Page last updated: 2024-11-06

imiquimod

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Description

Imiquimod is an immune response modifier. It is a synthetic imidazoquinoline derivative that activates Toll-like receptor 7 (TLR7) on immune cells, triggering the production of cytokines such as interferon-alpha (IFN-α). Imiquimod is used topically to treat certain skin conditions, such as actinic keratosis, superficial basal cell carcinoma, and genital warts. It is also being studied for its potential to treat other diseases, such as cancer and viral infections. Imiquimod is synthesized through a multi-step chemical process involving a series of reactions to form the imidazoquinoline core structure. Its effects on the immune system are primarily mediated through its activation of TLR7, which leads to the induction of various immune responses. It is important because it offers a novel therapeutic approach to treating various skin conditions, including those that are difficult to treat with conventional therapies. Imiquimod is studied because of its unique mechanism of action and its potential to treat a wide range of diseases.'

Imiquimod: A topically-applied aminoquinoline immune modulator that induces interferon production. It is used in the treatment of external genital and perianal warts, superficial CARCINOMA, BASAL CELL; and ACTINIC KERATOSIS. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

imiquimod : An imidazoquinoline fused [4,5-c] carrying isobutyl and amino substituents at N-1 and C-4 respectively. A prescription medication, it acts as an immune response modifier and is used to treat genital warts, superficial basal cell carcinoma, and actinic keratosis. [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 CID57469
CHEMBL ID1282
CHEBI ID36704
SCHEMBL ID26136
MeSH IDM0158430

Synonyms (138)

Synonym
BIDD:GT0859
AC-529
R837 ,
9050-31-1
dz-2636
mtd-39
zyclara
tmx-101
beselna
zartra
vyloma
aldara
cellulose, hydrogen 1,2-benzenedicarboxylate, 2-hydroxypropyl methyl ether
smr000048307
MLS000083577
imiquimod, >=98% (hplc), solid
4-amino-1-isobutyl-1h-imidazo(4,5-c)quinoline
imiquimod (jan/usp/inn)
CHEBI:36704 ,
zyclara (tn)
1-isobutyl-1h-imidazo[4,5-c]quinolin-4-amine
1-(2-methylpropyl)-1h-imidazo[4,5-c]quinolin-4-amine
imiquimodum
r 837
D02500
aldara (tn)
s-26308
99011-02-6
imiquimod
1h-imidazo[4,5-c]quinolin-4-amine, 1-(2-methylpropyl)-
r-837
1-isobutylimidazo[4,5-c]quinolin-4-amine
imiquimod acetate
DB00724
1-(2-methylpropyl)-1h-imidazole[4,5-c]quinoline-4-amine
NCGC00070736-02
c14h16n4
s 26308
1h-imidazo(4,5-c)quinolin-4-amine, 1-(2-methylpropyl)-
nsc-369100
1h-imidazo[4, 1-(2-methylpropyl)-
nsc369100
1-isobutyl-1h-imidazo(4,5-c)quinolin-4-amine
HMS2090M14
bdbm50240849
I0747
4-amino-1-isobutyl-1h-imidazo[4,5-c]quinoline
nsc741062
CHEMBL1282 ,
nsc-759651
s26308 ,
1-(2-methylpropyl)imidazo[4,5-c]quinolin-4-amine
A845945
1-(2-methylpropyl)-4-imidazo[4,5-c]quinolinamine
nsc 759651
unii-p1qw714r7m
nsc 741062
nsc 369100
tmx 101
hsdb 8129
p1qw714r7m ,
imiquimod [usan:inn:ban]
BBL010772
pharmakon1600-01502351
nsc759651
cas-99011-02-6
dtxsid7041047 ,
tox21_110985
dtxcid5021047
BRD-K26657438-001-13-7
IMIQUIMOD - ALDARA
STK583860
HMS2232G07
AKOS005507352
FT-0602727
NCGC00070736-04
imiquimod [mart.]
imiquimod [vandf]
imiquimod [usp monograph]
imiquimod [who-dd]
imiquimod [usp-rs]
imiquimod [orange book]
imiquimod [ema epar]
imiquimod [usan]
imiquimod [jan]
imiquimod [inn]
imiquimod [mi]
S1211
HMS3373B13
gtpl5003
CCG-208015
CS-2058
HY-B0180
1-(2-methylpropyl)-1himidazo[4,5-c]quinolin-4-amine
DOUYETYNHWVLEO-UHFFFAOYSA-N
1-isobutyl-1h-imidazo[4,5-c]quinoline-4-amine
1-isobutyl-1h-imidazo[4,5-c]quinolin-4-ylamine
1-(2-methylpropyl)-1h-imidazo[4,5-c]-quinolin-4-amine
1-isobutyl-1h-imidazo [4,5-c]quinolin-4-amine
SCHEMBL26136
NCGC00070736-03
tox21_110985_1
KS-5218
AB00399298-06
AB00399298-05
AB00399298-07
SY017571
mfcd00866946
HB3109
AB00399298_09
AB00399298_08
6t0 ,
SR-01000611320-3
SR-01000611320-2
sr-01000611320
imiquimod, united states pharmacopeia (usp) reference standard
HMS3715N19
BCP05151
Q423417
imiquimod - cas 99011-02-6
imiquimod,(s)
BRD-K26657438-001-01-2
HMS3747A13
imiquimod 100 microg/ml in acetonitrile
YH44175
(hydroxypropyl)methyl cellulose phthalate
EN300-6477856
BI164576
imiquimod- bio-x
nsc-811538
nsc811538
4-amino-1-(2-methylpropyl)-1h-imidazo(4,5-c)quinoline
1-(2-methylpropyl)-1h-imidazo(4,5-c)quinolin-4-amine
d06bb10
imiquimod (mart.)
imiquimod (usp monograph)
imiquimod (usp-rs)
Z2588038940

