least Squares Mean)
BaselineChange from Baseline at Day 365
Asenapine45.312.4
Olanzapine42.311.7

[back to top]

BMI

BMI at baseline and at end of 15 months for Risperidone LAI and oral AAP groups (NCT00177164)
Timeframe: baseline to end of 15 months

,
Interventionkg / m^2 (Mean)
BaselineFinal
Oral AAP29.8632.0
Risperidone LAI31.0532.27

[back to top]

Number of Participants With Treatment Emergent Hyperlipidemia

Number of participants with Hyperlipidemia as determined by safety labs (NCT00177164)
Timeframe: from baseline to end of 15 months

Interventionparticipants (Number)
Risperidone LAI0
Oral AAP0

[back to top]

Number of Participants With Treatment - Emergent Hyperglycemia

Number of participants with hyperglycemia based on safety labs (NCT00177164)
Timeframe: from baseline to end of 15 months

Interventionparticipants (Number)
Risperidone LAI0
Oral AAP0

[back to top]

Evaluate the Number of Clinical Events (Pooled) Occurring Between 3-15 Months Following a Switch/Stabilization of the Antipsychotic Agents Among Patients Who Receive Either Risperidal Consta or One of the 4 Marketed 2nd Generation Antipsychotic Agents.

(NCT00177164)
Timeframe: Upto 15 months

InterventionNumber of clinical events (Mean)
Risperidone LAI0.86
Oral AAP1.61

[back to top]

Total Weeks Worked

(NCT00183625)
Timeframe: 24 months

InterventionWeeks (Mean)
Individual Placement and Support (IPS)51.53
Individual Placement and Support With Workplace Fundamentals41.37

[back to top]

Body Mass Index

Intent was to compare medication and not work group conditions. This was initially assessed at baseline and includes total time on either risperidone or olanzapine up to 18 months. (NCT00183625)
Timeframe: First 18 months of study

Interventionkg/m^2 (Least Squares Mean)
Risperidone Treatment29.21
Olanzapine Treatment30.4

[back to top]

Mean Change in Hamilton Anxiety Rating Scales (HAM-A)

"The HAM-A was one of the first rating scales developed to measure the severity of anxiety symptoms, and is still widely used today in both clinical and research settings. The scale consists of 14 items, each defined by a series of symptoms, and measures both psychic anxiety (mental agitation and psychological distress) and somatic anxiety (physical complaints related to anxiety). The HAM-A does not provide any standardized probe questions. Despite this,the reported levels of interrater reliability for the scale appear to be acceptable.~Each item is scored on a scale of 0 (not present) to 4 (severe), with a total score range of 0-56, where <17 indicates mild severity, 18-24 mild to moderate severity and 25-30 moderate to severe." (NCT00186017)
Timeframe: Baseline, 1 Week

Interventionunits on a scale (Mean)
Olanzapine/Zyprexa-7.9
Placebo-3.8

[back to top]

Mean Change in MADRS After 1 Week of Treatment.

Montgomery-Asberg Depression Rating Scales (MADRS) is a multi-item clinician tool assessing depression. Each item yields a score of 0 to 6. The overall score ranges from 0 to 60. Higher MADRS score indicates more severe depression. (NCT00186017)
Timeframe: Baseline, 1 week

Interventionunits on a scale (Mean)
Olanzapine/Zyprexa-12.3
Placebo-6.8

[back to top]

Mean Change in CGI-BP-OS After 1 Week of Treatment

The Clinical Global Impression - bipolar version - overall severity scale (CGI-S) is a 7-point scale that requires the clinician to rate the severity of the patient's illness at the time of assessment, relative to the clinician's past experience with patients who have the same diagnosis. Considering total clinical experience, a patient is assessed on severity of mental illness at the time of rating 1, normal, not ill; 2, minimally ill; 3, mildly ill; 4, moderately ill; 5, markedly ill; 6, severely ill; or 7, very severely ill (NCT00186017)
Timeframe: Baseline, 1 Week

Interventionunits on a scale (Mean)
Olanzapine/Zyprexa-1.4
Placebo.8

[back to top]

Mean Change in YMRS After 1 Week of Treatment

"The Young Mania Rating Scale (YMRS) scale has 11 items and is based on the patient's subjective report of his or her clinical condition over the previous 48 hours. Responses to each item are summed with a higher score indicating more mania symptoms endorsed.~Scale:0-60 0=Good 60=Bad" (NCT00186017)
Timeframe: Baseline, 1 week

Interventionunits on a scale (Mean)
Olanzapine/Zyprexa-6.0
Placebo-3.3

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Brief Psychiatric Rating Scale Scores.

Normalized insulin senstivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in Brief Psychiatric Rating Scale scores (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine0.035
Risperidone0.066

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Body Mass Index (BMI)

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in BMI (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.182
Risperidone-0.195

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Abnormal Involuntary Movement Scale Scores.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in Abnormal Involuntary Movement Scale scores (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine0.001
Risperidone-0.134

[back to top]

Pairwise Correlation Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Barnes Akathisia Scale Scores.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in Barnes Akathisia scores (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.120
Risperidone0.006

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Visceral Fat Area.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in visceral fat area (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.048
Risperidone-0.057

[back to top]

Change From Baseline to 12 Week Endpoint in Abnormal Involuntary Movement Scale Scores

A 12-item instrument assesses observed abnormal movements in different parts of body. Seven items are scored in a 5-point scale (0 = none/normal, 4 = severe) which evaluates abnormal movements in 3 main anatomic areas (orofacial area, extremities, and trunk). Total scores range from 0 to 28. Five collected elements are not used in this total. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionunits on a scale (Mean)
BaselineChange to last observation
Olanzapine0.480.04
Risperidone0.530.04

[back to top]

Pairwise Correlations Between Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Eating Behavior Assessment Scale Scores.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in Eating Behavior Assessment Scale scores (NCT00190749)
Timeframe: 12 weeks

,
Interventioncorrelation (Number)
Item 1: How Hungry?Item 2: How Strong Appetite?Item 3: Craved Sweets or Other Carbohydrates?Item 4: Craved Fatty Foods?Item 5: Felt Full or Satisfied After Meal?Item 6:Excessive Amount of Food to Feel Satisfied?Item 7: Thinking About Food?Item 8: Overeating?Item 9: Feel Eating is Out of Control?
Olanzapine-0.137-0.137-0.009-0.068-0.1170.134-0.172-0.032-0.075
Risperidone-0.371-0.2690.035-0.184-0.0600.0670.045-0.165-0.354

[back to top]

Change in Baseline to Last Observation In Normalized Insulin Sensitivity Index at Low Insulin Phase Using Change in Weight as a Covariate

Normalized insulin sensitivity index (Mffm/I) was defined as the ratio of whole body glucose disposal rate normalized to fat-free mass (Mffm) divided by the plasma insulin concentration (I) during steady-state conditions of the clamp procedure. Units:[(mg glucose)*min*mL] / [(kg fat free body mass)*(micro IU insulin)] (NCT00190749)
Timeframe: baseline and 12 weeks

,
InterventionMffm/I (Mean)
BaselineChange to Last Observation
Olanzapine0.1664-0.0149
Risperidone0.1937-0.0327

[back to top]

Change From Baseline to 12 Week Endpoint in Weight

Weight change from baseline to last visit (last observation carried forward) (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionkilograms (Mean)
BaselineChange to Last Observation
Olanzapine85.932.98
Risperidone86.551.23

[back to top]

Change From Baseline to 12 Week Endpoint in Waist Circumference

Waist circumference change from baseline to last observation carried forward. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventioncentimeters (Mean)
BaselineChange to Last Observation
Olanzapine99.132.38
Risperidone98.490.17

[back to top]

Change From Baseline to 12 Week Endpoint in Visceral Fat Area

Visceral fat area change from baseline to last observation carried forward, all randomized patients, double-blind treatment period (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionsquare centimeters (cm2) (Mean)
BaselineChange to Last Observation
Olanzapine101.464.70
Risperidone102.178.70

[back to top]

Change From Baseline to 12 Week Endpoint in the Ratio of the Visceral Fat Area to the Subcutaneous Fat Area

Ratio of the visceral fat area to the subcutaneous fat area change from baseline to last observation carried forward, all randomized patients, double-blind treatment period (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionratio in square centimeters (cm2) (Mean)
BaselineChange to last observation
Olanzapine0.410.01
Risperidone0.430.00

[back to top]

Change From Baseline to 12 Week Endpoint in Subcutaneous Fat Area

Subcutaneous fat area change from baseline to last observation carried forward, all randomized patients, double-blind treatment period (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionsquare centimeters (cm2) (Mean)
BaselineChange to last observation
Olanzapine281.074.94
Risperidone317.1635.15

[back to top]

Change From Baseline to 12 Week Endpoint in Simpson Angus Scale Scores

Measures neuroleptic-induced parkinsonism. Total score of Simpson Angus Scale consists of the sum of 10 items rated on a 5-point severity scale where 0=normal and 4=extreme. The total score ranges from 0 to 40. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionunits on a scale (Mean)
BaselineChange to last observation
Olanzapine1.13-0.06
Risperidone0.940.30

[back to top]

Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Triglycerides

Changes in fasting lipid parameters including triglycerides last observation carried forward (LOCF) mean change from baseline (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionmillimoles per Liter (mmol/L) (Mean)
BaselineChange to Last Observation
Olanzapine1.680.34
Risperidone1.55-0.10

[back to top]

Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Total Cholesterol

Fasting lipid parameters including total cholesterol, change from baseline to last observation carried forward. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionmillimoles per Liter (mmol/L) (Mean)
BaselineChange to Last Observation
Olanzapine4.910.18
Risperidone4.970.01

[back to top]

Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Lipoprotein Subclasses

Changes in lipid parameters and subclass lipoproteins last observation carried forward (LOCF) mean change from baseline. HDL=High Density Lipoprotein, IDL=Intermdiate Density Lipoprotein, LDL=Low Density Lipoprotein, VLDL=Very Low Density Lipoprotein. (NCT00190749)
Timeframe: baseline and 12 weeks.

,
Interventionnanomoles per Liter (nmol/L) (Mean)
HDL particles, total, baselineHDL particles, total, change to last observationIDL, baselineIDL, change to last observationMedium small LDL, baselineMedium small LDL, change to last observationSmall LDL, baselineSmall LDL, change to last observationVery small LDL, baselineVery small LDL, change to last observationVLDL mean particle size, baselineVLDL mean particle size, change to last observ.
Olanzapine28.391.7153.1821.40175.1535.70878.68128.55703.6392.7551.214.09
Risperidone29.81-1.0952.56-2.69197.00-11.47977.84-74.09780.78-62.5051.051.80

[back to top]

Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including High Density Lipoprotein (HDL)

Fasting lipid parameters including HDL change from baseline to last observation carried forward. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionmillimoles per Liter (mmol/L) (Mean)
BaselineChange to last observation
Olanzapine1.080.06
Risperidone1.180.05

[back to top]

Change From Baseline to 12 Week Endpoint in Fasting Lipid Parameters Including Direct Low Density Lipoprotein (LDL)

Fasting lipid parameters including Direct LDL, change from baseline to last observation carried forward. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionmillimoles per Liter (mmol/L) (Mean)
BaselineChange to last observation
Olanzapine3.18-0.03
Risperidone3.11-0.02

[back to top]

Change From Baseline to 12 Week Endpoint in Eating Behavior Assessment Scale Scores

Eating Behavior Assessment Scale is a 9-item self-rated tool used to evaluate appetite and eating behaviors. Item scores range from 0 (never) to 4 (always). (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionunits on a scale (Mean)
Item 1 Baseline (How Hungry?)Item 1 Change to Last ObservationItem 2 Baseline (How Strong Appetite?)Item 2 Change to Last ObservationItem 3 Baseline (Craved Sweets or Other Carbos?)Item 3 Change to Last ObservationItem 4 Baseline (Craved Fatty Foods?)Item 4 Change to Last ObservationItem 5 Baseline (Felt Full After Meal?)Item 5 Change to Last ObservationItem 6 Baseline(Excessive Food to Feel Satisfied?)Item 6 Change to Last ObservationItem 7 Baseline (Thinking About Food?)Item 7 Change to Last ObservationItem 8 Baseline (Overeating?)Item 8 Change to Last ObservationItem 9 Baseline (Feel Eating is Out of Control?)Item 9 Change to Last Observation
Olanzapine1.420.251.540.171.000.190.800.312.59-0.170.860.170.900.120.420.170.100.25
Risperidone1.320.421.320.380.830.360.740.252.550.000.790.280.770.130.530.150.260.11

[back to top]

Change From Baseline to 12 Week Endpoint in Clinical Global Impression - Severity of Illness Scores

Measures severity of illness at the time of assessment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionunits on a scale (Mean)
BaselineChange to last observation
Olanzapine3.65-0.22
Risperidone3.61-0.23

[back to top]

Change From Baseline to 12 Week Endpoint in Brief Psychiatric Rating Scale (BPRS) Scores

Brief Psychiatric Rating Scale (BPRS) is an 18-item clinician-administered scale used to assess the degree of severity of a subject's general psychopathological symptoms. Item scores range from 0 (not present) to 6 (extremely severe). Total Scores range from 0 to 108; Positive Subscale Scores range from 0 to 24. Negative Subscale Scores range from 0 to 18. Anxiety-Depression Subscale Scores range from 0 to 24. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionunits on a scale (Mean)
Total Score BaselineTotal Score Change to Last ObservationPositive Subscale Score BaselinePositive Subscale Score Change to Last ObservationNegative Subscale Score BaselineNegative Subscale Score Change to Last ObservationAnxiety-Depression BaselineAnxiety-Depression Change to Last Observation
Olanzapine13.32-1.985.22-0.822.32-0.384.33-0.78
Risperidone13.96-1.485.27-1.201.88-0.023.73-0.32

[back to top]

Change From Baseline to 12 Week Endpoint in Body Mass Index

Within-and Between-Treatment Group changes in Body Mass Index from baseline to last observation carried forward. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionkilograms per square meter (kg/m2) (Mean)
BaselineChange to Last Observation
Olanzapine28.961.02
Risperidone28.790.39

[back to top]

Change From Baseline to 12 Week Endpoint in Barnes Akathisia Rating Scale (BARS) Scores

The BARS is a 4-item instrument that evaluates akathisia associated with use of antipsychotic medications. Item 4 is the Global clinical assessment and is rated 0 to 5 (0 = absent, 5 = severe). The other 3 items (related to objective and subjective assessments) are not used for these analyses. (NCT00190749)
Timeframe: baseline and 12 weeks

,
Interventionunits on a scale (Mean)
BaselineChange to last observation
Olanzapine0.240.02
Risperidone0.36-0.02

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Weight.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in weight (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.212
Risperidone-0.188

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Waist Circumference.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in waist circumference (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.206
Risperidone-0.263

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in the Simpson Angus Scale Scores.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in the Simpson Angus Scale scores (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine0.184
Risperidone0.249

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Subcutaneous Fat Area.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in subcutaneous fat area (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.043
Risperidone-0.085

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Ratio of Visceral Fat Area to the Subcutaneous Fat Area.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in ratio of visceral far area to subcutaneous fat area (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine-0.055
Risperidone0.101

[back to top]

Pairwise Correlations Between Changes in Normalized Insulin Sensitivity Index at Low Insulin Phase and Changes in Clinical Global Impression - Severity of Illness Scale Scores.

Normalized insulin sensitivity index (Mffm/I) at low insulin phase-pairwise correlations between changes in Mffm/I and changes in Clinical Global Impression-Severity of Illness scale scores (NCT00190749)
Timeframe: 12 weeks

Interventioncorrelation (Number)
Olanzapine0.068
Risperidone0.234

[back to top]

Difference in Migraine Headache Periods During the Active Treatment Period as Compared to the Placebo Treatment Period, Per Subject.

"Definition of migraine headache period: One migraine period is defined as a 24-hour period starting at the time of onset of the migraine headache, during which the migraine headache is present*.~Definition of time frames: First treatment period: Day 1 to 84. Second treatment period: day 113-196. Washout phase is day 85-112." (NCT00203307)
Timeframe: 84 day period on placebo compared to 84 day period on olanzapine

Interventionheadache periods (Mean)
Olanzapine First, Then Placeb0

[back to top]

Change in DEXA % Body Fat

This study hypothesized that antipsychotic treatment would increase percent total body fat, as measured by whole body dual energy x-ray absorptiometry (DEXA), with larger adverse effects for olanzapine. (NCT00205699)
Timeframe: 12 weeks

Interventionpercent body fat (Mean)
Risperidone1.81
Olanzapine4.12
Aripiprazole1.66

[back to top]

Change in Insulin-stimulated Glucose Rate of Appearance (Glucose Ra)

This study hypothesized that antipsychotic treatment would decrease hepatic insulin sensitivity, as measured by the rate of appearance of glucose (glucose Ra), with larger adverse effects for olanzapine. (NCT00205699)
Timeframe: 12 weeks

Interventionpercentage of % change (Mean)
Risperidone-2.50
Olanzapine-6.57
Aripiprazole-3.27

[back to top]

Change in Insulin-stimulated Glucose Rate of Disappearance (Glucose Rd)

This study hypothesized that antipsychotic treatment would decrease insulin sensitivity at muscle, as measured by the insulin-stimulated rate of disappearance of glucose (glucose Rd), with larger adverse effects for olanzapine. (NCT00205699)
Timeframe: 12 weeks

Interventionpercentage of % change (Mean)
Risperidone2.30
Olanzapine-29.34
Aripiprazole-30.26

[back to top]

Change in Insulin-stimulated Glycerol Rate of Appearance (Glycerol Ra)

This study hypothesized that antipsychotic treatment would decrease insulin sensitivity at adipose tissue, as measured by the insulin-stimulated rate of disappearance of glycerol (glycerol Ra), with larger adverse effects for olanzapine. (NCT00205699)
Timeframe: 12 weeks

Interventionpercentage of % change (Mean)
Risperidone-3.65
Olanzapine-8.29
Aripiprazole1.70

[back to top]

Change in MRI-measured Visceral Abdominal Fat

This study hypothesized that antipsychotic treatment would increase visceral abdominal fat, as measured by abdominal magnetic resonance imaging (MRI), with larger adverse effects for olanzapine. (NCT00205699)
Timeframe: 12 weeks

InterventionChange in cm-squared (Mean)
Risperidone6.85
Olanzapine10.73
Aripiprazole12.04

[back to top]

Change in MRI-measured Subcutaneous Abdominal Fat

This study hypothesized that antipsychotic treatment would increase subcutaneous abdominal fat, as measured by abdominal magnetic resonance imaging (MRI), with larger adverse effects for olanzapine. (NCT00205699)
Timeframe: 12 weeks

InterventionChange in cm-squared (Mean)
Risperidone18.21
Olanzapine34.27
Aripiprazole15.84

[back to top]

Working Memory

"California Verbal Learning Test (CVLT) trials 1 through 5 is a well established neuropsychological test of working memory. The maximum score is 80 which reflects a better outcome and the minimum score is 0 which reflects a worse outcome.~The only meaningful analyses with adequate statistical power that could be reported were of the 10 schizophrenia patients who met nonresponse criteria to ziprasidone. The overall enrollment of 35 subjects was insufficient to perform the originally planned analyses in a statistically valid manner." (NCT00225498)
Timeframe: 3 months

Interventionunits on a scale (Mean)
Ziprasidone44.8

[back to top]

Baseline MATHYS Assessment - Principal Component Analysis and Orthogonal Transformation Matrix

This analysis indicates whether the total score is correct and provides enough information, or if subscores need to be calculated. Eigen value, proportion and cumulative are statistical parameters from the Principal Component Analysis, given for each factor. (NCT00259272)
Timeframe: Baseline

,,
Interventionvalue (Number)
Factor 1Factor 2Factor 3Factor 4Factor 5Factor 6Factor 7Factor 8Factor 9Factor 10Factor 11Factor 12Factor 13Factor 14Factor 15Factor 16Factor 17Factor 18Factor 19Factor 20
Cumulative0.43830.53890.59840.65050.69950.73920.77390.80610.83410.86080.88360.90550.92410.94120.95510.96820.97820.98730.99441.0000
Eigen Value8.772.011.191.0420.980.790.690.640.560.540.450.440.370.340.280.260.200.180.140.11
Proportion0.43830.10060.05940.05210.04900.03970.03470.03220.02800.02680.02270.02190.01860.01710.01390.01310.01000.00910.00710.0056

[back to top]

Change From Baseline to 6 Week and 24 Week Endpoints in HAMA Total Scores - According to Thymic Reactivity Assessment

The 14-item HAMA assesses the severity of anxiety. The investigator talked to the patient about their symptoms over the previous week before the study visit. Each item was scored using a 5-point scale, i.e. 0 = absent to 4 = severe. The total score of HAMA-14 may range from 0 (not present) to 56 (very severe). (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 Weeks

,,
Interventionunits on a scale (Mean)
Baseline (n=30, 101, 10)Change from 6 Week Endpoint (n=29, 93, 10)Change from 24 Week Endpoint (n=30, 99, 10)
Neither11.40-4.30-6.90
Thymic Hyper-Reactivity12.63-5.96-5.65
Thymic Hypo-Reactivity12.87-4.93-4.83

[back to top]

Mean Change From Baseline to 6 Week and 24 Week Endpoints in the Hamilton Anxiety Scale (HAMA) Total Score

The 14-item HAMA assesses the severity of anxiety. The investigator talked to the patient about their symptoms over the previous week before the study visit. Each item was scored using a 5-point scale, i.e. 0 = absent to 4 = severe. The total score of HAMA-14 may range from 0 (not present) to 56 (very severe). (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 Weeks

,,,
Interventionunits on a scale (Mean)
Baseline (n=36, 31, 26, 48)Change from 6 Week Endpoint (n=31, 31, 25, 45)Change from 24 Week Endpoint (n=35, 31, 26, 47)
Depressive Episode15.08-6.76-6.83
Hypomanic Episode11.94-5.48-5.65
Manic Episode7.78-2.68-2.26
Mixed Episode15.46-7.32-7.62

[back to top]

Increases and Decreases in Fasting Glucose Levels

(NCT00259272)
Timeframe: over 24 weeks

,,,
Interventionparticipants (Number)
At Least One Increase in Fasting Glucose (FG)At Least One Decrease in FGAt Least One Increase/Decrease in FGPatients Who Increase and Decrease During Study
Depressive Episode1011156
Hypomanic Episode98107
Manic Episode5472
Mixed Episode3131

[back to top]

Increases and Decreases in Lipid Levels

(NCT00259272)
Timeframe: over 24 weeks

,,,
Interventionparticipants (Number)
At Least One Increase for Total Cholesterol (TC)At Least One Decrease for TCAt Least One Increase/Decrease for TCPatients Who Increase & Decrease in TC≥1 Increase for High Density Lipoprotein (HDL)At Least One Decrease for HDLAt Least One Increase/Decrease for HDLPatients Who Increase & Decrease in HDL≥1 Increase for Low Density Lipoprotein (LDL)At Least One Decrease for LDLAt Least One Increase/Decrease for LDLPatients Who Increase & Decrease in LDLAt Least One Increase for Triglycerides (TG)At Least One Decrease for TGAt Least One Increase/Decrease for TGPatients Who Increase & Decrease in TG
Depressive Episode2016261011812717172591113168
Hypomanic Episode7912456838712377113
Manic Episode1811191084931581761112158
Mixed Episode111014765741171266785

[back to top]

Mean Change From Baseline to 24 Week Endpoint in Glycaemia Levels (Glucose Fasting Levels)

(NCT00259272)
Timeframe: baseline and 24 weeks

,,,
Interventionmilligrams per deciliter (Mean)
Baseline (n=33, 30, 23, 47)Change from 24 Week Endpoint (n=26, 28, 23, 40)
Depressive Episode88.527.31
Hypomanic Episode85.994.65
Manic Episode89.27-3.07
Mixed Episode85.943.89

[back to top]

Mean Change From Baseline to 6 Week and 24 Week Endpoints in the Hamilton 17-Items Depression Scale (HAMD-17) Total Score

The 17-item HAMD measures depression severity. Each item was evaluated and scored using either a 5-point scale (e.g. absent, mild, moderate, severe, very severe) or a 3-point scale (e.g. absent, mild, marked). The total score of HAMD-17 may range from 0 (not at all depressed) to 52 (severely depressed). (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 Weeks

,,,
Interventionunits on a scale (Mean)
Baseline (n=35, 30, 26, 48)Change from 6 Week Endpoint (n=29, 29, 25, 45)Change from 24 Week Endpoint (n=34, 30, 26, 47)
Depressive Episode16.06-8.51-7.96
Hypomanic Episode8.43-3.10-3.20
Manic Episode6.46-1.79-1.74
Mixed Episode12.65-5.60-5.50

[back to top]

Mean Changes From Baseline to 6 Week and 24 Week Endpoints in the Multidimensional Assessment of THYmic States Scale (MATHYS) Total Score

A visual analogic scale consisting of 20 items. Item scores vary from 0 (inhibition of the state evaluated by the item) to 10 (excitation for the evaluated state), except for items 5 to 10 and 17 and 18 which are inversed and are consequently to be reversed before the analysis. Total score is sum of the 20 items and can vary from 0 to 200. (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 weeks

,,,
Interventionunits on a scale (Mean)
Baseline (n=34, 31, 25, 48)6 Week Endpoint (n=31, 31, 25, 44)Change from 6 Week Endpoint (n=30, 31, 24, 44)24 Week Endpoint (n=35, 31, 26, 47)Change from 24 Week Endpoint (n=34, 31, 25, 47)
Depressive Episode76.8893.4117.1794.5817.04
Hypomanic Episode136.52105.15-31.37103.16-33.36
Manic Episode140.55115.37-22.91115.15-24.67
Mixed Episode116.74101.58-13.3291.56-26.08

[back to top]

Change From Baseline to 6 Week and 24 Week Endpoints in HAMD-17 Total Scores - According to Thymic Reactivity Assessment

The 17-item HAMD measures depression severity. Each item was evaluated and scored using either a 5-point scale (e.g. absent, mild, moderate, severe, very severe) or a 3-point scale (e.g. absent, mild, marked). The total score of HAMD-17 may range from 0 (not at all depressed) to 52 (severely depressed). (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 Weeks

,,
Interventionunits on a scale (Mean)
Baseline (n=29, 100, 10)Change from 6 Week Endpoint (n=28, 90, 10)Change from 24 Week Endpoint (n=28, 98, 10)
Neither9.50-4.00-3.80
Thymic Hyper-Reactivity10.64-4.89-4.55
Thymic Hypo-Reactivity14.48-6.61-6.48

[back to top]

Mean Change From Baseline to 24 Week Endpoint in Lipids

Baseline, change from baseline, and percent change for the following lipids are presented: Total Cholesterol (TC), High Density Lipoproteins (HDL), Low Density Lipoproteins (LDL), and Triglycerides (TG). (NCT00259272)
Timeframe: Baseline and 24 Weeks

,,,
Interventionmilligrams per deciliter (Mean)
TC Baseline (n=33, 30, 24, 46)Change in TC from 24 Week Endpoint (n=26,28,23,41)Percent Change in TC (n=26, 28, 23, 41)HDL Baseline (n=33, 30, 23, 46)Change in HDL from Endpoint (n=26, 28, 22, 41)Percent Change in HDL (n=26, 28, 22, 41)LDL Baseline (n=34, 30, 23, 46)Change in LDL from Endpoint (n=27, 27, 22, 41)Percent Change in LDL (n=27, 27, 22, 41)TG Baseline (n=35, 30, 23, 46)Change in TG from 24 Week Endpoint (n=27,28,22,41)Percent Change in TG (n=27, 28, 22, 41)
Depressive Episode203.774.414.6850.783.258.87128.81-1.193.41120.1513.8525.95
Hypomanic Episode191.552.263.1056.871.576.17112.161.285.15110.6625.8640.06
Manic Episode182.8823.6414.9650.211.246.04112.7614.2220.54115.818.3720.65
Mixed Episode210.517.034.4157.46-0.453.78129.709.4611.37131.37-1.164.10

[back to top]

Change From Baseline to 6 Week and 24 Week Endpoints in YMRS Total Scores - According to Thymic Reactivity Assessment

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 Weeks

,,
Interventionunits on a scale (Mean)
Baseline (n=27, 101, 10)Change from 6 Week Endpoint (n=26, 93, 10)Change from 24 Week Endpoint (n=27, 99, 10)
Neither10.00-6.50-7.60
Thymic Hyper-Reactivity16.50-10.45-11.29
Thymic Hypo-Reactivity4.48-2.38-1.70

[back to top]

Mean Change From Baseline to 6 Week and 24 Week Endpoints in the Young Mania Rating Scale (YMRS) Total Score

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00259272)
Timeframe: Baseline, 6 Weeks, 24 Weeks

,,,
Interventionunits on a scale (Mean)
Baseline (n=36, 31, 25, 46)Change from 6 Week Endpoint (n=31, 31, 24, 43)Change from 24 Week Endpoint (n=35, 31, 25, 45)
Depressive Episode2.78-0.86-0.82
Hypomanic Episode17.84-13.13-14.45
Manic Episode24.50-13.65-14.00
Mixed Episode12.96-9.67-10.60

[back to top]

Weight Gain Compared to Baseline

Weight gain at anytime more than 7%-15% or 25% of body weight compared to baseline (NCT00259272)
Timeframe: over 24 weeks

,,,
Interventionparticipants (Number)
No Significant Gain>25%>15%>7%Missing Data
Depressive Episode420051
Hypomanic Episode260230
Manic Episode300150
Mixed Episode180170

[back to top]

Wellness Interventional Program for Weight Gain Management in Patients (for Those Who Gain at Anytime More Than 7% of Body Weight, Compared to Baseline)

(NCT00259272)
Timeframe: 24 weeks

Interventionparticipants (Number)
Advised to Consult Dietician - NoAdvised to Consult Dietician - YesPerformed a Wellness Program - NoPerformed a Wellness Program - YesNumber of Wellnes Program Consults - 1Number of Wellnes Program Consults - 2Number of Wellnes Program Consults - 3Patients Losing Weight After ConsultationPatients Gaining Weight After ConsultationPatients with Stable Weight After Consultation
Weight Gain Subgroup816610523880

[back to top]

MATHYS Total Score at Baseline - According to Thymic Reactivity Assessment

A visual analogic scale consisting of 20 items. Items scores vary from 0 (inhibition of the state evaluated by the item) to 10 (excitation for the evaluated state), except for items 5 to 10 and 17 and 18, which are inversed and are consequently to be reversed before the analysis. Total score is sum of the 20 items and can vary from 0 to 200. (NCT00259272)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Thymic Hypo-Reactive81.24
Thymic Hyper-Reactivity122.49
Neither117.26

[back to top]

Mean Change From Baseline to 24 Week Endpoint in Weight

(NCT00259272)
Timeframe: Baseline and 24 weeks

Interventionkilograms (Mean)
Manic Episode1.37
Hypomanic Episode1.91
Mixed Episode1.78
Depressive Episode2.15

[back to top]

Obsessions

Obsessions subscale of the Yale-Brown Obsessive Compulsive Scale. Minimum score is 0 and maximum score is 20. Higher scores indicate higher levels of obsessions. (NCT00260962)
Timeframe: Pretreatment (Week 1) and Posttreatment (Week 13)

,
Interventionunits on a scale (Mean)
PretreatmentPosttreatment
Olanzapine Plus Day Hospital11.066.54
Placebo Plus Day Hospital9.115.86

[back to top]

Body Mass Index (BMI) (kg/m^2)

Body Mass Index (BMI) measured in kg/m^2 units. Measured at Baseline (week 2) and post-treatment (week 13). (NCT00260962)
Timeframe: Baseline (week 2) and post-treatment (week 13)

,
Interventionkg/m^2 (Mean)
Week 2 baselineWeek 13
Olanzapine Plus Day Hospital20.3020.30
Placebo Plus Day Hospital19.6619.66

[back to top]

Long-term Change in Negative Symptoms of Schizophrenia Measured by the Negative Symptom Assessment (NSA) Scale

Decrease from baseline in the NSA scores indicates improvement of efficacy. Range NSA total score is 16 [best]-96 [worst]. (NCT00265343)
Timeframe: Baseline of Protocol 25543 (NCT 00212836) to 365 days (total time for both protocols 25543 & 25544)

InterventionUnits on a Scale (Least Squares Mean)
Asenapine-16.9
Olanzapine-15.4

[back to top]

Change in Quality of Life Measured by Quality of Life Scale (QLS)

Increase from baseline in the QLS scores indicates improvement of efficacy. Range QLS total score is 0 [worst]-126 [best]. (NCT00265343)
Timeframe: Baseline of Protocol 25543 (NCT 00212836) to 365 days (total time for both protocols 25543 & 25544)

InterventionUnits on a Scale (Least Squares Mean)
Asenapine18.7
Olanzapine16.4

[back to top]

Number of Participants With Response of Manic Symptoms - Olanzapine Monotherapy Arm Only

Defined by a 50% or more reduction in YMRS total score from baseline in Study BMAC to endpoint. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. The primary objective was only interested in the effects in the olanzapine monotherapy arm. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy97

[back to top]

Number of Participants With Treatment-Emergent Dyskenisia Based on DIEPSS Scores

DIEPSS assesses the extrapyramidal symptoms attributable to antipsychotics. Consists of 9 items (8 to assess individual symptoms and 1 to assess global severity). Each item is assessed from 0 (none, normal) to 4 (severe). The total points of 8 items are defined as DIEPSS total (0 to 32 points). The items are classified into 4 categories of parkinsonism, akathisia, dystonia and dyskinesia. Treatment-emergent dyskenisia was defined as a score of equal or more than 2 or an increase of equal to or more than 2 points from baseline on the dyskenisia item (total score possible 0 to 4 points). (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy0
Olanzapine + Mood Stabilizer0

[back to top]

Number of Participants With Treatment-Emergent Dystonia Based on DIEPSS Scores

DIEPSS assesses the extrapyramidal symptoms attributable to antipsychotics. Consists of 9 items (8 to assess individual symptoms and 1 to assess global severity). Each item is assessed from 0 (none, normal) to 4 (severe). The total points of 8 items are defined as DIEPSS total (0 to 32 points). The items are classified into 4 categories of parkinsonism, akathisia, dystonia and dyskinesia. Treatment-emergent dystonia was defined as a score equal or more than 2 or an increase of equal or more than 2 points from baseline on the dystonia item (total score possible 0 to 4 points). (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy0
Olanzapine + Mood Stabilizer1

[back to top]

Number of Participants With Treatment-Emergent Parkinsonism Based on DIEPSS Scores

DIEPSS assesses the extrapyramidal symptoms attributable to antipsychotics. Consists of 9 items (8 to assess individual symptoms and 1 to assess global severity). Each item is assessed from 0 (none, normal) to 4 (severe). The total points of 8 items are defined as DIEPSS total (0 to 32 points). Parkinsonism is assessed by the total points of items 1 to 5 (total score of 0 to 20). Treatment-emergent parkinsonism was defined as a score of equal or greater than 3 on 1 item, equal or greater than 2 on 2 items, or an increase of equal or greater than 3 from baseline on the parkinsonism total. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy1
Olanzapine + Mood Stabilizer3

[back to top]

Clinical Global Impressions - Bipolar Version, Severity of Illness (CGI-BP) Overall, Visit Data

Measures severity of the patient's overall severity of bipolar symptoms (1=normal, not at all ill; 7=among the most extremely ill patients). (NCT00266630)
Timeframe: baseline, Weeks 1, 2, 4, 6, 10, 14, 18

,
Interventionunits on a scale (Mean)
baseline1 week2 weeks4 weeks6 weeks10 weeks14 weeks18 weeks endpoint
Olanzapine + Mood Stabilizer4.74.13.73.53.43.03.02.9
Olanzapine Monotherapy1.91.81.81.71.71.71.81.7

[back to top]

Number of Participants With Treatment-emergent Abnormal, High, or Low Laboratory Values

High density lipoprotein: males low 40 milligram/deciliter (mg/dL), high 80 mg/dL; females low 40 mg/dL, high 90 mg/dL. Low density lipoprotein (LDL): males and females low 70 mg/dL, high 139 mg/dL. Hemoglobin A1C (HBA1C): males and females low 4.3%, high 5.8%. (NCT00266630)
Timeframe: baseline through 18 weeks

,
Interventionparticipants (Number)
Low high density lipoprotein (HDL); n=93, n=36High high density lipoprotein (HDL); n=95, n=37Low low density lipoprotein (LDL); n=97; n=37High low density lipoprotein (LDL); n=71, n=31Low hemoglobin A1C (HBA1C); n=100, n=39High hemoglobin A1C (HBA1C); n=97, n=38
Olanzapine + Mood Stabilizer3111110
Olanzapine Monotherapy10512412

[back to top]

Change From Baseline to Endpoint on the YMRS Total Score - Olanzapine + Mood Stabilizer Only

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionunits on a scale (Mean)
Olanzapine + Mood Stabilizer-19.8

[back to top]

Positive and Negative Syndrome Scale Positive Scores - Visit Data

Assesses positive symptoms associated with schizophrenia. 7 items make up the Positive scale. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). Total Positive Subscale scores range from 7 to 49. For the analysis, the score was converted to 0 to 6 for each item range; hence, the total score ranges from 0 to 42. (NCT00266630)
Timeframe: baseline, Weeks 1, 2, 4, 6, 10, 14, 18

,
Interventionunits on a scale (Mean)
baseline1 week2 weeks4 weeks6 weeks10 weeks14 weeks18 week endpoint
Olanzapine + Mood Stabilizer12.510.510.110.110.19.99.99.9
Olanzapine Monotherapy7.77.57.57.47.37.47.47.4

[back to top]

Number of Participants With Potentially Clinically Significant Changes in Vital Signs and Weight

Low systolic blood pressure (SBP): <=90 millimeter mercury (mmHg) and decrease of >=20 mmHg; High SBP: >=180 mmHg and increase of >=20 mmHg; Low diastolic blood pressure (DBP): <=50 mmHg and decrease of >=15 mmHg; High DBP: >=105 mmHg and increase of >=15 mmHg; Low pulse: <50 beats per minute (bpm) and decrease of >=15 bpm; High pulse: >120 bpm and an increase of >=15 bpm; Low weight: decrease of >=7%; High weight: increase of >=7%; (NCT00266630)
Timeframe: baseline through 18 weeks

,
Interventionparticipants (Number)
Low systolic blood pressureHigh systolic blood pressureLow diastolic blood pressureHigh diastolic blood pressureLow weightHigh weightLow pulseHigh pulse
Olanzapine + Mood Stabilizer201011000
Olanzapine Monotherapy604131700

[back to top]

Number of Participants With Potentially Clinically Significant Changes in Laboratory Analytes

Triglycerides: high limit equal to or more than 500 milligram/deciliter (mg/dL); Glucose (non-fasting): low limit 2.4975 mmol/liter (L); high limit 13.875 mmol/L; Glucose (fasting): low limit 2.4975 mmol/L; high limit 6.993 mmol/L. (NCT00266630)
Timeframe: baseline through 18 weeks

,
Interventionparticipants (Number)
High triglycerides; n=100, n=38Low glucose (non-fasting); n=64, n=28High glucose (non-fasting); n=64, n=28Low glucose (fasting); n=40, n=6High glucose (fasting); n=40, n=6
Olanzapine + Mood Stabilizer20000
Olanzapine Monotherapy50003

[back to top]

Maximum Change From Baseline to Endpoint on the Drug Induced Extra-Pyramidal Symptoms Scale (DIEPSS) - Total Score

A scale used to assess the extrapyramidal symptoms attributable to antipsychotics. Consists of 9 items (8 to assess individual symptoms and 1 to assess global severity). Each item is assessed from 0 (none, normal) to 4 (severe). The total points of 8 items are defined as DIEPSS total (0 to 32 points). The items for the assessment of individual symptoms are classified into 4 categories of parkinsonism, akathisia, dystonia and dyskinesia. Parkinsonism is assessed by the total points of items 1 to 5; akathisia, dystonia and dyskinesia are assessed by the points given to the corresponding items. (NCT00266630)
Timeframe: baseline through 18 weeks

,
Interventionunits on a scale (Mean)
BaselineMaximum Change from baseline to endpoint
Olanzapine + Mood Stabilizer0.180.64
Olanzapine Monotherapy0.350.05

[back to top]

Number of Participants With Relapse of Depressive Symptoms

Assessed were participants meeting remission criteria for bipolar disorder in Study BMAC and have a HAMD-17 total score greater than or equal to 13 at any time. The 17-item HAMD measures depression severity. Each item was evaluated and scored using a 3-point scale (e.g. absent, mild, marked) or a 5-point scale (e.g. absent, mild, moderate, severe, very severe). The total score of HAMD-17 may range from 0 (normal) to 52 (severe). (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy4

[back to top]

Number of Participants With Potentially Clinically Significant Changes in Electrocardiograms - High Fridericia Corrected QT Interval (QTcF)

High QTcF: more than or equal to 450 milliseconds (msec) for males; more than or equal to 470 milliseconds (msec) for females (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy0
Olanzapine + Mood Stabilizer0

[back to top]

Number of Participants Who Switched to Syndromic Depression

As defined as a shift from a Manic Episode at baseline to a Major Depressive Episode, at any post baseline visit, based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text Revision. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy8
Olanzapine + Mood Stabilizer4

[back to top]

Number of Participants Who Experienced Switch to Symptomatic Depression as Measured by the Hamilton Depression Scale - 17 Item Version (HAMD-17)

Incidence of depressive symptoms was defined as a score of equal to or more than 13 points on the HAMD-17. The 17-item HAMD measures depression severity. Each item was evaluated and scored a 3-point scale (e.g. absent, mild, marked) or a 5-point scale (e.g. absent, mild, moderate, severe, very severe). The total score of HAMD-17 may range from 0 (normal) to 52 (severe). (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy4
Olanzapine + Mood Stabilizer1

[back to top]

Change From Baseline to Endpoint in Young Mania Rating Scale (YMRS) Total Scores - Olanzapine Monotherapy Arm Only

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. The primary objective was only interested in the effects in the olanzapine monotherapy arm. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionunits on a scale (Mean)
Olanzapine Monotherapy-3.0

[back to top]

Number of Participants With Treatment-Emergent Akathisia Based on DIEPSS Scores

DIEPSS assesses the extrapyramidal symptoms attributable to antipsychotics. Consists of 9 items (8 to assess individual symptoms and 1 to assess global severity). Each item is assessed from 0 (none, normal) to 4 (severe). The total points of 8 items are defined as DIEPSS total (0 to 32 points). The items are classified into 4 categories of parkinsonism, akathisia, dystonia and dyskinesia. Treatment-emergent akathisia was defined as a score of equal or more than 2 or an increase of equal or more than 2 points from baseline on the akathisia item (total score possible 0 to 4 points). (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy3
Olanzapine + Mood Stabilizer2

[back to top]

Number of Participants With Relapse of Manic Symptoms - Olanzapine Monotherapy Arm Only

Patients achieved remission in Study BMAC (defined as YMRS total score <=12 and HAMD-17 total score <=7) and obtained YMRS total score of >=15 at any time during Study BMEX. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. The primary objective was only interested in the effects in the olanzapine monotherapy arm. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy3

[back to top]

Number of Participants With Remission of Mania - Olanzapine Monotherapy Arm Only

Remission of Mania was defined as a YMRS total score of less than or equal to 12 at endpoint. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. The primary objective was only interested in the effects in the olanzapine monotherapy arm. (NCT00266630)
Timeframe: baseline through 18 weeks

Interventionparticipants (Number)
Olanzapine Monotherapy93

[back to top]

Number of Participants Who Experienced Remission of Bipolar Disorder

Participants who had equal to or less than 12 points in YMRS total score and equal to or less than 7 points in HAMD-17 total score at 18 weeks. YMRS: 11-item scale, measures the severity of manic episodes. 4 items are rated from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total: 0 to 60. The 17-item HAMD measures depression severity. Each item was evaluated and scored using a 3-point scale or a 5-point scale. HAMD-17 total score: 0 (normal) to 52 (severe). (NCT00266630)
Timeframe: Week 18

Interventionparticipants (Number)
Olanzapine Monotherapy54
Olanzapine + Mood Stabilizer12

[back to top]

Change in Brain Metabolism From Baseline to Eight Weeks as Seen in PET Scan

The primary aim of this imaging study was to examine the effect of olanzapine on brain metabolism over the eight weeks of administration. To compare the baseline PET scan to the endpoint scan, (NCT00275301)
Timeframe: Baseline to 8 weeks

InterventionStandard uptake value (Mean)
All Subjects Were Open-label and Took the Same Dose.11.5

[back to top]

Mean Change From Baseline to 16 Week Endpoint in the Clinical Global Impression-Severity (CGI-S) Scale