Research Excerpts

Overview

Imiquimod is a safe, effective, and well accepted alternative to surgery for women with vHSIL and can be considered as first-line treatment. ImiquIMod topical cream is a promising therapy but experience with it is limited to small series or case reports.

ExcerptReferenceRelevance
"Imiquimod appears to be a versatile option for treating LM in suitable candidates."( Series of Fourteen Cases of Topical Imiquimod 5% in Lentigo Maligna: Treatment Modalities and Clues for Detecting Recurrences.
Álvarez-Chinchilla, P; Bañuls-Roca, J; Hispán-Ocete, P; Poveda-Montoyo, I; Schneller-Pavelescu, L, 2022
)
1.72
"Imiquimod is a safe, effective, and well accepted alternative to surgery for women with vHSIL and can be considered as first-line treatment."( Topical imiquimod versus surgery for vulvar intraepithelial neoplasia: a multicentre, randomised, phase 3, non-inferiority trial.
Boandl, A; Bogner, G; Ciresa-König, A; Holter, M; Jan, Z; Joura, EA; Kalteis, MS; Regauer, S; Reich, O; Schauer, C; Tamussino, K; Trutnovsky, G; Widschwendter, A, 2022
)
2.6
"Imiquimod appears to be a versatile option for treating LM in suitable candidates."( Series of Fourteen Cases of Topical Imiquimod 5% in Lentigo Maligna: Treatment Modalities and Clues for Detecting Recurrences.
Álvarez-Chinchilla, P; Bañuls-Roca, J; Hispán-Ocete, P; Poveda-Montoyo, I; Schneller-Pavelescu, L, 2022
)
1.72
"Imiquimod topical cream is a promising therapy; however, experience with it is limited to small series or case reports."( Vulvar Paget's disease: outcomes of 51 patients treated with imiquimod cream.
Benedetto, C; Bertero, L; Borella, F; Gallio, N; Micheletti, L; Pérez-López, FR; Preti, M; Vieira-Baptista, P, 2022
)
1.68
"Imiquimod is a topical immunomodulator that acts as an inducer of interferon (IFN)-a expression through Toll-like receptor (TLR)7 signaling with indications for the treatment of non-hyperkeratotic actinic keratosis of the face or scalp, superficial basal cell carcinoma (BCC), and external genital and perianal warts. "( Imiquimod-induced hypertrophic lupus erythematosus-like reaction.
Hassan, S; Patel, V; Safadi, MG; Viglione, M; Zahner, SL, 2022
)
3.61
"Imiquimod is a topically applied immunomodulator which is often used in the management of several premalignant and malignant cutaneous disorders."( Imiquimod as Local Immunotherapy in the Management of Premalignant Cutaneous Conditions and Skin Cancer.
Alonso-Martinez de Salinas, L; Azcarraga-Llobet, C; Bea-Ardebol, S; Berna-Rico, E; de Nicolas-Ruanes, B; Garcia-Mouronte, E, 2023
)
3.07
"Imiquimod (IMQ) is an immunostimulating agent used in the treatment of basal cell carcinoma and actinic keratosis. "( Nanoformulations for dermal delivery of imiquimod: The race of "soft" against "hard".
Balouch, M; Chvíla, S; Petrová, E; Štěpánek, F; Zbytovská, J, 2023
)
2.62
"Imiquimod is a topical agent that acts as a Toll-like receptor 7/8 agonist, stimulating the innate and adaptive immune system to exert antitumor and antiviral effects."( Recent advances in treating female genital human papillomavirus related neoplasms with topical imiquimod.
Benedetto, C; Bertero, L; Borella, F; Cassoni, P; Gallio, N; Mangherini, L; Preti, M, 2023
)
1.85
"Imiquimod (IMQ) is a synthetic ligand of toll-like receptor 7 that exerts antitumor activity by stimulating cell-mediated immunity or by directly inducing apoptosis."( Imiquimod Exerts Antitumor Effects by Inducing Immunogenic Cell Death and Is Enhanced by the Glycolytic Inhibitor 2-Deoxyglucose.
Chang, SH; Chen, YJ; Chuang, KC; Huang, SW; Kao, JK; Kao, SH; Liang, SM; Shieh, JJ; Wang, HY; Wang, ST; Wu, CY, 2020
)
2.72