Measures severity of illness at the time of assessment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionunits on a scale (Least Squares Mean)
SODO-0.26
SOT-0.09

[back to top]

Number of Participants Discontinuing the Trial by Visit (Week)

The number of participants who discontinued by visit (non-cumulative). (NCT00303602)
Timeframe: Visit 2 (Baseline) to Visit 7 (Week 16)

,
Interventionparticipants (Number)
Visit 3 (Week 2) DiscontinuationsVisit 4 (Week 4) DiscontinuationsVisit 5 (Week 8) DiscontinuationsVisit 6 (Week 12) DiscontinuationsVisit 7 (Week 16) Discontinuations
SODO33553
SOT11661

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Glycosylated Hemoglobin

(NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionpercent (Mean)
SODO0.0
SOT0.0

[back to top]

Number of Participants Meeting a Definition for the Presence of Metabolic Syndrome as Defined by Adult Treatment Panel III (ATP III) Criteria at Baseline and 16 Week Endpoint

Patient meets definition of metabolic syndrome if they have >=3 risk factors: Waist circumference (men>102cm, women>88cm); triglycerides >=1.7mmol/L; HDL cholesterol (men<1.04mmol/L, women<1.30mmol/L); blood pressure >135/>=85 mmHg; Fasting glucose >=6.1mmol/L (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

,
Interventionparticipants (Number)
Baseline - Metabolic Syndrome (N=82, N=65)Endpoint - Metabolic Syndrome (N=70, N=52)
SODO1818
SOT1610

[back to top]

Number of Patients Achieving at Least 5% Loss of Body Weight in Any Post-Baseline Period

Percentage loss of body weight = 100*(postbaseline weight - baseline weight)/baseline weight (NCT00303602)
Timeframe: Visit 2 (Baseline) to Visit 7 (Week 16)

,
Interventionparticipants (Number)
Up to Week 2 (N=82, N=63)Up to Week 4 (N=79, N=63)Up to Week 8 (N=75, N=58)Up to Week 12 (N=70, N=54)Up to Week 16 (N=67, N=51)
SODO00234
SOT01246

[back to top]

Time Course of Change From Baseline in Body Mass Index (BMI)

Body mass index is an estimate of body fat based on body weight divided by height squared. Comparison of changes at various time points throughout the study. Change = Time point value minus baseline (Visit 2) value. (NCT00303602)
Timeframe: Visit 2 (Baseline) to Visit 7 (16 Weeks)

,
Interventionkilograms/square meters (Least Squares Mean)
Week 2 (N=82, N=63)Week 4 (N=79, N=63)Week 8 (N=75, N=58)Week 12 (N=70, N=54)Week 16 (N=67, N=51)
SODO0.090.250.340.470.52
SOT0.160.270.320.540.72

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Blood Pressure

Sitting blood pressure, taken from the same arm. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

,
Interventionmm Hg (Mean)
Systolic Blood PressureDiastolic Blood Pressure
SODO0.10.3
SOT-0.10.8

[back to top]

Change From Baseline to 16 Week Endpoint in Fasting Plasma Glucose

Patients should be fasting a minimum of eight hours prior to plasma glucose measurement. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionmillimole/Liter (Mean)
SODO0.2
SOT0.1

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Fasting Lipoproteins (Total Cholesterol, High-Density Lipoprotein Cholesterol [HDL-Cholesterol], Low-Density Lipoprotein Cholesterol [LDL-Cholesterol] [Calculated], and Triglycerides)

Patients should be fasting a minimum of eight hours prior to lipoprotein measurements. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

,
Interventionmillimole/Liter (Mean)
Total CholesterolHigh-Density Lipoprotein CholesterolLow-Density Lipoprotein Cholesterol (N=73, N=57)Triglycerides
SODO0.1-0.00.10.1
SOT0.2-0.00.20.0

[back to top]

Mean Changes From Baseline to 16 Week Endpoint Homeostasis Model Assessments of Insulin Sensitivity HOMA-S (Calculated)

HOMA-S is an estimate of insulin sensitivity. The HOMA model is a computer model of the glucose insulin feedback system in the fasted state. The model consists of a number of non-linear empirical equations describing the functions of organs and tissues involved in glucose regulation. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionpercent sensitivity (Mean)
SODO-18.5
SOT-9.8

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Waist Circumference

Waist circumference is measured on a bare abodomen just above the hip bone. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventioncentimeters (Mean)
SODO1.13
SOT0.77

[back to top]

Change From Baseline to 16 Week Endpoint in Subjective Appetite Using a Visual Analog Scale

Participant chooses where they think their appetite lies on a 10 centimeter line between two anchors (0 - very poor appetite and 10 - very strong appetite). The possible range of scores is 0 to 100 and represents millimeters on the 10 centimeter line. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionunits on a scale (Least Squares Mean)
SODO-8.21
SOT-5.02

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Weight

Weight of undressed patient (undergarments allowed), measured preferably at the same time each day. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (16 Weeks)

Interventionkilograms (Least Squares Mean)
SODO1.42
SOT2.08

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Body Mass Index (BMI) for the Treatment Completers

Body mass index is an estimate of body fat based on body weight divided by height squared. Comparisons of change from baseline to endpoint between participants who completed their treatment. Change = Endpoint value minus Baseline value. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (16 Weeks)

Interventionkilograms/square meters (Mean)
SODO0.56
SOT0.79

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Body Mass Index (BMI)

Body mass index is an estimate of body fat based on body weight divided by height squared. Comparison of change from baseline to endpoint. Change = Endpoint (Week 16) minus Baseline (Week 0) (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionkilograms/square meters (Mean)
SODO0.52
SOT0.67

[back to top]

Mean Change From Baseline to 16 Week Endpoint in Fasting Serum Insulin

Patients should be fasting a minimum of eight hours prior to serum insulin measurement. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

InterventionmicroIU/milliliter (Mean)
SODO2.4
SOT-0.1

[back to top]

Mean Change From Baseline to 16 Week Endpoint in the Subjective Well-Being Under Neuroleptics (SWN) Scale

Measures subjective well-being for previous 7 days. 20 items covering 5 health domains (subscales) (4 items each): emotional regulation, self-control, mental functioning, social integration, and physical functioning. Individual scores range from 1 (not at all) to 6 (very much). Subscale scores range from 1 to 24. Total score ranges from 1 to 120. (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionunits on a scale (Least Squares Mean)
SODO4.79
SOT1.60

[back to top]

Mean Change From Baseline to 16 Week Endpoint in the Global Assessment of Functioning (GAF) Scale

Measures physician's judgment of a patient's overall level of functioning. Ratings are based on a scale of 1 to 100, with the following classification range: 1-10 (severely impaired) to 91-100 (superior functioning). (NCT00303602)
Timeframe: Visit 2 (Baseline) and Visit 7 (Week 16)

Interventionunits on a scale (Least Squares Mean)
SODO4.61
SOT2.72

[back to top]

Change From Baseline in Clinical Global Impression - Severity of Illness (CGI-S) Scale Scores at 104 Weeks

Measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00320489)
Timeframe: Baseline, 104 weeks

InterventionUnits on a Scale (Least Squares Mean)
Olanzapine Pamoate Depot-0.36
Oral Olanzapine-0.27

[back to top] [back to top]

Median Time to Relapse

Relapse is defined as any 1 of the following: 1) hospitalization for symptoms related to schizophrenia; 2) increase of 25% from baseline in PANSS total score (range:30-210) (if baseline score was >40) or increase of 10 points (if baseline score was ≤40), and ≥1-point increase from baseline on CGI-S score (range:1-7), provided that increase results in CGI-S ≥4; 3) deliberate self-injury or injury to others deemed clinically to be associated with worsening of psychosis; 4) discontinuation from the study because of worsening of psychosis. On PANSS and CGI-S higher scores indicate greater illness. (NCT00320489)
Timeframe: Baseline to time of relapse (up to 104 weeks)

InterventionDays (Median)
Olanzapine Pamoate Depot539.00
Oral Olanzapine623.50

[back to top] [back to top]

Participants With Treatment-Emergent High Alanine Transaminase (ALT), Aspartate Transaminase (AST), and Total Bilirubin

Treatment-emergent (TE) high ALT is defined as a baseline value of <3 times the upper limit of normal (ULN) to >=3 times the ULN at endpoint. TE high AST is defined as a baseline value of <5 times the ULN to >=5 times the ULN at endpoint. TE high total bilirubin is defined as a baseline value of <2 times the ULN to >=2 times the ULN at endpoint. Hy's Rule is defined as ALT >=3 times the ULN and total bilirubin >=2 times the ULN. (NCT00320489)
Timeframe: Baseline through 104 Weeks

,
InterventionParticipants (Number)
ALT (n=255,251)AST (n=256,252)Total bilirubin (n=256,253)Hy's Rule (n=255,251)
Olanzapine Pamoate Depot11300
Oral Olanzapine12420

[back to top]

Participants With Normal to High Fasting Glucose, Fasting Total Cholesterol, and Fasting Triglycerides

Normal to high fasting glucose = <100 milligrams per deciliter (mg/dL) baseline; >=126 mg/dL any time post baseline (or endpoint). Normal to high fasting total cholesterol =<200 mg/dL baseline; >=240 mg/dL any time post baseline or endpoint. Fasting triglycerides <150 mg/dL baseline; >=200 mg/dL and <500 mg/dL any time post baseline or endpoint. (NCT00320489)
Timeframe: Baseline through 104 weeks

,
InterventionParticipants (Number)
Fasting Glucose (n=243,241)Fasting Total Cholesterol (n=242,231)Fasting Triglycerides (n=242,231)
Olanzapine Pamoate Depot251248
Oral Olanzapine171444

[back to top]

Change From Baseline in Working Alliance Inventory (WAI) Total Score at 104 Weeks

Self-rated scale assessing patients' level of alliance with their therapist, including agreement on goals, tasks, and emotional bond. Each of 12 items is rated from 1 ('never') to 7 ('always'), with higher scores indicating greater alliance. Total Scores range from 12-84. LS Mean values were adjusted for investigator and treatment at baseline, and the change values were also adjusted for baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
BaselineChange from Baseline to Week 104
Olanzapine Pamoate Depot63.83-0.92
Oral Olanzapine63.21-0.07

[back to top]

Change From Baseline in Weight at 104 Weeks

(NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionKilograms (Mean)
BaselineChange from Baseline to Week 104
Olanzapine Pamoate Depot81.562.04
Oral Olanzapine79.842.18

[back to top]

Change From Baseline in Schizophrenia Objective Functioning Instrument (SOFI) Global Score at 104 Weeks

Interviewer-rated 49-item scale used to assess 4 functional domains in patients with schizophrenia : 1) living situation, 2) instrumental activities of daily living, 3) productive activities and role functioning, and 4) social/recreational functioning. Possible responses and scoring vary by item and by domain, with higher scores representing better functioning. Range of possible scores is 1-100. LS Mean values were adjusted for investigator and treatment at baseline, and the change values were also adjusted for baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
BaselineChange from Baseline to Week 104
Olanzapine Pamoate Depot60.683.92
Oral Olanzapine60.473.26

[back to top]

Change From Baseline in Scale to Assess Unawareness of Mental Disorder (SUMD) Total Score at 104 Weeks

Interviewer-rated scale that assesses patients' awareness of and insight into their illness. SUMD can either be based on 4 items or 5 items. Items 1 through 4 are rated from 1 (aware) to 5 (unaware); item 5 assesses correct attribution of symptoms to a mental disorder and is rated from 1 (symptoms correctly attributed) to 5 (symptoms incorrectly attributed). Total Scores for Items (1-4) range from 4 to 20 and Total Scores for Items (1-5) range from 5 to 25. LS Mean values were adjusted for investigator and treatment at baseline, and the change values were also adjusted for baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
Total Score (Items 1-5) BaselineTotal Score (Items 1-5) Change to Week 104Total Score (Items 1-4) BaselineTotal Score (Items 1-4) Change to Week 104
Olanzapine Pamoate Depot11.12-0.728.81-0.39
Oral Olanzapine10.73-0.508.52-0.29

[back to top]

Change From Baseline in Overall Health Status Assessment Using the EuroQol: 5 Dimensions Questionnaire (EQ-5D) at 104 Weeks

Generic, multidimensional, health-related, quality-of-life instrument. Overall health status is self-reported using a visual analogue scale marked on a scale of 0 to 100 with 0 representing worst imaginable health state and 100 representing best imaginable health state. LS Mean values were adjusted for investigator and treatment at baseline; change values were also adjusted for baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
Baseline (n=193,192)Change from Baseline to Week 104 (n=128,130)
Olanzapine Pamoate Depot66.510.07
Oral Olanzapine72.180.09

[back to top]

Patient Satisfaction With Medication Questionnaire-Modified (PSMQ) at 104 Weeks (All Items)

Self-rated scale which measures patient's level of satisfaction with current antipsychotic medication. Consists of 3 items assessing satisfaction with current study medication (scored from 1-'very dissatisfied' to 5-'very satisfied'), preference comparing current study medication versus previous medications (scored from 1-'much prefer previous medication' to 5-'much prefer study medication'), and side effects of current study medication compared with previous medications (scored from 1-'much less side effects' to 5-'much more side effects'). Range of possible scores is 3-15. (NCT00320489)
Timeframe: 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
Overall satisfaction with current medicationPreference current/previous medication (n=139,145)Side effects - current vs previous medication
Olanzapine Pamoate Depot4.203.681.91
Oral Olanzapine3.963.831.99

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total and Subscale Scores at 104 Weeks

Assesses the positive symptoms, negative symptoms, and general psychopathology specifically associated with schizophrenia. The scale consists of 30 items. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). The sum of the 30 items is defined as the PANSS total score and ranges from 30 to 210. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
PANSS Total ScorePANSS Positive ScorePANSS Negative ScorePANSS General Psychopathology Score
Olanzapine Pamoate Depot-0.82-0.48-0.20-0.51
Oral Olanzapine-1.14-0.42-0.41-0.61

[back to top]

Change From Baseline in Brief Psychiatric Rating Scale (BPRS) Total Score at 104 Weeks

BPRS is an 18-item clinician-administered scale used to assess the degree of severity of a subject's general psychopathological symptoms. For this study, the BPRS total score was derived from 18 PANSS questions. To calculate the score, the score of the 18 questions was added then 18 was subtracted from the total. As an example, if a subject had a score=1 (absent) on all 18 items, the resulting total=zero. Responses range from 0 (absent) to 6 (extremely severe); the Total Score range is 0-108. (NCT00320489)
Timeframe: Baseline, 104 weeks

InterventionUnits on a scale (Least Squares Mean)
Olanzapine Pamoate Depot-0.96
Oral Olanzapine-0.91

[back to top]

Change From Baseline in Heinrich-Carpenter Quality of Life in Schizophrenia Scale (QLS) Total Score at 104 Weeks

Interviewer-rated scale which measures the impact of negative symptoms on occupational, social, and psychological functioning in patients with schizophrenia or schizoaffective disorder. Each of 21 items is rated on a scale from 0 (severely impaired functioning) to 6 (normal or adequate functioning). Total score range is 0-126. Least Squares Mean (LS Mean) values were adjusted for investigator and treatment at baseline, and the change values were also adjusted for baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
Baseline (n=193,193)Change from Baseline at Week 104 (n=130,135)
Olanzapine Pamoate Depot60.098.15
Oral Olanzapine57.737.24

[back to top]

Change From Baseline in Burden Assessment Scale (BAS) Total Score at 104 Weeks

"Self-rated scale completed by patient's caregiver which measures level of burden placed on the caregiver by caring for the patient. Each of 19 items is rated on a scale from 0 (no impact) to 3 (high negative impact). Total Score range is 0-57. If any of the 19 questions were answered not applicable, then a Total Score of 9 was entered. LS Mean values were adjusted for investigator and treatment at baseline, and the change values were also adjusted for baseline." (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
Baseline (n=104,103)Change from Baseline to Week 104 (n=68,64)
Olanzapine Pamoate Depot20.06-5.02
Oral Olanzapine20.90-4.14

[back to top]

Change From Baseline in 36-Item Short Form Health Survey (SF-36) at 104 Weeks, All Domains and Summary Scores

SF-36 Health Status Survey is a generic, health-related scale assessing subjects' quality of life on 8 domains. Domains and scores: general health=5-25; physical functioning=10-30; role-physical=4-8; role-emotional=3-6; social functioning=2-10; bodily pain=2-11; vitality=4-24; mental health=5-30. There are 2 summary scores (mental component summary [MCS] and physical component summary [PCS]). MCS and PCS scores=0-100 (higher scores indicate better health status). LS Mean values were adjusted for investigator and treatment at baseline; change values were also adjusted for baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

,
InterventionUnits on a Scale (Least Squares Mean)
Mental Score Detail at Baseline (n=188,193)Mental Score Detail Change at Week 104 (n=124,134)Physical Score Detail at Baseline (n=188,193)Physical Score Detail Change Week 104 (n=124,134)Physical Functioning at Baseline (n=193,194)Physical Functioning Change Week 104 (n=129,134)Role-Physical at Baseline (n=192,194)Role-Physical Change at Week 104 (n=130,134)Mental Health at Baseline (n=192,194)Mental Health Change at Week 104 (n=129,134)Bodily Pain at Baseline (n=193,194)Bodily Pain Change at Week 104 (n=131,134)General Health at Baseline (n=191,194)General Health Change at Week 104 (n=128,134)Social Functioning at Baseline (n=193,194)Social Functioning Change at Week 104 (n=131,134)Vitality at Baseline (n=193,194)Vitality Change at Week 104 (n=129,134)Role-Emotional at Baseline (n=191,193)Role-Emotional Change at Week 104 (n=129,134)
Olanzapine Pamoate Depot42.124.8747.800.4376.181.3563.6010.7061.185.8173.133.2360.502.6964.028.1354.077.9561.4516.38
Oral Olanzapine40.564.5247.910.8475.632.4460.7413.7660.105.2775.61-0.6059.575.3262.615.1049.679.0155.3417.59

[back to top]

Resource Utilization: Number of Outpatient Surgeries During the Study, 24 Months After Randomization

Number of outpatient surgeries during the study, post-baseline through 104 weeks. (NCT00320489)
Timeframe: Baseline through 104 Weeks

InterventionSurgeries (Mean)
Olanzapine Pamoate Depot0.00
Oral Olanzapine0.04

[back to top]

Resource Utilization: Number of Outpatient Physician Visits During the Study

Number of outpatient physician visits during the study, post-baseline through 104 weeks. (NCT00320489)
Timeframe: Baseline through 104 weeks

InterventionOutpatient physician visits (Mean)
Olanzapine Pamoate Depot0.32
Oral Olanzapine0.65

[back to top]

Patient Attitude Toward Treatment Using the Drug Attitude Inventory (DAI) Scale Total Score at 104 Weeks

Self-rated scale which measures patient's subjective feelings about taking medications. Each of 10 items is rated as true or false. For items 1, 3, 4, 6, 7, 9, and 10, true is scored as 1; false is scored as 0. For items 2, 5, and 8, true is scored as 0; false is scored as 1. Possible total scores range from 0-10. A subject who answers all 10 questions false will have a score of 3; a subject who answers all 10 questions true will have a score of 7. For 7 out of 10 questions, false is represented by 0, the other 3 questions false is represented by a value=1. (NCT00320489)
Timeframe: 104 weeks

InterventionUnits on a Scale (Least Squares Mean)
Olanzapine Pamoate Depot7.44
Oral Olanzapine7.47

[back to top]

Participants With Treatment-Emergent Abnormal High Prolactin at 104 Weeks

The prolactin reference Range is: Female: 2.0 - 29.0 nanograms per milliliter (ng/mL); Male: 2.0 - 20.0 ng/mL. A treatment-emergent abnormally high value is defined as a change from a value less than or equal to the high limit at all baseline visits to a value greater than the high limit at any time after baseline. (NCT00320489)
Timeframe: Baseline, 104 weeks

InterventionParticipants (Number)
Olanzapine Pamoate Depot12
Oral Olanzapine12

[back to top]

Participants With Potentially Clinically Significant (PCS) Weight Gain at 104 Weeks

PCS weight gain is defined as a >=7% increase in weight from baseline at 104 weeks. (NCT00320489)
Timeframe: Baseline, 104 weeks

InterventionParticipants (Number)
Olanzapine Pamoate Depot106
Oral Olanzapine97

[back to top]

Participants Discontinuing Because of an Adverse Event (AE) or Death

(NCT00320489)
Timeframe: Baseline through 104 weeks

InterventionParticipants (Number)
Olanzapine Pamoate Depot26
Oral Olanzapine27

[back to top] [back to top]

Number of Participants Experiencing Relapse

Relapse is defined as any one of the following: 1) hospitalization for symptoms related to schizophrenia; 2) an increase of 25% from baseline in the total score on the PANSS (if the baseline score was >40), or an increase of 10 points (if baseline score was <=40) and >=1-point increase from baseline score on the CGI-S score, provided that the increase results in a CGI-S score >=4; 3) deliberate self-injury or injury to others that is deemed clinically to be associated with worsening of psychosis; 4) discontinuation from the study because of worsening of psychosis. (NCT00320489)
Timeframe: Baseline through 104 weeks

InterventionParticipants (Number)
Olanzapine Pamoate Depot53
Oral Olanzapine48

[back to top]

Number of Hospitalization Days

Mean - calculated based on total number of hospitalization days per patient within reporting interval. (NCT00320489)
Timeframe: Baseline through 104 weeks

InterventionDays (Mean)
Olanzapine Pamoate Depot0.43
Oral Olanzapine1.80

[back to top]

Number of Patients Discontinuing From the Study

(NCT00330863)
Timeframe: Measured throughout study up to 30 months

Interventionparticipants (Number)
Injectable81
Oral80

[back to top]

Substantial Clinical Deterioration Measured by Psychotic Symptoms

Brief Psychiatric Rating Scale (BPRS) psychosis cluster. Score range is based on the score range for individual items rather than the factor total because is factors have different numbers of items. Score range is 1 -7 where 1 + no symptomatology and 7 = very severe symptoms. (NCT00330863)
Timeframe: Measured throughout study up to 30 months

Interventionunits on a scale (Least Squares Mean)
Injectable1.8
Oral2.0

[back to top]

Side Effects and Metabolic Measures

The highest severity of each of 24 adverse event (AE) that was assessed.over the 30 month study period. The mean severity on a scale of 1 (none) to 4 very severe symptom was recorded at each biweekly visit. Results for each variable are summarized over time so that each subject has a single mean severity rating for each AE. There is no named scale. Each of the side effects measured is named in ways that are clear to medical readers e.g anorexia. The range is 1 none to 4 very severe. Therefore, a higher scale score is worse. (NCT00330863)
Timeframe: Measured throughout study up to 30 months

,
Interventionunits on a scale (Mean)
Bruising easilyRashUrticaria (hives, itching)Blurred visionsedation/drowsinessRestlessnessInsomniaMalaise (weakness, fatigue)StiffnessTremorDizzinessHeadacheFeverSore ThroatDry MouthHypersalivationEnuresisConstipationDiarrheaAnorexia (loss of appetite)NauseaVomitingMenstrual IrregularityBreast tenderness/galactorrhea
Injectable1.431.531.601.762.342.482.382.222.011.771.821.991.271.642.361.761.631.751.651.891.781.481.621.39
Oral1.481.441.711.912.532.432.362.141.971.751.781.891.241.572.251.841.561.641.681.691.721.511.551.32

[back to top]

Vital Signs - Change From Baseline to 10 Week Endpoint in Standing Diastolic Blood Pressure

Change from Study Period III baseline to endpoint in standing blood pressure. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 and Week 12

,,
Interventionmm Hg (Mean)
BaselineChange from Baseline
EO-RIS80.29-1.73
NEO-OLZ78.691.01
NEO-RIS78.57-0.20

[back to top]

Vital Signs - Change From Baseline to 10 Week Endpoint in Standing Mean Arterial Pressure

Change from Study Period III baseline to endpoint in standing mean arterial pressure. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 and Week 12

,,
Interventionmm Hg (Mean)
BaselineChange from Baseline
EO-RIS94.60-1.94
NEO-OLZ93.530.68
NEO-RIS93.81-0.58

[back to top]

Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Body Mass Index

Body mass index is an estimate of body fat based on body weight divided by height squared. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 to Week 12

,,
Interventionkilogram per square meter (Mean)
BaselineChange from Baseline
EO-RIS31.130.10
NEO-OLZ29.970.63
NEO-RIS31.050.43

[back to top]

Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Body Weight

Change from Study Period III baseline to endpoint in body weight. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 and Week 12

,,
Interventionkilograms (Mean)
BaselineChange from Baseline
EO-RIS90.670.30
NEO-OLZ88.281.85
NEO-RIS90.251.29

[back to top]

Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Sitting Pulse Rate

Changes from Study Period III baseline to endpoint in sitting pulse rate. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 and Week 12

,,
Interventionbeats per minute (Mean)
BaselineChange from Baseline
EO-RIS77.90-0.94
NEO-OLZ80.49-0.98
NEO-RIS80.84-2.52

[back to top]

Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Standing Systolic Blood Pressure

Change from Study Period III baseline to endpoint in standing systolic blood pressure. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 and Week 12

,,
Interventionmm Hg (Mean)
BaselineChange from Baseline
EO-RIS123.20-2.36
NEO-OLZ123.200.01
NEO-RIS124.30-1.35

[back to top]

Mean Change From Baseline to 10 Week Endpoint in Extrapyramidal Symptoms as Measured by the Barnes Akathisia Rating Scale - Total Score

Evaluates akathisia associated with use of antipsychotic medications, includes objective and subjective component plus global impression rating for overall disorder. Components rated on scale of 0 to 3 for objective and subjective items and 0 to 5 for global clinical assessment, for total score of 0 (absence of akathisia) to 11 (severe akathisia). (NCT00337662)
Timeframe: Week 2 to Week 12

Interventionunits on a scale (Mean)
NEO-OLZ-0.31
NEO-RIS-0.13
EO-RIS-0.24

[back to top]

Mean Change From Baseline to 10 Week Endpoint in Extrapyramidal Symptoms as Measured by the Modified Simpson-Angus Scale

Measures neuroleptic-induced parkinsonism. Total score consists of the sum of 10 items: 7 items (items 1, 3, 4, 7, 8, 9, 10) rated on a 4-point severity scale where 0=normal and 4=extreme, and 3 items (items 2, 5, 6) rated on a 2-point severity scale where 0=normal and 2=definitely abnormal/present. The total score ranges from 0 to 34. (NCT00337662)
Timeframe: Week 2 to Week 12

Interventionunits on a scale (Mean)
NEO-OLZ-0.06
NEO-RIS-0.03
EO-RIS-0.02

[back to top]

Vital Signs - Mean Change From Baseline to 10 Week Endpoint in Standing Pulse Rate

Change from Study Period III baseline to endpoint in standing pulse rate. Change = Endpoint minus baseline. (NCT00337662)
Timeframe: Week 2 and Week 12

,,
Interventionbeats per minute (Mean)
BaselineChange from Baseline
EO-RIS82.39-0.56
NEO-OLZ85.57-1.13
NEO-RIS85.32-2.05

[back to top]

Changes From Study Period II Baseline (Week 0) to Weeks 3, 4, 6, 8, and 12 in Positive and Negative Syndrome Scale (PANSS) Total Score in Early Onset Response and Not Early Onset Response-Risperidone Patients

Assesses positive symptoms, negative symptoms, and general psychopathology specifically associated with schizophrenia. Scale consists of 30 items. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). Sum of 30 items is PANSS total score and ranges from 30 to 210. Change = time point - single-blind baseline (Week 0). (NCT00337662)
Timeframe: Weeks 0, 3, 4, 6, 8, 12

,
Interventionunits on a scale (Least Squares Mean)
Change from Week 0 to Week 3Change from Week 0 to Week 4Change from Week 0 to Week 6Change from Week 0 to Week 8Change from Week 0 to Week 12
EO-RIS-30.80-32.53-32.90-34.10-35.09
NEO-RIS-11.90-14.81-16.23-18.10-18.62

[back to top]

Changes From Study Period III Baseline (Week 2) to Weeks 3, 4, 6, 8, and 12 in Positive and Negative Syndrome Scale Total Score in Not Early Onset Response-Risperidone and Not Early Onset Response-Olanzapine Patients

Assesses positive symptoms, negative symptoms, and general psychopathology specifically associated with schizophrenia. Scale consists of 30 items. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). Sum of 30 items is PANSS total score and ranges from 30 to 210. Change = time point - double-blind baseline (Week 2). (NCT00337662)
Timeframe: Weeks 2, 3, 4, 6, 8, 12

,
Interventionunits on a scale (Least Squares Mean)
Change from Week 2 to Week 3Change from Week 2 to Week 4Change from Week 2 to Week 6Change from Week 2 to Week 8Change from Week 2 to Week 12
NEO-OLZ-5.85-9.67-13.06-14.73-17.02
NEO-RIS-6.94-9.82-11.25-13.13-13.53

[back to top]

Number of Participants in the Early Onset and Not Early Onset-Risperidone Groups Who Show a 50% or Greater Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Baseline or Meet 'a Priori' Specified Criteria for Remission

'a priori' specified criteria for remission defined as a score of 3 (mild), 2 (minimal), or 1 (absent) on all of the following 8 PANSS items: delusions, conceptual disorganization, hallucinatory behavior, unusual thought content, mannerisms and posturing, blunted effect, passive/apathetic withdrawal, lack of spontaneity and flow of conversation. (NCT00337662)
Timeframe: Week 0 to Week 12

,
Interventionparticipants (Number)
>=50% Reduction - Yes>=50% Reduction - No
EO-RIS8751
NEO-RIS67122

[back to top]

Number of Participants in the Not Early Onset-Risperidone and Not Early Onset-Olanzapine Groups Who Show a 50% or Greater Reduction in Positive and Negative Syndrome Scale Total Score From Baseline or Meet 'a Priori' Specified Criteria for Remission

'a priori' specified criteria for remission defined as a score of 3 (mild), 2 (minimal), or 1 (absent) on all of the following 8 PANSS items: delusions, conceptual disorganization, hallucinatory behavior, unusual thought content, mannerisms and posturing, blunted effect, passive/apathetic withdrawal, lack of spontaneity and flow of conversation. (NCT00337662)
Timeframe: Week 2 to Week 12

,
Interventionparticipants (Number)
>=50% Reduction - Yes>=50% Reduction - No
NEO-OLZ67112
NEO-RIS67122

[back to top]

Number of Participants With Psychiatric Hospitalizations in the Early Onset and Not Early Onset-Risperidone Groups

Psychiatric Hospitalizations were measured by the Modified Schizophrenia Care and Assessment Program Health Questionnaire (SCAP-HQ) from which it could be determined the number of patients with a psychiatric episode that required an overnight stay in a hospital. (NCT00337662)
Timeframe: Week 2 to Week 12

,
Interventionparticipants (Number)
Required overnight stay in hospital: YesRequired overnight stay in hospital: No
EO-RIS10127
NEO-RIS9175

[back to top]

Mean Change From Baseline to 10 Week Endpoint in Extrapyramidal Symptoms as Measured by the Abnormal Involuntary Movement Scale (AIMS)- Non-Global Total Score

A 12-item instrument assesses observed abnormal movements in different parts of body. Ten items are scored in a 5-point scale (0 = none/normal, 4 = severe) which evaluates abnormal movements in three main anatomic areas (orofacial area, extremities, and trunk). Two items are yes/no questions regarding dentures. Total scores range from 0 to 42. (NCT00337662)
Timeframe: Week 2 to Week 12

Interventionunits on a scale (Mean)
NEO-OLZ-0.38
NEO-RIS0.11
EO-RIS-0.16

[back to top]

Number of Participants With Treatment-Emergent Abnormal Fasting Laboratory Analytes Reported in >=2% of All Participants

Number of participants who experienced abnormal fasting laboratory values at any time during Study Period III. Laboratory reference ranges are dependent on the patient's gender, origin, and age. (NCT00337662)
Timeframe: Week 2 to Week 12

,,
Interventionparticipants (Number)
Low total bilirubinHigh creatine phosphokinaseHigh creatinineHigh hemoglobin A1cLow sodiumHigh prolactin
EO-RIS253247
NEO-OLZ562647
NEO-RIS314748

[back to top]

The Number of Participants in the Early Onset (EO) and Not Early Onset-Risperidone (NEO-RIS) Groups Who Show a 20% or Greater Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score

The number of participants who experienced a 20% or greater reduction in their PANSS Total score during the 12 weeks they were on risperidone. (NCT00337662)
Timeframe: Week 0 to Week 12

,
Interventionparticipants (Number)
>=20% Reduction - Yes>=20% Reduction - No
EO-RIS11919
NEO-RIS9495

[back to top]

The Number of Participants in the Not Early Onset-Risperidone (NEO-RIS) and Not Early Onset-Olanzapine (NEO-OLZ) Groups Who Show a 20% or Greater Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score

The number of not early onset participants who experienced a 20% or greater reduction in PANSS Total Score at any time during the 12 weeks of combined Study Period II and Study Period III. (NCT00337662)
Timeframe: Week 0 to Week 12

,
Interventionparticipants (Number)
>=20% Reduction - Yes>=20% Reduction - No
NEO-OLZ9485
NEO-RIS9495

[back to top]

Change in Visceral Fat Mass From Baseline to Week 26

CT measured change in visceral fat mass from baseline to week 26 (mm^3) (NCT00338949)
Timeframe: Baseline and Week 26

Interventionmm^3 (Mean)
Control315
Switch392

[back to top]

Change in Insulin Sensitivity Index From Baseline to Week 26 ((1/mU/L) x 1/Min)

As measured by frequently sampled intravenous glucose tolerance testing (units: 1/mU/L) x 1/Min) (NCT00338949)
Timeframe: Measured at Baseline and Week 26

Intervention(1/mU/L) x 1/Min (Mean)
Control0.072
Switch0.407

[back to top]

Change in Positive Symptoms by Treatment Assignment

"The Brief Psychiatric Rating Scale (BPRS) consists of 20 items, with 6 of these items used to assess positive symptom change. The BPRS positive symptom items are: somatic concern, conceptual disorganization, hostility, suspiciousness, hallucinatory behavior, and unusual thought content. Each scale ranges from 1=Not Present to 7=Very Severe. A higher score indicates a more severe positive symptom rating." (NCT00349973)
Timeframe: Baseline and follow-up

,
Interventionunits on a scale (Mean)
Baseline - Somatic ConcernFollow-Up - Somatic ConcernBaseline - Conceptual DisorganizationFollow-Up - Conceptual DisorganizationBaseline - HostilityFollow-Up - HostilityBaseline - SuspiciousnessFollow-Up - SuspiciousnessBaseline - HallucinationFollow-Up - HallucinationBaseline - Unusual Thought ContentFollow-Up - Unusual Thought Content
Dipyridamole2.2221.602.6672.001.2221.004.113.0002.672.6003.1112.800
Olanzapine1.4001.002.6002.001.2002.003.401.5003.802.5003.4001.500

[back to top]

The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)

The RBANS is a brief, individually administered test designed to evaluate neuropsychological status of adults, ages 20-89. The 12 subtests measure attention, language, visuospatial/constructional abilities, and immediate and delayed memory. The raw scores from the subtests are scaled together to create index scores, and these are summed for conversion to a total scale score. Higher score equals a better outcome. The total index score range for the RBANS is 40-160. (NCT00349973)
Timeframe: Baseline and Follow-Up

,
Interventionunits on a scale (Mean)
Baseline (Phase 1/Week 1)Follow-Up (Phase 3/Week 6)
Dipyridamole73.0077.40
Olanzapine59.0065.00

[back to top]

Change in Negative Symptoms by Treatment Assignment

The Scale for the Assessment of Negative Symptoms (SANS) total score, minus the global items, inappropriate affect, poverty of content of speech, and attention items, used to measure negative symptoms. Mean SANS total score by treatment and week. SANS total score range = 0-85. Higher scores indicate more severe negative symptoms. (NCT00349973)
Timeframe: Baseline and Follow-Up

,
Interventionunits on a scale (Mean)
Baseline (Phase 1/Week 1)Follow-Up (Phase 4/Week 1)
Dipyridamole23.325.8
Olanzapine25.627.0

[back to top]

Weight in Kilograms at Baseline, Weeks 1, 4, 6, and 8

Change in weight from baseline to endpoint in kilograms. Reported as weight in Kilograms at Baseline, Weeks 1, 4, 6, and 8 (NCT00384332)
Timeframe: 10 weeks

,
Interventionkilograms (Mean)
BaselineWeek 1Week 4Week 6Week 8
Arm 1- ODT76.077.477.878.979.1
Arm 2- SOT76.177.678.379.480.1

[back to top]

Change From Baseline Montgomery Asberg Depression Rating Scale

Montgomery Asberg Depression Rating Scale (MADRS) total score. Construct: Depression severity. Scores below represent mean change scores, endpoint minus baseline. Minimum total score: 0 (no depression). Maximum total score: 60 (severe depression). Lower (more negative) scores indicate a better outcome. There are no subscales. (NCT00384332)
Timeframe: 10 weeks

Interventionunits on a scale (Mean)
Arm 1-15.5
Arm 2-15.5

[back to top]

Change From Double-blind Baseline to Endpoint in Montgomery Åsberg Depression Rating Scale (MADRS)

The MADRS was assessed by an adequately trained clinician who did not provide psychotherapy or psycho-education to the patient. The scale consists of 10 items that cover all of the core depressive symptoms. Each item is scored from 0 to 6 and a total score is calculated by adding the scores of all 10 items. For each individual item as well as for the total score, a higher score represents a more severe condition. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventionunits on a scale (Mean)
Risperidone LAI5.1
Placebo6.1
Olanzapine2.0

[back to top]

Change From Double-blind Baseline to Endpoint in Young Mania Rating Scale (YMRS)

The 11-item YMRS was administered by an adequately trained clinician who did not provide psychotherapy or psycho-education to the patient. A severity rating was assigned to each of the items, based on the patient's subjective report of his or her condition over the previous 7 days or since the last visit (whichever was shorter) and the clinician's behavioral observations during the interview, with emphasis on the latter. The total YMRS score included the score of all 11 items ranging from 0 to 60, a higher score indicating a more severe condition. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventionunits on a scale (Mean)
Risperidone LAI2.9
Placebo8.0
Olanzapine1.7

[back to top]

Time to Early Study Discontinuation for Any Reason

The robustness of the primary outcome analysis was tested by means of a sensitivity analysis: patients who discontinued the study during Period III for any reason were analyzed as having a recurrence of a mood episode at the time of their study discontinuation. The same survival analysis method as for the primary outcome was applied. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventiondays (Mean)
Risperidone LAI252.45
Placebo236.14
Olanzapine365.64

[back to top]

Time to Recurrence of a Mood Episode (Exploratory/Olanzapine)

Recurrence was defined as for the risperidone LAI and placebo arms (meeting any of 5 criteria). Since the study was designed to compare the efficacy of risperidone LAI versus placebo, this olanzapine analysis was exploratory in nature. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventiondays (Mean)
Olanzapine414.04

[back to top]

Time to Recurrence of an Elevated Mood (Hypomanic, Manic, or Mixed) Episode

Recurrences were classified as elevated mood or depressive by the investigator based on the patient's data at the time of the event. Time to recurrence of an elevated mood episode was estimated by means of the same survival analysis method as for the primary outcome. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventiondays (Mean)
Risperidone LAI357.41
Placebo323.14
Olanzapine448.03

[back to top]

Time to Recurrence of a Mood Episode (Risperidone LAI Versus Placebo)

Recurrence was estimated using the Kaplan-Meier method and defined as meeting any of the following: DSM-IV-TR criteria for a hypomanic, manic, mixed, or depressive episode; in need of mood stabilizer, antipsychotic medication, benzodiazepine or antidepressant; requiring hospitalization for mood episode; either Young Mania Rating Scale (YMRS) >12 or Montgomery-Åsberg Depression Rating Scale (MADRS) >12 combined with Clinical Global Impression - Severity (CGI-S) >=4; in need of increase in study medication dose or supplementation with oral risperidone or another antipsychotic or mood stabilizer. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventiondays (Mean)
Risperidone LAI293.39
Placebo270.47

[back to top]

Time to Recurrence of a Depressive Episode

Recurrences were classified as elevated mood or depressive by the investigator based on the patient's data at the time of the event. Time to recurrence of a depressive episode was estimated by means of the same survival analysis method as for the primary outcome. (NCT00391222)
Timeframe: Assessed at every visit from the moment of randomization to a treatment arm (baseline Period III) until the end of treatment (Month 21 or earlier)

Interventiondays (Mean)
Risperidone LAI213.86
Placebo300.20
Olanzapine356.11

[back to top]

Change From Baseline in the Total Positive and Negative Syndrome Scale (PANSS).

PANSS is a medical scale that assesses various symptoms of schizophrenia. The symptoms are rated on a 7-point scale from 1 (absent) to 7 (extreme psychopathology). The total score is the sum of all 30 PANSS items, with a range of 30 (absent) to 210 (extreme ill). (NCT00396565)
Timeframe: Baseline and 6 weeks

Interventionscores on a scale (Mean)
Paliperidone Extended Release (ER) (JNS007ER)-9.1
Placebo3.8
Olanzapine-9.9

[back to top]

Change From Baseline in Clinical Global Impression Scale (CGI-S)

The CGI-S rating scale is a 7-point global assessment with scores as follows: 1 - Not ill, 2 - Very Mild, 3 - Mild, 4 - Moderate, 5 - Marked, 6 - Severe, and 7 - Extremely Severe. (NCT00396565)
Timeframe: Baseline and 6 weeks

Interventionscores on a scale (Mean)
Paliperidone Extended Release (ER) (JNS007ER)-0.4
Placebo0.2
Olanzapine-0.3

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) - General Psychopathology Subscale Score

The PANSS General Psychopathology Subscale Score assesses 16 general psychopathology symptoms. The symptoms are rated on a 7-point scale, with a range of 16 (absent) to 112 (extreme psychopathology). (NCT00396565)
Timeframe: Baseline and 6 weeks

Interventionscores on a scale (Mean)
Paliperidone Extended Release (ER) (JNS007ER)-4.1
Placebo2.2
Olanzapine-4.7

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) - Negative Subscale Score

The PANSS Negative Subscale assesses seven negative-symptoms of schizophrenia. Negative symptoms represent a diminution or loss of normal functions. The symptoms are rated on a 7-point scale, with a range of 7 (absent) to 49 (extreme psychopathology). (NCT00396565)
Timeframe: Baseline and 6 weeks

Interventionscores on a scale (Mean)
Paliperidone Extended Release (ER) (JNS007ER)-2.4
Placebo0.0
Olanzapine-2.8

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) - Positive Subscale Score

The PANSS Positive Subscale assesses seven positive-symptoms of schizophrenia. Positive symptoms refer to an excess or distortion of normal functions. The symptoms are rated on a 7-point scale, with a range of 7 (absent) to 49 (extreme psychopathology). (NCT00396565)
Timeframe: Baseline and 6 weeks

Interventionscores on a scale (Mean)
Paliperidone Extended Release (ER) (JNS007ER)-2.6
Placebo1.6
Olanzapine-2.4

[back to top]

Proportion of Responders (≥30% Decrease in Total Positive and Negative Syndrome Scale [PANSS])

Responders are subjects with 30% or more reduction from baseline in total PANSS score. PANSS is a medical scale that assesses various symptoms of schizophrenia. The symptoms are rated on a 7-point scale from 1 (absent) to 7 (extreme psychopathology). The total score is the sum of all 30 PANSS items, with a range of 30 (absent) to 210 (extreme ill). (NCT00396565)
Timeframe: Baseline and 6 weeks

InterventionPercentage of participants (Number)
Paliperidone Extended Release (ER) (JNS007ER)25.4
Placebo9.4
Olanzapine26.1

[back to top]

Mean Change From Baseline to Endpoint in Fasting Triglycerides

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimoles per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine1.580.33
Olanzapine + Amantadine1.610.35
Olanzapine + Metformin1.680.06

[back to top]

Mean Change From Baseline to Endpoint in Hemoglobin A1c

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionpercent hemoglobin A1c (Mean)
BaselineChange from Baseline
Olanzapine5.510.09
Olanzapine + Amantadine5.480.10
Olanzapine + Metformin5.53-0.03

[back to top]

Mean Change From Baseline to Endpoint in Fasting Low Density Lipoprotein (LDL) Cholesterol

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine3.020.16
Olanzapine + Amantadine3.06-0.04
Olanzapine + Metformin2.91-0.02

[back to top]

Change From Baseline to Endpoint in Weight

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

Interventionkilograms (Least Squares Mean)
Olanzapine2.76
Olanzapine + Amantadine2.40
Olanzapine + Metformin0.65

[back to top]

Change From Baseline to Endpoint in Brief Psychiatric Rating Scale (BPRS) Total Score

The BPRS is an 18-item clinician-administered scale used to assess the degree of severity of a subject's general psychopathological symptoms. Each item is rated on a scale from 1 (symptom not present) to 7 (symptom extremely severe). The BPRS total score ranges from 18 to 126. (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Olanzapine48.24-13.89
Olanzapine + Amantadine45.90-9.90
Olanzapine + Metformin47.00-9.72

[back to top]

Change From Baseline to Endpoint in Clinical Global Impression - Severity Scale (CGI-S)

Measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Olanzapine4.06-0.98
Olanzapine + Amantadine4.03-0.72
Olanzapine + Metformin4.00-0.79

[back to top]

Change From Baseline to Endpoint in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score

The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionunits on a scale (Mean)
BaselineChange from Baseline
Olanzapine12.76-6.39
Olanzapine + Amantadine14.22-4.12
Olanzapine + Metformin15.40-4.36

[back to top]

Correlations Between Weight Changes and Changes in Eating Inventory (EI) and Food Craving Inventory (FCI) at 2 Weeks and 22 Weeks

To understand the drivers of weight gain as indicated by the correlation between weight changes and changes in the Eating Inventory (EI) and Food Craving Inventory (FCI). The EI is a 51-item inventory that measures dietary restraint, disinhibition, and perceived hunger. The FCI is a 28-item instrument measuring the frequency over the past month of general cravings and cravings for specific types of foods, namely: high fats, sweets, carbohydrates/starches, and fast-food fats. Correlations were computed on the combined treatment groups. (NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,
Interventioncorrelation (Number)
EI: DisinhibitionEI: Cognitive RestraintEI: HungerFCI: Carbohydrates/Starches (N=186, N=141)FCI: Fast Food Fats (N=188, N=140)FCI: High Fats (N=186, N=138)FCI: Sweets (N=187, N=140)FCI: Total Score (N=184, N=137)
2 Weeks-0.034-0.273-0.1500.013-0.0190.0510.0220.039
22 Weeks0.285-0.0380.148-0.0640.0470.043-0.008-0.000

[back to top]

Mean Change From Baseline to Endpoint in Fasting Glucose

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine5.320.26
Olanzapine + Amantadine5.250.10
Olanzapine + Metformin5.280.01

[back to top]

Mean Change From Baseline to Endpoint in Fasting High Density Lipoprotein (HDL) Cholesterol

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine1.25-0.00
Olanzapine + Amantadine1.26-0.11
Olanzapine + Metformin1.22-0.08

[back to top]

Mean Change From Baseline to Endpoint in Fasting Total Cholesterol

(NCT00401973)
Timeframe: Baseline to endpoint (22 weeks)

,,
Interventionmillimole per Liter (mmol/L) (Mean)
BaselineChange from Baseline
Olanzapine5.010.36
Olanzapine + Amantadine5.030.01
Olanzapine + Metformin4.91-0.08

[back to top]

Mean Change in Hamilton Depression Rating Scale-21 (HAMD) Scores From Baseline to Endpoint.