"Imiquimod is a topical immune response modifier and constitutes a noninvasive alternative for the treatment of anogenital condylomata acuminata."( Successful topical treatment of anal giant condylomata acuminata in an infant.
Carnevale, C; D'Argenio, P; Diociaiuti, A; El Hachem, M; Giancristoforo, S; Lucchetti, MC; Rotunno, R; Tchidjou, HK, 2020
)
1.28
"Imiquimod is an immune-stimulator that activates TLR 7 and can be used to enhance the innate and adaptive immunity."( Imiquimod - A toll like receptor 7 agonist - Is an ideal option for management of COVID 19.
Alexandris, N; Angelopoulou, A; Farsalinos, K; Konstantinou, E; Mesiakaris, K; Poulas, K; Zanidis, C, 2020
)
2.72
"Imiquimod is a toll-like receptor agonist with proven antitumor activity as a topical treatment for skin cancer. "( A phase 2 study of TMX-101, intravesical imiquimod, for the treatment of carcinoma in situ bladder cancer.
Belkoff, LH; Belldegrun, AS; Chamie, K; Donin, NM; Hakim, G; Holden, S; Holldack, J; Karsh, LI; Kivlin, D; Lamm, DL; Lenis, AT; Pantuck, AJ; Pozzi, R; Reddy, M; Shore, N, 2017
)
2.16
"Imiquimod is a topical agent whose efficacy has been documented in treating MF patches and plaques as well as one case of tumor-stage disease."( Complete resolution of mycosis fungoides tumors with imiquimod 5% cream: a case series.
Byekova, YA; Duvic, M; Emge, DA; Lewis, DJ, 2017
)
1.43
"Imiquimod is a topically applicable Toll-like receptor (TLR)-7/8 agonist, which is capable of stimulating the innate cutaneous immunity and the cellular arm of the adaptive immune response and of exerting potent anti-viral, anti-tumor and immunoregulatory effects (1)."( Topical Imiquimod is an Effective and Safe Drug for Molluscum Contagiosum in Children.
Badavanis, G; Georgiou, S; Monastirli, A; Pasmatzi, E; Tsambaos, D, 2017
)
1.61
"Imiquimod is a Toll-like receptor-7 agonist that regulates immunity and can be used as an immune adjuvant. "( Therapeutic effect of imiquimod on dextran sulfate sodium-induced ulcerative colitis in mice.
Chen, L; Chen, N; Xiang, H; Yang, Y; Zhou, Z, 2017
)
2.21
"Imiquimod is an excellent option for patients with actinic keratosis, although its use may be limited by the long course of treatment required (4 weeks) and the likelihood of local skin reactions. "( A 12-Day Course of Imiquimod 5% for the Treatment of Actinic Keratosis: Effectiveness and Local Reactions.
Calomarde, L; Guillén, C; Llombart, B; Nagore, E; Requena, C; Sanmartín, O; Serra-Guillén, C, 2018
)
2.25
"Imiquimod is an imidazoquinoline, approved for some skin pathologies other than hemangioma."( Selective hemangioma cell dysfunction and apoptosis triggered by in vitro treatment with imiquimod.
Alegre, N; Gazzaniga, S; Pozner, R; Rocco, R; Wainstok, R, 2018
)
1.42
"Imiquimod application is an established mouse model of psoriasis-like skin inflammation."( Imiquimod-Induced Psoriasis-Like Skin Lesions Do Not Accelerate Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice.
Cardoso, RM; Hansen, PR; Madsen, M; Nielsen, LB; Pedersen, TX; van Eck, M, 2018
)
2.64
"Imiquimod was found to be a direct but weak TRPA1 agonist that activated a subset of TRPA1 expressing neurons."( A zebrafish and mouse model for selective pruritus via direct activation of TRPA1.
Condon, L; Curtright, A; Dhaka, A; Esancy, K; Feng, J; Kimball, C, 2018
)
1.2
"Imiquimod is a topical immunomodulating medication approved by the US Food and Drug Administration for the treatment of condyloma acuminata, actinic keratoses (AKs), and superficial basal cell carcinoma (BCC). "( Imiquimod-induced hypopigmentation following treatment of periungual verruca vulgaris.
Edgar, N; Hogan, DJ; Pilkington, S, 2018
)
3.37