The 21-item HAMD measures depression severity. Items are rated on a scale from 0 (symptoms not present) to a maximum of 2 to 4 (symptom extremely severe) for a total score range of 0 to 60. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionunits on a scale (Least Squares Mean)
Olanzapine-9.37
Placebo-7.69

[back to top]

Mean Change in Clinical Global Impression for Bipolar Illness Severity (CGI-BP) From Baseline to Endpoint

CGI-BP Severity is used by the clinician to record the severity of illness at the time of assessment. The score ranges from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionunits on a scale (Least Squares Mean)
Olanzapine-1.34
Placebo-1.06

[back to top]

Clinically Significant Vital Signs - Percentage of Participants With Baseline-to-Endpoint Weight Increase of at Least Seven Percent (7%)

Percentages of participants in each group who experienced an increase in weight of at least 7% from baseline to endpoint. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionpercentage of participants (Number)
Olanzapine22
Placebo3

[back to top]

Clinically Significant Vital Signs - Body Mass Index Change From Baseline

Change from baseline to endpoint in body mass index (an estimate of body fat derived by dividing body weight by height squared): Value of body mass index measure at endpoint minus value at baseline. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionkilograms per square meters (Least Squares Mean)
Olanzapine1.18
Placebo0.26

[back to top]

Clinically Significant Vital Signs - Weight Change From Baseline

Change from baseline to endpoint: Value of weight measure at endpoint minus value at baseline. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionkilograms (Least Squares Mean)
Olanzapine3.34
Placebo0.70

[back to top]

Clinically Significant Laboratory Values - Bilirubin Total Change From Baseline

Change from baseline to endpoint in bilirubin total: Value of bilirubin total measure at endpoint minus value at baseline. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

,
Interventionmicromoles per Liter (Mean)
BaselineChange from Baseline
Olanzapine6.50-1.56
Placebo6.65-0.74

[back to top]

Clinically Significant Laboratory Values - Fasting Triglycerides Change From Baseline

Change from baseline to endpoint in triglycerides: Value of triglyceride measure at endpoint minus value at baseline. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

,
Interventionmilligrams per deciliter (Mean)
BaselineChange from Baseline
Olanzapine111.4622.91
Placebo139.7516.80

[back to top]

Clinically Significant Laboratory Values - Fasting Cholesterol Change From Baseline

Change from Baseline to endpoint in cholesterol: value of cholesterol measure at endpoint minus the value at baseline. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

,
Interventionmilligrams per deciliter (Mean)
Total Cholesterol BaselineTotal Cholesterol Change from BaselineLow Density Lipoprotein Baseline (N=62,N=64)Low Density Lipoprotein Change (N=62,N=64)High Density Lipoprotein BaselineHigh Density Lipoprotein Change from Baseline
Olanzapine191.37-7.80115.32-9.2253.76-3.24
Placebo192.25-8.72111.01-9.7751.48-1.22

[back to top]

Clinically Significant Laboratory Values - Fasting Blood Glucose Change From Baseline

Change from baseline to endpoint in fasting blood glucose: Value of fasting blood glucose measure at endpoint minus value at baseline. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

,
Interventionmilligrams per deciliter (Mean)
BaselineChange from Baseline
Olanzapine91.816.93
Placebo91.90-0.55

[back to top]

Number of Patients Hospitalized Due to Relapse of Mania or Depression.

Number of participants hospitalized as a result of relapse of mania or depression. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionparticipants (Number)
Olanzapine1
Placebo0

[back to top]

Number of Participants Meeting the Criteria for Mixed Response

The original outcome measure was Time to Mixed Response(at least a 50% reduction on HAMD and YMRS total scores from baseline); however since upper limit of measure of dispersion could not be computed by observed data, which is not allowed on this system, number of patients with event are presented instead. (NCT00402324)
Timeframe: baseline to endpoint (6 weeks)

Interventionparticipants (Number)
Olanzapine54
Placebo40

[back to top]

Number of Participants Meeting the Criteria for Mixed Onset of Action

The original outcome measure was Time to Mixed Onset of Action (at least a 25% reduction on HAMD and YMRS total scores from baseline); however since upper limit of measure of dispersion could not be computed by observed data, which is not allowed on this system, number of patients with event are presented instead. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionparticipants (Number)
Olanzapine81
Placebo71

[back to top]

Mean Change in Young Mania Rating Scale (YMRS) Scores From Baseline to Endpoint.

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00402324)
Timeframe: Baseline to endpoint (6 weeks)

Interventionunits on a scale (Least Squares Mean)
Olanzapine-10.15
Placebo-7.68

[back to top]

Change in Non-HDL Cholesterol Level for Patients Assigned to Stay and Patients Assigned to Switch Over 24 Weeks

Change in non-HDL cholesterol measured at baseline and every 4 weeks for 24 weeks. The efficacy analysis corresponded to a comparison of change in non-HDL cholesterol from baseline to 24 weeks between treatment groups (stay versus switch). Repeated measurements mixed effects linear models were fit for the primary analysis. (NCT00423878)
Timeframe: 24 weeks

Interventionmg/dL non-HDL cholesterol (Least Squares Mean)
Switch Group-20.2
Stay Group-10.8

[back to top]

Efficacy Failure, Defined as Psychiatric Hospitalization, a 25 Percent Increase From Baseline on the Positive and Negative Syndrome Scale or Substantial Clinical Deterioration on the Clinical Global Impressions-Change (CGI-C)

(NCT00423878)
Timeframe: Measured at Month 6

Interventionparticipants (Number)
Switch Group22
Stay Group18

[back to top]

Triglycerides

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionmg/dL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group80.198.73107.2115.4113.47

[back to top]

Body Mass Index

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionkg/m^2 (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group22.123.524.224.324.6

[back to top]

Cholesterol Total

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionmg/dL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group163.2184.9186.5188.1188.1

[back to top]

LDL

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionmg/dL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group96.6115.07116.0116.0117.7

[back to top]

Fasting Glucose

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionmg/dL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group82.183.286.085.389.1

[back to top]

HDL

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionmg/dL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group49.850.149.749.748.4

[back to top]

Hemoglobin A1c

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionpercentage (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group4.44.44.34.44.3

[back to top]

IL-6

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionpg/mL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group3.53.96.43.82.3

[back to top]

Fasting Insulin

(NCT00446992)
Timeframe: Baseline and 4 week intervals

Interventionmg/dL (Mean)
BaselineWeek 4Week 8Week 12Week 16
Open Trial Group9.712.110.511.110.7

[back to top]

Clinical Global Impression - Bipolar Disorder - Severity of Illness (CGI-BP-S): Change From Baseline

The CGI-BP-S rating scale is used to rate the severity of bipolar disorder, including both depressed and manic components, on a 7-point scale ranging from 1 (not ill) to 7 (very severely ill). This scale permits a global evaluation of the subject's bipolar condition at a given time. Negative Change in Score Indicates Improvement. (NCT00490971)
Timeframe: From 1st randomization into acute phase to end of acute/continuation phase (ie, up to 15 weeks after 1st randomization), or from randomization into maintenance (MA) phase to the end of MA phase (ie, up to 175 weeks (or 41 months) after 2nd randomization).

InterventionScores on the scale (Median)
Paliperidone ER-2
Olanzapine-3
Pali/Placebo2
Pali/Pali0
Olan/Olan0

[back to top]

Global Assessment of Functioning (GAF): Change From Baseline

This scale is used when the clinical progress of a subject needs to be assessed in global terms, using a single measure. The GAF scale is rated with respect to psychological, social, and occupational functioning at the time of the assessment only. A higher score indicates a better functioning, with an overall range from 1 to 100. Positive Change in Score Indicates Improvement. (NCT00490971)
Timeframe: From 1st randomization into acute phase to end of acute/continuation phase (ie, up to 15 weeks after 1st randomization), or from randomization into maintenance (MA) phase to the end of MA phase (ie, up to 175 weeks (or 41 months) after 2nd randomization).

InterventionScores on the scale (Mean)
Paliperidone ER19.6
Olanzapine20.8
Pali/Placebo-15.2
Pali/Pali-8.9
Olan/Olan-4.2

[back to top]

Montgomery-Asberg Depression Rating Scale (MADRS)

The MADRS consists of 10 items covering all the important complaints which patient with depression have (apparent sadness, reported sadness, inner tension, reduced sleep, reduced appetite, concentration difficulties, lassitude, inability to feel, pessimistic thoughts, and suicidal thoughts). Item is scored from 0 (normal) to 6 (severe). Total score (0 to 60) is calculated by adding the scores of all 10 items. A higher score represents a more severe condition. Negative Change in Score Indicates Improvement. (NCT00490971)
Timeframe: From 1st randomization into acute phase to end of acute/continuation phase (ie, up to 15 weeks after 1st randomization), or from randomization into maintenance (MA) phase to the end of MA phase (ie, up to 175 weeks (or 41 months) after 2nd randomization).

InterventionScores on the scale (Mean)
Paliperidone ER-2.7
Olanzapine-2.7
Pali/Placebo6.0
Pali/Pali6.1
Olan/Olan2.5

[back to top]

Time to Recurrence of Depressive Symptoms Associated With Bipolar I Disorder

Pali/Pali and Pali/Placebo were compared with each other with respect to time to recurrence of depressive symptoms. The criterias used for this analysis were similar to criterias used for primary analysis. (NCT00490971)
Timeframe: Date of randomization into the maintenance phase until the first occurrence of recurrence of depressive symptoms or discontinuation from the study, assessed over a period of 41 months.

InterventionDays (Number)
Pali/Placebo503.0
Pali/Pali448.0
Olan/OlanNA

[back to top]

Young Mania Rating Scale (YMRS): Change From Baseline

This is method by which condition of patient suffering with mania is checked. In this scale patient's condition is assessed using 11 items. A severity rating is assigned to each of 11 items based on the how subject feels of his or her condition and the physicians observation of patients behavior. The range of the scale is 0 to 60. A higher score indicates a more severe condition. Change from baseline (Day 105) in the double-blind maintenance phase to the last postbaseline assessment. (NCT00490971)
Timeframe: From 1st randomization into acute phase to end of acute/continuation phase (ie, up to 15 weeks after 1st randomization), or from randomization into maintenance (MA) phase to the end of MA phase (ie, up to 175 weeks (or 41 months) after 2nd randomization).

InterventionScores on the scale (Mean)
Paliperidone ER-19.2
Olanzapine-19.3
Pali/Placebo9.0
Pali/Pali4.2
Olan/Olan1.3

[back to top]

Time to Recurrence of Manic Symptoms Associated With Bipolar I Disorder

This was the key secondary efficacy end-point. Pali/Pali and Pali/Placebo were compared with each other with respect to time to recurrence of manic symptoms. The criterias used for this analysis were similar to criterias used for primary analysis. (NCT00490971)
Timeframe: Date of randomization into the maintenance phase until the first occurrence of recurrence of manic symptoms or discontinuation from the study, assessed over a period of 41 months.

,,
InterventionDays (Number)
25% Quantile of Time to RecurrenceMedian Time to Recurrence
Olan/OlanNANA
Pali/Pali498.0NA
Pali/Placebo194.0550.0

[back to top]

Time to Recurrence of Any Mood Symptoms (Manic or Depressive) Associated With Bipolar I Disorder

Time to first recurrence of any mood symptoms (ie, manic or depressive) associated with bipolar I disorder during the maintenance phase, after maintaining clinical stability during continued treatment with paliperidone ER over a period of 15 weeks. The time period was from occurrence of acute manic or mixed episode to Week 15. This outcome was measured using combination of various scales, hospitalization for any mood symptoms, use of any medicines for an mood episode and clinical events suggestive of recurrent mood episode associated with bipolar I disorder. (NCT00490971)
Timeframe: Date of randomization into the maintenance phase until the first occurrence of recurrence of any symptoms or discontinuation from the study, assessed over a period of 41 months.

,,
InterventionDays (Number)
25% Quantile of Time to RecurrenceMedian Time to Recurrence
Olan/Olan541NA
Pali/Pali140.0558.0
Pali/Placebo85.0283.0

[back to top]

Number of Participants Remaining on Metabolic Syndrome at Week 16

Metabolic syndrome is defined as the presence of at least 3 out of the following Adult Treatment Panel III-A (ATP III-A) criteria (all of which are to be assessed at the same visit): waist >102 cm in males, >88 cm in females; blood pressure (BP) systolic BP ≥130 or diastolic BP ≥85 mm Hg; fasting HDL <40 mg/dL in males, <50 mg/dL in females; fasting triglycerides ≥150 mg/dL; fasting glucose ≥100 mg/dL, and/or the start of a treatment for any of the parameters of metabolic syndrome during the course of the study. (NCT00508157)
Timeframe: Week 16

Interventionparticipants (Number)
Control Group22
Aripiprazole16

[back to top]

Mean Percent Change From Baseline in Fasting Non-high Density Lipoprotein (HDL) Cholesterol at Week 16

Non-HDL cholesterol was calculated as fasting Total Cholesterol minus fasting HDL Cholesterol. (NCT00508157)
Timeframe: Baseline, Week 16

Interventionpercent change (Mean)
Control Group10.06
Aripiprazole-2.3

[back to top]

Clinical Global Impression

The score for each subject was the mean rating on the severity item. The score of the item ranged from 1 (normal) to 7 (among most severely ill). (NCT00509067)
Timeframe: Measured at Baseline and Weeks 4, 8, 12, and 16

,
Interventionunits on a scale (Mean)
BaselineWeek 4Week 8Week 12Week 16
Galantamine and CDP-choline Group4.3243.673.873.8
Placebo Group4.383.924.0443.68

[back to top]

MATRICS Verbal Learning and Memory

The measure of verbal learning and memory is the Hopkins Verbal Learning Test. The score for each subject is the sum of the total number of words recalled correctly for Trials 1, 2, and 3. The measure is the mean of these scores at baseline, Week 8, and Week 16. (NCT00509067)
Timeframe: Measured at Baseline and Weeks 8 and 16

,
Interventionraw scores (Mean)
BaselineWeek 8Week 16
Galantamine and CDP-choline Group20.521.823.0
Placebo Group20.621.220.4

[back to top]

Negative Symptoms Measured on Positive and Negative Syndrome Scale (PANSS)

The score for each subject was the sum of the ratings for five items on the negative-symptom subscale of the PANSS: 1) blunted affect, 2) emotional withdrawal, 3) poor rapport, 4) passive/apathetic social withdrawal, and 5) lack of spontaneity and flow of conversation. Each item (symptom) is rated on a scale from 1 = absence of negative symptom to 7 = extreme negative symptom. The sum of the ratings for the five items range from 5 to 35, with higher scores indicating more severe symptoms. The primary outcome measure is the mean of the sum of these ratings across subjects. (NCT00509067)
Timeframe: Measured at Baseline and Weeks 4, 8, 12, and 16

,
Interventionunits on a scale (Mean)
BaselineWeek 4Week 8Week 12Week 16
Galantamine/CDP Choline17.6317.0613.9314.9313.93
Placebos for Galantamine/CDP Choline18.2917.0817.2617.3216.05

[back to top]

Percentage of Participants With Psychotic Disorders and Mood Disorders With Psychotic Features at Endpoint on MINI Psychotic Disorders Module (Acute Phase)

In the MINI Psychotic Features Episode module, participants are asked a series of Yes/No questions to determine whether or not they are currently experiencing mood disorder with psychotic features or current psychotic disorders. (NCT00510146)
Timeframe: Endpoint (Week 6)

,
Interventionpercentage of participants (Number)
Mood Disorder with Psychotic FeaturesPsychotic Disorders
Olanzapine3.60.0
Placebo2.40.6

[back to top]

Percentage of Participants With Extra-Pyramidal Symptoms (EPS) At Endpoint As Measured by Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS) (Acute Phase)

EPS symptoms measured by DIEPSS are grouped into 4 categories: parkinsonism, akathisia, dystonia, and dyskinesia. Severity is assessed at 5 levels, from level 0 (none, normal) to level 4 (severe). For Parkinsonism, normal baseline is defined as a score not >=3 on 1 item nor >=2 on 2 items; abnormal endpoint is defined as a score >=3 on 1 item or >=2 on 2 items, or an increase of 3 on Parkinsonism total. Baseline akathisia, dystonia and dyskinesia is defined as a score <2; abnormal endpoint is a score >=2 or an increase >= 2 from that baseline score. (NCT00510146)
Timeframe: Endpoint (Week 6)

,
Interventionpercentage of participants (Number)
Akathisia (N=335, 169)Dyskinesia (N=337, 169)Dystonia (N=337, 169)Parkinsonism (N=337, 169)
Olanzapine2.70.00.00.9
Placebo1.20.00.00.6

[back to top]

Percentage of Participants With Extra-Pyramidal Symptoms (EPS) at Endpoint As Measured by Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS) (Open-Label Phase)

EPS symptoms measured by DIEPSS are grouped into 4 categories: parkinsonism, akathisia, dystonia, and dyskinesia. Severity is assessed at 5 levels, from level 0 (none, normal) to level 4 (severe). For Parkinsonism, normal baseline is defined as a score not >=3 on 1 item nor >=2 on 2 items; abnormal endpoint is defined as a score >=3 on 1 item or >=2 on 2 items, or an increase of 3 on Parkinsonism total. Baseline akathisia, dystonia and dyskinesia is defined as a score <2; abnormal endpoint is a score >=2 or an increase >= 2 from that baseline score. (NCT00510146)
Timeframe: Endpoint (Week 24)

Interventionpercentage of participants (Number)
Akathisia (N=378)Dyskinesia (N=385)Dystonia (N=385)Parkinsonism (N=385)
Olanzapine (Open-label Treatment Period)0.80.30.01.0

[back to top]

Percentage of Participants With Major Depressive Episode at Endpoint on Mini International Neuropsychiatric Interview (MINI), Depressive Episode Module (Acute Phase)

In the MINI Major Depressive Episode module, participants are asked a series of Yes/No questions to determine whether or not they are experiencing a major depressive episode or a major depressive episode with melancholic features. (NCT00510146)
Timeframe: Endpoint (Week 6)

,
Interventionpercentage of participants (Number)
Major Depressive EpisodeMajor Depressive Episode with Melancholic Features
Olanzapine55.577.8
Placebo60.474.1

[back to top]

Percentage of Participants With Non-Alcohol Psychoactive Substance Use Disorder at Endpoint on MINI Substance Dependence/Abuse Module (Acute Phase)

In the MINI Substance Dependence and Abuse Module, participants are asked a series of Yes/No questions to determine whether or not they are currently experiencing symptoms indicating current non-alcohol substance use dependence or abuse. (NCT00510146)
Timeframe: Endpoint (Week 6)

,
Interventionpercentage of participants (Number)
DependenceAbuse
Olanzapine0.00.0
Placebo0.00.0

[back to top]

Percentage of Participants With High Suicidality at Endpoint (Open-Label Phase)

The MINI module C (MINI-C) is a rating scale for severity of suicidal thoughts and behaviors. The MINI-C is composed of 12 Yes/No questions with variable scores assigned to each question. The scale ranges from 0 to 52 with higher scores indicating a greater presence of suicidal thoughts and/or behaviors. Based upon scores, suicidality is defined as Low (1-8), Medium (9-16), and High (>=17). (NCT00510146)
Timeframe: Endpoint (Week 24)

Interventionpercentage of participants (Number)
Olanzapine (Open-label Treatment Period)1.3

[back to top]

Percentage of Participants With Current Hypomanic Episode at Endpoint on MINI Manic Episode Module (Acute Phase)

In the MINI Manic Episode module, participants are asked a series of Yes/No questions to determine whether or not they are currently experiencing hypomanic or manic episodes. (NCT00510146)
Timeframe: Endpoint (Week 6)

Interventionpercentage of participants (Number)
Olanzapine2.1
Placebo0.6

[back to top]

Percentage of Participants With Emergence of Mania During the Study (Acute Phase)

Emergence of mania is defined as first occurrence of score of >=15 in the YMRS total score in the post-baseline period of Acute Phase. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00510146)
Timeframe: Baseline through Endpoint (Week 6)

Interventionpercentage of participants (Number)
Olanzapine0.6
Placebo2.9

[back to top]

Percentage of Participants With Emergence of Mania During the Study (Open-Label Phase)

Emergence of mania is defined as first occurrence of score of >=15 in the YMRS total score in the Open-Label Extension. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6) through Endpoint (Week 24)

Interventionpercentage of participants (Number)
Olanzapine (Open-label Treatment Period)0.8

[back to top]

Percentage of Participants With Recovery (Acute Phase)

Percentage of participants with recovery defined as a value of less than or equal to 12 in the MADRS total score for at least 4 weeks of post-baseline treatment. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00510146)
Timeframe: Baseline through Endpoint (Week 6 )

Interventionpercentage of participants (Number)
Olanzapine13.7
Placebo9.4

[back to top]

Percentage of Participants With Recovery (Open-Label Phase)

Percentage of participants with recovery defined as a value of less than or equal to 12 in the MADRS total score for at least 4 weeks of post-baseline treatment. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6) through Endpoint (Week 24)

Interventionpercentage of participants (Number)
Olanzapine (Open-label Treatment Period)69.9

[back to top]

Percentage of Participants With Symptomatic Remission At Any Time (Acute Phase)

Percentage of participants with symptomatic remission at any time as defined as a score of less than or equal to 12 in the MADRS total score. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00510146)
Timeframe: Baseline through Endpoint (Week 6)

Interventionpercentage of participants (Number)
Olanzapine53.9
Placebo49.7

[back to top]

Percentage of Participants With Symptomatic Remission in the MADRS Total Score (Open-Label Phase)

Percentage of participants with symptomatic remission at any time as defined as a score of less than or equal to 12 in the MADRS total score. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6) through Endpoint (Week 24)

Interventionpercentage of participants (Number)
Olanzapine (Open-label Treatment Period)85.1

[back to top]

Percentage of Participants With Symptomatic Response at Endpoint (Acute Phase)

Response is defined as a reduction (from baseline to endpoint) of 50% or more in the MADRS total score. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00510146)
Timeframe: Endpoint (Week 6)

Interventionpercentage of participants (Number)
Olanzapine52.5
Placebo43.3

[back to top]

Percentage of Participants With Symptomatic Response in Montgomery-Asberg Depression Rating (MADRS) Depression Rating (Open-Label Phase)

The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). Response is defined as a reduction (from baseline to endpoint) of 50% or more in the MADRS total score. (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6) through Endpoint (Week 24)

Interventionpercentage of participants (Number)
Olanzapine (Open-label Treatment Period)43.7

[back to top]

Change From Baseline to Endpoint in Alanine Amino Transferase/Serum Glutamate Pyruvate Transaminase (ALT/SGPT), Aspartate Aminotransferase/Serum Glutamic Oxaloacetic Transaminase (AST/SGOT), Gamma Glutamyl Transferase (GGT)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionunits/Liter (Mean)
Baseline (ALT/SGPT)Change (ALT/SGPT)Baseline (AST/SGOT)Change (AST/SGOT)Baseline (GGT)Change (GGT)
Olanzapine21.688.3421.614.3124.875.36
Placebo21.180.0020.251.2623.63-1.21

[back to top]

Change From Baseline to Endpoint in Albumin (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventiongram/Liter (Mean)
BaselineChange
Olanzapine43.07-0.81
Placebo43.470.03

[back to top]

Change From Baseline to Endpoint in Albumin and Total Protein (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventiongram/Liter (Mean)
Baseline- AlbuminChange- AlbuminBaseline- Total ProteinChange- Total Protein
Olanzapine (Open-label Treatment Period)42.640.5373.240.56

[back to top]

Change From Baseline to Endpoint in Alkaline Phosphatase, Creatinine Phosphokinase (CPK), GGT (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionunits/Liter (Mean)
Baseline- Alkaline PhosphataseChange- Alkaline PhosphataseBaseline- CPKChange- CPKBaseline- GGTChange- GGT
Olanzapine (Open-label Treatment Period)68.582.37107.36-1.7328.900.78

[back to top]

Change From Baseline to Endpoint in Blood Pressure (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
InterventionmmHg (millimeters of mercury) (Mean)
Baseline- Standing Systolic (N=320, 159)Change- Standing Systolic (N=320, 159)Baseline- Sitting Systolic (N=340, 169)Change- Sitting Systolic (N=340, 169)Baseline- Standing Diastolic (N=320, 159)Change- Standing Diastolic (N=320, 159)Baseline- Sitting Diastolic (N=340, 169)Change- Sitting Diastolic (N=340, 169)Baseline- Orthostatic Change-Systolic (N=320, 159)Change- Orthostatic Change-Systolic (N=320, 159)Baseline- Orthostatic Change-Diastolic (N=320, 159Change- Orthostatic Change-Diastolic (N=320, 159)
Olanzapine112.39-0.99112.35-0.3674.77-0.4873.07-0.110.54-0.651.92-0.52
Placebo115.65-0.67114.390.0476.87-0.1473.920.391.21-0.452.96-0.47

[back to top]

Change From Baseline to Endpoint in Blood Pressure (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmillimeters of mercury (Mean)
Baseline-Standing Diastolic (N=361)Change- Standing Diastolic (N=361)Baseline- Sitting Diastolic (N=383)Change- Sitting Diastolic (N=383)Baseline- Standing Systolic (N=361)Change- Standing Systolic (N=361)Baseline- Sitting Systolic (N=383)Change- Sitting Systolic (N=383)Baseline- Orthostatic Change-Diastolic (N=358)Change- Orthostatic Change- Diastolic (N=358)Baseline- Orthostatic Change- Systolic (N=358)Change- Orthostatic Change- Systolic (N=358)
Olanzapine (Open-label Treatment Period)74.980.1573.32-0.03112.060.96112.260.271.750.160.190.65

[back to top]

Change From Baseline to Endpoint in Chloride (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmillimole/Liter (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)103.620.33

[back to top]

Change From Baseline to Endpoint in Clinical Global Improvement- Bipolar (CGI-BP) Severity of Illness Scores-Mania, Depression, Overall Bipolar Illness Scores (Acute Phase)

CGI-BP is a measure of illness severity especially adapted for bipolar illness. It allows rating of mania, depression, and overall illness. The score ranges from 1 (normal, not ill) to 7 (very seriously ill). (NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionunits on a scale (Mean)
Baseline-ManiaChange-ManiaBaseline-DepressionChange-DepressionBaseline- OverallChange- Overall
Olanzapine1.070.004.54-1.454.45-1.40
Placebo1.110.094.53-1.204.44-1.08

[back to top]

Change From Baseline to Endpoint in Creatinine (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmicromole/Liter (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)67.482.05

[back to top]

Change From Baseline to Endpoint in Direct Bilirubin, Total Bilirubin, Uric Acid (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionmicromole/Liter (Mean)
Baseline- Direct BilirubinChange- Direct BilirubinBaseline- Total BilirubinChange- Total BilirubinBaseline- Uric AcidChange- Uric Acid
Olanzapine2.45-0.219.74-0.68307.1919.55
Placebo2.400.129.420.47314.38-1.86

[back to top]

Change From Baseline to Endpoint in ECG (Open-Label Phase)

Time from electrocardiogram Q wave to the end of the T wave corresponding to electrical systole, fixed correction factor (QTcF interval); Bazett-Corrected QT Interval (QTcB interval). (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmilliseconds (Mean)
Baseline- QTcFChange- QTcFBaseline- QTcBChange- QTcB
Olanzapine (Open-label Treatment Period)410.091.80421.721.76

[back to top]

Change From Baseline to Endpoint in Erythrocyte Count (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventiontrillion cells per liter ( TRIL/L) (Mean)
BaselineChange
Olanzapine4.65-0.05
Placebo4.710.02

[back to top]

Change From Baseline to Endpoint in Erythrocyte Count (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventiontrillion cells per liter (Tril/L) (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)4.640.03

[back to top]

Change From Baseline to Endpoint in Glucose and Lipids (Cholesterol, Triglycerides, HDL Cholesterol, LDL Cholesterol)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionmillimole/Liter (Mean)
Baseline- Fasting Glucose (N=320, 155)Change- Fasting Glucose (N=320, 155)Baseline- Cholesterol (N=329, 160)Change- Cholesterol (N=329, 160)Baseline-Triglycerides (N=329, 160)Change- Triglycerides (N=329, 160)Baseline- LDL Cholesterol (N=328, 159)Change- LDL Cholesterol (N=328, 159)Baseline- HDL Cholesterol (N=329, 160)Change- HDL Cholesterol (N=329, 160)
Olanzapine5.110.104.830.241.390.262.770.171.43-0.03
Placebo5.120.024.81-0.071.340.032.83-0.091.360.02

[back to top]

Change From Baseline to Endpoint in Glucose and Lipids (Cholesterol, Triglycerides, HDL Cholesterol, LDL Cholesterol) (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmillimole/Liter (Mean)
Baseline- Fasting Glucose (N=375)Change- Fasting Glucose (N=375)Baseline- Cholesterol (N=380)Change- Cholesterol (N=380)Baseline- Triglycerides (N=380)Change- Triglycerides (N=380)Baseline- LDL Cholesterol (N=378)Change- LDL Cholesterol (N=378)Baseline- HDL Cholesterol (N=380)Change- HDL Cholesterol (N=380)
Olanzapine (Open-label Treatment Period)5.200.064.960.051.550.102.880.061.39-0.05

[back to top]

Change From Baseline to Endpoint in Hamilton Depression Rating Scale-17 (HAMD-17) Total Score (Acute Phase)

The 17-item HAMD measures depression severity. Each item was evaluated and scored using either a 5-point scale (e.g. absent, mild, moderate, severe, very severe) or a 3-point scale (e.g. absent, mild, marked). The total score of HAMD-17 may range from 0 (normal) to 52 (severe). (NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionunits on a scale (Mean)
BaselineChange
Olanzapine22.62-11.44
Placebo22.35-9.12

[back to top]

Change From Baseline to Endpoint in Heart Rate (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionbeats per minute (bpm) (Mean)
BaselineChange
Olanzapine69.633.49
Placebo70.510.87

[back to top]

Change From Baseline to Endpoint in Heart Rate (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionbeats per minute (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)71.850.06

[back to top]

Change From Baseline to Endpoint in Hematocrit (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionproportion of blood volume (Mean)
BaselineChange
Olanzapine0.42-0.01
Placebo0.430.00

[back to top]

Change From Baseline to Endpoint in Hemoglobin (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionmillimole/Liter of iron (Fe) (Mean)
BaselineChange
Olanzapine8.65-0.11
Placebo8.730.05

[back to top]

Change From Baseline to Endpoint in Hemoglobin (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmillimole/Liter of iron (Fe) (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)8.610.04

[back to top]

Change From Baseline to Endpoint in Hemoglobin A1c (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionpercent of glycosylated hemoglobin (Mean)
BaselineChange
Olanzapine5.340.04
Placebo5.37-0.03

[back to top]

Change From Baseline to Endpoint in MINI Suicidality Total Scores (Acute Phase)

The MINI module C (MINI-C) is a rating scale for severity of suicidal thoughts and behaviors. The MINI-C is composed of 12 Yes/No questions with variable scores assigned to each question. The scale ranges from 0 to 52 with higher scores indicating a greater presence of suicidal thoughts and/or behaviors. (NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionunits on a scale (Mean)
BaselineChange
Olanzapine2.09-0.42
Placebo2.40-0.59

[back to top]

Change From Baseline to Endpoint in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score (Acute Phase)

The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionunits on a scale (Mean)
BaselineChange
Olanzapine29.36-14.26
Placebo28.69-11.71

[back to top]

Change From Baseline to Endpoint in Platelet Count (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionbillion cells per liter (BILL/L) (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)257.96-4.56

[back to top]

Change From Baseline to Endpoint in Prolactin (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionmicrogram/Liter (Mean)
BaselineChange
Olanzapine15.4012.07
Placebo15.86-1.18

[back to top]

Change From Baseline to Endpoint in Prolactin (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmicrogram/Liter (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)21.64-3.41

[back to top]

Change From Baseline to Endpoint in Uric Acid (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionmicromole/Liter (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)324.7414.73

[back to top]

Change From Baseline to Endpoint in Urinalysis (UA)- Specific Gravity (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionratio (Mean)
BaselineChange
Olanzapine1.02-0.00
Placebo1.020.00

[back to top]

Change From Baseline to Endpoint in Weight (Acute Phase)

(NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionkilograms (Mean)
BaselineEndpoint
Olanzapine66.112.45
Placebo68.30-0.13

[back to top]

Change From Baseline to Endpoint in Weight (Open-Label Phase)

(NCT00510146)
Timeframe: Baseline (End of Acute Phase/ Week 6), Endpoint (Week 24)

Interventionkilograms (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)68.312.27

[back to top]

Change From Baseline to Endpoint in Young Mania Rating Scale (YMRS) Total Score (Acute Phase)

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionunits on a scale (Mean)
BaselineChange
Olanzapine2.14-0.78
Placebo1.950.31

[back to top]

Change From Baseline to Endpoint in Young Mania Rating Scale (YMRS) Total Score (Open-Label Phase)

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6), Endpoint (Week 24)

Interventionunits on a scale (Mean)
BaselineChange
Olanzapine (Open-label Treatment Period)1.11-0.03

[back to top]

Change in Electrocardiogram (ECG) From Baseline to Endpoint (Acute Phase)

Time from electrocardiogram Q wave to the end of the T wave corresponding to electrical systole, fixed correction factor (QTcF interval); Bazett-Corrected QT Interval (QTcB interval). (NCT00510146)
Timeframe: Baseline, Endpoint (Week 6)

,
Interventionmilliseconds (Mean)
Baseline- QTcFChange- QTcFBaseline- QTcBChange- QTcB
Olanzapine406.852.82415.796.58
Placebo408.100.50418.421.21

[back to top]

Number of Participants With Adverse Events (Acute Phase)

Please refer to the Adverse Event overview for details regarding adverse events and serious adverse events. (NCT00510146)
Timeframe: Baseline through Week 6 (Acute Phase)

,
Interventionparticipants (Number)
SeriousNon-Serious
Olanzapine6238
Placebo788

[back to top]

Number of Participants With Adverse Events (Open-Label Phase)

Please refer to the Adverse Event overview for details regarding adverse events and serious adverse events. (NCT00510146)
Timeframe: Baseline (End of Acute Phase/Week 6) through Endpoint (Week 24)

Interventionparticipants (Number)
SeriousNon-Serious
Olanzapine (Open-label Treatment Period)14209

[back to top]

Percentage of Participants With Alcohol Dependence and Abuse at Endpoint on MINI Alcohol Dependence/Abuse Module (Acute Phase)

In the MINI Alcohol Abuse and Dependence Module, participants are asked a series of Yes/No questions to determine whether or not they are currently experiencing symptoms indicating current alcohol dependence or abuse. (NCT00510146)
Timeframe: Endpoint (Week 6)

,
Interventionpercentage of participants (Number)
DependenceAbuse
Olanzapine0.60.6
Placebo0.60.0

[back to top]

DEXA Total Fat

This study hypothesized that antipsychotic treatment would increase total body fat, as measured by whole body dual energy x-ray absorptiometry (DEXA), with larger adverse effects for olanzapine. (NCT00515723)
Timeframe: The relevant time points include baseline, week 6 and week 12.

,,,,
Interventionkilograms of body fat (Mean)
Baseline6 Weeks12 Weeks
Olanzapine32.2434.3835.45
Quetiapine28.8329.6030.10
Risperidone27.6628.2929.23
Total30.2531.0531.52
Ziprasidone31.6031.1830.66

[back to top]

Clamp Derived Insulin Sensitivity (mg/kg/Min)

This study hypothesized that antipsychotic treatment would decrease insulin sensitivity, with larger adverse effects for olanzapine. Insulin sensitivity describes how sensitive the body is to the effects of insulin. (NCT00515723)
Timeframe: The relevant time points include baseline and week 12.

,,,,
Interventionmg/kg/min (Mean)
BaselineWeek 12
Olanzapine4.393.62
Quetiapine5.285.08
Risperidone5.535.01
Total4.824.50
Ziprasidone4.334.45

[back to top]

Change in Total PANSS (Positive and Negative Syndrome Scale)Score From Baseline to the End of the Double Blind Treatment Period.

The PANSS is a 30-item rating instrument evaluating the presence/absence and severity of positive, negative and general psychopathology of schizophrenia. The scale was developed from the BPRS and the Psychopathology Rating Scale. All 30 items are rated on a 7-point scale (1=absent; 7=extreme). The total score can range from 30 to 210. Lower scores represent less severity of illness. (NCT00615433)
Timeframe: Baseline and 6 weeks

InterventionUnits on a scale (Least Squares Mean)
40mg-25.7
120mg-23.6
15mg Olz-28.7
Placebo-16.0

[back to top]

CGI-S (Clinical Global Impression - Severity) Change From Baseline to the End of the Double-blind Treatment.