"Imiquimod is a toll-like receptor that modifies the immune response via the up-regulation of cytokines and has the capacity to improve a person's immune response."( A Review on Imiquimod Therapy and Discussion on Optimal Management of Basal Cell Carcinomas.
Arora, H; Darwin, E; Kamath, P; Nouri, K, 2018
)
1.58
"Imiquimod is an immunomodulatory agent, which has received approval in the topical treatment of superficial BCCs."( Successful treatment of multifocal pigmented basal cell carcinomas with the application of topical 5% imiquimod cream.
Balasis, S; Georgiou, S; Koumoundourou, D; Mallioris, AF; Plachouri, KM, 2018
)
1.42
"Imiquimod is an immunomodulatory drug with a tested efficacy against L."( EAPB0503: An Imiquimod analog with potent in vitro activity against cutaneous leishmaniasis caused by Leishmania major and Leishmania tropica.
Bastien, P; Bonnet, PA; Bou Youness, H; El Hajj, H; El Hajj, R; Khalifeh, I; Lachaud, L; Masquefa, C, 2018
)
1.57
"Imiquimod 3.75% is a field-directed treatment for actinic keratosis that can detect and treat clinical and subclinical lesions across an entire sun-exposed field. "( Imiquimod 3.75% for field-directed therapy of actinic keratosis: results of a prospective case-series study in Greece.
Antoniou, C; Befon, A; Chasapi, V; Panagiotopoulos, A; Stratigos, AJ; Tzanetakou, V, 2019
)
3.4
"Imiquimod (IMQ) is a selective toll-like receptor 7 (TLR7) agonist. "( The TLR7 agonist imiquimod selectively inhibits IL-4-induced IgE production by suppressing IgG1/IgE class switching and germline ε transcription through the induction of BCL6 expression in B cells.
Kim, PH; Park, SR; Shim, YS; Yoon, HK, 2019
)
2.3
"Imiquimod (Imiq) is a synthetic imizoquinoline compound which can act on Toll-like receptor (TLR)7 and transduce signals involved in cell activation. "( Imiquimod enhances DNFB mediated contact hypersensitivity in mice.
Dong, X; Liu, M; Qin, X; Ren, S; Song, Y; Wang, Q; Zhang, B; Zhang, W; Zhang, Y; Zhao, C, 2019
)
3.4
"Imiquimod is an immunomodulatory agent with antiviral, antitumoural, and antiangiogenic properties that is expedient against Kaposi sarcoma."( Imiquimod 5% Cream Versus Cryotherapy in Classic Kaposi Sarcoma.
Bayramgürler, D; Bilen, N; Çağlayan, Ç; Kıran, R; Odyakmaz Demirsoy, E; Şikar Aktürk, A,
)
2.3
"Imiquimod is a topical toll-like receptor approved by the Food and Drug Administration (FDA) for genital warts, actinic keratosis, and primary superficial basal cell carcinoma."( Complete Resolution of Primary Cutaneous Anaplastic Large Cell Lymphoma With Topical Imiquimod
Aung, PP; Duvic, M; Kubicki, SL; Park, KE, 2019
)
1.46
"Imiquimod is a topical toll-like-receptor-7 agonist currently used for treating basal cell carcinoma. "( Transcriptomic profiles conducive to immune-mediated tumor rejection in human breast cancer skin metastases treated with Imiquimod.
Adams, S; Bedognetti, D; Chiriboga, L; Darvishian, F; Demaria, S; Egeblad, M; Heguy, A; Hendrickx, W; Loomis, C; Marincola, FM; Ray, K; Rozenblit, M, 2019
)
2.16
"Imiquimod (IQ) 5% cream is a synthetic imidazoquinolin heterocyclic amine that enhances, through cytokine induction, both the innate and acquired immune pathways, resulting in immunomodulating, antiviral and antitumor effects; it is currently used in adults in the treatment of various skin disorders."( Two pediatric cases of pyogenic granuloma treated with imiquimod 5% cream: combined clinical and dermatoscopic evaluation and review of the literature.
Anfuso, R; Lacarrubba, F; Li Calzi, M; Micali, G; Musumeci, ML, 2013
)
1.36
"Imiquimod 5% is a suitable treatment for patients with EQ, and the treatment response can be evaluated using OCT."( Optical coherence tomography imaging of erythroplasia of Queyrat and treatment with imiquimod 5% cream: a case report.