The CGI-S is a clinician-rated assessment of the subject's current illness state on a 7-point scale, where a higher score is associated with greater illness severity. (NCT00615433)
Timeframe: 6 weeks

Interventionscale (Least Squares Mean)
40mg-1.5
120mg-1.4
15mg Olz-1.5
Placebo-1.1

[back to top]

Change From Baseline in Prolactin at Week 24 or Week 48 Endpoint

(NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionmicrogram/Liter (Mean)
Pre-Olanzapine-1.669
Pre-Placebo-0.388
New Olanzapine3.383

[back to top]

Change From Baseline in Glucose and Lipid Panel at Week 24 or Week 48 Endpoint

(NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

,,
Interventionmillimole/Liter (Mean)
Glucose, FastingCholesterolLow-density lipoprotein ( LDL) CholesterolHigh-density lipoprotein ( HDL) CholesterolTriglycerides
New Olanzapine0.680.0860.008-0.0740.382
Pre-Olanzapine0.030.0330.141-0.036-0.108
Pre-Placebo0.370.040-0.034-0.0460.485

[back to top]

Change From Baseline in Hemoglobin (HbA1c) at Week 24 or Week 48 Endpoint

HbA1c is a test that measures the amount of glycated hemoglobin in the blood over prolonged periods of time. (NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionpercentage of glycated hemoglobin (Mean)
Pre-Olanzapine-0.016
Pre-Placebo0.036
New Olanzapine0.180

[back to top]

Change From Baseline in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score at Week 24 or Week 48 Endpoint

The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionunits on a scale (Mean)
Pre-Olanzapine-0.2
Pre-Placebo-0.4
New Olanzapine-5.8

[back to top]

Change From Baseline to in QTcF at Week 24 or Week 48 Endpoint

Time from electrocardiogram Q wave to the end of the T wave corresponding to electrical systole, fixed correction factor (QTcF interval) (NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionmillisecond (msec) (Mean)
Pre-Olanzapine-1.7
Pre-Placebo-8.5
New Olanzapine-3.4

[back to top]

Percentage of Participants With Adverse Events Leading to Discontinuation

An adverse event (AE) is an untoward medical event associated with the use of the study drug or study procedure, whether or not it is considered related to the study drug or study procedure. Results presented are the percentage of participants who experienced an adverse event that resulted in the discontinuation of the study. (NCT00618748)
Timeframe: Baseline through 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionpercentage of participants (Number)
Pre-Olanzapine7.1
Pre-Placebo12.0
New Olanzapine40.0

[back to top]

Percentage of Participants With Emergence of Mania at Week 24 or Week 48

Emergence of mania is defined as first occurrence of score of >=15 in the YMRS total score in the post-baseline period of Acute Phase. The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00618748)
Timeframe: 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionpercentage of participants (Number)
Pre-Olanzapine0
Pre-Placebo0
New Olanzapine0

[back to top]

Percentage of Participants With High Suicidality at Week 24 or Week 48

The MINI module C (MINI-C) is a rating scale for severity of suicidal thoughts and behaviors. The MINI-C is composed of 12 Yes/No questions with variable scores assigned to each question. The scale ranges from 0 to 52 with higher scores indicating a greater presence of suicidal thoughts and/or behaviors. Based upon scores, suicidality is defined as Low (1-8), Medium (9-16), and High (>=17). (NCT00618748)
Timeframe: 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionpercentage of participants (Number)
Pre-Olanzapine3.6
Pre-Placebo0
New Olanzapine0

[back to top]

Percentage of Participants With Extra-Pyramidal Symptoms (EPS) at Week 24 or Week 48

EPS symptoms measured by DIEPSS are grouped into 4 categories: Parkinsonism, akathisia, dystonia, and dyskinesia. Severity ranges from level 0 (none, normal) to 4 (severe). A participant is deemed to have EPS at endpoint if they have an abnormal endpoint. Normal baseline Parkinsonism is defined as a score not ≥3 on 1 item or ≥2 on 2 items; abnormal endpoint is a score ≥3 on 1 item or ≥2 on 2 items, or an increase of 3 on Parkinsonism total. Normal baseline akathisia, dystonia and dyskinesia is defined as a score <2; abnormal endpoint is a score ≥2 or an increase ≥2 from that baseline score. (NCT00618748)
Timeframe: 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

,,
Interventionpercentage of participants (Number)
AkathisiaDyskinesiaDystoniaParkinsonism
New Olanzapine0005.0
Pre-Olanzapine0003.6
Pre-Placebo0000

[back to top]

Change From Baseline in Clinical Global Improvement- Bipolar (CGI-BP) at Week 24 or Week 48 Endpoint

CGI-BP is a measure of illness severity especially adapted for bipolar illness. It allows rating of mania, depression, and overall illness. The scores for mania, depression, and overall illness each range from 1 (normal, not ill) to 7 (very seriously ill). (NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

,,
Interventionunits on a scale (Mean)
CGI-BP ManiaCGI-BP DepressionCGI-BP Overall Bipolar Illness
New Olanzapine0.1-1.1-0.9
Pre-Olanzapine-0.1-0.3-0.3
Pre-Placebo0.1-0.0-0.1

[back to top]

Change From Baseline in Young Mania Rating Scale (YMRS) Total Score at Week 24 or Week 48 Endpoint

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionunits on a scale (Mean)
Pre-Olanzapine0.4
Pre-Placebo-0.2
New Olanzapine-0.1

[back to top]

Change From Baseline in Weight at Week 24 or Week 48 Endpoint

(NCT00618748)
Timeframe: baseline, 24 weeks (pre-olanzapine and pre-placebo) or 48 weeks (new olanzapine)

Interventionkilograms (Mean)
Pre-Olanzapine0.29
Pre-Placebo0.92
New Olanzapine5.36

[back to top]

Number of Participants With Scores of 4 to 7 in the Agitation-Calmness Evaluation Scale (ACES) at Each Timepoint

The ACES differentiates agitation, calmness, and sleep-state, using a 9-point scale: 1 (Marked Agitation) to 9 (Unarousable). Scores of 4 (Normal) to 7 (Marked Calmness) were used for this outcome measure. (NCT00640510)
Timeframe: 30 min, 60 min, 90 min and 2 hours post first IM injection

,
Interventionparticipants (Number)
30 Minutes60 Minutes90 Minutes2 Hours
IM Olanzapine 10mg1123
IM Placebo1122

[back to top]

Change From Baseline to Each Timepoint in Positive and Negative Syndrome Scale-Excited Component (PANSS-EC)

Measures excitability and consists of the following 5 items from the PANSS: Excitement, Hostility, Tension, Uncooperativeness, and Poor Impulse Control. Each item is rated on a scale from 1 (Absent) to 7 (Extreme). The sum of the 5 items is defined as the PANSS-EC total score which ranges from 5 to 35. (NCT00640510)
Timeframe: 15 min, 30 min, 60 min, 90 min post first IM injection

,
Interventionunits on a scale (Mean)
Change from Baseline to 15 minutesChange from Baseline to 30 minutesChange from Baseline to 60 minutesChange from Baseline to 90 minutes
IM Olanzapine 10mg-1.2-2.9-3.8-5.1
IM Placebo-1.2-2.4-3.4-4.6

[back to top]

Number of Responders at 2 Hours After First Intramuscular (IM) Injection

A responder was defined ast he patient with ≥ 40% decrease in the PANSS-EC total score at 2 hours after the first IM injection in comparison with baseline. (See outcome measure 1 for description of PANSS-EC). (NCT00640510)
Timeframe: 2 hours post first IM injection

Interventionparticipants (Number)
IM Olanzapine 10mg3
IM Placebo4

[back to top]

Change From Baseline to 2 Hours Post the First Intramuscular (IM) Injection in Positive and Negative Syndrome Scale-Excited Component (PANSS-EC)

Measures excitability and consists of the following 5 items from the PANSS: Excitement, Hostility, Tension, Uncooperativeness, and Poor Impulse Control. Each item is rated on a scale from 1 (Absent) to 7 (Extreme). The sum of the 5 items is defined as the PANSS-EC total score which ranges from 5 to 35. (NCT00640510)
Timeframe: 2 hours post first intramuscular (IM) injection

Interventionunits on a scale (Mean)
IM Olanzapine 10mg-4.7
IM Placebo-4.6

[back to top]

Change From Baseline at End Point in Body Weight

Patients were weighed lightly clothed. The same amount of clothing had to be worn each time. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionkg (Mean)
Paliperidone ER1.16
Olanzapine3.81

[back to top]

Change From Baseline at End Point in Waist Circumference

Patients had to be instructed to stand erect with abdomen relaxed, arms at sides, feet together, and weight divided equally over both legs. The tape measure was placed around the bare abdomen midway between the palpated iliac crest and the palpated lowest rib margin in the left and right mid-axillary lines. A nonstretchable tape was evenly placed around the natural waist covering the left and right natural-waist marks. The measurement scale had to face outward, and there could not be any twists in the tape. The tape had to be just touching the skin but not compressing the soft tissue. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventioncm (Mean)
Paliperidone ER0.70
Olanzapine3.38

[back to top]

Change From Baseline at End Point of Mari-Type Analysis of Glucose Sensitivity for Insulin

As another measure of beta-cell function, the relationship between plasma insulin and glucose concentrations during the OGTT was calculated using a simplified version of the method described by Mari et al. (Mari A, Sallas WM, He YL, Watson C, Ligueros-Saylan M, Dunning BE, Deacon CF, Holst JJ, Foley JE. Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed beta-cell function in patients with type 2 diabetes. J Clin Endocrinol Metab. 2005; 90:4888-4894.). (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

InterventionpM/mM (Mean)
Paliperidone ER8.63
Olanzapine17.28

[back to top]

Change From Baseline at End Point of the Insulinogenic Index

The insulinogenic index, defined as (insulin at 30 min - insulin at 0)/(glucose at 30 min [G(30)] - glucose at 0 [G(0)]) was used as a measure of early insulin secretion in response to the OGTT. Because the index is undefined when G(30)-G(0)=0, and poorly defined when G(30)-G(0)<0, the index was only calculated when G(30)>G(0). (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

InterventionpM/mM (Mean)
Paliperidone ER2.21
Olanzapine33.78

[back to top]

Change From Baseline to End Point in Converted Insulin

The insulin level was assessed under fasted conditions. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionpmol/L (Mean)
Paliperidone ER2.7397
Olanzapine17.2327

[back to top]

Change From Baseline to End Point in Fasting Glucose

(NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionmmol/L (Mean)
Paliperidone ER-0.2071
Olanzapine0.0769

[back to top]

Change From Baseline to End Point in High Density Lipoprotein

The HDL level was assessed under fasted conditions. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionmmol/L (Mean)
Paliperidone ER0.01
Olanzapine-0.04

[back to top]

Change From Baseline to End Point in Homeastatic Model Assessment of Insulin Resistance (HOMA-IR)

HOMA-IR is used to assess insulin resistance (IR). HOMA-IR is a dimensionless measure of insulin resistance (higher values present more insulin resistance. HOMA-IR are normalized so that lean, healthy individuals will have values of HOMA-IR close to 1. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventiondimensionless (Mean)
Paliperidone ER0.28
Olanzapine0.43

[back to top]

Change From Baseline to End Point in Homeostatic Model Assessment of Beta-cell Function (HOMA-%B)

"HOMA-%B is used to assess beta-cell function. HOMA-%B is a dimensionless measure of beta-cell function (higher values present increased insulin secretion for a given glucose level).~HOMA-%B is normalized so that lean, healthy individuals will have values of HOMA-%B close to 100%." (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventiondimensionless (Mean)
Paliperidone ER-7.54
Olanzapine18.82

[back to top]

Change From Baseline to End Point in Low Density Lipoprotein Cholesterol (Friedwald QT)

The level of low density lipoprotein cholesterol was calculated using the Friedwald QT formula. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionmmol/L (Mean)
Paliperidone ER-0.0029
Olanzapine0.1892

[back to top]

Change From Baseline to End Point in the Triglycerides (TG) to High Density Lipoprotein (HDL) Ratio (TG:HDL Ratio)

Plasma fasting TG and HDL concentrations were measured to determine the TG:HDL ratio. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

InterventionRatio (Mean)
Paliperidone ER-0.08
Olanzapine0.42

[back to top]

Change From Baseline to End Point in Total Cholesterol

The total cholesterol level was assessed under fasted conditions. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionmmol/L (Mean)
Paliperidone ER0.0263
Olanzapine0.2886

[back to top]

Change From Baseline to End Point in Total Positive and Negative Syndrome Scale Score (PANSS)

PANSS is an investigator-rated 30-item scale to assess the neuropsychiatric symptoms of schizophrenia. The PANSS provided a total score and scores for 3 subscales, the positive subscale (7 items), the negative subscale (7 items), and the general psychopathology subscale (16 items), each rated on a scale of 1 (absent) to 7 (extreme). (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionpoints on a scale (Mean)
Paliperidone ER-13.50
Olanzapine-16.60

[back to top]

Change From Baseline to End Point in Triglycerides

The TG level was assessed under fasted conditions. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionmmol/L (Mean)
Paliperidone ER-0.01
Olanzapine0.36

[back to top]

Number of Patients First Meeting the NCEP/ATP III Criteria for Metabolic Syndrome During Follow-up

"Metabolic syndrome is defined according the Third Report of the National Cholesterol Education Program Expert Panel on~Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP/ATPIII) of which 3 out of 5 criteria must be met:~waist circumference men > 102 cm; waist circumference women > 88 cm~TG ≥ 150 mg/dL~HDL cholesterol men <40 mg/dL; HDL cholesterol women <50 mg/dL~Blood pressure systolic ≥ 130 mmHg; Blood pressure diastolic ≥ 85 mmHg~Fasting glucose ≥ 110 mg /dL" (NCT00645099)
Timeframe: 6 months

InterventionParticipants (Number)
Paliperidone ER23
Olanzapine38

[back to top]

Number of Patients Meeting the Criteria for Type 2 Diabetes Mellitus During Follow-up

Fasting plasma glucose ≥126 mg/dL or 2-hour post-load plasma glucose ≥200 mg/dL during an oral glucose tolerance test (OGTT) or initiated use of glucose-lowering agents during the course of the study. (NCT00645099)
Timeframe: 6 months

InterventionParticipants (Number)
Paliperidone ER21
Olanzapine23

[back to top]

Number of Patients With Impaired Fasting Glucose

Post-baseline glucose level under fasted conditions ≥100 mg/dL but <126 mg/dL. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

InterventionParticipants (Number)
Paliperidone ER68
Olanzapine66

[back to top]

Number of Patients With Onset of Impaired Glucose Tolerance

Glucose ≥140 mg/dL, <200 mg/dL after a 75g OGTT. (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

InterventionParticipants (Number)
Paliperidone ER36
Olanzapine33

[back to top]

Change From Baseline at End Point in Body Mass Index (BMI)

BMI is calculated by dividing the body weight (in kg) by the square of height (in meters). (NCT00645099)
Timeframe: Baseline to End Point (up to 6 months)

Interventionkg/m² (Mean)
Paliperidone ER0.43
Olanzapine1.32

[back to top]

Change From Baseline in Weight (Lbs.) at 12 Weeks

This study looked at change in weight before and after medication use. (NCT00685334)
Timeframe: baseline and 12 weeks

Interventionlbs (Mean)
Olanzapine2.2
Aripiprazole-1.2

[back to top]

Tolerability

This study addressed the benefits, tolerability, acceptability, safety, and appropriate dosage of olanzapine and aripiprazole, as determined by clinical evaluation and self report. The outcome measure reported here is the number of patients who did not experience untoward side effects while taking the medication. (NCT00685334)
Timeframe: Measured at Week 12

InterventionParticipants (Number)
Olanzapine8
Aripiprazole9

[back to top]

Positive and Negative Syndrome Scale (PANSS) Total Score Change From Baseline

PANSS total score, sum of 30 item scores (each on a 0 to 7 scale), assesses positive and negative symptoms of psychopathology on a continuous scale from 0 (the best) to 210 (the worst). Day 28 value was calculated using last observation carried forward (LOCF). Change from baseline was calculated as Day 28 value minus baseline value. (NCT00686998)
Timeframe: Baseline, Day 28

InterventionPoints on a scale (Mean)
AZD26241.40
Placebo4.51
Olanzapine-8.79

[back to top]

Symptom Severity Assessed by Yale Brown Cornell-Eating Disorders Scale

The Yale Brown Cornell-Eating Disorders Scale was used.This scale assesses severity of preoccupations and rituals. There are 8 questions that can be scored between 0-4 to indicate severity of symptoms, with 0 representing less severe and 4 representing most severe symptoms. The scores were summed, with possible results totaling 0-32. (NCT00692185)
Timeframe: Measured at Week 8

Interventionscore on a scale (Mean)
Olanzapine19.4
Placebo18.9

[back to top]

Weight Gain

(NCT00692185)
Timeframe: Measured at Week 8

Interventionlbs (Mean)
Olanzapine6.2
Placebo1.5

[back to top]

Systolic Blood Pressure

Systolic Blood Pressure (NCT00741026)
Timeframe: 3 Days

InterventionmmHg (Mean)
Placebo113.3
Olanzapine111.7

[back to top]

Plasma Leptin

Leptin following placebo or olanzapine treatment (NCT00741026)
Timeframe: 3 Days

Interventionng/ml (Mean)
Placebo6.8
Olanzapine8.4

[back to top]

Plasma Free Fatty Acid

Plasma Free Fatty Acid (NCT00741026)
Timeframe: 3 Days

InterventionmM (Mean)
Placebo0.38
Olanzapine0.26

[back to top]

Diastolic Blood Pressure

Diastolic Blood Pressure (NCT00741026)
Timeframe: 3 Days

InterventionmmHg (Mean)
Placebo68.3
Olanzapine69.5

[back to top]

Oral Glucose Tolerance

Oral Glucose Tolerance (NCT00741026)
Timeframe: 3 Days

Interventionmin*mg/dl (Mean)
Placebo2808
Olanzapine3984

[back to top]

LDL Cholesterol

LDL Cholesterol (NCT00741026)
Timeframe: 3 Days

Interventionmg/dl (Mean)
Placebo82.7
Olanzapine81.7

[back to top]

Heart Rate

Heart Rate (NCT00741026)
Timeframe: 3 Days

Interventionbeats per minute (Mean)
Placebo69.9
Olanzapine67.6

[back to top]

Body Weight

Body Weight (NCT00741026)
Timeframe: 3 Days

Interventionkg (Mean)
Placebo68.2
Olanzapine68.9

[back to top]

BMI

BMI (NCT00741026)
Timeframe: 3 Days

Interventionkg / m2 (Mean)
Placebo23.0
Olanzapine23.0

[back to top]

HDL Cholesterol

HDL Cholesterol (NCT00741026)
Timeframe: 3 Days

Interventionmg/dl (Mean)
Placebo54.2
Olanzapine48.9

[back to top]

Triglycerides

Triglycerides (NCT00741026)
Timeframe: 3 Days

Interventionmg/dl (Mean)
Placebo88.9
Olanzapine108.2

[back to top]

Total Cholesterol

Total Cholesterol (NCT00741026)
Timeframe: 3 Days

Interventionmg/dl (Mean)
Placebo156.8
Olanzapine152.6

[back to top]

Drinks Per Drinking Day

"Drinks are measured as the number of standard alcoholic beverages consumed each day, assessed in varying lengths of time (i.e., 2 weeks, 4 weeks, 6 weeks, etc.). A standard alcoholic beverage is equivalent to: 1, 12 oz. regular beer; 1, 5 oz. glass of wine; 1, mixed drink with one1.5 oz shot; or 1, 1.5 oz shot. A drinking day is measured as any day of the week in which an alcoholic beverage is consumed. Data for drinks per drinking day is gathered using the Time Line Follow Back method in which participants are asked to recall their alcohol consumption day by day for a pre-defined set of time." (NCT00746785)
Timeframe: up to 36 weeks

InterventionDrinks per drinking day (Mean)
A - 2.5 mg Olanzapine8.7
B - 5 mg Olanzapine8.9
C - Placebo9.2

[back to top]

Change of the Agitation-Calmness Evaluation Scale (ACES) Score From Baseline to 120 Minutes After 1st Injection

Agitation was further assessed by the Agitation Calmness Evaluation Scale (ACES) (Copyright 1998, Eli Lilly and Company), a single-item scale developed by Eli Lilly and Company on which 1 indicates marked agitation; 2, moderate agitation; 3, mild agitation; 4, normal; 5, mild calmness; 6, moderate calmness; 7, marked calmness; 8, deep sleep; and 9, unable to be aroused. (NCT00797277)
Timeframe: from baseline to 120 minutes after first injection

Interventionunits on a scale (Mean)
1. IM Olanzapine2.14
2. IM Haloperidol Pus Lorazepam2.23

[back to top]

The Change of the Positive and Negative Symptom Scale Excited Component (PANSS-EC) Score From Baseline to 120 Minutes After First Injection

The primary efficacy measure was PANSS-EC, which was derived from the PANSS by its originators using a principal-components factor analysis, and includes the items of tension, uncooperativeness, hostility, poor impulse control and excitement.22 The score of each item ranges from 1 (normal) to 7 (most severe), with a total sum score ranging from 5 to 35. The changes in PANSS-EC from baseline to 2 hours after the first injection were compared. (NCT00797277)
Timeframe: from baseline to 120 minutes after first injection

Interventionunits on a scale (Mean)
1. IM Olanzapine-10.2
2. IM Haloperidol Plus Lorazepam-9.9

[back to top]

Feasibility of Randomizing a Cohort of Participants Meeting the Inclusion and Exclusion Criteria of the Study

Goal was to randomize 60 participants who met eligibility criteria. (NCT00802100)
Timeframe: Baseline

Interventionparticipants (Number)
Overall Study21

[back to top]

Antipsychotic Efficacy, Defined as Completion of the Trial Without Psychiatric Hospitalization, Clinician Decision to Discontinue Treatment, or Patient Decision to Discontinue Treatment

(NCT00802100)
Timeframe: Measured over 28 weeks of study visits

,,
Interventionparticipants (Number)
InefficacyUnacceptable side effectsPatient refusalDrop-out, no information availableAdministrativeCompleted trial without discontinuing
Aripiprazole100032
Olanzapine003210
Perphenazine100152

[back to top]

Triglyceride Levels

(NCT00806234)
Timeframe: Change from baseline to 24 weeks

Interventionmg/dL (Least Squares Mean)
Healthy Lifestyle Information0.2
Switch Treatment + Healthy Lifestyle Instruction16.6
Metformin Treatment + Healthy Lifestyle Instruction14.7

[back to top]

Change in Whole Body Insulin Sensitivity Index

(NCT00806234)
Timeframe: Change from baseline to 24 weeks

InterventionmU/L (Least Squares Mean)
Healthy Lifestyle Information0.74
Switch Treatment + Healthy Lifestyle Instruction0.42
Metformin Treatment + Healthy Lifestyle Instruction-0.34

[back to top]

Body Mass Index (BMI) Z-score Change

(NCT00806234)
Timeframe: Change from baseline to 24 weeks

InterventionZ Score (Least Squares Mean)
Healthy Lifestyle Information0.040
Switch Treatment + Healthy Lifestyle Instruction-0.112
Metformin Treatment + Healthy Lifestyle Instruction-0.088

[back to top]

Change in Low Density Lipoprotein (LDL) Cholesterol Level

(NCT00806234)
Timeframe: From Baseline to Week 24

Interventionmg/dL (Least Squares Mean)
Healthy Lifestyle Information3.6
Switch Treatment + Healthy Lifestyle Instruction-8.1
Metformin Treatment + Healthy Lifestyle Instruction-4.1

[back to top]

Mean Change From Baseline in Clinical Global Impression - Severity of Illness Scale (CGI-S) at Week 4

CGI-S is a commonly used measure of symptom severity in treatment studies of participants with mental disorders. CGI-S is a 7-point scale that requires the clinician to rate the severity of the participant's illness at the time of assessment, relative to the clinician's past experience with participants who have the same diagnosis. Considering total clinical experience, a participant is assessed on severity of mental illness at the time of rating 1 = normal, not at all ill; 2 = borderline mentally ill; 3 = mildly ill; 4 = moderately ill; 5 = markedly ill; 6 = severely ill; or 7 = extremely ill. (NCT00827918)
Timeframe: Baseline and Week 4

InterventionUnits on a scale (Least Squares Mean)
MK-8998-0.9
Olanzapine-0.8
Placebo Comparator-0.9

[back to top]

Mean Change From Baseline in PANSS Negative Subscale at Week 4

PANSS Negative scale assesses emotional withdrawal, lack of motivation, and similar symptoms. The Negative scale has 7 items with an anchored Likert scale from 1 to 7 to score each item. Values of 2 and above indicate the presence of progressively more severe symptoms. A total score ranges from 7 to 49. (NCT00827918)
Timeframe: Baseline and Week 4

InterventionUnits on a scale (Least Squares Mean)
MK-8998-3.3
Olanzapine-3.1
Placebo Comparator-2.9

[back to top]

Mean Change From Baseline in the Positive and Negative Syndrome Scale (PANSS) at Week 4

PANSS is a medical scale used for measuring symptom severity of participants with schizophrenia. PANSS measure is composed of 3 scales: Positive scale, Negative scale, and General Psychopathology scale. Positive scale assesses hallucinations, delusions and related symptoms; Negative scale assesses emotional withdrawal, lack of motivation, and similar symptoms; and General Psychopathology scale addresses other symptoms such as anxiety, somatic concern and disorientation. The PANSS has 30 items in its 3 scales and an anchored Likert scale from 1 to 7 is used to score each item. Values of 2 and above indicate the presence of progressively more severe symptoms. The Positive scale has 7 items with a score from 7 to 49, the Negative scale has 7 items with a score from 7 to 49, and the General Psychopathology scale has 16 items with a score from 16 to 112. A total score is the sum of the 3 scores for the 3 scales. (NCT00827918)
Timeframe: Baseline and Week 4

InterventionUnits on a scale (Least Squares Mean)
MK-8998-13.3
Olanzapine-17.0
Placebo Comparator-12.7

[back to top]

Percentage of Participants With Response at Week 4

Responders were defined as participants who demonstrated ≥ 20% improvement from baseline on the PANSS total score. PANSS measure is composed of 3 scales: Positive scale, Negative scale, and General Psychopathology scale. Positive scale assesses hallucinations, delusions and related symptoms; Negative scale assesses emotional withdrawal, lack of motivation, and similar symptoms; and General Psychopathology scale addresses other symptoms such as anxiety, somatic concern and disorientation. The PANSS has 30 items in its 3 scales and an anchored Likert scale from 1 to 7 is used to score each item. Values of 2 and above indicate the presence of progressively more severe symptoms. The Positive scale has 7 items with a score from 7 to 49, the Negative scale has 7 items with a score from 7 to 49, and the General Psychopathology scale has 16 items with a score from 16 to 112. A total score is the sum of the 3 scores for the 3 scales. (NCT00827918)
Timeframe: Week 4

InterventionPercentage of participants (Number)
MK-899857.4
Olanzapine66.7
Placebo Comparator48.3

[back to top]

Number of Participants Who Experienced at Least One Adverse Event

An adverse event (AE) is any unfavorable and unintended change in the structure, function or chemistry of the body temporally associated with study drug administration whether or not considered related to the use of the study drug. (NCT00827918)
Timeframe: Up to 6 Weeks

InterventionParticipants (Number)
MK-899841
Olanzapine23
Placebo Comparator33

[back to top]

Number of Participants Who Discontinued Study Drug Due to an Adverse Event

An AE is any unfavorable and unintended change in the structure, function or chemistry of the body temporally associated with study drug administration whether or not considered related to the use of the study drug. (NCT00827918)
Timeframe: Up to 4 Weeks

InterventionParticipants (Number)
MK-89989
Olanzapine1
Placebo Comparator1

[back to top]

Mean Change From Baseline in PANSS Positive Subscale at Week 4

PANSS Positive scale assesses hallucinations, delusions and related symptoms. The Positive scale has 7 items with an anchored Likert scale from 1 to 7 to score each item. Values of 2 and above indicate the presence of progressively more severe symptoms. A total score ranges from 7 to 49. (NCT00827918)
Timeframe: Baseline and Week 4

InterventionUnits on a scale (Least Squares Mean)
MK-8998-4.2
Olanzapine-5.6
Placebo Comparator-4.2

[back to top]

Change From Baseline in Weight Up to Week 8

Weight LS mean was adjusted for baseline and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionkilogram (kg) (Least Squares Mean)
Olanzapine/Fluoxetine Combination4.37
Placebo0.50

[back to top]

Change From Baseline in the YMRS Total Score at Week 8

The YMRS is an 11-item scale measuring the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total scores ranges: 0 to 60. LS mean was adjusted for baseline, country, treatment, visit, and treatment * visit interaction. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination-2.02
Placebo-1.57

[back to top]

Change From Baseline in the Quality of Life Questionnaire for Children and Adolescents (KINDL) Parent Scale Up to Week 8

The KINDL consists of 24 Likert-scale items. Total scores were standardized to a 0 (lowest quality of life) to 100 (highest quality of life). LS mean was adjusted for baseline, country, and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination15.98
Placebo10.88

[back to top]

Change From Baseline in the Quality of Life Questionnaire for Children and Adolescents (KINDL) Kid and Kiddo Combined Scale Up to Week 8

The KINDL consists of 24 Likert-scale items. Kid-KINDL was administered to ages 8-11 and Kiddo-KINDL to ages 12-16. Total scores were standardized to a 0 (lowest quality of life) to 100 (highest quality of life). LS mean was adjusted for baseline, country, and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination12.83
Placebo7.91

[back to top]

Change From Baseline in the Clinical Global Impression Scale - Bipolar Version (CGI-BP) Score at Week 8

CGI-BP measures severity of illness for bipolar illness. Scores range: 1 (normal, not ill at all) to 7 (among the most extremely ill patients). LS mean was adjusted for baseline, country, treatment, visit, and treatment * visit interaction. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination-2.21
Placebo-1.83

[back to top]

Change From Baseline in the Children's Depression Rating Scale Revised (CDRS-R) Total Score at Week 8

CDRS-R Total score measures the presence and severity of depression in children. The scale consists of 17 items scored on a 1-to-5- or 1-to-7-point scale. A rating of 1 indicates normal functioning. Total scores range from 17 to 113. In general, scores below 20 indicate an absence of depression, scores of 20 to 30 indicate borderline depression, and scores of 40 to 60 indicate moderate depression. Least Square (LS) mean was adjusted for baseline, country, treatment, visit, and treatment times (*) visit interaction. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination-28.43
Placebo-23.40

[back to top]

Change From Baseline in Symptoms of Attention-Deficit/Hyperactivity Disorder Up to Week 8

Attention Deficit/Hyperactivity Disorder Rating Scale-IV-Parent Version (ADHDRS-IV-PI): Investigator Administered and Scored measures the 18 symptoms contained in the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition, Text Revision (DSM-IV-TR) diagnosis of Attention-Deficit/Hyperactivity Disorder. Individual item scores range from 0 (none/never or rarely) to 3 (severe/very often). Scores range: 0 to 54. The LS mean was adjusted for baseline and treatment. (NCT00844857)
Timeframe: Baseline up to Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination-4.31
Placebo-3.57

[back to top]

Change From Baseline in Prolactin Up to Week 8

Prolactin LS mean was adjusted for baseline and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionmicrogram/Liter (μg/L) (Least Squares Mean)
Olanzapine/Fluoxetine Combination8.66
Placebo0.70

[back to top]

Change From Baseline in Electrocardiogram (ECG) QTcF Interval Up to Week 8

QTcF is defined as ECG QT interval corrected for heart rate using the Fridericia correction factor. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionmillisecond (msec) (Least Squares Mean)
Olanzapine/Fluoxetine Combination8.19
Placebo-1.07

[back to top]

Change From Baseline in Alanine Aminotransferase/Serum Glutamic-Pyruvic Transaminase (ALT/SGPT) Up to Week 8

ALT/SGPT LS mean was adjusted for baseline and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits/Liter (U/L) (Least Squares Mean)
Olanzapine/Fluoxetine Combination7.63
Placebo0.46

[back to top]

Change From Baseline in the CDRS-R Total Score Up to Week 8

CDRS-R Total score measure the presence and severity of depression in children and consists of 17 items scored on a 1-to-5- or 1-to-7-point scale. Rating of 1 indicates normal function. Total scores range from 17 to 113. In general, scores < 20 indicate an absence of depression, scores of 20 to 30 indicate borderline depression, and scores of 40 to 60 indicate moderate depression. LS mean was adjusted for baseline, country, and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Fluoxetine Combination-28.57
Placebo-23.38

[back to top]

Percentage of Participants With Treatment Emergent Suicidal Ideation or Behavior Up to Week 8

"Columbia-Suicide Severity Rating Scale (C-SSRS) captures occurrence, severity, and frequency of suicide-related thoughts and behaviors. Percentage of participants with suicidal ideation, behavior, and acts are provided. Suicidal ideation: a yes answer to any 1 of 5 suicidal ideation questions, which includes wish to be dead, and 4 different categories of active suicidal ideation. Suicidal behavior: a yes answer to any of 5 suicidal behavior questions: preparatory acts or behavior, aborted attempt, interrupted attempt, actual attempt, and completed suicide. Suicidal act: a yes answer to actual attempt or completed suicide." (NCT00844857)
Timeframe: Baseline up to Week 8

,
Interventionpercentage of participants (Number)
Total Suicidal Ideation (1 - 5)Total Suicidal Behavior (6 - 10)Total Suicidal Ideation or Behavior (1 - 10)
Olanzapine/Fluoxetine Combination10.61.810.6
Placebo15.52.415.5

[back to top]

Percentage of Participants in Each Improvement Category Up to Week 8

CDRS-R scores: No/low improvement is < 25 percent (%) of maximum reduction from baseline. Mild improvement: maximum reduction from baseline on CDRS-R score ≥ 25% up to <50% and YMRS elevated mood score ≤ 2. Moderate improvement: maximum reduction from baseline on CDRS-R score ≥50% and <75% and YMRS elevated mood score ≤ 2. Major improvement: maximum reduction from baseline on CDRS-R score ≥75% and YMRS elevated mood score ≤ 2. CDRS-R measures presence/severity of depression in children. Scale is 17 items scored 1-to-5- or 1-to-7. Rating of 1 indicates normal function. Scores range: 17 to 113. Scores < 20 absence of depression, scores 20 to 30 borderline depression, scores 40 to 60 indicate moderate depression. YMRS is an 11-item scale that measures severity of manic episodes. Four items rated 0 (symptoms not present) to 8 (symptom extremely severe). Remaining items rated 0 (symptoms not present) to 4 (symptom extremely severe). Score range: 0 to 60. (NCT00844857)
Timeframe: Baseline up to Week 8

,
Interventionpercentage of participants (Number)
No or Low ImprovementMild ImprovementModerate ImprovementMajor Improvement
Olanzapine Plus Fluoxetine Combination12.89.021.856.4
Placebo22.418.418.440.8

[back to top]

Change From Baseline in Fasting Metabolic Parameters Up to Week 8

Fasting glucose, fasting cholesterol and fasting triglycerides. LS means were adjusted for baseline and treatment. (NCT00844857)
Timeframe: Baseline, Week 8

,
Interventionmillimoles/liter (mmol/L) (Least Squares Mean)
Fasting Glucose (157, 79)Fasting Cholesterol (158, 81)Fasting Triglycerides (158, 81)
Olanzapine/Fluoxetine Combination0.030.420.40
Placebo0.03-0.11-0.04

[back to top]

Percentage of Participants With Response Up to Week 8

Response is defined as a CDRS-R total score greater than or equal to (≥)50% reduction from baseline and YMRS elevated mood score ≤2. CDRS-R Total score measure the presence and severity of depression in children. The scale consists of 17 items scored on a 1-to-5- or 1-to-7-point scale. Rating of 1 indicates normal function. Scores range: 17 to 113. In general, <20 indicate an absence of depression, scores 20 to 30 indicate borderline depression, and scores of 40 to 60 indicate moderate depression. YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptoms not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptoms not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. (NCT00844857)
Timeframe: Baseline up to Week 8

Interventionpercentage of participants (Number)
Olanzapine/Fluoxetine Combination78.2
Placebo59.2

[back to top]

Percentage of Participants With Remission Up to Week 8

Remission is defined as a CDRS-R total score less than or equal to (≤)28, and Young Mania Rating Scale (YMRS) total score ≤ 8 and Clinical Global Impressions-Bipolar Version (CGI-BP) total score ≤3. CDRS-R is a 17-item scale measuring presence/severity of depression in children and is scored on a 1-to-5- or 1-to-7-point scale. Rating of 1 indicates normal function. Scores range: 17 to 113. Scores <20 indicate an absence of depression, scores 20 to 30 indicate borderline depression, scores 40 to 60 indicate moderate depression. The YMRS is an 11-item scale measuring severity of manic episodes; 4 items are rated on a scale from 0 (symptoms not present) to 8 (symptom extremely severe) with remaining items rated on a scale from 0 (symptoms not present) to 4 (symptom extremely severe). YMRS score ranges from 0 to 60. CGI-BP measures participant's overall severity of bipolar symptoms. Scores range: 1 (normal, not at all ill ) to 7 (among the most extremely ill participants). (NCT00844857)
Timeframe: Baseline up to Week 8

Interventionpercentage of participants (Number)
Olanzapine/Fluoxetine Combination59.0
Placebo43.4

[back to top]

Percentage of Participants With at Least One Treatment-Emergent Incident of Parkinsonism Up to Week 8

Parkinsonism was measured using the Simpson-Angus Scale with a total scores range from 0 to 40. A score > 3 was considered abnormal. Simpson-Angus Scale consists of 10 items, each rated on a 5-point scale, 0 (complete absence of the condition) to 4 (presence of the condition in extreme form). (NCT00844857)
Timeframe: Baseline, Week 8

Interventionpercentage of participants (Number)
Olanzapine/Fluoxetine Combination0.6
Placebo1.3

[back to top]

Percentage of Participants With at Least One Treatment-Emergent Incident of Dyskinesia Up to Week 8

Dyskinesia was measured using the Abnormal Involuntary Movement Scale (AIMS) a 12-item scale designed to record the occurrence of dyskinetic movements. Items 1 through 10 are rated on a 5-point scale: 0 (no dyskinetic movements) to 4 (severe dyskinetic movements). Items 11 and 12 are yes/no questions regarding the dental condition of a patient. Total score (0-40) is obtained by adding the scores of the first 10 items. An abnormal result is defined as having a score ≥3 for at least 1 of the first 7 items or a score ≥2 for at least two of the first 7 items. (NCT00844857)
Timeframe: Baseline, Week 8

Interventionpercentage of participants (Number)
Olanzapine/Fluoxetine Combination0.6
Placebo0.0

[back to top]

Percentage of Participants With at Least One Treatment-Emergent Incident of Akathisia Up to Week 8

Akathisia was measured using the Barnes Akathisia Rating Scale where the global scores range from 0 (absent) to 5 (severe) and a score ≥ 2 is considered abnormal. (NCT00844857)
Timeframe: Baseline up to Week 8

Interventionpercentage of participants (Number)
Olanzapine/Fluoxetine Combination1.3
Placebo0.0

[back to top]

Percentage of Participants With at Least One Incident of Worsening of Mania Up to Week 8

Worsening of mania was defined as YMRS score of ≥20 and a CGI severity of mania score of ≥ 5 at the same visit. The YMRS is an 11-item scale measuring severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe) with remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 to 60. CGI measures severity of the participant's overall severity of bipolar symptoms and scores range from 1 (normal) to 7 (among the most extremely ill participants). (NCT00844857)
Timeframe: Baseline up to Week 8

Interventionpercentage of participants (Number)
Olanzapine/Fluoxetine Combination1.2
Placebo0.0

[back to top]

Change From Baseline in 16-Item Negative Symptoms Assessment (NSA-16) Total Score at 52 Weeks Endpoint

"The NSA-16 is used to rate behaviors (not psychopathology) associated with negative symptoms of schizophrenia and rates patients on 16 anchors, each of which is rated 1 to 6. The total score is their sum and ranges from 16 to 96. Higher scores indicate greater severity of illness. LS Mean of change from baseline is from a MMRM model which includes treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline score and baseline-by-visit interaction." (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY2140023-2.86
Standard-of-Care (SOC)-7.81

[back to top]

Change From Baseline in Abnormal Involuntary Movement Scale (AIMS) Total Score at 52 Weeks Endpoint

The AIMS is a 12-item scale designed to record the occurrence of dyskinetic movements. Items 1 to 10 are rated 0 - 4, with 0 being no dyskinetic movements and 4 being severe dyskinetic movements. Items 11 and 12 are yes/no questions regarding the dental condition of a subject. The total score is the sum of items 1-7 and ranges from 0-28. LS means of change from baseline in the AIMS total score is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY21400230.13
Standard-of-Care (SOC)-0.23

[back to top]

Change From Baseline in Barnes Akathisia Scale (BAS) Global Score at 52 Weeks Endpoint

The BAS rates drug induced akathisia symptoms. Akathisia is rated on a 4-point scale, with 0 being no akathisia and 3 being severe akathisia. A global clinical assessment of akathisia is then scored on a 6-point scale, with 0 being no evidence of akathisia and 5 being severe akathisia. LS mean of change from baseline in BAS global score is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY2140023-0.06
Standard-of-Care (SOC)-0.08

[back to top]

Change From Baseline in Clinical Global Impression Severity Scale (CGI-S) at 52 Weeks Endpoint

The CGI-S scale measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill patients). LS Mean of change from baseline is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline score and baseline-by-visit interaction. Higher CGI-S score means worse symptoms. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY2140023-0.27
Standard-of-Care (SOC)-0.81

[back to top]

Change From Baseline in Measurement and Treatment Research to Improve Cognition in Schizophrenia Consensus Cognitive Battery (MCCB): Overall Composite T-Score at 52 Weeks Endpoint

The MCCB assesses cognitive function in 7 domains important in schizophrenia. The MCCB overall composite score is calculated by summing age- and gender-corrected T-scores of all the domains and then standardizing the sum to a T-score, where the mean is 50 and a standard deviation is 10. A higher score indicates better performance. LS Mean of change from baseline is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline score and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY21400235.29
Standard-of-Care (SOC)8.19

[back to top]

Change From Baseline in Montgomery-Asberg Depression Rating Scale (MADRS) Total Score at 52 Weeks Endpoint

The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist. Items are rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). LS Mean of changes from baseline is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline score and baseline-by-visit interaction. Higher MADRS scores mean worse symptoms. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY21400232.72
Standard-of-Care (SOC)-2.82

[back to top]

Change From Baseline in Number of Psychiatric Visits at 24 Weeks Endpoint

Change in number of psychiatric visits between the 6 months prior to the active treatment phase and psychiatric visits reported during the active treatment phase was summarized. Treatment groups were compared on change using the analysis of covariance (ANCOVA) model. The model has baseline as a covariate, and investigative site, gender, and treatment as fixed effects. (Analysis for Study Period III only) (NCT00845026)
Timeframe: Baseline, 24 weeks

Interventionvisits (Least Squares Mean)
LY2140023-2.60
Standard-of-Care (SOC)-2.95

[back to top]

Change From Baseline in Personal and Social Performance (PSP) at 52 Weeks Endpoint

The Personal and Social Performance (PSP) scale is a 100-point, single-item, clinician-rated scale to assess 4 domains of functioning, including personal and social relationships, socially useful activities, self care, and disturbing and aggressive behaviors. Score ranges from 1-100. The higher score indicates a better health state. LS Mean of changes from baseline is from a MMRM model which includes the effects of treatment, gender, investigator site, visit, treatment-by-visit interaction, baseline score and baseline score by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY21400236.47
Standard-of-Care (SOC)10.71

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) at 52 Weeks Endpoint

Assesses the positive and negative symptoms and general psychopathology associated with schizophrenia. The scale consists of 30 items. Each item is rated on a scale from 1 (symptom not present) to 7 (symptoms extremely severe). The sum of the 30 items is defined as the PANSS total score and ranges from 30 to 210. LS Mean of change from baseline is from a mixed model repeated measures (MMRM) model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline score and baseline-by-visit interaction. Higher PANSS scores mean worse symptoms. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY2140023-4.54
Standard-of-Care (SOC)-21.47

[back to top]

Change From Baseline in Subjective Well-Being Under Neuroleptic Treatment-Short Form (SWN-S) Total Score at 52 Weeks Endpoint

Measures subjective well-being for previous 7 days. 20 items covering 5 health domains (subscales) (4 items each): emotional regulation, self-control, mental functioning, social integration, and physical functioning. Individual scores range from 1 (not at all) to 6 (very much). Subscale scores range from 4 to 24. Total score ranges from 20 to 120. LS mean of change from baseline is from a MMRM model which includes the effects of treatment, gender, investigator site, visit, treatment-by-visit interaction, baseline score and baseline score by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY21400231.11
Standard-of-Care (SOC)4.15

[back to top]

Percentage of Participants With Response (Rate of Response) at 6 and 24 Weeks Endpoints

Response is defined as reduction ≥ 30% from baseline on PANSS Total Score (Each PANSS item transformed to a 0-6 scale first). PANSS assesses the positive symptoms, negative symptoms, and general psychopathology specifically associated with schizophrenia. The scale consists of 30 items. Each item is rated on an original scale from 1 (symptom not present) to 7 (symptoms extremely severe). The sum of the 30 items is defined as the PANSS total score and ranges from 30 to 210. Higher scores indicate greater severity of illness. (Analysis for Study Period III only) (NCT00845026)
Timeframe: 6 and 24 weeks

,
Interventionpercentage of participants (Number)
6 weeks24 weeks
LY214002335.026.7
Standard-of-Care (SOC)31.337.5

[back to top]

Number of Participants With Treatment-Emergent Change in Neurological Examination

An increase in score from baseline was considered a treatment-emergent change, unless stated otherwise. Tremor: 0 (absent) - 3 (interferes with motor function); Nystagmus: 0 (absent) - 3 (present on forward gaze); Reflexes: 0 (absent) - 4 (clonic) with normal being a score 2, decrease or increase in score was considered change. Finger-nose and gait tests: 0 (normal) - 1(abnormal); Romberg's sign: (0) absent - (1) present; Muscular strength: 0 (no contraction)-5 (full/normal resistance), decrease in score was considered change; Myoclonic jerks: 0 (absent) - 3 (frequent). (NCT00845026)
Timeframe: Baseline through 52 weeks

,
Interventionparticipants (Number)
TremorNystagmusIncreased reflexesDecreased reflexesAbnormal finger-nose testRomberg's signAbnormal GaitDecreased muscle strengthMyoclonus
LY2140023161792020471
Standard-of-Care (SOC)2312628011110

[back to top]

Number of Participants With Suicidal Behaviors and Ideations Baseline Through 52 Weeks

"Columbia Suicide Rating Scale (C-SSRS): scale capturing occurrence, severity, and frequency of suicide-related thoughts and behaviors. Number of participants with suicidal behaviors and ideations are provided. Suicidal behavior: a yes answer to any of 5 suicidal behavior questions: preparatory acts or behavior, aborted attempt, interrupted attempt, actual attempt, and completed suicide. Suicidal ideation: a yes answer to any one of 5 suicidal ideation questions, which includes wish to be dead, and 4 different categories of active suicidal ideation. There are no scores on a scale reported, rather, number of patients who reported yes as described above." (NCT00845026)
Timeframe: Baseline through 52 weeks

,
Interventionparticipants (Number)
Suicidal ideationSuicidal behavior/acts
LY214002380
Standard-of-Care (SOC)162

[back to top]

Change From Baseline in Pulse Rate at 52 Weeks Endpoint

LS Mean of change from baseline in pulse rate is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline value and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

,
Interventionbeats per minute (bpm) (Least Squares Mean)
Supine PulseStanding Pulse
LY2140023-1.62-2.16
Standard-of-Care (SOC)-2.44-2.41

[back to top]

Number of Participants With Potentially Clinical Significant Change in Lipids Level

Treatment-emergent changes in lab results on lipids level were analyzed using the American Diabetes Association (ADA 2001) and National Cholesterol Education Program (NCEP ATP III) guidelines. Total cholesterol Normal to High is <200 mg/dL at baseline and ≥240 mg/dL post-baseline. Low-density lipoprotein (LDL) cholesterol Normal to High is <100 mg/dL at baseline and ≥160 mg/dL post-baseline. High-density lipoprotein (HDL) cholesterol Normal to Low is ≥40 mg/dL at baseline and <40 mg/dL post-baseline. Triglycerides Normal to High is <150 mg/dL at baseline and ≥200 mg/dL post-baseline. (NCT00845026)
Timeframe: Baseline through 52 weeks

,
Interventionparticipants (Number)
Total cholesterol Normal to High (n=56, 59)LDL cholesterol Normal to High (n=20, 22)HDL cholesterol Normal to Low (n=74, 91)Triglycerides Normal to High (n=58, 77)
LY214002330167
Standard-of-Care (SOC)602321

[back to top]

Number of Participants With Shift From Baseline to Maximum Post-Baseline Grading in Electroencephalograms (EEGs)

EEG scoring by a central neurologist is done by the following definitions: E0=Normal; E1(within normal)=fewer than 3 focal abnormalities or non-epileptiform abnormalities; E2(questionably epileptiform)=3-10 focal discharges and/or 1-10 multifocal or generalized discharges; E3=(clearly epileptiform)= Sharp/slow complex, runs of epileptiform abnormalities, greater than 10 total epileptiform discharges; and E4= seizure. Decreased= maximum (max) post-baseline (PB) EEG grading< baseline EEG grading; Increased= max PB EEG grading> baseline EEG grading; Same=no change from baseline to max PB result. (NCT00845026)
Timeframe: Baseline through 52 weeks

,
Interventionparticipants (Number)
DecreasedSameIncreased
LY2140023117418
Standard-of-Care (SOC)87733

[back to top]

Change From Baseline in EuroQoL Questionnaire-5 Dimension (EQ-5D) at 52 Weeks Endpoint

The EQ-5D is a quality-of-life (QoL) instrument with 2 parts: a health status profile and a visual analog scale (VAS). The profile rates patients' health state in 5 domains and each of them ranges 1-3. The outcomes on the 5 domains are mapped to an index with range 0-1. The higher score indicates a better health state. The VAS is used to indicate the patient's health status with range 0=worst and 100=best. LS means are from a MMRM model with the effects of treatment, gender, investigator site, visit, treatment-by-visit interaction, baseline score and baseline score by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

,
Interventionunits on a scale (Least Squares Mean)
Visual Analog Scale (n=107, 120)Index Score (n=107, 119)
LY21400234.830.03
Standard-of-Care (SOC)12.840.10

[back to top]

Change From Baseline in Blood Pressure (BP) at 52 Weeks Endpoint

Least Square (LS) Mean of change from baseline in BP is from a mixed model repeated measures (MMRM) model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline value and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

,
Interventionmillimeters of mercury (mmHg) (Least Squares Mean)
Supine Diastolic BPStanding Diastolic BPSupine Systolic BPStanding Systolic BP
LY21400232.495.572.844.65
Standard-of-Care (SOC)0.871.103.471.93

[back to top]

Change From Baseline in Simpson-Angus Scale (SAS) Total Score at 52 Weeks Endpoint

The SAS is used to measure Parkinsonian type symptoms in patients exposed to antipsychotics. The scale consists of 10 items each rated on a 5-point scale, with 0 meaning complete absence of the condition and 4 meaning the presence of the condition in extreme form. The range of possible total score is 0-40. LS Mean of change from baseline in the SAS total score is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY2140023-0.87
Standard-of-Care (SOC)-0.82

[back to top]

Time to Discontinuation Due to Adverse Event (AE)

(NCT00845026)
Timeframe: Baseline through 24 weeks

Interventiondays (Mean)
LY214002393.02
Standard-of-Care (SOC)116.86

[back to top]

Percentage of Participants With Remission (Rate of Remission) at Week 24 Endpoint

Remission is defined as endpoint score of mild or better (≤3) for each of the following PANSS items: delusions, conceptual disorganization, hallucinatory behavior, social withdrawal, blunted affect, lack of spontaneity and flow of conversation, mannerisms and posturing, and unusual thought content. PANSS assesses the positive and negative symptoms and general psychopathology specifically associated with schizophrenia. The scale consists of 30 items. Each item is rated from 1 (symptom not present) to 7 (extremely severe). The sum of the 30 items is the PANSS total score and ranges 30 - 210. (Analysis for Study Period III only) (NCT00845026)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
LY214002315.0
Standard-of-Care (SOC)22.7

[back to top]

Percentage of Participants With Relapse (Rate of Relapse)

Relapse is defined as an increase in at least one PANSS positive item to a score>5 and an absolute increase of ≥2 points on that item post randomization , or hospitalization for any psychiatric condition, or active suicidal ideation or suicidal behavior as captured by the C-SSRS. PANSS assesses the positive and negative symptoms and general psychopathology specifically associated with schizophrenia. The scale consists of 30 items. Each item is rated from 1 (symptom not present) to 7 (symptoms extremely severe). The sum of the 30 items is defined as the PANSS total score and ranges from 30-210. (NCT00845026)
Timeframe: Baseline through 52 weeks

Interventionpercentage of participants (Number)
LY214002326.2
Standard-of-Care (SOC)16.8

[back to top]

Number of Participants With Potentially Clinically Significant Changes in QT Intervals Electrocardiograms (ECGs)

"A potentially clinically significant QT interval (high) is defined as a value meeting the criteria of (> 450 millisecond [ms]) at anytime during the active treatment phase, provided it does not meet the criteria at baseline.~(analysis for Study Period III only)" (NCT00845026)
Timeframe: Baseline through 24 weeks

Interventionparticipants (Number)
LY21400233
Standard-of-Care (SOC)4

[back to top]

Number of Participants With Potentially Clinical Significant Change in Fasting Glucose Level

Treatment-emergent changes in lab results on fasting glucose were analyzed using the American Diabetes Association (ADA 2001) and National Cholesterol Education Program (NCEP ATP III) guidelines. Glucose Normal to High is <100 milligram/deciliter (mg/dL) at baseline and ≥126mg/dL post-baseline. (NCT00845026)
Timeframe: Baseline through 52 weeks

Interventionparticipants (Number)
LY21400238
Standard-of-Care (SOC)13

[back to top]

Change From Baseline in Weight at 52 Weeks Endpoint

LS Mean of change from baseline in weight is from a MMRM model which includes the effects of treatment, gender, investigative site, visit, treatment-by-visit interaction, baseline weight and baseline-by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionkilogram (kg) (Least Squares Mean)
LY2140023-4.76
Standard-of-Care (SOC)3.88

[back to top]

Change From Baseline in University of California-San Diego (UCSD) Performance-Based Skills Assessment-B (UPSA-B) Total Score at 52 Weeks Endpoint

The UPSA-B is a performance-based assessment of improvement in functional capacity. Patients are asked to role-play tasks in 2 areas of functioning: communication and finances. Scores are assigned for each of the 2 subscales and a provided formulae is used to calculated an UPSA-B Total Score (range = 0-100). The higher score indicates a better performance. LS mean of change from baseline is from a MMRM model which includes the effects of treatment, gender, investigator site, visit, treatment-by-visit interaction, baseline score and baseline score by-visit interaction. (NCT00845026)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
LY214002311.82
Standard-of-Care (SOC)12.84

[back to top]

Change in Glucose Disposition

Ratio of post-antipsychotic/pre-antipsychotic glucose disposition as measured using the hyperglycemic clamp technique. This method allows one to measure either how well an individual metabolizes glucose or how sensitive an individual is to insulin. (NCT00895921)
Timeframe: Measured over 6 hours

Interventionratio of post/pre values (Mean)
Aripiprazole1.18
Olanzapine1.42

[back to top]

Change in Percent of Insulin Suppression of Endogenous Glucose Production

Ratio of Post-Antipsychotic/Pre-Antipsychotic Percent of Insulin Suppression of Endogenous Glucose Production (NCT00895921)
Timeframe: Measured over 6 hours

Interventionratio of post/pre values (Mean)
Aripiprazole1.0594
Olanzapine1.312

[back to top]

Akathisia

Number of subjects reporting mild or greater complaints of akathisia after antipsychotic administration (NCT00895921)
Timeframe: 6 hours

Interventionparticipants (Number)
Aripiprazole1
Olanzapine7

[back to top]

Adipose Tissue Insulin Sensitivity

To evaluate, using a within-subject placebo-controlled comparison, the acute effects of olanzapine or ziprasidone administration on insulin sensitivity in antipsychotic-naïve healthy young men, measured as free fatty acid release (glycerol rate of appearance [Ra]). (NCT00910988)
Timeframe: approximately 3 hours

Intervention% change from basal to insulin phase (Mean)
Olanzapine, to be Followed by Normal Saline43.3
Normal Saline, Following Olanzapine45.2
Normal Saline, to be Followed by Olanzapine52.8
Olanzapine, Following Normal Saline53.1
Normal Saline, to be Followed by Ziprasidone39.5
Ziprasidone, Following Normal Saline37.6
Ziprasidone, to be Followed by Normal Saline47.8
Normal Saline, Following Ziprasidone44.4

[back to top]

Hepatic Insulin Sensitivity

To evaluate, using a within-subject placebo-controlled comparison, the acute effects of olanzapine or ziprasidone administration on insulin sensitivity in antipsychotic-naïve healthy young men, measured as hepatic glucose production (glucose rate of appearance [Ra]). (NCT00910988)
Timeframe: approximately 3 hours

Intervention% change from basal to insulin phase (Mean)
Olanzapine, to be Followed by Normal Saline81.0
Normal Saline, Following Olanzapine79.1
Normal Saline, to be Followed by Olanzapine73.1
Olanzapine, Following Normal Saline78.5
Normal Saline, to be Followed by Ziprasidone84.0
Ziprasidone, Following Normal Saline80.7
Ziprasidone, to be Followed by Normal Saline82.1
Normal Saline, Following Ziprasidone83.4

[back to top]

Peripheral Insulin Sensitivity

To evaluate, using a within-subject placebo-controlled comparison, the acute effects of olanzapine or ziprasidone administration on insulin sensitivity in antipsychotic-naïve healthy young men, measured as primarily muscle glucose utilization (glucose rate of disappearance [Rd]). (NCT00910988)
Timeframe: approximately 3 hours

Intervention% change from basal to insulin phase (Mean)
Olanzapine, to be Followed by Normal Saline152.2
Normal Saline, Following Olanzapine183.5
Normal Saline, to be Followed by Olanzapine157.0
Olanzapine, Following Normal Saline83.7
Normal Saline, to be Followed by Ziprasidone208.2
Ziprasidone, Following Normal Saline161.0
Ziprasidone, to be Followed by Normal Saline135.6
Normal Saline, Following Ziprasidone185.3

[back to top]

Whole Body Insulin Sensitivity

To evaluate, using a within-subject placebo-controlled comparison, the acute effects of olanzapine or ziprasidone administration on insulin sensitivity in antipsychotic-naïve healthy young men, measured as whole-body dextrose infusion rates (mg/kg/min). (NCT00910988)
Timeframe: approximately 3 hours

Interventionmg/kg/min (Mean)
Olanzapine (Drug/Placebo)-Drug4.9
Olanzapine (Drug/Placebo)-Placebo5.4
Olanzapine (Placebo/Drug)-Placebo4.1
Olanzapine (Placebo/Drug)-Drug2.9
Ziprasidone (Placebo/Drug)-Placebo5.8
Ziprasidone (Placebo/Drug)-Drug4.7
Ziprasidone (Drug/Placebo)-Drug4.5
Ziprasidone (Drug/Placebo)-Placebo5.3

[back to top]

Percent of Participants With Treatment-Emergent High Fasting Low-Density Lipoprotein (LDL) Cholesterol

Borderline to High fasting LDL cholesterol: ≥100 milligrams/deciliter (mg/dL) and <160 mg/dL at baseline and ≥160 mg/dL any time post baseline; Normal to Borderline fasting LDL cholesterol: <100 mg/dL at baseline, ≥100 mg/dL and <160 mg/dL any time post baseline; Normal to High fasting LDL cholesterol: <100 mg/dL at baseline and ≥160 mg/dL any time post baseline. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

,
Interventionpercent of participants (Number)
Borderline to High (n= 115, 134)Normal to Borderline (n=22, 26)Normal to High (n=22, 26)
Flu (SPIV)10.430.80.0
OFC (SPIV)17.422.74.5

[back to top]

Percent of Participants With Treatment-Emergent High Fasting Glucose

Impaired to High fasting glucose: ≥100 milligrams/deciliter (mg/dL) and <126 mg/dL at baseline and ≥126 mg/dL any time post baseline; Normal to High glucose: <100 mg/dL at baseline and ≥126 mg/dL any time post baseline; Normal to Impaired fasting glucose is <100 mg/dL at baseline, ≥100 mg/dL and <126 mg/dL any time post baseline; Normal/Impaired to High fasting glucose: <126 mg/dL at baseline and ≥126 mg/dL any time post baseline. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

,
Interventionpercentage of participants (Number)
Impaired to High (n=98, 97)Normal to High (n=90, 96)Normal to Impaired (n=90, 96)Normal/Impaired to High (n= 188, 193)
Flu (SPIV)7.25.228.16.2
OFC (SPIV)18.44.435.611.7

[back to top] [back to top]

Kaplan-Meier Estimate of Percentage of Subjects Not Relapsing at Week 27 (Day 189)

Relapse is defined as meeting any of the following criteria (Relapse-any reason): 50% increase in MADRS score from randomization with concomitant CGI-S of Depression score increase to a score of 4 or more (MADRS score/CGI-S Depression Score); Hospitalization for depression or suicidality; Discontinuation due to lack of efficacy/worsening of depression/suicidality. MADRS is a rating scale for severity of depressive mood symptoms with 10 items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (the most extremely ill). Lack of Efficacy/Worsening of depression was at the discretion of the investigator and based on clinical observation. Suicidality is thoughts or actions of self-harm as determined by the investigator. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 27

,
Interventionpercentage of participants (Number)
Relapse-any criteriaRelapse-MADRS score/CGI-S Depression ScoreRelapse-Hospitalization for depression/suicidalityRelapse-Discontinued for lack efficacy/worsening
Flu (SPIV)66.569.698.669.8
OFC (SPIV)83.685.397.787.4

[back to top]

Time to Relapse by Any Criteria

"Relapse defined as meeting any of these criteria: 50% increase in Montgomery-Asberg Depression Rating Scale (MADRS) score from randomization with a Clinical Global Impressions-Severity (CGI-S) of Depression score increase to a score of 4 or more; Hospitalized for depression or suicidality; Discontinued due to lack of efficacy/worsening of depression/suicidality. MADRS is a 10-item rating scale for depressive mood symptoms severity, items rated on 0-6 scale, with total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (the most extremely ill). Lack of Efficacy/Worsening of depression was at discretion of investigator based on clinical observation. Suicidality is thoughts or actions of self-harm as determined by the investigator. Those who did not relapse were censored at their last observation." (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventiondays (Median)
OFC (SPIV)NA
Flu (SPIV)NA

[back to top]

Time to Relapse Based on the Montgomery-Åsberg Depression Rating Scale (MADRS) Score With Concomitant Clinical Global Impressions-Severity (CGI-S) of Depression Score

"Relapse is defined as a 50% increase in the Montgomery-Asberg Depression Rating Scale (MADRS) score from randomization with concomitant Clinical Global Impressions-Severity (CGI-S) of Depression score increase to a score of 4 or more. The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (the most extremely ill). Those who did not relapse were censored at their last observation." (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventiondays (Median)
OFC (SPIV)NA
Flu (SPIV)NA

[back to top]

Time to Relapse as Measured by Hospitalization for Depression or Suicidality

"Those who did not relapse were censored at their last observation." (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventiondays (Median)
OFC (SPIV)NA
Flu (SPIV)NA

[back to top]

Time to Relapse as Measured by Discontinuation Due to Lack of Efficacy/Worsening of Depression/Suicidality

"Lack of Efficacy/Worsening of depression was at the discretion of the investigator and was based on clinical observation. Suicidality is thoughts or actions of self-harm as determined by the investigator. Those who did not relapse were censored at their last observation." (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventiondays (Median)
OFC (SPIV)NA
Flu (SPIV)NA

[back to top]

Resource Utilization - Average Number of Hours Worked for Pay Per Week at Week 47

(NCT00958568)
Timeframe: Week 47

Interventionhours (Mean)
OFC (SPIV)37.49
Flu (SPIV)37.76

[back to top]

Percent of Participants With Treatment-Emergent Dyskinesia

Abnormal Involuntary Movement Scale (AIMS) is a 12-item scale designed to record the occurrence of dyskinetic movements. Items 1 through 10 are rated on a 5-point scale, with 0 being no dyskinetic movements and 4 being severe dyskinetic movements. Items 11 and 12 are yes/no questions regarding the dental condition of the participants. Treatment emergent dyskinesia is defined as a score ≥3 on any one of the AIMS items 1-7 post-baseline (Weeks 21-47) or scores ≥2 on any two of the AIMS items 1-7 post-baseline (Weeks 21-47) among participants without either criteria at baseline (Week 20). (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)0.5
Flu (SPIV)0.0

[back to top]

Percentage of Participants Who Relapse by Any Criteria

Relapse is defined as meeting any of the following criteria: 50% increase in Montgomery-Asberg Depression Rating Scale (MADRS) score from randomization with concomitant Clinical Global Impressions-Severity (CGI-S) of Depression score increase to a score of 4 or more; Hospitalization for depression or suicidality; Discontinuation due to lack of efficacy/worsening of depression/suicidality. MADRS is a rating scale for severity of depressive mood symptoms with 10 items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (the most extremely ill). Lack of Efficacy/Worsening of depression was at the discretion of the investigator and based on clinical observation. Suicidality is thoughts or actions of self-harm as determined by the investigator. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)15.8
Flu (SPIV)31.8

[back to top]

Percentage of Participants Who Relapse Based on Montgomery-Åsberg Depression Rating Scale (MADRS) Score With Concomitant Clinical Global Impressions-Severity (CGI-S) of Depression Score

Relapse is defined as a 50% increase in the Montgomery-Asberg Depression Rating Scale (MADRS) score from randomization with concomitant Clinical Global Impressions-Severity (CGI-S) of Depression score increase to a score of 4 or more. The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (the most extremely ill). (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)14.0
Flu (SPIV)28.3

[back to top]

Percentage of Participants Who Relapse as Measured by Hospitalization for Depression or Suicidality

(NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)1.8
Flu (SPIV)1.3

[back to top]

Percentage of Participants Who Relapse as Measured by Discontinuation Due to Lack of Efficacy/Worsening of Depression/Suicidality

Lack of Efficacy/Worsening of depression was at the discretion of the investigator and was based on clinical observation. Suicidality is thoughts or actions of self-harm as determined by the investigator. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)10.9
Flu (SPIV)28.3

[back to top]

Percentage of Participants Responding to Treatment During Open-Label Acute Treatment Phase

A 50% or greater improvement from baseline on the Montgomery-Asberg Depression Rating Scale (MADRS) and a Clinical Global Impressions-Severity (CGI-S) of Depression score ≤3 will be considered as response criteria met. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill participants). (NCT00958568)
Timeframe: Week 0 to Week 8

Interventionpercentage of participants (Number)
OFC (SPII-Wk 0-8, Acute Open-label)78.0

[back to top]

Percentage of Participants Achieving Remission at Any Point During Stabilization Treatment Phase

Remission is defined as the Montgomery-Asberg Depression Rating Scale (MADRS) score ≤8. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00958568)
Timeframe: Week 8 to Week 20

Interventionpercentage of participants (Number)
OFC (SPIII)77.9

[back to top]

Percent of Participants With Week 20-to-Week 47 Endpoint Increase in Weight of at Least 7%

(NCT00958568)
Timeframe: Week 20 to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)11.8
Flu (SPIV)2.3

[back to top]

Percent of Participants With Treatment-Emergent Parkinsonism

Simpson-Angus Scale is used to measure Parkinsonian-type symptoms in participants exposed to neuroleptics. The scale consists of 10 items, each rated on a 5-point scale, with 0 meaning complete absence of the condition and 4 meaning the presence of the condition in extreme form. The total score is obtained by adding the items and ranges from 0-40 with higher scores indicating worse conditions. Treatment emergent parkinsonism is defined as total score ≤3 of items 1 through 10 of the Simpson-Angus scale at baseline (Week 20) and a total score >3 of items 1 through 10 post-baseline (Weeks 21-47). (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)1.4
Flu (SPIV)0.0

[back to top]

Percent of Participants With Treatment-Emergent Low Fasting High-Density Lipoprotein (HDL) Cholesterol

Normal to Low fasting HDL cholesterol is ≥40 milligrams/deciliter (mg/dL) at baseline and <40 mg/dL anytime post baseline. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)39.2
Flu (SPIV)25.5

[back to top]

Percent of Participants With Treatment-Emergent Hepatic Events

Participants with alanine aminotransferase (ALT) and aspartate aminotransferase (AST) <=3 times the upper limit of normal (ULN) at baseline, with ALT or AST >=3 times the ULN post-baseline and total bilirubin >=2 times ULN at the same time are considered having treatment-emergent hepatic events. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)0.0
Flu (SPIV)0.0

[back to top]

Percent of Participants With Treatment-Emergent Corrected (for Rate) Cardiac QT Interval Using Fridericia's Formula (QTcF) on Electrocardiogram ≥500 Milliseconds (Msec)

Data presented are the percent of participants whose baseline corrected (for rate) cardiac QT interval <500 msec with post-baseline corrected (for rate) cardiac QT interval ≥500 msec. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)0
Flu (SPIV)0

[back to top]

Percent of Participants With Treatment-Emergent Akathisia

Barnes Akathisia Scale (BAS) rates observable, restless movements of drug-induced akathisia as well as the subjective awareness of restlessness and any distress associated with the akathisia. It consists of 4 items. 3 items (objective akathisia, subjective awareness of restlessness and subjective distress related to restlessness) rated on a 4-point scale, with 0 being no akathisia and 3 being severe akathisia. Item 4 (global clinical assessment of Akathisia) is derived from the responses on Items 1-3 rated on a 6-point scale, with 0 being absence and 5 being extreme Akathisia. Treatment emergent akathisia is defined as a global clinical assessment score on BAS <2 at baseline (Week 20) and a global clinical assessment score on BAS ≥2 post-baseline (Weeks 21-47). (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)0.9
Flu (SPIV)0.9

[back to top]

Percent of Participants With a 60 Milliseconds (Msec) Increase in Fridericia-Corrected (for Rate) Cardiac QT Interval (QTcF) on Electrocardiogram

(NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)0
Flu (SPIV)0

[back to top]

Percentage of Participants Maintaining Remission

Remission is defined as the Montgomery-Asberg Depression Rating Scale (MADRS) score ≤8. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

Interventionpercentage of participants (Number)
OFC (SPIV)86.4
Flu (SPIV)78.9

[back to top]

Change From Week 20 to Week 47 Endpoint in the Sheehan Disability Scale (SDS)

The SDS is completed by the participant and is used to assess the effect of the participant's symptoms on their work or school (Item 1), social (Item 2), and family life and home responsibilities (Item 3). Each item is measured on a 0 (not at all) to 10 (extremely) point scale with higher values indicating greater disruption. Total scores is the sum of the 3 items and range from 0 to 30 with higher values indicating greater disruption in the participant's work/social/family life. Least Squares (LS) Mean values were controlled for baseline (Week 20), treatment and country. (NCT00958568)
Timeframe: Randomization (Week 20), up to Week 47

Interventionunits on a scale (Least Squares Mean)
OFC (SPIV)1.30
Flu (SPIV)3.24

[back to top]

Mean Change From Week 20 to Week 47 in Clinical Global Impressions - Severity (CGI-S) of Depression Using Mixed-Effects Model Repeated Measures (MMRM) Analysis

CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill participants). Least Squares (LS) Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionunits on a scale (Least Squares Mean)
OFC (SPIV)0.20
Flu (SPIV)0.54

[back to top]

Percentage of Participants Maintaining Response at Any Point During Stabilization Treatment Phase

A 50% or greater improvement from baseline on the Montgomery-Asberg Depression Rating Scale (MADRS) and a Clinical Global Impressions-Severity (CGI-S) of Depression score ≤3 will be considered as response criteria met. The MADRS is a rating scale for severity of depressive mood symptoms. The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). CGI-S measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill participants). (NCT00958568)
Timeframe: Week 8 to Week 20

Interventionpercentage of participants (Number)
OFC (SPIII)68.2

[back to top]

Resource Utilization (Number of Psychiatric Visits, Number of Emergency Room or Equivalent Facility Visits for Psychiatric Illness)

Resource utilization is defined as the average number of psychiatric visits and number of emergency room or equivalent facility visits for psychiatric illness. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

,
Interventionvisits per participant (Mean)
Psychiatric visits (n=136, 113)Emergency room or equivalent facility visits
Flu (SPIV)0.810.00
OFC (SPIV)0.650.00

[back to top]

Percent of Participants With Treatment-Emergent High Fasting Triglycerides

Borderline to High fasting triglycerides: ≥150 milligrams/deciliter (mg/dL) and <200 mg/dL at baseline and ≥200 mg/dL any time post baseline; Normal to Borderline fasting triglycerides: <150 mg/dL at baseline, ≥150 mg/dL and <200 mg/dL any time post baseline; Normal to High fasting triglycerides: <150 mg/dL at baseline and ≥200 mg/dL any time post baseline. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

,
Interventionpercentage of participants (Number)
Borderline to High (n=47, 41)Normal to Borderline (n= 68, 74)Normal to High (n=68, 74)
Flu (SPIV)26.86.85.4
OFC (SPIV)51.122.116.2

[back to top]

Percent of Participants With Treatment-Emergent High Fasting Total Cholesterol

Borderline to High fasting total cholesterol: ≥200 milligrams/deciliter (mg/dL) and <240 mg/dL at baseline and ≥240 mg/dL any time post baseline; Normal to Borderline fasting total cholesterol: <200 mg/dL at baseline, ≥200 mg/dL and <240 mg/dL any time post baseline; Normal to High fasting total cholesterol: <200 mg/dL at baseline and ≥240 mg/dL any time post baseline. (NCT00958568)
Timeframe: Randomization (Week 20) to Week 47

,
Interventionpercentage of participants (Number)
Borderline to High (n= 75, 83)Normal to Borderline (n=47, 59)Normal to High (n=47, 59)
Flu (SPIV)20.516.93.4
OFC (SPIV)28.017.02.1

[back to top]

Mean Change From Week 20 to Week 47 in Fasting Glucose

Mixed-effects model repeated measures (MMRM) analysis was used to calculate Least Squares (LS) Mean and standard error (SE). LS Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionmilligrams/deciliter (mg/dL) (Least Squares Mean)
OFC (SPIV)3.67
Flu (SPIV)-2.22

[back to top]

Mean Change in Corrected (for Rate) Cardiac QT Interval Using Fridericia's Formula (QTcF) on Electrocardiogram

Least Squares (LS) Mean values were obtained from a mixed model repeated measures (MMRM) analysis. Model includes baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionmilliseconds (msec) (Least Squares Mean)
OFC (SPIV)-3.12
Flu (SPIV)-1.55

[back to top]

Mean Change From Week 20 to Week 47 in Weight

Mixed-effects model repeated measures (MMRM) analysis was used to calculate Least Squares (LS) Mean and standard error (SE). LS Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionkilograms (kg) (Least Squares Mean)
OFC (SPIV)1.14
Flu (SPIV)-2.78

[back to top]

Mean Change From Week 20 to Week 47 in Montgomery-Asberg Depression Rating Scale (MADRS) Using Mixed-Effects Model Repeated Measures (MMRM) Analysis

The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). Least Squares (LS) Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionunits on a scale (Least Squares Mean)
OFC (SPIV)2.06
Flu (SPIV)4.97

[back to top]

Mean Change From Week 20 to Week 47 in Montgomery-Asberg Depression Rating Scale (MADRS) Using Last Observation Carried Forward (LOCF) Analysis

The MADRS has a 10-item checklist with items rated on a scale of 0-6, for a total score range of 0 (low severity of depressive symptoms) to 60 (high severity of depressive symptoms). Least Squares (LS) Mean values were controlled for baseline (Week 20), treatment and country. (NCT00958568)
Timeframe: Randomization (Week 20), up to Week 47

Interventionunits on a scale (Least Squares Mean)
OFC (SPIV)3.03
Flu (SPIV)6.84

[back to top]

Mean Change From Week 20 to Week 47 in Fasting Triglycerides

Mixed-effects model repeated measures (MMRM) analysis was used to calculate Least Squares (LS) Mean and standard error (SE). LS Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionmilligrams/deciliter (mg/dL) (Least Squares Mean)
OFC (SPIV)-8.24
Flu (SPIV)-21.51

[back to top]

Mean Change From Week 20 to Week 47 in Fasting Total Cholesterol

Mixed-effects model repeated measures (MMRM) analysis was used to calculate Least Squares (LS) Mean and standard error (SE). LS Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionmilligrams/deciliter (mg/dL) (Least Squares Mean)
OFC (SPIV)-2.65
Flu (SPIV)-1.74

[back to top]

Mean Change From Week 20 to Week 47 in Fasting Low-Density Lipoprotein (LDL) Cholesterol

Mixed-effects model repeated measures (MMRM) analysis was used to calculate Least Squares (LS) Mean and standard error (SE). LS Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionmilligrams/deciliter (mg/dL) (Least Squares Mean)
OFC (SPIV)-0.72
Flu (SPIV)0.85

[back to top]

Mean Change From Week 20 to Week 47 in Fasting High-Density Lipoprotein (HDL) Cholesterol

Mixed-effects model repeated measures (MMRM) analysis was used to calculate Least Squares (LS) Mean and standard error (SE). LS Mean values were controlled for baseline (Week 20), treatment, country, visit, and treatment by visit interaction. (NCT00958568)
Timeframe: Randomization (Week 20), Week 47

Interventionmilligrams/deciliter (mg/dL) (Least Squares Mean)
OFC (SPIV)-1.71
Flu (SPIV)2.02

[back to top]

Percentage of Participants With Treatment-Emergent Extrapyramidal Symptoms Based on the Drug Induced Extrapyramidal Symptoms Scale (DIEPSS) Score up to 24 Hours After the First Intramuscular (IM) Injection

Assesses extrapyramidal symptoms attributable to antipsychotics. Consists of 9 items (8 to assess individual symptoms; 1 to assess global severity). Each item is assessed from 0 (none, normal) to 4 (severe). Total points of 8 items are defined as DIEPSS total (0 to 32 points). Items for assessment of individual symptoms are classified into 4 categories of parkinsonism, akathisia, dystonia and dyskinesia. Parkinsonism is assessed by total points of items 1 to 5; akathisia, dystonia and dyskinesia are assessed by points given to corresponding items (item 6, item 7, and item 8, respectively). (NCT00970281)
Timeframe: Up to 24 hours after the first IM injection

,
Interventionpercentage of participants (Number)
Parkinsonism (N=43, 44)Akathisia (N=43, 45)Dystonia (N=44, 45)Dyskinesia (N=44, 45)
10 mg Olanzapine4.70.00.00.0
Placebo6.80.00.00.0

[back to top]

Percentage of Participants With Scores of 4 to 7 in the Agitation-Calmness Evaluation Scale (ACES) Score up to 24 Hours After the First Intramuscular (IM) Injection

The ACES differentiates agitation, calmness, and sleep-state, using a 9-point scale: 1 (Marked Agitation) to 9 (Unarousable). Scores of 4 (Normal) to 7 (Marked Calmness) were used for this outcome measure. (NCT00970281)
Timeframe: up to 24 hours after the first IM injection

,
Interventionpercentage of participants (Number)
0.5 hour after First IM Injection1 hour after First IM Injection1.5 hours after First IM Injection2 hours after First IM Injection24 hours after First IM Injection
10 mg Olanzapine24.431.140.040.028.9
Placebo11.415.913.613.615.9

[back to top]

Change From Baseline in the Positive and Negative Syndrome Scale - Excited Component (PANSS-EC) Total Score up to 24 Hours After the First Intramuscular (IM) Injection

Measures excitability and consists of the following 5 items from the PANSS: Excitement, Hostility, Tension, Uncooperativeness, and Poor Impulse Control. Each item is rated on a scale from 1 (absent) to 7 (extreme). The sum of the 5 items is defined as the PANSS-EC total score which ranges from 5 to 35. (NCT00970281)
Timeframe: Baseline, up to 24 hours after first IM injection

Interventionunits on a scale (Mean)
10 mg Olanzapine-5.6
Placebo-2.8

[back to top]

Percentage of Participants With 40% or Greater Percent Decrease in the Positive and Negative Syndrome Scale - Excited Component (PANSS-EC) Total Score up to 2 Hours After the First Intramuscular (IM) Injection

Measures excitability and consists of the following 5 items from the PANSS: Excitement, Hostility, Tension, Uncooperativeness, and Poor Impulse Control. Each item is rated on a scale from 1 (absent) to 7 (extreme). The sum of the 5 items is defined as the PANSS-EC total score which ranges from 5 to 35. (NCT00970281)
Timeframe: Up to 2 hours after the first (IM) injection

Interventionpercentage of participants (Number)
10 mg Olanzapine40.0
Placebo13.6

[back to top]

Change From Baseline in PANSS-EC Total Score up to 90 Minutes After the First Intramuscular (IM) Injection

Measures excitability and consists of the following 5 items from the PANSS: Excitement, Hostility, Tension, Uncooperativeness, and Poor Impulse Control. Each item is rated on a scale from 1 (absent) to 7 (extreme). The sum of the 5 items is defined as the PANSS-EC total score which ranges from 5 to 35. (NCT00970281)
Timeframe: Baseline, 15 minutes, 30 minutes, 60 minutes, and 90 minutes after the first injection

,
Interventionunits on a scale (Mean)
0.25 hour after First IM Injection0.50 hour after First IM Injection1 hour after First IM Injection1.5 hour after First IM Injection
10 mg Olanzapine-2.4-5.0-7.3-8.2
Placebo-1.0-1.9-3.0-2.7

[back to top]

Change From Baseline in the Positive and Negative Syndrome Scale-Excited Component (PANSS-EC) Total Score up to 2 Hours After the First Intramuscular (IM) Injection

Measures excitability and consists of the following 5 items from the PANSS: Excitement, Hostility, Tension, Uncooperativeness, and Poor Impulse Control. Each item is rated on a scale from 1 (absent) to 7 (extreme). The sum of the 5 items is defined as the PANSS-EC total score which ranges from 5 to 35. (NCT00970281)
Timeframe: Baseline, up to 2 hours after first IM injection

Interventionunits on a scale (Mean)
10 mg Olanzapine-9.2
Placebo-2.8

[back to top]

Body Composition: Percent Total Body Fat

Body composition estimated by percent total body fat as measured by a dual energy absorptiometry (DXA) scan in both experimental and placebo arms at 12 weeks. (NCT00981526)
Timeframe: 12 weeks

Interventionpercentage of body fat (Mean)
A: Telmisartan31.9
B: Placebo31.28

[back to top]

Body Composition: Waist to Hip Ratio

Body composition as estimated by waist to hip ratio in both experimental and placebo arms at 12 weeks. (NCT00981526)
Timeframe: 12 weeks

InterventionRatio (Mean)
A: Telmisartan0.99
B: Placebo0.95

[back to top]

Insulin Resistance

Insulin resistance as estimated by homeostasis model of assessment of insulin resistance (HOMA-IR) at week 12 in both the experimental and placebo arm. Insulin resistance is a condition in which cells fail to respond to the normal action of the hormone in the body. The HOMA-IR is calculated using a subject's fasting plasma insulin and glucose levels. The higher the score, the higher the level of insulin resistance. (NCT00981526)
Timeframe: 12 weeks

InterventionHOMA-IR scores (Mean)
A: Telmisartan1.9997
B: Placebo2.5824

[back to top]

Triglycerides

Fasting triglycerides assessed in both experimental and placebo arm at week 12. (NCT00981526)
Timeframe: 12 weeks

Interventionmg/dl (Mean)
A: Telmisartan154.15
B: Placebo176.72

[back to top]

Lipid Metabolism - LDL-cholesterol and HDL-cholesterol

Lipid metabolism - fasting low density lipoprotein (LDL) and high density lipoprotein (HDL) are estimated in both experimental and placebo arms at 12 weeks. (NCT00981526)
Timeframe: 12 weeks

,
Interventionmg/dl (Mean)
LDL-cholesterolHDL-cholesterol
A: Experimental10741.05
B: Placebo107.8543.18

[back to top]

Psychopathology - PANSS Total, PANSS - Negative Score, PANNS - Positive Score and SANS - Total Scores.

The Positive and Negative Syndrome Scale (PANSS) and Scale for the Assessment of Negative Symptoms (SANS) were used to assess the positive and negative symptoms in experimental and placebo arms at 12 weeks. The PANSS total scale includes positive and negative subscales. For both subscales, the score ranges from 7-49 and total PANSS score ranges from 30-210. The total scale is a summation of all the subscales. The SANS score ranges from 0-100. For all scales, a greater score represents a worse outcome. (NCT00981526)
Timeframe: 12 weeks

,
Interventionunits on a scale (Mean)
PANSS total scorePANSS negative scorePANSS positive scoreSANS total score
A: Experimental67.4119.5515.5027.82
B: Placebo71.0519.9516.6829.28

[back to top]

Mean Change From Baseline to 52 Weeks in Anchored Version of the Brief Psychiatric Rating Scale for Children (BPRS-C) for Participants With Schizophrenia

The BPRS-C characterizes psychopathology. A total of 21 items are rated on a scale from 0 (not present) to 6 (extremely severe) with a total score ranging from 0 to 126. A decrease in score indicates a reduction in psychopathology. (NCT00982020)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention-28.00
Olanzapine/Intense Behavioral Weight Intervention-30.96

[back to top]

Mean Change From Baseline to 52 Weeks in Body Mass Index (BMI) for All Participants

(NCT00982020)
Timeframe: Baseline, 52 weeks

Interventionkilograms per meter squared (kg/m^2) (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention3.64
Olanzapine/Intense Behavioral Weight Intervention2.83

[back to top]

Mean Clinical Global Impression of Improvement (CGI-I) at 52 Weeks for All Participants

The Clinical Global Impression of Improvement (CGI-I) is used by the clinician to record the improvement of illness at the time of assessment. The score ranges from 1 (very much improved) to 7 (very much worse). (NCT00982020)
Timeframe: 52 weeks

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention2.04
Olanzapine/Intense Behavioral Weight Intervention2.29

[back to top]

Mean Change From Baseline to Endpoint in Body Mass Index (BMI) for Participants With Duration of Treatment of at Least 6 Months

(NCT00982020)
Timeframe: Baseline, 52 weeks

Interventionkg/m^2 (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention3.36
Olanzapine/Intense Behavioral Weight Intervention2.99

[back to top]

Mean Change From Baseline to 52 Weeks in Waist Circumference for All Participants

(NCT00982020)
Timeframe: Baseline, 52 weeks

Interventioncentimeters (cm) (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention7.22
Olanzapine/Intense Behavioral Weight Intervention7.31

[back to top]

Mean Change From Baseline to 52 Weeks in Adolescent Structured Young Mania Rating Scale (YMRS) for Participants With Bipolar I Disorder

The YMRS is an 11-item scale that measures the severity of manic episodes. Four items are rated on a scale from 0 (symptom not present) to 8 (symptom extremely severe). The remaining items are rated on a scale from 0 (symptom not present) to 4 (symptom extremely severe). The YMRS total score ranges from 0 (symptom not present) to 60 (symptom extremely severe). (NCT00982020)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention-17.66
Olanzapine/Intense Behavioral Weight Intervention-12.05

[back to top]

Mean Change From Baseline to 52 Weeks in Clinical Global Impression - Severity (CGI-S) for All Participants

The CGI-S is used by the clinician to record the severity of illness at the time of assessment. The score ranges from 1 = normal, not at all ill to 7 = among the most extremely ill. (NCT00982020)
Timeframe: Baseline, 52 weeks

Interventionunits on a scale (Least Squares Mean)
Olanzapine/Standard Behavioral Weight Intervention-2.06
Olanzapine/Intense Behavioral Weight Intervention-1.74

[back to top]

Time to Event for 7%, 15%, and 25% Weight Gain for All Participants

Kaplan-Meier methodology used to estimate time to event. Participants who never reached the target weight gain contributed to the set of patients at risk up to the point at which they discontinued from the study and were then censored (i.e., removed from the risk set). (NCT00982020)
Timeframe: Baseline up to 52 weeks

,
Interventiondays (Median)
Time to First 7% Weight GainTime to First 15% Weight GainTime to First 25% Weight Gain
Olanzapine/Intense Behavioral Weight Intervention57198NA
Olanzapine/Standard Behavioral Weight Intervention57197NA

[back to top]

Time to First Psychiatric Hospitalization

"A time-to parameter looking only at 1 component event of treatment failure: psychiatric hospitalization. Time to first psychiatric hospitalization was admission date of the psychiatric hospitalization recorded in the Assessment of Treatment Failure - Psychiatric Hospitalization." (NCT01157351)
Timeframe: From date of randomization up to Month 15

InterventionDays (Median)
Paliperidone PalmitateNA
Oral AntipsychoticsNA

[back to top]

Change From Baseline in Personal and Social Performance (PSP) Total Score During Overall Treatment Duration

The PSP score assesses the degree of difficulty a participant exhibit over a 1 month period within 4 domains of behavior: a) socially useful activities, b) personal and social relationships, c) self-care, and d) disturbing and aggressive behavior. The investigators rate participants' degree of difficulty in each of the 4 domains using a 6-point Likert scale (from 0=absent to 5=very severe). The domain ratings were then transformed to PSP total score ranging from 1 to 100. Higher PSP total scores denote better functioning. A score between 71 and 100 represents normal to mild degree of dysfunction; a score between 31 and 70 represents varying degree of difficulty; and a score <=30 represents poor function that requires intensive supervision. (NCT01157351)
Timeframe: Baseline up to Month 15

InterventionUnits on a scale (Least Squares Mean)
Paliperidone Palmitate5.75
Oral Antipsychotics5.36

[back to top]

Change From Baseline in Clinical Global Impression - Severity (CGI-S) Score During Overall Treatment Duration

The CGI-S rating scale was a 7-point global assessment of symptom severity with scores determined by clinician as follows: 1=Not ill, 2=Very Mild, 3= Mild, 4= Moderate, 5= Marked, 6= Severe, and 7= Extremely Severe. The higher the score the worse the illness. (NCT01157351)
Timeframe: Baseline up to Month 15

InterventionUnits on a scale (Least Squares Mean)
Paliperidone Palmitate-0.48
Oral Antipsychotics-0.43

[back to top]

Time to First Psychiatric Hospitalization or Arrest/Incarceration

A time to parameter looking only at 2 component events of treatment failure: arrest or incarceration, and psychiatric hospitalization. An arrest was defined as the taking of a participant into custody by legal authority, for any reason. Incarceration was defined as involuntary confinement by an officer of the law. Psychiatric hospitalization was an inpatient psychiatric hospitalization that occurred due to the participant's clinically significant worsening of symptoms of schizophrenia. (NCT01157351)
Timeframe: From date of randomization up to Month 15

InterventionDays (Median)
Paliperidone PalmitateNA
Oral Antipsychotics274

[back to top]

Percentage of Participants in Each Event Category of First Treatment Failure

First treatment failure was a composite endpoint consisting of any of the following events: arrest/incarceration, psychiatric hospitalization, discontinuation (D/C) of antipsychotic treatment due to safety or tolerability, treatment supplementation with another antipsychotic due to inadequate efficacy, discontinuation of antipsychotic treatment due to inadequate efficacy, increase in level of psychiatric services to prevent imminent psychiatric hospitalization, suicide. A Treatment Failure Event Monitoring Board (EMB), blinded to individual participant treatment assignment, determined the occurrence and date of the first treatment failure event. Percentage of participants who experienced treatment failure due to any event and for each specific category of event were assessed. (NCT01157351)
Timeframe: From date of randomization up to Month 15

,
Interventionpercentage of participants (Number)
Treatment Failure Due to Any EventArrest/incarcerationPsychiatric hospitalizationD/C due to safety/tolerabilityTreatment supplementationD/C due to inadequate efficacyIncrease in level of psychiatric servicesSuicide
Oral Antipsychotics53.729.411.93.72.84.11.80
Paliperidone Palmitate39.821.28.06.62.20.41.30

[back to top]

Time to First Treatment Failure

Time to first treatment failure was the time from participant randomization to the first treatment failure, which was a composite endpoint consisting of any of the following events: arrest/incarceration, psychiatric hospitalization, discontinuation of antipsychotic treatment due to safety or tolerability, treatment supplementation with another antipsychotic due to inadequate efficacy, discontinuation of antipsychotic treatment due to inadequate efficacy, increase in level of psychiatric services to prevent imminent psychiatric hospitalization, suicide. A Treatment Failure Event Monitoring Board (EMB), blinded to individual participant treatment assignment, determined the occurrence and date of the first treatment failure event. (NCT01157351)
Timeframe: From date of randomization up to Month 15

InterventionDays (Median)
Paliperidone Palmitate416
Oral Antipsychotics226

[back to top]

Rate of Weight Change

Comparison of rate of weight change between patients receiving olanzapine and those receiving placebo (NCT01170117)
Timeframe: Weekly during 16-week trial and twice during 8 weeks follow-up

Interventionkg/m^2 per month (Mean)
Placebo0.095
Olanzapine0.260

[back to top]

Psychological Change

Comparison of psychological change as measured by the Yale-Brown Obsessive Compulsive Scale (YBOCS), in patients receiving olanzapine compared with those receiving placebo. The Y-BOCS is divided into two sections: obsessive and compulsive. The scores for each section range from 1 to 20. The overall scores are obtained from adding scores for the two sections, to obtain a range between 2-40. A lower score reflects improvement/ fewer obsessive compulsive symptoms. A score of 25 or more is considered moderately severe, a score of 30 or more is considered severe, and a score of more than 35 is considered very severe. (NCT01170117)
Timeframe: Weekly during 16-week intervention and twice during 8-week follow-up

InterventionYBOCs score units per month (Mean)
Placebo0.762
Olanzapine0.800

[back to top]

Changes in Metabolic Measure: Cholesterol

Change in cholesterol from entry into randomized phase (baseline) and 36 weeks. (NCT01427608)
Timeframe: From entry into randomized phase (baseline) and 36 weeks

Interventionmg/dL (Mean)
Sertraline + Olanzapine-0.46
Sertraline + Placebo-22.28

[back to top]

Changes in Metabolic Measures: Triglycerides

Change in triglycerides from entry into randomized phase (baseline) and 36 weeks. (NCT01427608)
Timeframe: From entry into randomized phase (baseline) and 36 weeks

Interventionmg/dL (Mean)
Sertraline + Olanzapine-3.85
Sertraline + Placebo-18.18

[back to top]

Changes in Metabolic Measures: Weight

Change in weight from entry into randomized phase (baseline) and 36 weeks. (NCT01427608)
Timeframe: From entry into randomized phase (baseline) and 36 weeks

Interventionpounds (Mean)
Sertraline + Olanzapine5.70
Sertraline + Placebo-3.11

[back to top]

Number of Subjects at Risk of Relapse During the Randomized Phase.

"Relapse criteria include at least one of the following:~1)Structured Clinical Interview for Diagnostic Statistical Manual #4 Trade Revision (DSM-IV-TR) Axis 1 Disorders (SCID) symptoms of major depression maintained over two weeks 2)17-item Hamilton Depression Rating Scale score of >17 maintained for more than one week + a mean increase of 5 points from entry into randomized phase 3)Re-emergence of psychosis for more than one week, with a SADS (Schedule for Affective Disorders and Schizophrenia) score of >2 on delusion or hallucination severity items 4)Significant clinical worsening defined as either emergence of high-risk of suicide, and/or development of mania for greater than one week, and/or psychiatric hospitalization." (NCT01427608)
Timeframe: From entry into randomized phase (baseline) and 36 weeks or earlier relapse

InterventionParticipants (Count of Participants)
Sertraline + Olanzapine13
Sertraline + Placebo34

[back to top]

Physical Activity as Measured Using a Physical Activity Monitor

Change from baseline in physical activity. Physical activity was measured using an activity monitor that subjects wore around their waist throughout baseline and treatment days. Subjects were instructed to remove the monitor when sleeping or engaging in water-based activities, and to report on a daily log the times that they were wearing and removing the device. Physical activity was monitored during weekdays and weekend days. Physical activity data were collected in 60-second epochs. The results are reported as average counts per day of physical activity for weekdays and weekend days at baseline and 2 week treatment. (NCT01496183)
Timeframe: baseline and 2 week treatment

,
Interventioncounts per day (Mean)
baseline - weekdays2 week treatment - weekdaysbaseline - weekend days2 week treatment - weekend days
Olanzapine263,720263,757277,298198,382
Placebo410,029279,722279,149247,036

[back to top]

Change From Baseline in Leptin

Leptin (ng/ml) at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: Assessed at different time points: baseline and 2 weeks of treatment (olanzapine or placebo)

,
Interventionng/ml (Mean)
baseline2 weeks treatment
Olanzapine3.85.7
Placebo3.84.8

[back to top]

Change From Baseline in Resting Metabolic Rate

Resting metabolic rate at baseline and after 2 weeks of treatment (NCT01496183)
Timeframe: baseline and 2weeks of treatment

,
Interventionkcal/24 hours (Mean)
baseline2 weeks treatment
Olanzapine18551858
Placebo17021689

[back to top]

Change From Baseline Total Cholesterol

Total cholesterol at baseline and after 2 weeks treatment with olanzapine or placebo (NCT01496183)
Timeframe: baseline and 2 weeks treatment

,
Interventionmg/dl (Mean)
baseline2 weeks treatment
Olanzapine156.8167.0
Placebo153.2147.4

[back to top]

Change From Baseline Triglycerides

Triglycerides (mg/dl) at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: Assessed at different time points: baseline and 2 weeks of treatment (olanzapine or placebo)

,
Interventionmg/dl (Mean)
baseline2 weeks of treatment
Olanzapine93.0136.6
Placebo48.452.8

[back to top]

HDL

High-density lipoprotein at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: baseline and 2 weeks treatment

,
Interventionmg/dl (Mean)
baseline2 weeks treatment
Olanzapine51.346.1
Placebo54.655.0

[back to top]

Laboratory Breakfast Intake

Total kcal intake at breakfast in a laboratory setting at baseline and after 2 week of treatment with olanzapine or placebo (NCT01496183)
Timeframe: baseline and 2 week treatment

,
Interventionkcal (Mean)
Baseline2 week treatment
Olanzapine8641058
Placebo13961567

[back to top]

LDL

Low-density lipoprotein at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: baseline and 2 weeks treatment

,
Interventionmg/dl (Mean)
baseline2 weeks treatment
Olanzapine86.993.7
Placebo88.882.0

[back to top]

Change From Baseline in Weight

(NCT01496183)
Timeframe: Assessed at baseline and 2 weeks

InterventionKg (Mean)
Placebo0.2
Olanzapine1.7

[back to top]

Change From Baseline in 24-Hour Dietary Recall

24-hour dietary intake recall at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: Assessed at different time points: baseline and 2 weeks of treatment (olanzapine or placebo)

,
Interventionkcal/day (Mean)
baseline2 weeks of treatment
Olanzapine24102374
Placebo17481785

[back to top]

Change From Baseline in Body Composition

lean body mass (kg) and fat mass (kg) at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: baseline and 2 weeks of treatment (olanzapine or placebo)

,
Interventionkg (Mean)
lean body mass at baselinelean body mass at 2 weeks of treatmentfat mass at baselinefat mass at 2 weeks of treatment
Olanzapine65.867.016.517.4
Placebo60.160.117.918.5

[back to top]

Change From Baseline in Glucose

Glucose (mg/dl) at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: Assessed at different time points: baseline and 2 weeks of treatment (olanzapine or placebo)

,
Interventionmg/dl (Mean)
baseline2 weeks of treatment
Olanzapine78.682.2
Placebo82.485.0

[back to top]

Change From Baseline in Insulin

Insulin (µIU/ml) at baseline and after 2 weeks of treatment with olanzapine or placebo (NCT01496183)
Timeframe: Assessed at different time points: baseline and 2 weeks of treatment (olanzapine or placebo)

,
InterventionµIU/ml (Mean)
baseline2 weeks of treatment
Olanzapine6.210.1
Placebo5.05.8

[back to top]

Change From Baseline in PANSS Marder Factor Hostility/Excitement Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 4 items of the Marder hostility/excitement factor of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Marder factors are a modified grouping of the 30 PANSS items. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS Marder factor hostility/excitement symptom score for each participant was sum of rating assigned to each of the 4 applicable Marder factor items, and ranged from 4 to 28 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-0.4-0.5-0.9-0.8-0.5-1.4-1.1
Asenapine 5 mg BID-0.3-0.5-0.8-0.9-0.8-1.5-1.8
Olanzapine 15 mg QD-0.7-1.0-1.2-1.8-1.6-2.0-1.9
Placebo BID-0.5-0.7-0.9-1.0-1.0-1.4-1.1

[back to top]

Change From Baseline in PANSS Marder Factor Negative Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 7 items of the Marder negative symptoms factor of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Marder factors are a modified grouping of the 30 PANSS items. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS Marder factor negative symptom score for each participant was sum of the rating assigned to each of the 7 applicable Marder factor items, and ranged from 7 to 49 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-1.2-1.7-2.0-2.6-2.9-3.5-3.4
Asenapine 5 mg BID-0.8-1.9-2.8-3.2-3.8-3.9-4.7
Olanzapine 15 mg QD-0.8-1.8-2.2-2.6-3.2-4.1-4.3
Placebo BID-0.7-1.3-2.0-2.5-3.5-3.0-4.0

[back to top]

Change From Baseline in PANSS Marder Factor Positive Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 8 items of the Marder positive symptom factor of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Marder factors are a modified grouping of the 30 PANSS items. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS Marder factor positive symptom score for each participant was sum of rating assigned to each of the 8 applicable Marder factor items, and ranged from 8 to 56 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-1.3-2.5-3.9-4.5-4.8-6.1-6.8
Asenapine 5 mg BID-1.8-2.9-4.0-5.4-6.3-6.7-7.6
Olanzapine 15 mg QD-2.0-3.2-4.4-5.5-6.6-6.9-7.8
Placebo BID-2.0-2.8-4.1-5.1-5.6-6.1-6.2

[back to top]

Change From Baseline in PANSS Negative Subscale Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 7 items of the negative subscale of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Negative symptoms represent a diminution or loss of normal functions (e.g., emotional withdrawal). For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS negative subscale score for each participant was sum of the rating assigned to each of the 7 subscale items, and ranged from 7 to 49 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-0.7-1.2-1.6-2.3-2.5-3.3-3.3
Asenapine 5 mg BID-0.5-1.3-2.3-2.5-3.1-3.4-4.3
Olanzapine 15 mg QD-0.9-1.5-1.7-2.0-2.6-3.4-3.8
Placebo BID-0.8-1.1-1.8-2.3-3.0-2.6-3.2

[back to top]

Change From Baseline in PANSS Positive Subscale Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 7 items of the positive subscale of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Positive symptoms refer to an excess or distortion of normal mental status (e.g., delusions). For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS positive subscale score for each participant was sum of the rating assigned to each of the 7 subscale items, and ranged from 7 to 49 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-1.2-2.3-3.4-4.0-4.1-5.2-5.6
Asenapine 5 mg BID-1.6-2.8-3.9-5.0-5.7-6.3-7.2
Olanzapine 15 mg QD-2.3-3.6-4.4-5.7-6.2-6.8-7.5
Placebo BID-1.7-2.6-3.7-4.5-5.0-5.5-5.4

[back to top]

Change From Baseline in PANSS Total Score at Days 4, 7, 14, 21, 28 and 35

The PANSS is a 30-item clinician-rated instrument for assessing schizophrenia symptoms. It consists of 3 subscales: positive subscale (7 items), negative subscale (7 items), and general psychopathology subscale (16 items). For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. The PANSS total score for each participant was sum of the rating assigned to each of the 30 PANSS items, and ranged from 30 to 210 with a higher score indicating greater severity of symptoms. The reported measure is the change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28 and 35

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35
Asenapine 2.5 mg BID-4.0-7.2-9.9-12.0-12.3-17.0
Asenapine 5 mg BID-4.9-9.1-12.5-14.8-17.1-19.0
Olanzapine 15 mg QD-5.5-9.3-12.4-15.2-17.3-20.3
Placebo BID-4.8-7.1-10.7-13.2-15.5-15.4

[back to top]

Percentage of Participants Who Are Clinical Global Impression Scale-Improvement (CGI-I) Responders at Days 4, 7, 14, 21, 28, 35 and 42

A CGI-I responder was defined as a participant who had a CGI-I score of 1 (very much improved) or 2 (much improved) at a post-baseline assessment. CGI-I is a 7-point scale for assessing the global improvement of the participant's illness relative to baseline, with ratings from 1=very much improved to 7=very much worse. Missing data were imputed by LOCF. (NCT01617187)
Timeframe: Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionpercentage of participants (Number)
Day 4 (n = 95,108,44,98)Day 7 (n = 96,111,45,99)Day 14 (n = 96,111,45,99)Day 21 (n = 96,111,45,99)Day 28 (n = 96,111,45,99)Day 35 (n = 96,111,45,99)Day 42 (n = 96,111,45,99)
Asenapine 2.5 mg BID34.751.051.054.258.360.459.4
Asenapine 5 mg BID33.346.860.463.162.264.066.7
Olanzapine 15 mg QD43.260.071.175.673.382.284.4
Placebo BID37.845.554.558.660.664.662.6

[back to top]

Percentage of Participants Who Are PANSS Responders (≥30% Reduction From Baseline in PANSS Total Score) at Days 4, 7, 14, 21, 28 and 35

A PANSS responder was defined as a participant who had a reduction from baseline of at least 30% in the PANSS total score at a post-baseline assessment. The PANSS is a 30-item clinician-rated instrument for assessing schizophrenia symptoms. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. The Total score is the sum of the ratings for the individual items, and ranged from 30 to 210 with a higher score indicating greater severity of symptoms. Missing data were imputed by LOCF. (NCT01617187)
Timeframe: Days 4, 7, 14, 21, 28 and 35

,,,
Interventionpercentage of participants (Number)
Day 4 (n = 95,108,44,97)Day 7 (n = 96,111,45,99)Day 14 (n = 96,111,45,99)Day 21 (n = 96,111,45,99)Day 28 (n = 96,111,45,99)Day 35 (n = 96,111,45,99)
Asenapine 2.5 mg BID0.02.15.28.310.415.6
Asenapine 5 mg BID0.05.45.414.416.221.6
Olanzapine 15 mg QD0.00.04.411.115.615.6
Placebo BID2.15.17.113.114.117.2

[back to top]

Change From Baseline in Body Weight at Day 42

Change from baseline in body weight at Day 42 is the Key Safety Outcome Measure. (NCT01617187)
Timeframe: Baseline and Day 42

Interventionkg (Least Squares Mean)
Asenapine 2.5 mg BID1.3
Asenapine 5 mg BID1.3
Olanzapine 15 mg QD2.4
Placebo BID0.3

[back to top]

Change From Baseline in CGI-S Score at Day 42

Change from baseline in CGI-S score at Day 42 is a Key Secondary Outcome Measure. CGI-S is a 7-point scale for assessing the global severity of the participant's illness, with ratings from 1=normal, not ill to 7=very severely ill. The reported measure is the change from baseline at Day 42; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Day 42

Interventionscore on a scale (Least Squares Mean)
Asenapine 2.5 mg BID-0.9
Asenapine 5 mg BID-1.2
Olanzapine 15 mg QD-1.1
Placebo BID-1.0

[back to top]

Change From Baseline in PANSS General Psychopathology Subscale Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 16 items of the general psychopathology subscale of the PANSS, which is a 30-item clinician-rated instrument used to assess the symptoms of schizophrenia. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. The PANSS general psychopathology subscale score for each participant was calculated as the sum of the rating assigned to each of the 16 subscale items, and ranged from 16 to 112 with a higher score indicating greater severity of symptoms. The reported measure is the change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-2.2-3.8-5.1-5.9-5.9-8.8-8.9
Asenapine 5 mg BID-2.7-4.9-6.2-7.4-8.2-9.2-10.1
Olanzapine 15 mg QD-2.5-4.4-6.4-7.7-8.6-10.2-10.4
Placebo BID-2.4-3.6-5.4-6.7-7.7-7.6-8.0

[back to top]

Change From Baseline in PANSS Total Score at Day 42

The PANSS is a 30-item clinician-rated instrument for assessing schizophrenia symptoms. It consists of 3 subscales: positive subscale (7 items), negative subscale (7 items), and general psychopathology subscale (16 items). For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. The PANSS total score for each participant was sum of the rating assigned to each of the 30 PANSS items, and ranged from 30 to 210 with a higher score indicating greater severity of symptoms. The reported measure is the change from baseline at Day 42; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Day 42

Interventionscore on a scale (Least Squares Mean)
Asenapine 2.5 mg BID-17.4
Asenapine 5 mg BID-21.7
Olanzapine 15 mg QD-21.6
Placebo BID-16.2

[back to top]

Percentage of Participants Who Are PANSS Responders (≥30% Reduction From Baseline in PANSS Total Score) at Day 42

Rate of PANSS responders at Day 42 is a Key Secondary Outcome Measure. A PANSS responder was defined as a participant who had a reduction from baseline of at least 30% in the PANSS total score at a post-baseline assessment. The PANSS is a 30-item clinician-rated instrument for assessing schizophrenia symptoms. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. The Total score is the sum of the ratings for the individual items, and ranged from 30 to 210 with a higher score indicating greater severity of symptoms. Missing data were imputed by Last Observation Carried Forward (LOCF). (NCT01617187)
Timeframe: Baseline and Day 42

Interventionpercentage of participants (Number)
Asenapine 2.5 mg BID14.6
Asenapine 5 mg BID25.2
Olanzapine 15 mg QD26.7
Placebo BID19.2

[back to top]

Change From Baseline in CGI-S Score at Days 4, 7, 14, 21, 28 and 35

CGI-S is a 7-point scale for assessing the global severity of the participant's illness, with ratings from 1=normal, not ill to 7=very severely ill. The reported measure is the change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28 and 35

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35
Asenapine 2.5 mg BID-0.1-0.3-0.6-0.6-0.7-0.9
Asenapine 5 mg BID-0.2-0.3-0.6-0.8-0.9-1.1
Olanzapine 15 mg QD-0.2-0.3-0.6-0.8-0.8-1.0
Placebo BID-0.2-0.3-0.5-0.7-0.8-0.8

[back to top]

Change From Baseline in PANSS Marder Factor Anxiety/Depression Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 4 items of the Marder anxiety/depression factor of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Marder factors are a modified grouping of the 30 PANSS items. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS Marder factor anxiety/depression symptom score for each participant was sum of rating assigned to each of the 4 applicable Marder factor items, and ranged from 4 to 28 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-0.9-1.5-1.9-2.1-1.9-3.0-2.9
Asenapine 5 mg BID-1.2-2.2-2.9-3.0-3.2-3.6-3.4
Olanzapine 15 mg QD-1.0-1.8-2.5-2.7-2.8-3.2-3.1
Placebo BID-0.9-1.7-2.5-3.1-3.4-3.2-3.0

[back to top]

Change From Baseline in PANSS Marder Factor Disorganized Thought Symptom Score at Days 4, 7, 14, 21, 28, 35 and 42

This measure reports results for the 7 items of the Marder disorganized thoughts factor of the PANSS, which is a 30-item clinician-rated instrument used to assess schizophrenia symptoms. Marder factors are a modified grouping of the 30 PANSS items. For each item, symptom severity was rated on a 7-point scale, from 1=absent to 7=extreme. PANSS Marder factor disorganized thought symptom score for each participant was sum of rating assigned to each of the 7 applicable Marder factor items, and ranged from 7 to 49 with a higher score indicating greater severity of symptoms. Measure reports change from baseline; improvement in symptoms is represented by negative values. (NCT01617187)
Timeframe: Baseline and Days 4, 7, 14, 21, 28, 35 and 42

,,,
Interventionscore on a scale (Least Squares Mean)
Day 4Day 7Day 14Day 21Day 28Day 35Day 42
Asenapine 2.5 mg BID-0.3-1.0-1.3-2.3-2.4-3.5-3.8
Asenapine 5 mg BID-0.7-1.4-2.0-2.5-3.1-3.5-4.3
Olanzapine 15 mg QD-1.1-1.6-2.2-2.7-3.1-4.3-4.7
Placebo BID-0.7-0.7-1.5-2.1-2.4-2.4-2.7

[back to top]

Change in Mean Gastric Emptying Time

The investigators aim to test gastric motility, including gastric emptying and antroduodenal contractility parameters, by wireless motility capsule (WMC) before and at the completion of the study to determine if olanzapine has any pro-motility effects in gastroparesis. (NCT01625923)
Timeframe: 8 weeks

Interventionminutes (Mean)
Baseline GET (minutes)GET at Week 8 (minutes)
Olanzapine468.3563.3

[back to top]

Change in Mean Serum Glucose

Subjects will undergo regular testing of blood glucose, insulin, hemoglobin (Hgb) A1c, body mass index (BMI), liver enzymes, thyroid stimulating hormone (TSH), and prolactin levels during the study as well as after treatment completion to determine the safety of the medication. All adverse events will be compiled to investigate the tolerability of the medication. (NCT01625923)
Timeframe: 8 weeks

Interventionmg/dl (Mean)
Baseline Serum GlucoseSerum Glucose at Week 8
Olanzapine90.590.5

[back to top]

Change in Mean Ghrelin Levels Over Time

The investigators seek to determine whether olanzapine promotes secretion of ghrelin in gastroparesis. (NCT01625923)
Timeframe: 8 weeks

Interventionpg/ml (Mean)
Baseline plasma ghrelin (pg/ml)Plasma ghrelin at week 8 (pg/ml)
Olanzapine615.7577.0

[back to top]

Change in Mean BMI

Subjects will undergo regular testing of blood glucose, insulin, hemoglobin (Hgb) A1c, body mass index (BMI), liver enzymes, thyroid stimulating hormone (TSH), and prolactin levels during the study as well as after treatment completion to determine the safety of the medication. All adverse events will be compiled to investigate the tolerability of the medication. (NCT01625923)
Timeframe: 8 weeks

Interventionkg/m^2 (Mean)
Baseline BMIBMI at Week 8
Olanzapine23.524.9

[back to top]

Mean GCSI-DD Before/After Treatment With Olanzapine

The investigators will utilize the gastroparesis cardinal symptom index daily diary (GCSI-DD) to compare severity of symptoms before and after treatment with olanzapine. The total GCSI-DD is a validated questionnaire that measures the daily relevant symptoms of gastroparesis and ranges from 0 (no symptoms) to 5 (severe symptoms). (NCT01625923)
Timeframe: 8 weeks

Interventionscore on a scale (Mean)
Baseline GCSI-DD ScoreGCSI-DD Score After Intervention
Olanzapine3.112.17

[back to top]

Mean Change From Baseline to 8 Week Endpoint in the Barnes Akathisia Scale (BAS)

BAS is used to rate observable, restless movements of drug induced akathisia and the subjective awareness of restlessness and any distress associated with the akathisia. The BAS consists of the following 3 items: an objective assessment of akathisia symptoms; a subjective assessment of the patient's awareness of inner restlessness; and a global clinical assessment of akathisia. The first two items are rated on a 4-point scale ranging from 0 (no abnormal movements or the absence of inner restlessness) to 3 (severe akathisia or the awareness of intense compulsion to move most of the time). The last item, the global clinical assessment of akathisia, is rated on a 5-point scale, ranging from 0 (no evidence of akathisia) to 5 (severe akathisia). Total BAS score ranges from 0 to 14 with a higher score representing worse results. (NCT01687478)
Timeframe: Baseline, 8 Weeks

Interventionunits on a scale (Mean)
Olanzapine + Fluoxetine-0.01
Placebo + Fluoxetine-0.04

[back to top]

Percentage of Participants Who Achieve a Response Based on a ≥50% Reduction From Baseline in MADRS Total Score

The MADRS total score is the sum of the 10 items; therefore the possible MADRS total score ranges from 0 to 60. A higher MADRS total score indicates a greater severity of depressive symptoms. (NCT01687478)
Timeframe: Baseline,8 Weeks

InterventionPercent of participants (Number)
Olanzapine + Fluoxetine65.5
Placebo + Fluoxetine61.2

[back to top]

Percentage of Participants Who Achieve Remission Based on MADRS Total Score ≤10 at 8 Weeks

The MADRS consists of 10 items with each item rated on a scale ranging from 0 to 6. Fixed descriptors appear along the scale for each item at points 0, 2, 4, and 6, to standardize the gradation of response along the scale. The MADRS total score is the sum of the 10 items; therefore the possible MADRS total score ranges from 0 to 60. A higher MADRS total score indicates a greater severity of depressive symptoms. (NCT01687478)
Timeframe: Baseline, 8 Weeks

InterventionPercent of participants (Number)
Olanzapine + Fluoxetine37.9
Placebo + Fluoxetine38.8

[back to top]

Mean Change From Baseline to 8 Week Endpoint in the Sheehan Disability Scale (SDS)

SDS consists of 3 items (work/school, social life/leisure activities, and family life/home responsibilities). Total scores range from 0 to 30 with higher values indicating greater disruption. Individual Item scores range from 0 to 10 with higher values indicating greater disruption. (NCT01687478)
Timeframe: Baseline, 8 Weeks

,
InterventionUnits on a scale (Mean)
Work/School (n=68,65)Social Life (n=79,79)Family Life (n=79,78)SDS Total Score (68,64)
Olanzapine + Fluoxetine-1.34-1.70-1.63-4.57
Placebo + Fluoxetine-1.55-1.49-1.53-4.41

[back to top]

Mean Change From Baseline to 8 Week Endpoint in the Short-Form 36 Health Survey (SF-36)

SF-36, version 2 is a generic participant-rated questionnaire and consists of 36 questions covering the following 8 health domains (subscales): general health, role limitations because of physical problems, role limitations due to emotional problems, physical functioning, bodily pain, mental health, social functioning, and vitality. Each subscale is scored by summing the individual items and transforming the scores into a 0 to 100 scale, with higher scores indicating better health status or functioning. Two summary scores, the physical component summary (PCS) and the mental component summary (MCS) were constructed based on the eight SF-36 subscales. Both PCS and MCS range from 0-100 with higher scores indicating better health or functioning. (NCT01687478)
Timeframe: Baseline, 8 Weeks

,
Interventionunits on a scale (Mean)
Physical FunctioningRole-PhysicalBodily PainGeneral HealthVitalitySocial FunctioningRole-EmotionalMental HealthMental Component ScorePhysical Component Score
Olanzapine + Fluoxetine2.203.996.815.827.436.136.618.988.872.87
Placebo + Fluoxetine0.703.930.022.845.044.566.718.438.73-0.65

[back to top]

Mean Change From Baseline to 8 Week Endpoint in the Simpson-Angus Scale (SAS)

SAS scale consists of 10 items including 7 items that address bradykinesia-rigidity and additional single items for tremor, glabellar tap,and salivation. Each item represents a specific physical condition and is rated on a 5-point category rating scale ranging from 0 (complete absence of the condition) to 4 (the condition is present to an extreme degree).The total score is obtained by adding the scores for the 10 individual items making the maximum possible score is 40. Higher scores are indicative of more severe Parkinsonian-type symptoms. (NCT01687478)
Timeframe: Baseline, 8 Weeks

Interventionunits on a scale (Mean)
Olanzapine + Fluoxetine0.03
Placebo + Fluoxetine-0.14

[back to top]

Mean Change From Baseline to 8 Week Endpoint in Clinical Global Impressions-Severity of Depression (CGI-S) Scale

CGI-S scale measures severity of illness at the time of assessment compared with start of treatment. Scores range from 1 (normal, not at all ill) to 7 (among the most extremely ill participants). The LS mean (LSM) change from baseline, standard error was derived using MMRM methodology with factors for treatment , Pooled Investigator , Visit , (Baseline + Treatment)*Visit. (NCT01687478)
Timeframe: Baseline, 8 Weeks

InterventionUnits on a scale (Least Squares Mean)
Olanzapine + Fluoxetine-1.43
Placebo + Fluoxetine-1.63

[back to top]

Mean Change From Baseline to 8 Week Endpoint in Montgomery-Äsberg Depression Rating Scale (MADRS)

The MADRS total score is the sum of the 10 items; therefore the possible MADRS total score ranges from 0 to 60. A higher MADRS total score indicates a greater severity of depressive symptoms. Least square means (LSM) change from baseline, standard error was derived using mixed model repeated measures (MMRM) methodology with factors for treatment, Pooled Investigator, Visit, (Baseline + Treatment)*Visit. (NCT01687478)
Timeframe: Baseline, 8 Weeks

InterventionUnits on a scale (Least Squares Mean)
Olanzapine + Fluoxetine-15.92
Placebo + Fluoxetine-14.30

[back to top]

Mean Change From Baseline to 8 Week Endpoint in the Abnormal Involuntary Movement Scale (AIMS)

AIMS is a 12-item scale. Items 1 to 8 are rated on a 5-point scale ranging from 0 (no dyskinetic movements) to 4 (severe dyskinetic movements). Item 9 assesses the participant's incapacitation due to abnormal movements, and item 10 assesses the participant's awareness of the abnormal movements and associated distress. Items 9 and 10 are rated on 5-point scales ranging from 0 (none or no awareness) to 4 (severe or aware, severe distress). Items 11 and 12 are yes/no questions regarding the dental status of the participant. The total score is the sum of the scores for the 12 items and the possible total score ranges from 0 to 42. A higher total score is indicative of more severe dyskinetic movements. (NCT01687478)
Timeframe: Baseline, 8 Weeks

Interventionunits on a scale (Mean)
Olanzapine + Fluoxetine-0.16
Placebo + Fluoxetine-0.31

[back to top]

Hamilton Depression Rating Scale (HAM-D)

"Depression rating scale: Range 0-53, higher scores indicate worse depression. 0-7 = Normal 8-13 = Mild Depression 14-18 = Moderate Depression 19-22 = Severe Depression~≥ 23 = Very Severe Depression" (NCT01833897)
Timeframe: 8 weeks

Interventionunits on a scale (final score) (Mean)
Ketamine and DCS Treatment9.5

[back to top]

Beck's Depression Inventory

Range 0-63, with higher scores worse. Total score of 0-13 is considered minimal range, 14-19 is mild, 20-28 is moderate, and 29-63 is severe. (NCT01833897)
Timeframe: 8 weeks

Interventionunits on a scale (final score) (Mean)
Ketamine and DCS Treatment10.8

[back to top]

Hamilton Anxiety Scale

Each item is scored on a scale of 0 (not present) to 4 (severe), with a total score range of 0-56, where <17 indi- cates mild severity, 18-24 mild to moderate severity and 25-30 moderate to severe. (NCT01833897)
Timeframe: 8 weeks

Interventionunits on a scale (final score) (Mean)
Ketamine and DCS Treatment6.4

[back to top]

HAM-D Suicide Item

Ham-D suicide item: range 0-4, higher scores indicate worse symptoms (NCT01833897)
Timeframe: 8 weeks

Interventionunits on a scale (final) (Mean)
Ketamine and DCS Treatment0.3

[back to top]

Loss of Motivated Behavior HAM-D Factor

includes the total of four HAM-D items: (Item 7: Work and activities, Item 12. Somatic symptoms (appetite), Item 14. Genital symptoms (libido), and Item 16. Weight loss). Range 0-11, higher scores indicate worse symptoms (NCT01833897)
Timeframe: 8 weeks

Interventionunits on a scale (final score) (Mean)
Ketamine and DCS Treatment1.6

[back to top]

Change in Clinical Global Impressions - Severity (CGI-S) From Baseline to Day 92

"Change in CGI-S score from baseline (Day 8) to the end of Part A (Week 12; Day 92).~The CGI-S is a 7-point scale intended to measure the severity of a patient's illness at the time of assessment. Scores range from 1 (normal) to 7(extremely ill), so a higher score is correlative to more severe illness." (NCT01903837)
Timeframe: Baseline (Day 8) to Day 92 (end of study Part A)

Interventionunits on a scale (Least Squares Mean)
Part A FAS 1 - OLZ + Placebo-0.0
Part A FAS 1 - Olz + Sam 5mg-0.1
Part A FAS 1- Olz + Sam 10mg-0.0
Part A FAS 1- Olz + Sam 20mg-0.1

[back to top]

Absolute Change in Total Positive and Negative Syndrome Scale (PANSS) Score

"Change from baseline (Day 8) to Day 92 (end of study Part A).~The PANSS is a 30-item scale measuring severity of schizophrenia symptoms. Symptom severity for each item is rated on a 7-point scale (1 = absent; 7 = extreme), and the total score is added together, with a minimum score of 30 and a maximum score of 210. A higher score indicates more severe symptoms, while a lower score indicates less severe symptoms." (NCT01903837)
Timeframe: Baseline (Day 8) to Day 92 (end of study Part A)

Interventionunits on a scale (Least Squares Mean)
Part A FAS 1 - Olz + Placebo-2.9
Part A FAS 1 - Olz + Sam 5mg-1.5
Part A FAS 1- Olz+ Sam 10mg-2.7
Part A FAS 1- Olz+ Sam 20mg-2.5

[back to top]

Absolute Change in Body Weight (kg) From Baseline to Day 92

Change from randomization (Day 8) to the end of Part A (Week 12; Day 92) (NCT01903837)
Timeframe: Baseline (Day 8) to Day 92 (end of study Part A)

Interventionkg (Least Squares Mean)
Part A FAS 1- Olz + Placebo2.9
Part A FAS 1- Olz + Sam 5mg2.1
Part A FAS 1- Olz + Sam 10mg1.5
Part A FAS 1- Olz + Sam 20mg2.2
Part A FAS 2- Olz + Placebo3.8
Part A FAS 2- Olz + Sam 5mg2.9
Part A FAS 2- Olz + Sam 10mg1.5
Part A FAS 2- Olz + Sam 20mg1.2

[back to top]

Percentage of Subjects Exhibiting Significant Weight Gain at Day 92

Significant weight gain will include a >=5%, >= 7%, or >=10% gain in body weight from baseline (Day 8) to Day 92 (end of study Part A) (NCT01903837)
Timeframe: Baseline (Day 8) to Day 92 (end of study Part A)

,,,,,,,
InterventionParticipants (Count of Participants)
>= 5% weight gain>= 7% weight gain>=10% weight gain
Part A FAS 1- Olz + Placebo201410
Part A FAS 1- Olz + Sam 10mg1694
Part A FAS 1- Olz + Sam 20mg16125
Part A FAS 1- Olz + Sam 5mg1883
Part A FAS 2- Olz + Placebo14118
Part A FAS 2- Olz + Sam 10mg843
Part A FAS 2- Olz + Sam 20mg871
Part A FAS 2- Olz + Sam 5mg1373

[back to top]

Percent Change in Body Weight (Kilogram) From Baseline to Day 92

Percent change from baseline (Day 8) to the end of Part A (Day 92) (NCT01903837)
Timeframe: Baseline (Day 8) to Day 92 (end of study Part A)

Interventionpercent change (Least Squares Mean)
Part A FAS 1 - Olz + Placebo4.1
Part A FAS 1 - Olz + Sam 5mg2.8
Part A FAS 1- Olz + Sam 10mg2.1
Part A FAS 1- Olz + Sam 20mg2.9
Part A FAS 2- Olz + Placebo5.3
Part A FAS 2- Olz + Sam 5mg3.8
Part A FAS 2- Olz + Sam 10mg2.2
Part A FAS 2- Olz + 20mg1.6

[back to top]

Change in Adiposity

Total fat mass (excluding head) from baseline to Day 28 (NCT01920802)
Timeframe: Baseline to Day 28

,,
Interventiongrams (Mean)
BaselineDay 28
Iloperidone1474116366
Olanzapine1194213312
Placebo1169012081

[back to top]

Change in Food Intake

Total grams of food consumed (NCT01920802)
Timeframe: Baseline to Day 28

,,
Interventiongrams (Mean)
BaselineDay 28
Iloperidone1196.65571154.1286
Olanzapine1101.77151198.4071
Placebo1567.5261458.108

[back to top]

Change in Insulin

Change in Insulin levels from baseline to Day 28 (NCT01920802)
Timeframe: Baseline to Day 28

,,
InterventionmlU/L (Mean)
BaselineDay 28
Iloperidone9.931610.873
Olanzapine9.774912.0862
Placebo10.961910.785

[back to top]

Change in Lipid Metabolism

Change in lipid metabolism as measured by cholesterol/HDL ratio (NCT01920802)
Timeframe: Baseline to Day 28

,,
Interventionratio (Mean)
BaselineDay 28
Iloperidone2.572.57
Olanzapine2.713.14
Placebo2.72.5

[back to top]

Insulin Resistance

Homeostatic model assessment for Insulin Resistance (HOMA-IR) is a method for assessing β-cell function and insulin resistance (IR) from basal (fasting) glucose and insulin. (NCT01920802)
Timeframe: Baseline to Day 28

,,
InterventionHOMA-IR score (Mean)
BaselineDay 28
Iloperidone2.06612.4733
Olanzapine2.04772.6147
Placebo2.29882.3362

[back to top]

Change Glucose in People Taking Olanzapine or Iloperidone

To quantify, prospectively, change in glucose from baseline to Day 28 (NCT01920802)
Timeframe: Baseline to study termination (about 12 weeks)

,,
Interventionmg/dL (Mean)
BaselineDay 28
Iloperidone1443013975
Olanzapine11500.7111276.43
Placebo10925.512179.5

[back to top]

Change in Leptin

Leptin levels measured at Day 3 compared to baseline (NCT01920802)
Timeframe: change in baseline to Day 3

Interventionng/dL (Mean)
Olanzapine2.47
Iloperidone1.76
Placebo1.16

[back to top]

Change in Body Weight

Delineate a pathophysiological mechanism of antipsychotic induced weight gain (NCT01920802)
Timeframe: baseline and 6 week visit

Interventionkg (Mean)
Olanzapine3.2
Iloperidone0.8
Placebo0.4

[back to top]

Number of Participants With Adverse Events.

Olanzapine will be considered tolerable if less than 10% of patients experience a grade III or IV adverse event attributable to olanzapine. (NCT02097823)
Timeframe: Ongoing, throughout the study. Will be fully evaluated in approximately 1 year, at the conclusion of data collection. Each patient will be followed during 2 cycles of chemotherapy, an expected average of 6 weeks.

Interventionparticipants (Number)
Aprepitant0
Olanzapine0

[back to top]

Feasibility of Recruitment and Data Collection.

Primary objective of this study is to determine the feasibility of recruitment and data collection for conducting a larger trial. Recruitment and data collection will be feasible if at least 20 subjects can be recruited in 1 year and there is a 90% form completion rate. (NCT02097823)
Timeframe: Approximately 1 year after study opens, at the conclusion of data collection. Participants will be followed during 2 cycles of chemotherapy, an expected average of 6 weeks. Data will be collected over 5 days during each cycle.

Interventionpercentage of completed forms (Number)
All Participants70.4

[back to top]

Complete Response in Overall Phase

This will measure what percentage of patients have a complete response (no emesis or use of breakthrough medications) in the overall phase (0-120 hours). (NCT02097823)
Timeframe: Participants will be followed during 2 cycles of chemotherapy, an expected average of 6 weeks. Data will be collected over 5 days during each cycle.

Interventionpercentage of participants with CR (Number)
Aprepitant23.1
Olanzapine28.6

[back to top]

Complete Response in Delayed Phase

This will measure what percentage of patients have a complete response (no emesis or use of breakthrough medications) in the delayed phase (25-120 hours). (NCT02097823)
Timeframe: Participants will be followed during 2 cycles of chemotherapy, an expected average of 6 weeks. Data will be collected over 5 days during each cycle.

Interventionpercentage of participants with CR (Number)
Aprepitant23.1
Olanzapine28.6

[back to top]

Complete Response in Acute Phase

This will measure what percentage of patients have a complete response (no emesis or use of breakthrough medications) in the acute phase (0-24 hours). (NCT02097823)
Timeframe: Participants will be followed during 2 cycles of chemotherapy, an expected average of 6 weeks. Data will be collected over 5 days during each cycle.

Interventionpercentage of participants with CR (Number)
Aprepitant76.9
Olanzapine78.6

[back to top]

Good Control of Nausea

"Good control of nausea will be ratings <25 on visual analog scale by parents and <2 on baxter retching faces scale by patients. Will look at the proportions of patients with good control of nausea.~The visual analog scale ranged from 0-100, with 0 being no nausea and 100 being very very severe nausea. The Baxter retching faces scale ranged from 0-10 using only even numbers (0,2,4,6,8,10) and each number has a corresponding face depicting someone experiencing varying levels of nausea, with 0 being no nausea and 10 being a picture of face vomiting." (NCT02097823)
Timeframe: Participants will be followed during 2 cycles of chemotherapy, an expected average of 6 weeks. Data will be collected over 5 days during each cycle.

,
Interventionpercentage of participant w/good control (Number)
Visual Analog Scale/ParentsBARF scale/Patients
Aprepitant54.554.5
Olanzapine5050

[back to top] [back to top]

Median Nausea Scores

Nausea scores was measured using a visual-analogue scale ranging from 0 (none) to 10 (as bad as it can be). (NCT02116530)
Timeframe: Baseline and Day 2 to Day 6 after chemotherapy

,
Interventionunits on a scale (Median)
BaselineDay 2Day 3Day 4Day 5Day 6
Olanzapine000000
Placebo011111

[back to top]

Proportion of Patients With Complete Response

Complete response was defined as no emetic episodes and no use of rescue medication during the acute (0-24 hours), delayed (25-120 hours) and overall (0-120 hours) periods as measured by the Nausea and Vomiting Daily Diary/Questionnaire. (NCT02116530)
Timeframe: 0 to 120 hours after chemotherapy

,
Interventionpercentage of participants (Number)
0-24 hours after chemotherapy25-120 hours after chemotherapy0-120 hours after chemotherapy
Olanzapine85.766.963.6
Placebo64.652.440.6

[back to top]

Proportion of Patients With no Nausea

No nausea was defined as a response of 0 in the nausea item of Nausea and Vomiting Daily Diary/Questionnaire in the acute (0-24 hours), delayed (25-120 hours) and overall (0-120 hours) periods after chemotherapy. (NCT02116530)
Timeframe: 0 to 120 hours after chemotherapy

,
Interventionpercentage of participants (Number)
0-24 hours after chemotherapy25-120 hours after chemotherapy0-120 hours after chemotherapy
Olanzapine73.842.437.3
Placebo45.325.421.9

[back to top]

Frequency of Rescue Medication

Patients were asked to record daily number of extra nausea/vomiting pills taken because they developed nausea/vomiting in the following categories: None, One, Two, More than two in Nausea and Vomiting Daily Diary Questionnaire. (NCT02116530)
Timeframe: Day 2 to Day 6 after chemotherapy

InterventionParticipants (Count of Participants)
Day 272213840Day 272213839Day 372213839Day 372213840Day 472213839Day 472213840Day 572213840Day 572213839Day 672213839Day 672213840
More than twiceTwiceNoneOnce
Olanzapine156
Placebo117
Olanzapine21
Placebo35
Placebo19
Olanzapine2
Olanzapine158
Placebo124
Olanzapine11
Placebo24
Olanzapine7
Placebo20
Olanzapine4
Placebo10
Olanzapine141
Olanzapine16
Olanzapine10
Placebo17
Olanzapine3
Placebo11
Olanzapine145
Placebo131
Olanzapine19
Placebo23
Olanzapine5
Placebo7
Olanzapine143
Placebo130
Olanzapine12
Placebo16
Placebo14

[back to top]

Patient Outcomes

Our primary study outcome evaluated the feasibility of a future trial of olanzapine that would evaluate the contribution of olanzapine to chemotherapy-induced nausea and vomiting (CINV) control in pediatric oncology patients. A future trial was considered feasible if the following patient outcomes were met: mean time to enroll 15 patients was 12 months or less per site, 12 or more patients took at least half of the planned olanzapine doses, and 3 or less patients experienced significant sedation or dizziness despite dose reduction. (NCT02129478)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Participants enrolled at 12 monthsPatients taking half olanzapine doses at 12 monthsPatients with sedation or dizziness at half dose
Olanzapine15150

[back to top]

Number of Participants With Adverse Events as a Measure of Safety and Tolerability

All early discontinuation of olanzapine or dose reduction cases will be reported. (NCT02129478)
Timeframe: Every day for 30 days after the last dose of the study drug

InterventionParticipants (Count of Participants)
# patients with reduced dose# patients with drug discontinuation
Olanzapine62

[back to top]

Proportion of Patients With Complete CINV Control

The proportion of children achieving complete CINV control (no nausea, vomiting, or retching and no use of breakthrough antiemetic agents) during the acute (24 hours after the last dose of chemotherapy is administered) and delayed phases (the 7 days following the acute phase) will be described. The duration of assessment will depend on the number of days each individual patient receives chemotherapy. Nausea will be assessed using the Pediatric Nausea Assessment Tool (PeNAT). (NCT02129478)
Timeframe: During the acute (24 hours) and delayed (7 days after acute phase) phases, up to 2 weeks

InterventionParticipants (Count of Participants)
Olanzapine0

[back to top]

Number of Participants With Independent Adjudication Committee (IAC) Adjudicated Event of Exacerbation of Disease (EEDS)

"EEDS was defined as any of the following occurring during the double-blind period & was related to worsening of disease symptoms, as confirmed by the Independent Adjudication Committee (IAC):~Hospitalization (includes psychiatric& treatment of alcohol intoxication/withdrawal)~>= 25% or >= 15 point increase from randomization in PANSS total score~PANSS items score of P1, P2, P3, P6, P7 or G8 that meets 1 of the following:~3a. Score >= 5 for subjects at a 2nd ad hoc visit with a score <=3 at randomization 3b. Score >= 6 for subjects at a 2nd ad hoc visit with a score =4 at randomization 4. Engagement in self injury, aggressive behavior, or suicidal/homicidal ideation 5. Initiation of rescue medication, including increase in olanzapine dosage initially prescribed at randomization 6. ER visit 7. Subject withdraws or PI discontinues subject for lack of efficacy, lost to follow-up, or withdrawal by subject 8. Arrest or incarceration related to subject's underlying disease" (NCT02161718)
Timeframe: Up to 15 months

,
InterventionParticipants (Count of Participants)
Number of Subjects with IAC Adjudicated EEDSNumber of Subjects Censored
ALKS 38312587
Olanzapine + Placebo2988

[back to top]

Number of Events of Exacerbation of Disease (EEDS)

"EEDS was defined as any of the following occurring during the double-blind period & was related to worsening of disease symptoms, as confirmed by the Independent Adjudication Committee (IAC):~Hospitalization(includes psychiatric & treatment of alcohol intoxication/withdrawal)~>= 25% or >= 15 point increase from randomization in PANSS total score~PANSS items score of P1, P2, P3, P6, P7 or G8 that meets 1 of the following:~3a. Score >= 5 for subjects at a 2nd ad hoc visit with a score <=3 at randomization 3b. Score >= 6 for subjects at a 2nd ad hoc visit with a score =4 at randomization 4. Engagement in self injury, aggressive behavior, or suicidal/homicidal ideation 5. Initiation of rescue medication, including increase in olanzapine dosage initially prescribed at randomization 6. ER visit 7. Subject withdraws or PI discontinues subject for lack of efficacy, lost to follow-up, or withdrawal by subject 8. Arrest or incarceration related to subject's underlying disease" (NCT02161718)
Timeframe: Up to 15 months

InterventionEvents (Number)
ALKS 383135
Olanzapine + Placebo49

[back to top]

Part 3 (EDP): Number of Participants With Change From Baseline in Severity of Psychotic Symptoms, as Measured by CRDPSS

The CRDPSS is an 8-item measure that assesses the severity of mental health symptoms that are important across psychotic disorders, including delusions, hallucinations, disorganized speech, abnormal psychomotor behavior, negative symptoms. Each item on the measure is rated on a 5-point scale (0=none; 1=equivocal; 2=present, but mild; 3=present and moderate; and 4=present and severe). Total Score is taken as summation. A higher score indicates a more severe condition. Worsened or improved is defined as increase or decrease compared to baseline. (NCT02431702)
Timeframe: Baseline, up to 18 Months

InterventionParticipants (Count of Participants)
Hallucinations72513609Hallucinations72513610Delusions72513609Delusions72513610Disorganized Speech72513609Disorganized Speech72513610Abnormal Psychomotor Behavior72513609Abnormal Psychomotor Behavior72513610Negative Symptoms72513609Negative Symptoms72513610Impaired Cognition72513609Impaired Cognition72513610Mania72513609Mania72513610Depression72513609Depression72513610
WorsenedUnchangedImproved
Part 3-PP to PP3
Part 3-OAP to OAP8
Part 3-PP to PP27
Part 3-OAP to OAP29
Part 3-PP to PP11
Part 3-OAP to OAP10
Part 3-PP to PP6
Part 3-PP to PP21
Part 3-OAP to OAP20
Part 3-PP to PP14
Part 3-OAP to OAP17
Part 3-PP to PP2
Part 3-OAP to OAP36
Part 3-PP to PP12
Part 3-PP to PP4
Part 3-OAP to OAP2
Part 3-PP to PP32
Part 3-OAP to OAP37
Part 3-PP to PP5
Part 3-OAP to OAP4
Part 3-OAP to OAP22
Part 3-PP to PP19
Part 3-OAP to OAP21
Part 3-PP to PP10
Part 3-OAP to OAP9
Part 3-OAP to OAP23
Part 3-PP to PP17
Part 3-OAP to OAP15
Part 3-PP to PP0
Part 3-OAP to OAP3
Part 3-PP to PP40
Part 3-OAP to OAP39
Part 3-PP to PP1
Part 3-OAP to OAP5
Part 3-PP to PP7
Part 3-OAP to OAP6
Part 3-PP to PP26
Part 3-PP to PP8
Part 3-OAP to OAP12

[back to top]

Part 2 (Disease Progression): Change From Baseline in Adjusted Intracortical Myelin (ICM) Fraction Score as Measured by Inversion Recovery (IR) and Spin Echo Magnetic Resonance Imaging (MRI)

"The adjusted ICM fraction score is quantified as: 1. The volume of myelinated brain tissue is measured separately on co-localized IR and proton density (PD) MRI images, by outlining the boundary between gray matter and white matter on each image. 2. ICM is calculated from the difference of IR volume minus PD volume. 3. ICM is then expressed as a fraction of the total intracranial volume (ICM divided by intracranial volume). 4. The ICM fraction is then adjusted for effects of age, gender, and race/ethnicity in the sample of treated participants and healthy controls. A decrease in the adjusted ICM fraction score may be a sign of disease progression." (NCT02431702)
Timeframe: Baseline and Day 260

Interventionratio (Mean)
Part-2: Paliperidone Palmitate (PP)-0.001
Part-2: OAP-0.004

[back to top]

Part 2 (Disease Progression): Change From Baseline in Attention/Vigilance Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess attention/vigilance score of participants. The range of attention/vigilance score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)3.2
Part-2: OAP0.7

[back to top]

Part 2 (Disease Progression): Change From Baseline in Clinical Global Impression Severity (CGI-S) Score

"The Clinical Global Impression Severity (CGI-S) rating scale is used to rate the severity of a participant's overall clinical condition on a 7 point scale. The score ranges from 1 to 7, where 1 is equivalent to Normal, not at all ill and a rating of 7 is equivalent to Among the most extremely ill participants. Higher scores indicate worsening." (NCT02431702)
Timeframe: Baseline, up to 9 Months of Part 2

Interventionunits on a scale (Mean)
Part-2: Paliperidone Palmitate (PP)-0.2
Part-2: OAP-0.3

[back to top]

Part 2 (Disease Progression): Change From Baseline in Cognition as Measured by the MATRICS Consensus Cognitive Battery (MCCB) Composite Score

The MATRICS Consensus Cognitive Battery is an instrument that contains 10 tests to measure cognitive performance in 7 cognitive domains: speed processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition. The composite score combines the individual scores of the 10 tests and scores them on a normative scale to derive a T-score and composites scores. The range of T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Month 9

InterventionT-score (Least Squares Mean)
Part-2: Paliperidone Palmitate (PP)2.0
Part-2: OAP2.8

[back to top]

Part 2 (Disease Progression): Change From Baseline in Functioning as Measured by the Personal and Social Performance (PSP) Total Score

The Personal and Social Performance (PSP) scale assesses degree of a participant's dysfunction within 4 domains of behavior: 1) socially useful activities, 2) personal and social relationships, 3) self-care, and 4) disturbing and aggressive behavior. Each domain was assessed on a 6-point scale, from 1 (absent) to 6 (very severe) (1 = absent, 2 = mild, 3 = manifest, 4 = marked, 5 = severe, and 6 = very severe). PSP total score was calculated as sum of all the domain scores and ranges from 1 to 100. Participants with score of 71 to 100 have mild degree of difficulty; from 31 to 70, varying degrees of disability; less than or equal to 30, functioning so poorly as to require intensive supervision. Higher score indicate better performance. (NCT02431702)
Timeframe: Baseline and Month 9

Interventionunits on a scale (Mean)
Part-2: Paliperidone Palmitate (PP)2.5
Part-2: OAP2.9

[back to top]

Part 2 (Disease Progression): Change From Baseline in Medication Satisfaction Questionnaire (MSQ) Total Score

The Medication Satisfaction Questionnaire (MSQ) is a 7-point, verbally administered, Likert-type scale rated as follows: 1=Extremely Dissatisfied, 2=Very Dissatisfied, 3=Somewhat Dissatisfied, 4=Neither Satisfied Nor Dissatisfied, 5=Somewhat Satisfied, 6=Very Satisfied, 7=Extremely Satisfied. Worst value is 1 (Extremely Dissatisfied) and best value is 7 (Extremely Satisfied). Total score ranges from 1 to 7. Higher score indicate improvement. (NCT02431702)
Timeframe: Baseline and endpoint Part 2 (up to 9 Months)

Interventionunits on a scale (Mean)
Part-2: Paliperidone Palmitate (PP)-0.2
Part-2: OAP0.1

[back to top]

Part 2 (Disease Progression): Change From Baseline in Reasoning and Problem Solving: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess reasoning and problem solving of participants. The range of reasoning and problem solving T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)0.2
Part-2: OAP2.8

[back to top]

Part 2 (Disease Progression): Change From Baseline in Social Cognition Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess social cognition score of participants. The range of social cognition score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)0.3
Part-2: OAP1.6

[back to top]

Part 2 (Disease Progression): Change From Baseline in Speed of Processing Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess speed of processing score of participants. The range of speed of processing T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)1.8
Part-2: OAP3.5

[back to top]

Part 2 (Disease Progression): Change From Baseline in Verbal Learning Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess verbal learning score of participants. The range of verbal learning score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)1.3
Part-2: OAP1.0

[back to top]

Part 2 (Disease Progression): Change From Baseline in Visual Learning Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess visual learning score of participants. The range of visual learning score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)1.3
Part-2: OAP1.4

[back to top]

Part 3 (EDP): Change From Baseline in Reasoning and Problem Solving: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess reasoning and problem solving score of participants. The range of reasoning and problem solving T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP3.4
Part 3-OAP to OAP4.7

[back to top]

Part 3 (EDP): Change From Baseline in Social Cognition Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess social cognition score of participants. The range of social cognition score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP-0.2
Part 3-OAP to OAP1.4

[back to top]

Part 3 (EDP): Change From Baseline in Speed of Processing Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess speed of processing score of participants. The range of speed of processing score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP2.5
Part 3-OAP to OAP4.9

[back to top]

Part 2 (Disease Progression): Change From Baseline in Working Memory Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess working memory of participants. The range of working memory score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part-2: Paliperidone Palmitate (PP)-0.2
Part-2: OAP-0.8

[back to top]

Part 3 (Disease Modification): Change From Baseline in Adjusted Intracortical Myelin Fraction Score as Measured by Inversion Recovery (IR) and Spin Echo Magnetic Resonance Imaging (SE MRI)

"The adjusted ICM fraction score is quantified as: 1. The volume of myelinated brain tissue is measured separately on co-localized IR and proton density (PD) MRI images, by outlining the boundary between gray matter and white matter on each image. 2. ICM is calculated from the difference of IR volume minus PD volume. 3. ICM is then expressed as a fraction of the total intracranial volume (ICM divided by intracranial volume). 4. The ICM fraction is then adjusted for effects of age, gender, and race/ethnicity in the sample of treated participants and healthy controls. A decrease in the adjusted ICM fraction score may be a sign of disease progression." (NCT02431702)
Timeframe: Baseline and Month 9 of Part 3

Interventionratio (Least Squares Mean)
Part 3-PP to PP-0.7
Part 3- OAP to PP (or Delayed-Start PP)-0.2
Part 3-OAP to OAP0.5

[back to top]

Part 3 (Disease Modification): Change From Baseline in Cognition as Measured by the MATRICS Consensus Cognitive Battery (MCCB) Composite Score

The MATRICS Consensus Cognitive Battery is an instrument that contains 10 tests to measure cognitive performance in 7 cognitive domains: speed processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition. The composite score combines the individual scores of the 10 tests and scores them on a normative scale to derive a T-score and composites scores. The range of T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and Day 260

InterventionT-score (Mean)
Part 3- PP to PP-0.7
Part 3- OAP to PP (or Delayed-Start PP)-0.2
Part 3-OAP to OAP0.5

[back to top]

Part 3 (Disease Modification): Personal and Social Performance (PSP) Total Observed Score

The Personal and Social Performance (PSP) scale assesses degree of a participant's dysfunction within 4 domains of behavior: 1) socially useful activities, 2) personal and social relationships, 3) self-care, and 4) disturbing and aggressive behavior. Score ranges from 1 to 100, divided into 10 equal intervals to rate degree of difficulty (1 = absent, 2 = mild, 3 = manifest, 4 = marked, 5 = severe, and 6 = very severe) in each of the 4 domains. Based on 4 domains there will be 1 transformed total score. Participants with score of 71 to 100 have mild degree of difficulty; from 31 to 70, varying degrees of disability; less than or equal to 30, functioning so poorly as to require intensive supervision. (NCT02431702)
Timeframe: Month 9 of Part 3

Interventionunits on a scale (Least Squares Mean)
Part 3-PP to PP67.6
Part 3- OAP to PP (or Delayed-Start PP)66.1
Part 3-OAP to OAP66.6

[back to top]

Part 3 (EDP): Change From Baseline in Adjusted Intracortical Myelin Fraction Score as Measured by Inversion Recovery (IR) and Spin Echo Magnetic Resonance Imaging (MRI)

"The adjusted ICM fraction score is quantified as: 1. The volume of myelinated brain tissue is measured separately on co-localized IR and proton density (PD) MRI images, by outlining the boundary between gray matter and white matter on each image. 2. ICM is calculated from the difference of IR volume minus PD volume. 3. ICM is then expressed as a fraction of the total intracranial volume (ICM divided by intracranial volume). 4. The ICM fraction is then adjusted for effects of age, gender, and race/ethnicity in the sample of treated participants and healthy controls. A decrease in the adjusted ICM fraction score may be a sign of disease progression." (NCT02431702)
Timeframe: Baseline and 18 Months

Interventionratio (Mean)
Part 3-PP to PP-0.001
Part 3-OAP to OAP-0.003

[back to top]

Part 3 (EDP): Change From Baseline in Visual Learning Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess visual learning score of participants. The range of visual learning score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP0.2
Part 3-OAP to OAP-0.2

[back to top]

Part 3 (EDP): Change From Baseline in Clinical Global Impression Severity (CGI-S) Score

"The Clinical Global Impression Severity (CGI-S) rating scale is used to rate the severity of a participant's overall clinical condition on a 7 point scale. The total score ranges from 1 to 7, where 1 is equivalent to Normal, not at all ill and a rating of 7 is equivalent to Among the most extremely ill participants. Higher scores indicate worsening." (NCT02431702)
Timeframe: Baseline, up to 18 Months

Interventionunits on a scale (Mean)
Part 3-PP to PP-0.7
Part 3-OAP to OAP-0.7

[back to top]

Part 3 (EDP): Change From Baseline in Functioning as Measured by the Personal and Social Performance (PSP) Total Score

The Personal and Social Performance (PSP) scale assesses degree of a participant's dysfunction within 4 domains of behavior: 1) socially useful activities, 2) personal and social relationships, 3) self-care, and 4) disturbing and aggressive behavior. Each domain was assessed on a 6-point scale, from 1 (absent) to 6 (very severe) (1 = absent, 2 = mild, 3 = manifest, 4 = marked, 5 = severe, and 6 = very severe). PSP total score was calculated as sum of all the domain scores and ranges from 1 to 100. Participants with score of 71 to 100 have mild degree of difficulty; from 31 to 70, varying degrees of disability; less than or equal to 30, functioning so poorly as to require intensive supervision. Higher score indicate better performance. (NCT02431702)
Timeframe: Baseline and 18 Months

Interventionunits on a scale (Mean)
Part 3-PP to PP7.5
Part 3-OAP to OAP7.0

[back to top]

Part 3 (EDP): Change From Baseline in Medication Satisfaction Questionnaire (MSQ) Score

The Medication Satisfaction Questionnaire (MSQ) is a 7-point, verbally administered, Likert-type scale rated as follows: 1=Extremely Dissatisfied, 2=Very Dissatisfied, 3=Somewhat Dissatisfied, 4=Neither Satisfied Nor Dissatisfied, 5=Somewhat Satisfied, 6=Very Satisfied, 7=Extremely Satisfied. Worst value is 1 (Extremely Dissatisfied) and best value is 7 (Extremely Satisfied). Total score ranges from 1 to 7. Higher score indicate improvement. (NCT02431702)
Timeframe: Baseline, up to 18 Months

Interventionunits on a scale (Mean)
Part 3-PP to PP0.3
Part 3-OAP to OAP0.4

[back to top]

Part 3 (EDP): Change From Baseline in Attention/Vigilance Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess attention/vigilance score of participants. The range of attention/vigilance score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP2.4
Part 3-OAP to OAP0.7

[back to top]

Part 3 (EDP): Change From Baseline in Working Memory Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess working memory of participants. The range of working memory score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP-1.7
Part 3-OAP to OAP0.7

[back to top]

Part 3 (EDP): Time to First Treatment Failure

Treatment failure is defined as the time from participant's randomization to first treatment failure, which was a composite endpoint consisting of any of the following: 1) Psychiatric hospitalization due to worsening symptoms; 2) Any deliberate self-injury, suicidal ideation or behavior, homicidal ideation or violent behavior that is clinically significant and needs immediate intervention as determined by the study physician; 3) New arrest/incarceration; 4) Discontinuation of antipsychotic treatment due to inadequate efficacy as determined by the study physician; 5) Discontinuation of antipsychotic treatment due to safety or tolerability as determined by the study physician; 6) Treatment supplementation with another antipsychotic due to inadequate efficacy as determined by the study physician; 7) Increase in the level of psychiatric services in order to prevent imminent psychiatric hospitalization as determined by the study physician. (NCT02431702)
Timeframe: From Day 1 Up to 18 Months

Interventiondays (Median)
Part 3-PP to PPNA
Part 3-OAP to OAPNA

[back to top]

Part 3 (Extended Disease Progression [EDP]): Change From Baseline in Cognition as Measured by the MATRICS Consensus Cognitive Battery (MCCB) Composite Score

The MATRICS Consensus Cognitive Battery is an instrument that contains 10 tests to measure cognitive performance in 7 cognitive domains: speed processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition. The composite score combines the individual scores of the 10 tests and scores them on a normative scale to derive a T-score and composites scores. The range of T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP1.6
Part 3-OAP to OAP3.2

[back to top]

Part-2 (Disease Progression): Time to First Treatment Failure

Treatment failure is defined as the time from participant's randomization to first treatment failure, which was a composite endpoint consisting of any of the following: 1) Psychiatric hospitalization due to worsening symptoms; 2) Any deliberate self-injury, suicidal ideation or behavior, homicidal ideation or violent behavior that is clinically significant and needs immediate intervention as determined by the study physician; 3) New arrest/incarceration; 4) Discontinuation of antipsychotic treatment due to inadequate efficacy as determined by the study physician; 5) Discontinuation of antipsychotic treatment due to safety or tolerability as determined by the study physician; 6) Treatment supplementation with another antipsychotic due to inadequate efficacy as determined by the study physician; 7) Increase in the level of psychiatric services in order to prevent imminent psychiatric hospitalization as determined by the study physician. (NCT02431702)
Timeframe: From Day 1 up to 9 Months

Interventiondays (Median)
Part-2: Paliperidone Palmitate (PP)NA
Part-2: OAPNA

[back to top]

Part 2 (Disease Progression): Number of Participants With Change From Baseline in Severity of Psychotic Symptoms, as Measured by Clinician-Rated Dimensions of Psychosis Symptom Severity Scale (CRDPSS)

The CRDPSS is an 8-item measure that assesses the severity of mental health symptoms that are important across psychotic disorders, including delusions, hallucinations, disorganized speech, abnormal psychomotor behavior, negative symptoms. Each item on the measure is rated on a 5-point scale (0=none; 1=equivocal; 2=present, but mild; 3=present and moderate; and 4=present and severe). Total Score is taken as summation. A higher score indicates a more severe condition. Worsened or improved is defined as increase or decrease compared to baseline. (NCT02431702)
Timeframe: Baseline, up to 9 Months

InterventionParticipants (Count of Participants)
Hallucinations72513608Hallucinations72513614Delusions72513614Delusions72513608Disorganized Speech72513614Disorganized Speech72513608Abnormal Psychomotor Behavior72513614Abnormal Psychomotor Behavior72513608Negative Symptoms72513608Negative Symptoms72513614Impaired Cognition72513614Impaired Cognition72513608Mania72513608Mania72513614Depression72513608Depression72513614
UnchangedImprovedWorsened
Part-2: OAP19
Part-2: Paliperidone Palmitate (PP)29
Part-2: OAP73
Part-2: Paliperidone Palmitate (PP)14
Part-2: OAP33
Part-2: Paliperidone Palmitate (PP)10
Part-2: OAP20
Part-2: Paliperidone Palmitate (PP)23
Part-2: OAP70
Part-2: OAP35
Part-2: OAP13
Part-2: Paliperidone Palmitate (PP)36
Part-2: OAP85
Part-2: Paliperidone Palmitate (PP)12
Part-2: OAP27
Part-2: Paliperidone Palmitate (PP)9
Part-2: OAP14
Part-2: Paliperidone Palmitate (PP)37
Part-2: OAP86
Part-2: Paliperidone Palmitate (PP)4
Part-2: OAP25
Part-2: Paliperidone Palmitate (PP)16
Part-2: OAP61
Part-2: Paliperidone Palmitate (PP)17
Part-2: OAP39
Part-2: Paliperidone Palmitate (PP)13
Part-2: OAP29
Part-2: Paliperidone Palmitate (PP)22
Part-2: OAP52
Part-2: Paliperidone Palmitate (PP)15
Part-2: OAP44
Part-2: Paliperidone Palmitate (PP)1
Part-2: OAP7
Part-2: Paliperidone Palmitate (PP)47
Part-2: OAP107
Part-2: Paliperidone Palmitate (PP)2
Part-2: OAP11
Part-2: Paliperidone Palmitate (PP)7
Part-2: OAP28
Part-2: Paliperidone Palmitate (PP)33
Part-2: OAP74
Part-2: OAP23

[back to top]

Part 3 (EDP): Change From Baseline in Verbal Learning Score: MCCB Domain

MCCB measures cognitive function across cognitive domains and is comprised of 10 independent tests assessing 7 cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition). A subset of the MCCB cognitive domain was used to assess verbal learning score of participants. The range of verbal learning score T-scores for a normal control population is between 0 to 100 with a mean of 50 and standard deviation of 10. Higher scores indicate better cognitive functioning. (NCT02431702)
Timeframe: Baseline and 18 Months

InterventionT-score (Mean)
Part 3-PP to PP0.3
Part 3-OAP to OAP0.8

[back to top]

Patient Satisfaction Survey (PSS) Total Score at Week 0 and 12

The PSS is a brief scale designed to capture a psychiatric patient's satisfaction with a clinician. The scale covers 6 domains: Trust (3 items), Communication (3 items), Exploration of Ideas/Options (2 items), Body Language (2 items), Active Listening (4 items), and Miscellaneous Items (6 items). Out of the 20 items, the first 19 are scored on a 5-point Likert Scale (1=strongly disagree, 2=disagree, 3=satisfactory, 4=agree, 5=strongly agree). The last question (6f) is a free-response question asking for input on how the clinician might improve. Sum of scores of individual items give a total score (range 9-95). Higher scores indicate greater degree of satisfaction. Due to early study termination collected data was not summarized. Hence, individual data for each participant was reported. (NCT02462473)
Timeframe: Week 0, Week 12

Interventionunits on a scale (Number)
Participant 1 (Week 0)Participant 1 (Week 12)Participant 2 (Week 0)Participant 2 (Week 12)Participant 3 (Week 0)Participant 3 (Week 12)Participant 4 (Week 0)Participant 5 (Week 0)Participant 5 (Week 12)Participant 6 (Week 0)Participant 6 (Week 12)Participant 7 (Week 0)Participant 7 (Week 12)Participant 8 (Week 0)Participant 8 (Week 12)Participant 9 (Week 0)Participant 9 (Week 12)
Cohort 17676525757574866647676767263727176

[back to top]

Adherence to Antipsychotic Medication as Assessed by Brief Adherence Rating Scale (BARS) at Week 0 and 12

The BARS is a 4-item scale that includes 3 questions and an overall visual analog rating scale that assesses participant's knowledge about his/her medication. The key measure of adherence is the visual analog scale and assesses the percentage of doses taken by the participants in the past month (0 percent [%] - 100%). The 3 questions include: number of prescribed doses per day, number of days in the past month when the participant did not take the prescribed doses, and the number of days in the past month when the participant took less than the prescribed dose. Due to early study termination collected data was not summarized. Hence, individual data for each participant was reported. (NCT02462473)
Timeframe: Week 0, Week 12

Interventionpercent adherence (Number)
Participant 1 (Week 0)Participant 1 (Week 12)Participant 2 (Week 0)Participant 2 (Week 12)Participant 3 (Week 0)Participant 3 (Week 12)Participant 4 (Week 0)Participant 5 (Week 0)Participant 5 (Week 12)Participant 6 (Week 0)Participant 6 (Week 12)Participant 7 (Week 0)Participant 7 (Week 12)Participant 8 (Week 0)Participant 8 (Week 12)Participant 9 (Week 0)Participant 9 (Week 12)
Cohort 110010010010010010097939090969095100100100100

[back to top]

Antipsychotic Medication Plasma Levels (AMPL) During the Active Assessment Phase at Week 12

AMPL of the individual participant during the active assessment phase was reported. (NCT02462473)
Timeframe: Week 12

Interventionnanogram per milliliter (Number)
Participant 1- ARIPIPRAZOLEParticipant 1- DEHYDROARIPIPRAZOLEParticipant 2- OLANZAPINEParticipant 2- PALIPERIDONEParticipant 3- 7-OH QUETIAPINEParticipant 3-NORQUETIAPINEParticipant 3-QUETIAPINEParticipant 3-QUETIAPINE SULFOXIDEParticipant 5-7-OH QUETIAPINEParticipant 5-NORQUETIAPINEParticipant 5-QUETIAPINEParticipant 5-QUETIAPINE SULFOXIDEParticipant 6-ARIPIPRAZOLEParticipant 6-DEHYDROARIPIPRAZOLEParticipant 7-PALIPERIDONEParticipant 7-RISPERIDONEParticipant 8-ARIPIPRAZOLEParticipant 8-DEHYDROARIPIPRAZOLEParticipant 9- 7-OH QUETIAPINEParticipant 9- NORQUETIAPINEParticipant 9- PALIPERIDONEParticipant 9- QUETIAPINEParticipant 9- QUETIAPINE SULFOXIDEParticipant 9- RISPERIDONE
Cohort 1596.00139.0027.3045.1043.10660.00280.00660.007.72153.0050.30321.00464.00112.0031.0026.20168.0033.000.2002.000.1002.002.000.100

[back to top]

Clinical Global Impression-Severity (CGI-S) Score at Week 0 and 12

Clinical Global Impression-Severity (CGI-S) rating scale used to rate the severity of a participant's overall clinical condition on a 7-point scale ranging from 1 (not ill) to 7 (extremely severe). Due to early study termination collected data was not summarized. Hence, individual data for each participant was reported. (NCT02462473)
Timeframe: Week 0, Week 12

Interventionunits on a scale (Number)
Participant 1 (Week 0)Participant 1 (Week 12)Participant 2 (Week 0)Participant 2 (Week 12)Participant 3 (Week 0)Participant 3 (Week 12)Participant 4 (Week 0)Participant 5 (Week 0)Participant 5 (Week 12)Participant 6 (Week 0)Participant 6 (Week 12)Participant 7 (Week 0)Participant 7 (Week 12)Participant 8 (Week 0)Participant 8 (Week 12)Participant 9 (Week 0)Participant 9 (Week 12)
Cohort 143434453333344333

[back to top]

Clinician's Rating Scale of Adherence (CRS) Score at Week 0 and 12

The CRS is an ordinal scale filled by the clinician. The scores range from 1 to 7 that were used to quantify the clinician's assessment of treatment adherence by the patient. Higher scores indicate greater adherence. Due to early study termination collected data was not summarized. Hence, individual data for each participant was reported. (NCT02462473)
Timeframe: Week 0, Week 12

Interventionunits on a scale (Number)
Participant 1 (Week 0)Participant 1 (Week 12)Participant 2 (Week 0)Participant 2 (Week 12)Participant 3 (Week 0)Participant 3 (Week 12)Participant 4 (Week 0)Participant 5 (Week 0)Participant 5 (Week 12)Participant 6 (Week 0)Participant 6 (Week 12)Participant 7 (Week 0)Participant 7 (Week 12)Participant 8 (Week 0)Participant 8 (Week 12)Participant 9 (Week 0)Participant 9 (Week 12)
Cohort 177777777777777777

[back to top]

Number of Participants With Medication Treatment Modifications (MTM)

Information on MTMs derived from data collected in the clinical assessment of the schizophrenia patient (CASP) questionnaire. The CASP captured changes in medications, changes in psychosocial treatments, visit frequency, and the need for any acute interventions. The CASP comprised of 3 sections covering several parameters. The CASP captured changes in treatment options which was used to compute MTM, as well as factors in clinical decision making and the influence of antipsychotic medication plasma levels (AMPL), when they were available, on clinical decision making. (NCT02462473)
Timeframe: Up to Week 12

InterventionParticipants (Number)
Cohort 14

[back to top]

Number of Participants With Factors Considered in Clinical Decision as Assessed by Clinical Assessment of the Schizophrenia Patient (CASP)

The CASP and data on concomitant medications and psychosocial treatments were used to evaluate the impact of AMPL results on other aspects of clinical decision making. (NCT02462473)
Timeframe: Up to Week 12

Interventionparticipants (Number)
Side Effects Of MedicationAttitude Toward TreatmentReport of Increased SymptomsReport of Decrease in SymptomsPatient Still SymptomaticPatient Ideation
Cohort 1324311

[back to top]

Dimensions of Psychosis Symptom Severity Scale (DPSS) Total Score at Week 0 and 12

The DPSS is a clinician-rated scale used to rate 8 domains commonly seen in patients with psychotic disorders. Each domain was rated on a 5-point scale (0 to 4) with anchored description of endpoints. Total score was computed by summing the scores of individual items (range of 0-32). Higher scores represent more severe condition. Due to early study termination collected data was not summarized. Hence, individual data for each participant was reported. (NCT02462473)
Timeframe: Week 0, Week 12

Interventionunits on a scale (Number)
Participant 1 (Week 0)Participant 1 (Week 12)Participant 2 (Week 0)Participant 2 (Week 12)Participant 3 (Week 0)Participant 3 (Week 12)Participant 4 (Week 0)Participant 5 (Week 0)Participant 5 (Week 12)Participant 6 (Week 0)Participant 6 (Week 12)Participant 7 (Week 0)Participant 7 (Week 12)Participant 8 (Week 0)Participant 8 (Week 12)Participant 9 (Week 0)Participant 9 (Week 12)
Cohort 11248288149474584446

[back to top]

Proportion of Participants Receiving HEC With Complete Response in Overall Phase

"Overall phase was defined as 0 to 120 hours following initiation of chemotherapy.~Complete response was defined as no vomiting with no rescue therapy." (NCT02484911)
Timeframe: 0 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen20
Control Regimen15

[back to top]

Proportion of Participants Receiving HEC With Complete Response in the Acute Phase

Acute phase was defined as 0 to 24 hours following initiation of chemotherapy. Complete response was defined as no vomiting with no rescue therapy. (NCT02484911)
Timeframe: 0 to 24 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen20
Control Regimen17

[back to top]

Proportion of Participants Receiving HEC With Complete Response in the Delayed Phase

"Delayed phase was defined as 24 to 120 hours following initiation of chemotherapy.~Complete response was defined as no vomiting with no rescue therapy." (NCT02484911)
Timeframe: 24 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen20
Aprepitant Regimen15

[back to top]

Proportion of Participants Receiving HEC With No Vomiting in the Acute Phase

"Overall Phase was defined as 0 to 120 hours following initiation of chemotherapy.~No vomiting was defined as no vomiting or retching or dry heaves (included participants who received rescue )" (NCT02484911)
Timeframe: 0 to 24 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen18
Control Regimen15

[back to top]

Proportion of Participants Receiving HEC With No Vomiting in the Delayed Phase

"Overall Phase was defined as 24 to 120 hours following initiation of chemotherapy.~No vomiting was defined as no vomiting or retching or dry heaves (included participants who received rescue therapy)." (NCT02484911)
Timeframe: 24 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen17
Control Regimen7

[back to top]

Proportion of Participants Receiving HEC With No Vomiting in the Overall Phase

"Overall phase was defined as 0 to 120 hours following initiation of chemotherapy.~No vomiting was defined as no vomiting or retching or dry heaves (included participants who received rescue therapy)." (NCT02484911)
Timeframe: 0 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen17
Control Regimen6

[back to top]

Proportion of Participants Receiving MEC With Complete Response in Overall Phase

"Overall phase was defined as 0 to 120 hours following initiation of chemotherapy.~Complete response was defined as no vomiting with no rescue therapy." (NCT02484911)
Timeframe: 0 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen36
Control Regimen40

[back to top]

Proportion of Participants Receiving MEC With Complete Response in the Acute Phase

Acute phase was defined as 0 to 24 hours following initiation of chemotherapy. Complete response was defined as no vomiting with no rescue therapy. (NCT02484911)
Timeframe: 0 to 24 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen36
Control Regimen41

[back to top]

Proportion of Participants Receiving MEC With Complete Response in the Delayed Phase

"Delayed phase was defined as 24 to 120 hours following initiation of chemotherapy.~Complete response was defined as no vomiting with no rescue therapy." (NCT02484911)
Timeframe: 24 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen36
Control Regimen40

[back to top]

Proportion of Participants Receiving MEC With No Vomiting in the Acute Phase

"Overall Phase was defined as 0 to 24 hours following initiation of chemotherapy.~No vomiting was defined as no vomiting or retching or dry heaves (included participants who received rescue therapy)." (NCT02484911)
Timeframe: 0 to 24 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen35
Control Regimen40

[back to top]

Proportion of Participants Receiving MEC With No Vomiting in the Delayed Phase

"Overall Phase was defined as 24 to 120 hours following initiation of chemotherapy.~No vomiting was defined as no vomiting or retching or dry heaves (included participants who received rescue therapy)." (NCT02484911)
Timeframe: 24 to 120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen30
Control Regimen31

[back to top]

Proportion of Participants Receiving MEC With No Vomiting in the Overall Phase

"Overall Phase was defined as 0 to 120 hours following initiation of chemotherapy.~No vomiting was defined as no vomiting or retching or dry heaves (included participants who received rescue therapy)." (NCT02484911)
Timeframe: 0-120 hours

InterventionParticipants (Count of Participants)
Olanzapine Regimen30
Control Regimen30

[back to top]

Change in The Columbia Suicide Severity Rating Scale Score

Change in The Columbia Suicide Severity Rating Scale score, a self-report scale measuring suicidality. Only the total score, not subscale of suicidal ideation intensity, will be measured. Total scores can range from 0-10, with higher scores indicating increased suicidality. (NCT02536846)
Timeframe: baseline and 2, 5, 10, 15 days during medication period

Interventionscore on a scale (Mean)
BaselineAfter 2 days medicationAfter 5 days medicationAfter 10 days medicationAfter 15 days medication
Second Generation Antipsychotic Drug00000

[back to top]

Change in Surface Area of the Frontal, Parietal and Temporal Regions

Change in the cortical surface area (millimeters squared) of the frontal, parietal and temporal lobes as defined by Freesurfer's Desikan-Killiany Brain Atlas. Data was acquired using structural magnetic resonance imaging (MRI) at 3T. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionmm^2 (Mean)
Frontal lobeParietal lobe
Olanzapine-801.19-581.56

[back to top]

Change in LUNSERS (Liverpool University Neuroleptic Side Effect Rating Scale) Score

"Change in LUNSERS (Liverpool University Neuroleptic Side Effect Rating Scale) score, a self-report measure of antipsychotic side effects. The scale has 51 questions, 41 of which are about side-effects and 10 red herrings for validation purposes. The total neuroleptic side effect score is derived from the sum of the 41 side-effect questions, with a potential range of 0-164. Higher scores indicate more severe neuroleptic side effects." (NCT02536846)
Timeframe: baseline and 2, 5, 10 and 15 days (or final assessment) during medication period

Interventionscore on a scale (Mean)
Baseline2 days5 days10 daysEndpoint
Olanzapine0.204.502.112.223.90

[back to top]

Change in Hip Circumference

Change in the hip circumference measurement, taken as an average of 3 measures by tape measure (NCT02536846)
Timeframe: baseline and 2, 5, 10 and 15 days (or final assessment) during medication period

Interventioncm (Mean)
Baseline2 days5 days10 daysEndpoint
Olanzapine0-0.43-1.10-1.62-1.24

[back to top]

Change in Fractional Anisotropy (FA) Measured by Diffusion Tensor Imaging (DTI)

Change in fractional anisotropy (FA), a scalar measure of diffusivity, of water in the brain assessed by DTI at 3T. FA values range from 0 (isotropic, meaning diffusion is equally restricted in 3D space) to 1 (anisotrophic, meaning that diffusion is completely restricted to a single direction). (NCT02536846)
Timeframe: baseline and after 15 days medication period

InterventionUnits on a scale (Mean)
Core FAGenu of corpus callosumCingulumInferior fronto-occipital fasciculusAnterior thalamic radiation
Olanzapine0.0007-0.003-0.008-0.0020.002

[back to top]

Change in fMRI Resting State Functional Connectivity

Change in resting state functional connectivity to the medial prefrontal cortex and superior parietal lobules following olanzapine administration period. Whole-brain, seed-to-voxel analyses were conducted utilizing anatomically-defined seed regions and age-corrected within-subjects f-tests were run to determine the presence and size (in voxels) of clusters where connectivity changed significantly following olanzapine administration. Results are reported in units of voxels for each cluster meeting a threshold of voxel-level uncorrected p<.001 and cluster-level p-FDR<.05. A result of zero indicates that no clusters were identified within subjects as changed in connectivity relative to the seed regions. (NCT02536846)
Timeframe: baseline and after 15 days medication period

InterventionVoxels (Number)
medial prefrontal cortexsuperior parietal lobule
Olanzapine00

[back to top]

Change in Body Weight

Change in participant body weight in kg, as measured using a standing scale. (NCT02536846)
Timeframe: baseline and 2, 5, 10 and 15 days (or final assessment) during medication period

Interventionkg (Mean)
Baseline2 days5 days10 daysEndpoint
Olanzapine0-0.290.120.210.73

[back to top]

Change in Young Mania Rating Scale (YMRS) Score

Change in Young Mania Rating Scale (YMRS) score, an interview-based, 11-item scale that measures the severity of core features of clinical mania. 7 items are scored on a 0-4 point scale, while the remaining 4 are scored on a 0-8 point scale, for a total possible range of 0-64. Higher scores indicate more severe manic symptoms. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-0.875

[back to top]

Change in Total Caloric Intake

Change in total caloric intake as assessed by the ASA24 Dietary Recall and Food Frequency Questionnaire - Revised. The ASA24 is a self-administered 24-hour dietary recall assessment. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionkcal (Mean)
Olanzapine151.94

[back to top]

Change in the Symptoms Checklist - 90 - Revised Global Severity Score

Changes in the Symptoms Checklist - 90 - Revised scale, which measures 9 domains of psychological dysfunction, summing to create an overall psychological distress (Global Severity Score). The scores of each of the 9 domains - somatization, obsessive-compulsive, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideation and psychoticism - combine for a total of 90 items, each measured on a 5-point scale. The sums of all 90 item scores, ranging 0-360, creates the Global Severity score. Higher scores indicate greater psychopathology. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-2.33

[back to top]

Change in the Prodromal Questionnaire, Brief Version Total Score

Change in the Prodromal Questionnaire, Brief Version score, a 21 item self-report questionnaire designed to help identify those at ultra-high risk for developing psychotic symptoms. The total score is derived as the sum of all 21 items, with a possible range of 0-21. Higher scores indicate greater psychopathology. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine0

[back to top]

Change in Serum Insulin Levels

Change in insulin fasting serum levels (NCT02536846)
Timeframe: baseline and after 15 days medication period

InterventionuIU/mL (Mean)
Olanzapine-0.94

[back to top]

Change in Prolactin Levels

Change prolactin serum levels (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionng/mL (Mean)
Olanzapine11.77

[back to top]

Change in Pittsburgh Sleep Quality Index Score

Change in Pittsburgh Sleep Quality Index score, a measurement of sleep quality. The index measures 7 sleep components on a 0-3 scale; each of the 7 raw scores is summed to get a global score. The global score ranges from 0-21, with higher scores indicating poor sleep quality. Scores >5 are typically considered poor sleep quality. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-0.63

[back to top]

Change in Montgomery-Asberg Depression Rating Scale (MADRS) Score

Change in Montgomery-Asberg Depression Rating Scale (MADRS) score, a 0-60 point scale rating depressive symptoms. Higher scores indicate more severe clinical symptoms. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-0.88

[back to top]

Change in MATRICS Cognitive Consensus Battery (MCCB) Total Composite Score

Change in the MATRICS Cognitive Consensus Battery (MCCB), that includes 10 tasks that measure processing speed (Brief Assessment of Cognition in Schizophrenia - Symbol Coding, Animal Fluency, Trails A), attention (Continuous Performance Test), working memory (WMS-III Spatial Span, Letter-Number Span), verbal learning (Hopkins Verbal Learning Test - Revised), visual learning (Brief Visuospatial Memory Test - Revised), problem solving (Neuropsychological Assessment Battery Mazes) and social cognition (Mayer-Salovey-Caruso Emotional Intelligence Test). Scores from each subtest are normed and their T-scores are summed to yield a MCCB composite score, then the total composite T-score is standardized to normative data among a healthy population. The composite T-score has a mean of 50 and a standard deviation of 10. Higher total composite scores indicate better cognitive outcomes. (NCT02536846)
Timeframe: baseline and after 15 days medication period

InterventionScore on a scale (Mean)
Olanzapine3.63

[back to top]

Change in Brain Phosphocreatine (PCr)

Change in Phosphocreatine (PCr) metabolite concentration as measured by in vivo 31P magnetic resonance spectroscopy (NCT02536846)
Timeframe: Baseline and after 15 days medication period

Interventionratio (Mean)
Olanzapine0.01

[back to top]

Change in Fasting Total Cholesterol Level

Change in fasting total cholesterol level (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionmg/dL (Mean)
Olanzapine-1.75

[back to top]

Change in GABA Concentration

Change in GABA concentration measured by proton magnetic resonance spectroscopy. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionmmol (Mean)
Olanzapine0.11

[back to top]

Change in Glutamate Metabolite Concentration

Change in glutamate metabolite concentration measured by proton magnetic resonance spectroscopy. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionmillimoles (Mean)
Olanzapine0.13

[back to top]

Change in The Wisconsin Schizotypy Scales - Short Form Scores

"Change in Wisconsin Schizotypy Scales (WSS) Short Form score, a self-report questionnaire assessing schizotypy in clinical and non-clinical samples. The measure has four scales, each with 15 True/False questions. There are 13 red-herring questions, that, if answered True invalidate the test. Each false response is scored 0, and each true response is scored 1. Scores for each scale range from 0 - 15, with higher scores indicating greater schizotypy. The WSS positive schizotypy score consists of the summed score of the perceptual aberration and magical ideation scales and scores range from 0-30, with higher scores indicating greater positive schizotypy. The WSS negative schizotypy score sums scores from the physical anhedonia and social anhedonia scales and ranges from 0-30, with higher scores indicating greater negative schizotypy." (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Change in positive schizotypy subscalesChange in negative schizotypy subscales
Olanzapine0.060.09

[back to top]

Change in Hemoglobin A1c Level

Change in fasting, Hemoglobin A1c level (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionmmol/mol (Mean)
Olanzapine-0.01

[back to top]

Change in Beck Anxiety Inventory (BAI) Score

Change in Beck Anxiety Inventory (BAI) score, a self-report measure of anxiety symptoms. Scores range from 0-63, with higher scores indicating more severe anxiety. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-0.63

[back to top]

Change in Waist Circumference

Change in waist circumference measurements, taken as an average of 3 measures by tape measure. (NCT02536846)
Timeframe: baseline and 2, 5, 10 and 15 days (or final assessment) during medication period

Interventioncm (Mean)
BaselineAfter 2 days medicationAfter 5 days medicationAfter 10 days medicationEndpoint
Olanzapine0-0.470.22-0.23-0.15

[back to top]

Change in Volumes of the Frontal, Parietal and Temporal Lobe Regions

Change in the gray matter volumes (cubic millimeters) of the frontal, parietal and temporal lobes as defined by Freesurfer's Desikan-Killiany Brain Atlas. Data was acquired using structural magnetic resonance imaging (MRI) at 3T. (NCT02536846)
Timeframe: baseline and after 15 day medication period

Interventioncubic mm (Mean)
Frontal LobeParietal Lobe
Olanzapine-2500.44-600

[back to top]

Change in the World Health Organization Quality of Life Questionnaire Score

Change in the World Health Organization Quality of Life questionnaire score, a 26-item assessment of overall quality of life. The questionnaire encompasses 4 domains: physical health, psychological health, social relationships, and environment. There are two additional questions, which assess the participant's perceptions of their own quality of life and physical health. Higher scores indicate better quality of life. Scores are summed within each domain. Total score is obtained by transforming for a total range of 0-100 within each domain. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Change in physical health scoreChange in psychological health scoreChange in social relationships scoreChange in environment score
Olanzapine2.25-4.380.75-7.875

[back to top]

Change in the Early Psychosis Social Scale Survey Score

Change in the Early Psychosis Social Scale score item of missed absences from school or work. Scores range from 1-5, with higher scores indicating more absences from school or work. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-0.13

[back to top]

Change in the State-Trait Anxiety Inventory for Adults Scores

Change in the State-Trait Anxiety Inventory for Adults, which measures both state and trait anxiety using 2 subscales for a total of 40 items. Each subscale has a range of 20-80, with higher scores indicating greater state or trait anxiety, respectively. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Change in State-anxiety scaleChange in Trait-anxiety scale
Olanzapine-0.25-0.75

[back to top]

Change in Beck Depression Inventory (BDI) Score

Change in Beck Depression Inventory (BDI) score, a self-report questionnaire measuring depressive symptoms on a scale of 0-63. Scores ranging 0-9 generally indicate minimal depressive symptoms, while scores 10-18 indicate mild, 19-29 indicates moderate, and 30-63 indicates severe depressive symptoms, respectively. (NCT02536846)
Timeframe: baseline and after 15 days medication period

Interventionscore on a scale (Mean)
Olanzapine-0.63

[back to top]

Change in Blood Glucose Levels

Change in fasting serum glucose levels. (NCT02536846)
Timeframe: baseline and after 15 days during medication period

Interventionmg/dL (Mean)
Olanzapine0.75

[back to top]

Change in Brain Creatine Kinase (CK) Forward Reaction Rate

Change in forward reaction rate constant (kf) of the creatine kinase (CK) as measured by in vivo 31P magnetic resonance spectroscopy magnetization transfer (NCT02536846)
Timeframe: Baseline and after 15 days medication period

Interventions-1 (Mean)
Olanzapine-0.04

[back to top]

Change in Brain Nicotinamide Adenine Dinucleotide Metabolites NAD+/NADH

Change in brain nicotinamide adenine dinucleotide NAD+/NADH metabolite ratio as measured by in vivo 31P magnetic resonance spectroscopy (NCT02536846)
Timeframe: Baseline and after 15 days medication period

Interventionratio (Mean)
Olanzapine-0.79

[back to top]

Change in Brain Parenchymal pH

Change in brain parenchymal pH as measured by in vivo 31P magnetic resonance spectroscopy (NCT02536846)
Timeframe: baseline and after 15 days medication period

InterventionpH (Mean)
Olanzapine0.00

[back to top]

Change From Baseline in Positive and Negative Syndrome Scale (PANSS) Total Score at Week 4

This scale consists of symptom constructs (7 positive, 7 negative, 16 general psychopathology), each to be rated on a 7-point Likert-type scale of severity with 1 being absent to 7 being extreme. Minimum scores (best outcome) equals 30 (total scale); maximum scores (worst outcome) equals 210 (total scale). Change is calculated between the baseline visit and Week 4. (NCT02634346)
Timeframe: 4 weeks

Interventionunits on a scale (Least Squares Mean)
ALKS 3831-23.9
Olanzapine-22.8
Placebo-17.5

[back to top]

Incidence of Adverse Events

(NCT02634346)
Timeframe: Approximately 4 weeks

InterventionParticipants (Count of Participants)
ALKS 383173
Olanzapine73
Placebo60

[back to top]

Change From Baseline in Clinical Global Impressions-Severity (CGIS) Score at Week 4

"The CGI-S is a 7-point scale that requires the clinician to assess how mentally ill the patient is in a specific point in time. Results indicate participants evaluated at one of the following categories: 1: normal, not at all ill; 2: borderline mentally ill; 3: mildly ill; 4: moderately ill; 5: markedly ill; 6: severely ill; and 7: among the most extremely ill patients. Results indicate a change in CGI-S score from baseline to Week 4 based on the observed data. Change is calculated between the baseline visit and Week 4." (NCT02634346)
Timeframe: 4 weeks

Interventionunits on a scale (Least Squares Mean)
ALKS 3831-1.21
Olanzapine-1.27
Placebo-0.84

[back to top]

Percent of Patients Achieving Complete Protection in Overall Assessment Phase

(CP = no emesis, no breakthrough antiemetic use, no significant nausea). To be reported as overall phases [chemotherapy days plus 5 days after] (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo6
Triplet Therapy Plus Olanzapine13

[back to top]

Overall Percentage of Patients Who Had a Complete Response

Overall percentage of patients who had a complete response (CR) defined as no emesis and minimal nausea (< 25 mm on a 100 mm visual analog scale [VAS]) during the overall assessment period (starting day 1 of chemotherapy and continuing for 5 days after discontinuation of chemotherapy) for the first cycle of chemotherapy. (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo13
Triplet Therapy Plus Olanzapine28

[back to top]

Percent of Patients With Complete Response in Acute Phase

Complete response (no emesis and no more than minimal nausea, defined as < 25 mm on a 100 mm visual analog scale [VAS]) in acute phase (days of chemotherapy) (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo31
Triplet Therapy Plus Olanzapine39

[back to top]

Percent of Patients With Complete Response in Delayed Phase

Complete response (no emesis and no more than minimal nausea, defined as < 25 mm on a 100 mm visual analog scale [VAS]) in delayed phase (5 days after chemotherapy) (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo15
Triplet Therapy Plus Olanzapine31

[back to top]

Percent of Patients With no Nausea in Overall Assessment Period

No nausea (all VAS <5 mm) in overall assessment period (days of chemotherapy plus five days after) (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo6
Triplet Therapy Plus Olanzapine18

[back to top]

Percent of Patients With no Significant Nausea in Overall Assessment Period

Reported for overall phases [chemotherapy days plus 5 days after] where all VAS < 25 mm (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo14
Triplet Therapy Plus Olanzapine30

[back to top]

Percent of Participants With no Significant Nausea in Acute Phase

Reported as acute [chemotherapy days]. All assessment with all VAS < 25 mm on days of chemotherapy (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo33
Triplet Therapy Plus Olanzapine39

[back to top]

Percent of Participants With no Significant Nausea in Delayed Phase

Reported for delayed [5 days after chemotherapy administration] All assessment with all VAS < 25 mm (NCT02635984)
Timeframe: Until study completion; estimated 1.5 years

InterventionParticipants (Count of Participants)
Triplet Therapy Plus Placebo16
Triplet Therapy Plus Olanzapine34

[back to top]

Clinical Opiate Withdrawal Scale Score at 1 Hour Post Medication

"Opiate withdrawal scale score for all patients who received medication by one hour~The Clinical Opiate Withdrawal Scale (COWS) is an 11-item scale, ranging from 0 to 48 (5- 12 = mild; 13-24 = moderate; 25-36 = moderately severe; more than 36 = severe withdrawal).~This tool can be used to reproducibly rate common signs and symptoms of opiate withdrawal and monitor these symptoms over time. The summed score for the complete scale can be used to help clinicians determine the stage or severity of opiate withdrawal and assess the level of physical dependence on opioids. The 11 items on the scale include scores rate the following symptoms: pulse rate, GI upset, sweating, tremor, restlessness, yawning, pupil size, anxiety, bone or joint aches, gooseflesh skin, runny nose." (NCT02643355)
Timeframe: At 1 hour

Interventionunits on a scale (Mean)
Olanzapine5.3
Clonidine6.7

[back to top]

Clinical Opiate Withdrawal Scale Score at 2 Hours Post Medication

"Opiate withdrawal scale score for all patients who received medication by one hour~The Clinical Opiate Withdrawal Scale (COWS) is an 11-item scale, ranging from 0 to 48 (5- 12 = mild; 13-24 = moderate; 25-36 = moderately severe; more than 36 = severe withdrawal).~This tool can be used to reproducibly rate common signs and symptoms of opiate withdrawal and monitor these symptoms over time. The summed score for the complete scale can be used to help clinicians determine the stage or severity of opiate withdrawal and assess the level of physical dependence on opioids. The 11 items on the scale include scores rate the following symptoms: pulse rate, GI upset, sweating, tremor, restlessness, yawning, pupil size, anxiety, bone or joint aches, gooseflesh skin, runny nose." (NCT02643355)
Timeframe: 2 hours

Interventionunits on a scale (Mean)
Olanzapine4.8
Clonidine3.7

[back to top]

Clinical Opiate Withdrawal Scale Score at the Time of Disposition

"Opiate withdrawal scale score for all patients who received medication by one hour~The Clinical Opiate Withdrawal Scale (COWS) is an 11-item scale, ranging from 0 to 48 (5- 12 = mild; 13-24 = moderate; 25-36 = moderately severe; more than 36 = severe withdrawal).~This tool can be used to reproducibly rate common signs and symptoms of opiate withdrawal and monitor these symptoms over time. The summed score for the complete scale can be used to help clinicians determine the stage or severity of opiate withdrawal and assess the level of physical dependence on opioids. The 11 items on the scale include scores rate the following symptoms: pulse rate, GI upset, sweating, tremor, restlessness, yawning, pupil size, anxiety, bone or joint aches, gooseflesh skin, runny nose." (NCT02643355)
Timeframe: Time of Disposition (on average within 6 hours)

Interventionunits on a scale (Mean)
Olanzapine4.3
Clonidine3.6

[back to top]

Number of Participants That Received Rescue Medication for Withdrawal Symptoms Within 1 Hour

Rescue Medication (additional medications given for symptoms) within 1 hour of medication administration (NCT02643355)
Timeframe: 1 Hour

InterventionParticipants (Count of Participants)
Olanzapine9
Clonidine19

[back to top]

Number of Participants Experiencing of Adverse Events (AEs)

(NCT02694328)
Timeframe: 24 weeks

InterventionParticipants (Count of Participants)
Olanzapine227
ALKS 3831203

[back to top]

Percent Change From Baseline in Body Weight at Week 24

(NCT02694328)
Timeframe: Baseline and Week 24

InterventionPercent change in body weight (Least Squares Mean)
Olanzapine6.59
ALKS 38314.21

[back to top]

Percentage of Participants With >/= 7% Weight Gain at Week 24

(NCT02694328)
Timeframe: Baseline and Week 24

InterventionPercentage of participants (Number)
Olanzapine42.7
ALKS 383127.5

[back to top]

Percentage of Participants With >/= 10% Weight Gain at Week 24

(NCT02694328)
Timeframe: Baseline and Week 24

InterventionPercentage of participants (Number)
Olanzapine29.8
ALKS 383117.8

[back to top]

Change From Randomization to Week 10 in Global Clinical Impression - Severity of Illness (CGI-S) Score

CGI-S provides the clinician's impression of the patient's current state of mental illness. The clinician uses his or her clinical experience of this patient population to rate the severity of the patient's current mental illness on a 7-point scale ranging from 1 (Normal - not at all ill) to 7 (among the most extremely ill patients). Higher scores indicate worsening. (NCT02717195)
Timeframe: From Randomization to Week 10

Interventionunits on a scale (Mean)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg-0.59
DBT Period, Lu AF35700 20 mg-0.54
DBT Period, Continued Treatment From PC Period-0.57

[back to top]

Change From Randomization to Week 10 in Positive and Negative Syndrome Scale (PANSS) Total Score

PANSS total score administered by the investigator. It included 3 sub-scales with a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A higher score corresponded to a worse severity of schizophrenia. (NCT02717195)
Timeframe: From Randomization to Week 10

Interventionunits on a scale (Mean)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg-10.01
DBT Period, Lu AF35700 20 mg-8.22
DBT Period, Continued Treatment From PC Period-9.90

[back to top]

Change From Randomization to Week 10 in PSP Total Personal and Social Performance (PSP) Total Score

PSP is a clinician-rated scale designed and validated to measure a patient's current level of social functioning. It consists of 4 items: socially useful activities, personal and social relationships, self-care, and disturbing and aggressive behaviours. Each items were assessed on a 6-point scale, from 1 (absent) to 6 (very severe). PSP score was calculated as sum of all the items on the scale and ranged from 4 to 100. A higher score represents more severe functional impairment. (NCT02717195)
Timeframe: From Randomization to Week 10

Interventionunits on a scale (Mean)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg4.90
DBT Period, Lu AF35700 20 mg3.23
DBT Period, Continued Treatment From PC Period3.94

[back to top]

Response at Week 10, Defined as ≥20% Reduction in PANSS Total Score, PANSS (Positive and Negative Syndrome Scale) Total Score ≤70, CGI-S (Clinical Global Impression Scale - Severity of Illness) Score <4

"PANSS total score administered by the investigator. It included 3 sub-scales with a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A higher score corresponded to a worse severity of schizophrenia. A reduction in score indicates improvement.~The Clinical Global Impression scale - severity of illness (CGI-S) is administered by the investigator. The patient is rated on a 7-point scale ranging from 1 (Normal - not at all ill) to 7 (among the most extremely ill patients). A reduction in scale indicates improvement." (NCT02717195)
Timeframe: From Randomization to Week 10

InterventionParticipants (Count of Participants)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg21
DBT Period, Lu AF35700 20 mg18
DBT Period, Continued Treatment From PC Period12

[back to top]

Response at Week 10, Defined as ≥20% Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Randomization

PANSS total score administered by the investigator. It included 3 sub-scales with a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A higher score corresponded to a worse severity of schizophrenia. A reduction in score indicates improvement. (NCT02717195)
Timeframe: From Randomization to Week 10

InterventionParticipants (Count of Participants)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg82
DBT Period, Lu AF35700 20 mg59
DBT Period, Continued Treatment From PC Period77

[back to top]

Response at Week 10, Defined as ≥30% Reduction in PANSS Total Score From Randomization

Positive and Negative Syndrome Scale (PANSS) total score administered by the investigator. It included 3 sub-scales with a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A higher score corresponded to a worse severity of schizophrenia. A reduction in score indicates improvement. (NCT02717195)
Timeframe: From Randomization to Week 10

InterventionParticipants (Count of Participants)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg42
DBT Period, Lu AF35700 20 mg30
DBT Period, Continued Treatment From PC Period45

[back to top]

Response at Week 10, Defined as ≥40% Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Randomization

PANSS total score administered by the investigator. It included 3 sub-scales with a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A higher score corresponded to a worse severity of schizophrenia. A reduction in score indicates improvement. (NCT02717195)
Timeframe: From Randomization to Week 10

InterventionParticipants (Count of Participants)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg23
DBT Period, Lu AF35700 20 mg15
DBT Period, Continued Treatment From PC Period16

[back to top]

Response at Week 10, Defined as ≥50% Reduction in Positive and Negative Syndrome Scale (PANSS) Total Score From Randomization

PANSS total score administered by the investigator. It included 3 sub-scales with a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A higher score corresponded to a worse severity of schizophrenia. A reduction in score indicates improvement. (NCT02717195)
Timeframe: From Randomization to Week 10

InterventionParticipants (Count of Participants)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg10
DBT Period, Lu AF35700 20 mg4
DBT Period, Continued Treatment From PC Period6

[back to top]

Number of Participants With Severe PONV

Number of participants with severe PONV in first 24 hours after post-op.defined as numerical rating scale score greater than 3. (11-point numerical rating scale from 0-10, higher score indicating worse nausea) (NCT02755116)
Timeframe: first 24 hours post-op

InterventionParticipants (Count of Participants)
Olanzapine12
Placebo26

[back to top]

Number of Participants With Severe Nausea

Number of participants with severe postdischarge nausea, defined as numerical rating scale score greater than 3. (11-point numerical rating scale from 0-10, higher score indicating worse nausea) (NCT02755116)
Timeframe: in 24 hours after discharge

InterventionParticipants (Count of Participants)
Olanzapine4
Placebo14

[back to top]

Number of Participants With Postdischarge Vomiting

Number of participants with post discharge vomiting (NCT02755116)
Timeframe: in 24 hours after discharge

InterventionParticipants (Count of Participants)
Olanzapine2
Placebo8

[back to top]

Number of Participants With Nausea and/or Vomiting

Number of participants with post-discharge nausea and/or vomiting (NCT02755116)
Timeframe: in 24 hours after discharge

InterventionParticipants (Count of Participants)
Olanzapine10
Placebo26

[back to top]

Number of Participants With PONV

Number of participants with postoperative nausea and/or vomiting (PONV) in first 24 hours (NCT02755116)
Timeframe: first 24 hours post-op

InterventionParticipants (Count of Participants)
Olanzapine22
Placebo35

[back to top]

Number of Participants With Relapse

The definition of relapse is as follows 1.50% or greater increase in total DIEPSS score, 2. an increase in the total PANSS score of 25% or more from baseline, 3. deliberate self-injury, 4. emergence of clinically significant suicidal ideation, 5. violent behavior resulting in clinically significant injury to another person or property damage. (NCT03019887)
Timeframe: One year after the baseline cognitive function test or three months after the end of dose reduction, whichever came first.

InterventionParticipants (Count of Participants)
Dose Reduction130

[back to top]

Comparison of Duration of ED Length of Stay

The total time the patient spent in the ED after initially being seen by the physician (NCT03066622)
Timeframe: Length of Emergency Department stay (Time Frame: up to 12 hours)

InterventionMinutes (Mean)
Standard of Care179.57
Olanzapine180.28

[back to top]

Number of Participants That Receive Peripheral Intravenous Catheterization

Determining if patients randomized to rapidly dissolving Olanzapine eventually require IV access, defined as A successful cannulation (blood return or ability to infuse intravenous fluid without infiltration) on initial percutaneous needle puncture (NCT03066622)
Timeframe: Length of Emergency Department stay (Time Frame: up to 12 hours)

InterventionParticipants (Count of Participants)
Standard of Care55
Olanzapine28

[back to top]

Change in Pain Scores Based on Patient Questionnaire

Change in patient reported pain score from baseline using the Numeric Pain Rating Scale (PNRS) Minimum score = 0 Maximum score = 10 Lower score indicates lower pain level, with zero indicating no pain and 10 indicating the worst pain imaginable. (NCT03066622)
Timeframe: baseline, 30, 60, and 90 minutes post drug administration

,
Interventionunits on a scale of 1-10 (Mean)
Pain at 30 minutesPain at 60 minutesPain at 90 minutes
Olanzapine-1.79-2.65-3.88
Standard of Care-2.95-4.49-4.68

[back to top]

Mean Nausea Scores

"Daily nausea scores (the primary objective) on day 1 to 7 of treatment for each patient from the Olanzapine and Placebo group will be measured using the Visual Analogue Scale rankings from 0-10 where 0 is no nausea and 10 is the maximum nausea experienced by a patient. A Visual Analogue Scale is a psychometric response scale which can be used in questionnaires. It is a measurement instrument for subjective characteristics or attitudes that can't be directly measured.~Patients will be asked to record the average nausea score for each day in a diary and a study nurse will call the patient at the same time each day to remind the patient to record the nausea score and to inquire about any toxicities. The difference in the nausea scores for the patients in each group (Olanzapine and Placebo) will be compared." (NCT03137121)
Timeframe: Nausea score from the Visual Analogue Scale will be recorded each day daily for 7 days. An average value calculated will be reported for the 7 day period.

Interventionunits on a scale (Mean)
Olanzapine1
Placebo9

[back to top]

Number of Emetic Episodes

The number of emetic episodes (a secondary outcome) by each patient in each group, Olanzapine & Placebo, on each day of treatment will be recorded by each patient on each day of treatment in a diary. A study nurse will contact each patient at the same time of each day of the study to ask the patient to record the number of emetic episodes and report any toxicities.The number of emetic episodes for the patients in each Group for each day of the treatment will be compared. (NCT03137121)
Timeframe: Number of emetic episodes for each patient on each day of the seven day treatment.

,
Interventionepisodes (Number)
day 1day 2day 3day 4day 5day 6day 7
Olanzapine3000000
Placebo3333333

[back to top]

"Number of Treatment-related Adverse Events as Assessed by CTCAE v4.0."

Adverse events will be measured by patient-reported outcomes questionnaires and the Common Terminology Criteria for Adverse Events (CTCAE v4.0). A study nurse will contact each patient each day of the seven days of treatment to inquire about any toxicities, specifically sedation and appetite. Sedation and appetite will be reported by the patient in each Group on a Visual Analogue Scale of 0 to 10 with 0 being no sedation or no appetite to 10 indicating maximum sedation or maximum appetite. (NCT03137121)
Timeframe: Daily assessment for 7 days for each patient in Olanzapine & Placebo Groups.

InterventionEvents (Number)
Olanzapine3
Placebo21

[back to top]

Percentage of Subjects With ≥7% Weight Gain at Week 12

(NCT03187769)
Timeframe: Baseline and 12 weeks

InterventionPercentage of participants (Number)
ALKS 383133.1
Olanzapine44.8

[back to top]

Percent Change From Baseline in Body Weight at Week 12

The efficacy analyses were performed using the Final Analysis Set which is defined as all randomized subjects who received one dose of study drug and had at least 1 primary efficacy assessment after administration of study drug (NCT03187769)
Timeframe: Baseline and 12 weeks

InterventionPercentage of change in body weight (Least Squares Mean)
ALKS 38314.91
Olanzapine6.77

[back to top]

Percentage of Subjects With ≥10% Weight Gain at Week 12

Percentage of weight gain is analyzed based on the subject's assessment status (≥10% vs <10%) at Week 12 using a logistic regression model including treatment group, diagnosis (schizophrenia/schizophreniform disorder vs bipolar I disorder), region (US vs non-US), and baseline BMI (<25 vs ≥25) as factors and baseline weight as covariate. (NCT03187769)
Timeframe: Baseline and 12 weeks

InterventionPercentage of participants (Number)
ALKS 383121.9
Olanzapine30.4

[back to top]

Number of Participants Experiencing of Adverse Events (AEs)

(NCT03187769)
Timeframe: Up to 16 weeks

InterventionParticipants (Count of Participants)
ALKS 3831134
Olanzapine136

[back to top]

Change From Baseline in Waist Circumference at Week 12

(NCT03187769)
Timeframe: Baseline and Week 12

InterventionCentimeters (Least Squares Mean)
ALKS 38312.99
Olanzapine3.90

[back to top]

Change From Baseline in Clinical Global Impression-Severity (CGI-S) Score Within the ALKS 3831 Group at Week 12

"Clinical Global Impression-Severity (CGI-S) Score is a 3-item, clinician-rated scale used to assess global illness severity, overall improvement from the start of treatment, and therapeutic response. It is a 7-point scale that requires the clinician to assess how mentally ill the patient is at a specific point in time. Based on the scale, patients are categorized as follows: 1: normal, not at all ill; 2: borderline mentally ill; 3: mildly ill; 4: moderately ill; 5: markedly ill; 6: severely ill; and 7: among the most extremely ill patients." (NCT03187769)
Timeframe: Baseline and Week 12

Interventionunits on a scale (Least Squares Mean)
ALKS 3831-.82

[back to top]

Response

Response is defined as a ≥20% reduction in PANSS total score from Randomization (NCT03230864)
Timeframe: at Week 8

InterventionParticipants (Count of Participants)
DBT, Lu AF35700 10 mg6
DBT, Continued Treatment13

[back to top]

Change From Randomization to Week 8 in Global Clinical Impression - Severity of Illness (CGI-S) Score

CGI-S provides the clinician's impression of the patient's current state of mental illness. The clinician uses his or her clinical experience of this patient population to rate the severity of the patient's current mental illness on a 7-point scale ranging from 1 (normal - not at all ill) to 7 (among the most extremely ill patients). Higher scores indicate worsening (NCT03230864)
Timeframe: From Randomization to Week 8

Interventionunits on a scale (Mean)
DBT, Lu AF35700 10 mg-0.18
DBT, Continued Treatment-0.37

[back to top]

Change From Randomization to Week 8 in PANSS Marder Negative Factor Score

The PANSS Negative Factor score is a subset of the PANSS assessing negative symptoms of schizophrenia. The factor consist of the seven items: blunted affect, emotional withdrawal, poor rapport, passive social withdrawal, lack of spontaneity, motor retardation, and active social avoidance which are each rated on a 7-point scale, from 1=absent to 7=extreme. The PANSS Negative Factor score (7 items) range from 7 to 49 with a higher score indicating greater severity of symptoms. (NCT03230864)
Timeframe: From Randomization to Week 8

Interventionunits on a scale (Mean)
DBT, Lu AF35700 10 mg-1.51
DBT, Continued Treatment-1.74

[back to top]

Change From Randomization to Week 8 in Positive and Negative Syndrome Scale (PANSS) Total Score

PANSS total score administered by the investigator. It included a total of 30 items that evaluated the Positive Symptoms subscale, the Negative Symptoms subscale, the General Psychopathology subscale. Each item is rated from 1 (symptom not present) to 7 (symptom extremely severe). PANSS total score was calculated as sum of all the items on the scale and ranged from 30 to 210. A negative score indicates an improvement compared to Randomization. (NCT03230864)
Timeframe: From Randomization to Week 8

Interventionunits on a scale (Mean)
Double-blind Treatment (DBT) Period, Lu AF35700 10 mg-4.71
DBT, Continued Treatment From PC Period-10.19

[back to top]

Change From Randomization to Week 8 in 16-item Negative Symptom Assessment (NSA-16 Total) Score

The NSA-16 is a clinician-rated scale designed to assess the presence, severity, and range of negative symptoms associated with schizophrenia. The NSA-16 consists of 16 items arranged in 5 subdomains: communication dysfunction (items 1 to 4), emotional/affective dysfunction (items 5 to 7), dysfunction in sociality (items 8 to 10), motivational/hedonic dysfunction (items 11 to 14), and reduced psychomotor activity (items 15 and 16), and a Global Negative Symptom Rating. NSA-16 items are rated on a 6-point scale from 1 (behaviour is normal) to 6 (behaviour severely reduced), and a score of 9 if the item is not-rateable. The Global Negative Symptom Rating is rated from 1 (no evidence of symptoms) to 7 (extremely severe symptoms). The 16 items are summed to yield a total score ranging from 16 to 96 and the global rating ranges from 1 to 7. (NCT03230864)
Timeframe: From Randomization to Week 8

Interventionunits on a scale (Mean)
DBT, Lu AF35700 10 mg-2.99
DBT, Continued Treatment-3.14

[back to top]

Number of Participants With Adverse Event (AE)

Treatment emergent adverse event (TEAE) is defined as an AE observed after starting administration of the study drug and 28 days after the last dose of study drug. A study drug-related TEAE is defined as any TEAE with at least possible relationship to study treatment as assessed by the investigator or with missing assessment of the causal relationship. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. Safety was assessed by AEs, which included abnormalities identified during a medical test (e.g. laboratory tests, vital signs, electrocardiogram, metabolic parameters etc.) if the abnormality induced clinical signs or symptoms, needed active intervention, interruption or discontinuation of study medication or was clinically significant. (NCT03557931)
Timeframe: Baseline up to end of study (EoS) (week 14)

,,
Interventionparticipants (Number)
TEAEDrug-Related TEAEsSerious TEAEsDrug-Related Serious TEAE
ASP4345 150 mg281110
ASP4345 50 mg281330
Placebo451110

[back to top]

Number of Participants With Clinically Significant Differences in Abnormal Involuntary Movement Scale (AIMS) Values

AIMS is a 14-item scale. Items 1 to 8 are rated on a 5-point scale ranging from 0 (no dyskinetic movements) to 4 (severe dyskinetic movements). Item 9 assesses the participant's incapacitation due to abnormal movements, and item 10 assesses the participant's awareness of the abnormal movements and associated distress. Items 9 and 10 are rated on 5-point scales ranging from 0 (none or no awareness) to 4 (severe or aware, severe distress). Items 11 to 14 are yes/no questions regarding the global judgement and dental status of the participant. The total score is the sum of the scores for the 14 items and the possible total score ranges from 0 to 44. A higher total score is indicative of more severe dyskinetic movements. (NCT03557931)
Timeframe: Baseline, week 6 and week 12

,,
Interventionparticipants (Number)
BaselineWeek 6Week 12
ASP4345 150 mg000
ASP4345 50 mg000
Placebo000

[back to top]

Number of Participants With Clinically Significant Differences in Barnes Akathisia Rating Scale (BARS) Values

BARS is used to rate observable, restless movements of drug induced akathisia and subjective awareness of restlessness and any distress associated with the akathisia. BARS consists of the following 4 items: objective assessment of akathisia symptoms, subjective assessment of the participants's awareness of inner restlessness, distress restlessness, and global clinical assessment of akathisia. First three items are rated on a 4-point scale ranging from 0 (no abnormal movements or absence of inner restlessness or no distress) to 3 (severe akathisia or awareness of intense compulsion to move most of the time or severe distress). The last item, the global clinical assessment of akathisia, is rated on a 6-point scale, ranging from 0 (no evidence of akathisia) to 5 (severe akathisia). Total BARS score ranges from 0 to 14 with a higher score representing worse results. (NCT03557931)
Timeframe: Baseline, week 6 and week 12

,,
Interventionparticipants (Number)
BaselineWeek 6Week 12
ASP4345 150 mg000
ASP4345 50 mg000
Placebo000

[back to top]

Number of Participants With Clinically Significant Differences in Simpson Angus Scale (SAS) Values

SAS scale consists of 10 items including 7 items that address bradykinesia-rigidity and additional single items for tremor, glabellar tap, and salivation. Each item represents a specific physical condition and is rated on a 5-point category rating scale ranging from 0 (complete absence of the condition) to 4 (the condition is present to an extreme degree).The total score is obtained by adding the scores for the 10 individual items making the maximum possible score is 40. Higher scores are indicative of more severe Parkinsonian-type symptoms. (NCT03557931)
Timeframe: Baseline, week 6 and week 12

,,
Interventionparticipants (Number)
BaselineWeek 6Week 12
ASP4345 150 mg000
ASP4345 50 mg000
Placebo000

[back to top]

Change From Baseline to Week 12/End of Treatment (EoT) in Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery (MCCB) Neurocognitive Composite Score

The MCCB is a cognitive battery to assess 7 domains recommended by the MATRICS initiative (i.e., working memory, verbal learning, speed of processing, attention/vigilance, visual learning, social cognition, reasoning and problem solving). The MCCB neurocognitive composite score is a standardized mean of the six domain scores (excluding social cognition). Raw scores are converted to age and sex adjusted t-scores which are standardized to normative data, and have a mean of 50 and standard deviation of 10 in the general healthy population. A higher score indicates less impairment. (NCT03557931)
Timeframe: Baseline and week 12/end of treatment (EoT)

InterventionT-score (Least Squares Mean)
Placebo1.15
ASP4345 50 mg1.34
ASP4345 150 mg0.87

[back to top]

Change From Baseline to Week 12/EoT in University of California San Diego Performance-based Skills Assessment-2 Extended Range (UPSA-2-ER) Total Score

The UPSA-2-ER assesses the functional abilities of the participant with schizophrenia in 6 domains: household management, communication, financial skills, transportation, comprehension/planning and medication management. The UPSA-2-ER total score has a range from 0 to 105. A higher score indicates less impairment. (NCT03557931)
Timeframe: Baseline and week 12/EoT

Interventionunits on a scale (Least Squares Mean)
Placebo3.11
ASP4345 50 mg3.86
ASP4345 150 mg2.56

[back to top]

Number of Participants With Clinically Significant Differences in Columbia-Suicide Severity Rating Scale (C-SSRS) Values

The C-SSRS is a questionnaire used for suicide risk assessment. Affirmative or negative responses are provided to items 1 to 5 for suicidal ideation (1. Wish to be dead, 2. Non-specific active suicidal thoughts, 3. Active suicidal ideation with any methods [not plan] without intent to act, 4. Active suicidal ideation with some intent to act, without specific plan, 5. Active suicidal ideation with specific plan and intent) and items 6 to 10 for suicide behavior (6. Preparatory acts or behavior, 7. Aborted attempt, 8. Interrupted attempt, 9. Actual attempt, 10. Completed suicide). (NCT03557931)
Timeframe: Baseline up to EoS (week 14)

Interventionparticipants (Number)
Placebo0
ASP4345 50 mg0
ASP4345 150 mg0

[back to top]

Concentration at Trough Level (Ctrough) for ASP4345

Ctrough concentration for ASP4345 was reported. (NCT03557931)
Timeframe: Predose: day 7, day 14, day 21, day 42 and day 84/EoT

,
Interventionnanogram per milliliter (ng/mL) (Mean)
Day 7 Pre-doseDay 14 Pre-doseDay 21 Pre-doseDay 42 Pre-doseDay 84 Pre-dose
ASP4345 150 mg483.84428.88384.48471.78433.56
ASP4345 50 mg175.041182.903172.040207.145204.914

[back to top]

Percentage Of Days With Good Patch Coverage

The DMS includes a drug-device combination of a CoE product, a wearable sensor patch, and application software (smartphone) to record activity and rest and mark events through the act of ingestion. The CoE product consists of an approved antipsychotic medication enclosed with an Ingestible Sensor Pill (miniature ingestible event marker in tablet [MIT]). The sensor patch detects and records each MIT ingestion, as well as other physiologic and behavioral data. Good patch coverage for a specific day was defined as having either at least 80% patch data available (80% of the day the patch was worn and data was collected as noted via the accelerometer channel) or the MIT was detected within the 24-hour period, for each day while the participant was in the trial. The percentage of days was calculated as the number of days with good patch coverage divided by the total number of trial days for each participant. Descriptive statistics were performed for this outcome measure. (NCT03568500)
Timeframe: Up to 8 weeks

Interventionpercentage of days (Mean)
Schizophrenia64.34
Schizoaffective Disorder62.99
First Episode Psychosis62.51
Total63.37

[back to top]

Participant Adherence

The DMS includes a drug-device combination of a CoE product, a wearable sensor patch, and application software (smartphone) to record activity and rest and mark events through the act of ingestion. The CoE product consists of an approved antipsychotic medication enclosed with an Ingestible Sensor Pill (MIT). The sensor patch detects and records each MIT ingestion, as well as other physiologic and behavioral data. Participant adherence was measured as the detected MITs over the expected MITs ingested during the trial days with good patch coverage. The more the participant successfully engaged in a number of processes across the 8-week trial, the greater the measured adherence. Descriptive statistics were performed for this outcome measure. (NCT03568500)
Timeframe: Up to 8 weeks

Interventionpercentage of MITs (Mean)
Schizophrenia88.94
Schizoaffective Disorder72.29
First Episode Psychosis91.04
Total86.57

[back to top]

Potential Toxicities as Ascribed to Olanzapine as Measured by the Nausea and Vomiting Daily Diary/Questionnaire

Potential toxicities includes nausea, undesired sedation, and undesired appetite, measured by three individual items ( nausea, undesired sedation, undesired appetite) of the Nausea and Vomiting Daily Dairy/Questionnaire(scale 0-10, 0 is no symptoms, 10 is worst symptoms). Incidences of toxicities will be summarized by type and by treatment arm. Incidences of toxicities will be compared between arms using a Chi-squared test or the Fisher's exact test as appropriate. In addition, undesired sedation and appetite increase as collected in the Nausea and Vomiting Daily Diary/Questionnaire will be analyzed by repeated measures analyses including descriptive statistics, graphical approaches, and growth curve models to account for the factor of day and time trend. (NCT03578081)
Timeframe: Up to 120 hours

,
InterventionParticipants (Count of Participants)
Overall No Appetite IncreaseOverall Any Appetite IncreaseAcute No Appetite IncreaseAcute Any Appetite IncreaseDelayed No Appetite IncreaseDelayed Any Appetite Increase
Arm I (Fosaprepitant Dimeglumine, Olanzapine)14018623591147179
Arm II (Placebo, Olanzapine)13618423684143177

[back to top]

Average Nausea Scores (0-10) Repeatedly Measured by the Nausea and Vomiting Daily Diary/Questionnaire

The specific measure will be based on the by the single nausea item (scale 0-10, 0 is no symptoms, 10 is worst symptoms) of the Nausea and Vomiting Daily Diary/Questionnaire. Nausea scores (0-10) repeatedly measured by the Nausea and Vomiting Daily Diary/Questionnaire will be analyzed using the repeated measures analyses and growth curve models as described above for undesired sedation and increase in appetite. (NCT03578081)
Timeframe: Up to 1 year

Interventionscore on a scale (Mean)
Arm I (Fosaprepitant Dimeglumine, Olanzapine)0.8211364
Arm II (Placebo, Olanzapine)0.9177778

[back to top]

No Nausea Rate Defined as a Response of 0 in the Nausea Item of Nausea and Vomiting Daily Diary/Questionnaire in the Overall (0-120 Hours), Acute (0-24 Hours), and Delayed (24-120 Hours) Periods

The specific measure will be based on the proportion of patients with a value of 0, as measured by the single nausea item (scale 0-10, 0 is no symptoms, 10 is worst symptoms) of the Questionnaire. A modified intent-to-treat principle will be applied for statistical analysis of efficacy in evaluable patients. The proportions of patients with no nausea during the overall, the acute, and the delayed period will be summarized by treatment arm. They will be tested in a sequential manner, using a Simes gatekeeping procedure to maintain the overall significance level at the specified by the Lan-DeMets family of alpha spending function. The difference in no nausea proportions between arms will be estimated along with a one-sided 95% confidence interval. The tests and the confidence intervals will be constructed using normal approximation of the binomial distribution adjusted for the non-inferiority margin. (NCT03578081)
Timeframe: Up to 120 hours

,
InterventionParticipants (Count of Participants)
Overall No NauseaOverall Any NauseaAcute No NauseaAcute Any NauseaDelayed No NauseaDelayed Any Nausea
Arm I (Fosaprepitant Dimeglumine, Olanzapine)123203202124140186
Arm II (Placebo, Olanzapine)97223201119114206

[back to top]

Total Frequency of Rescue Medication as Measured by the Nausea and Vomiting Daily Diary/Questionnaire

The specific measure will be based on the single item : number of extra nausea/vomiting pills taken (None, One , Twice, More than twice) of the Nausea and Vomiting Daily Diary/Questionnaire. (NCT03578081)
Timeframe: Over 5 Days per each of the 4 cycles

,
Interventionepisodes (Number)
ZeroOneTwoMore than two
Arm I (Fosaprepitant Dimeglumine, Olanzapine)361435017056
Arm II (Placebo, Olanzapine)354140516274

[back to top]

Complete Response (CR) (no Emetic Episodes and no Use of Rescue Medication) During the Acute, Delayed and the Overall Periods as Measured by the Nausea and Vomiting Daily Diary/Questionnaire

"The specific measure will be based on the proportion of patients who answered None to both questions concerning Vomiting episode(None, Once, Twice, More than twice) and number of extra nausea/vomiting pills taken (None, One, Two, More than two) in the Nausea and Vomiting Daily Diary/Questionnaire. The CR rate for the overall, the acute, and the delayed period will be summarized by treatment arm and will be compared using a Chi-squared test. The difference in CR rates between arms will be estimated along with a 95% confidence interval." (NCT03578081)
Timeframe: Up to 120 hours

,
InterventionParticipants (Count of Participants)
Complete Response - >> OverallComplete Response - >> AcuteComplete Response ->> Delayed
Arm I (Fosaprepitant Dimeglumine, Olanzapine)179256193
Arm II (Placebo, Olanzapine)151247166

[back to top]

Frequency of Nausea in the Acute Phase

"Starting with the first dose of highly or moderately emetogenic conditioning chemotherapy and continuing for one day after the last dose of highly or moderately emetogenic conditioning chemotherapy.~Nausea was assessed using subjects' responses to the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE) nausea questions. Scale: Never, Rarely, Occasionally, Frequently, Almost constantly.~To meet this endpoint the score reported for the Pro-CTCAE question for nausea frequency cannot exceed rarely in the first 24 hours following receipt of chemotherapy." (NCT04535141)
Timeframe: End of day 1 following last chemotherapy administration (Up to day 2)

,
InterventionParticipants (Count of Participants)
Met endpointDid not meet endpoint
Olanzapine441
Usual Care433

[back to top]

Total Number of Rescue Medications Needed -Delayed

"The total number of rescue medications needed for breakthrough chemotherapy-induced nausea and vomiting were calculated, starting from the second day after the completion of highly or moderately emetogenic conditioning chemotherapy and continuing through the fifth day after the completion of highly or moderately emetogenic chemotherapy.~The rescue medication is defined as documented administration of an anti-emetic agent other than those that are scheduled for CINV prophylaxis." (NCT04535141)
Timeframe: Day 1 to 5 days after end of the chemotherapy ( Days 2-12).

Interventionnumber of rescue medication (Mean)
Usual Care0.47
Olanzapine1.17

[back to top]

Number of Subjects Achieved Nausea Endpoint in the Delayed Phase.

"Nausea was assessed using subjects' responses to the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE) nausea questions, starting the second day after the completion of highly or moderately emetogenic conditioning chemotherapy and continuing through the fifth day after the completion of highly or moderately emetogenic chemotherapy.~Scale: Never, Rarely, Occasionally, Frequently, Almost constantly.~The number of subjects who experienced never or rarely nausea were considered as met the endpoint while those who experienced occasionally, frequently or almost constantly were considered as not met the endpoint." (NCT04535141)
Timeframe: Day 1 to 5 days after end of the chemotherapy (Days 2-12).

,
InterventionParticipants (Count of Participants)
Met endpointDid not meet endpoint
Olanzapine2718
Usual Care1927

[back to top]

Number of Subjects Achieved Emesis Endpoint in Acute Phase.

: The number of subjects who did not experience emesis, starting from the first dose of highly or moderately emetogenic conditioning chemotherapy and continuing for one day after the last dose of highly or moderately emetogenic conditioning chemotherapy. Met endpoint = 0 emesis. (NCT04535141)
Timeframe: End of day 1 following last chemotherapy administration. (Up to day 2)

,
InterventionParticipants (Count of Participants)
Met endpointDid not meet endpoint
Olanzapine450
Usual Care451

[back to top]

Total Number of Rescue Medications Needed Acute

"The total number of rescue medications needed acute was calculated, starting from the first dose of highly or moderately emetogenic conditioning chemotherapy and continuing for one day after the last dose of highly or moderately emetogenic conditioning chemotherapy.~The rescue medication is defined as documented administration of an anti-emetic agent other than those that are scheduled for chemotherapy-induced nausea and vomiting (CINV) prophylaxis." (NCT04535141)
Timeframe: End of day 1 following last chemotherapy administration. (Up to day 2)

Interventionnumber of rescue medication (Mean)
Usual Care0.08
Olanzapin0.10

[back to top]

Frequency of Somnolence

The frequency of somnolence was determined as the number of patients who experienced somnolence based on Common Terminology Criteria for Adverse Events version 5 (CTCAE v5). The number of subjects has somnolence during the study period was counted. (NCT04535141)
Timeframe: Day 2-12

,
InterventionParticipants (Count of Participants)
subjects have somnolencesubjects do not have somnolence
Olanzapine142
Usual Care046

[back to top]

Number of Subjects Achieving Minimal Nausea

"To determine the number of subjects achieving minimal nausea was defined as the frequency of participants responded to the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO-CTCAE) nausea question In the last 24 hours, how often did you have nausea? as rarely or less Starting with the first dose of chemotherapy and continuing for one day after the last dose of highly or moderately emetogenic conditioning chemotherapy.~PRO-CTCAE of nausea scale includes categories: Never, Rarely, Occasionally, Frequently, Almost constantly To meet this endpoint the score reported for the Pro-CTCAE question for nausea frequency cannot exceed rarely and the score reported for the Pro-CTCAE question for nausea severity cannot exceed mild" (NCT04535141)
Timeframe: Day 2-12

,
InterventionParticipants (Count of Participants)
YesNo
Olanzapine2520
Usual Care1531

[back to top]

Safety Endpoint: Qtc Prolongation

Prolongation of corrected QTc interval graded as defined in Common Terminology Criteria for Adverse Events (CTCAE) v5.0. Corrected QTc was calculated using Fredericia's Formula. Corrected QT interval (QTc) = QT interval / (60/Heart rate)^0.33. (NCT04535141)
Timeframe: Day 1 to 5 days after end of the chemotherapy (Days 2- 12).

,,,,,
InterventionParticipants (Count of Participants)
Grade 1Grade 2Grade 3Grade 4Grade 5None
Baseline Olanzapine4000041
Baseline Usual Care3000043
Olanzapine Post-chemo Day 13000042
Olanzapine- End of Study3010041
Usual Care End of Study3010042
Usual Care Post-chemo Day 12000044

[back to top]

Severity of Nausea in Delayed Phase

"The severity of nausea in the delayed phase was defined as the response of the subject to the PRO- CTCAE nausea question.~Starting the second day after the completion of highly or moderately emetogenic conditioning chemotherapy and continuing through the fifth day after the completion of highly or moderately emetogenic chemotherapy (PRO-CTCAE) Scale: Never, Rarely, Occasionally, Frequently, Almost constantly~o meet the endpoint, the subject could not have answered a score as higher than mild in the period of time starting 24 hours after the last dose of chemotherapy and continuing until the 5th day following receipt of chemotherapy ." (NCT04535141)
Timeframe: Day 2-12

,
InterventionParticipants (Count of Participants)
Met endpointDid not meet endpoint
Olanzapine3124
Usual Care2323

[back to top]

Number of Emesis Episodes in Delayed Phase

The number of emesis episodes in acute phase was defined as the number of subjects with no emesis, 1 emesis, and 2 or more emesis. (NCT04535141)
Timeframe: Day 1 to 5 days after end of the chemotherapy ( Days 2-12).

,
InterventionParticipants (Count of Participants)
No emesis episodes1 emesis episode2 or more emesis episodes
Olanzapine3663
Usual Care3295

[back to top]