Bierhoff, E; Dirschka, T; Schmitz, L, 2014
)
1.35
"Imiquimod is an effective ligand for TLR7 (and TLR8 in humans) and also interferes with adenosine receptor signaling."( TLRs to cytokines: mechanistic insights from the imiquimod mouse model of psoriasis.
Flutter, B; Nestle, FO, 2013
)
1.37
"Imiquimod 5% cream is an immune-response-modifying drug with antiviral and anti-tumour activity."( Lichen planopilaris after imiquimod 5% cream for multiple BCC in basal cell naevus syndrome.
Argenziano, G; Drummond, A; Lallas, A; Longo, C; Moscarella, E; Piana, S; Pichler, J; Zalaudek, I, 2015
)
1.44
"Imiquimod is a good alternative to surgery in elderly patients who have unwillingness to surgery and are often poor candidates for surgery."( Treatment of various types of basal cell carcinoma with topical 5% imiquimod in the elderly who refused surgical intervention: a case series.
Erkan, F; Kaçar, SD; Karaca, Ş; Özuğuz, P, 2015
)
1.37
"Imiquimod (IMQ) is a synthetic Toll-like receptor (TLR7/8) ligand that can trigger antiviral and antitumor activities. "( Imiquimod inhibits melanoma development by promoting pDC cytotoxic functions and impeding tumor vascularization.
Aspord, C; Charles, J; Leccia, MT; Leloup, C; Molens, JP; Plumas, J; Tramcourt, L, 2014
)
3.29
"Imiquimod is a topically active immunomodulatory agent that has been shown to successfully treat pediatric anogenital warts."( Treatment of anogenital warts in an 18-month-old girl with 5% imiquimod cream.
Hiršl Hećej, V; Ljubojević Hadžavdić, S; Pustišek, N; Sikanić Dugić, N, 2014
)
1.36
"Imiquimod is a Toll-like receptor 7 agonist used topically to treat external genital warts and basal cell carcinoma. "( Toll-like receptor agonist imiquimod facilitates antigen-specific CD8+ T-cell accumulation in the genital tract leading to tumor control through IFNγ.
Chang, YN; Cheng, WF; He, L; Huh, W; Hung, CF; Knoff, J; Roden, RB; Song, L; Soong, RS; Trieu, J; Trimble, CL; Tsai, YC; Wu, TC, 2014
)
2.14
"Imiquimod 5% cream is a potentially effective treatment modality for lesions that are difficult to treat with surgical excision."( Bowenoid papulosis successfully treated with imiquimod 5% cream.
Ishikawa, O; Kato, M; Shimizu, A, 2014
)
1.38
"Imiquimod is an itch-promoting, small, synthetic compound that is generally used to treat genital warts and basal cell carcinoma. "( Imiquimod induces a Toll-like receptor 7-independent increase in intracellular calcium via IP(3) receptor activation.
Choi, SY; Hwang, H; Jung, SJ; Kim, D; Lee, SJ; Min, H; Yu, SW, 2014
)
3.29
"Imiquimod is an immune response modifier that is approved as a topical cream for the treatment of anogenital warts by the US Food and Drug Administration."( Imiquimod in the treatment of cutaneous warts: an evidence-based review.
Ahn, CS; Huang, WW, 2014
)
2.57
"Imiquimod (IMI) is a topical immune response modifier used in the treatment of actinic keratosis and cheilitis. "( A topical imiquimod-induced oral mucosal lichenoid reaction: a case report.
Brown, RS; Farquharson, AA, 2014
)
2.25
"Imiquimod 3.75% is a novel field-directed therapy which uniquely can detect and clear both clinical and subclinical lesions across a large sun-exposed field such as the full face or balding scalp, and so far is the only AK treatment to have had its efficacy assessed with the Lmax concept."( Lmax and imiquimod 3.75%: the new standard in AK management.
Stockfleth, E, 2015
)
1.56
"Imiquimod 3.75% is a field-directed AK treatment, which can detect and clear clinical and subclinical lesions across an entire sun-exposed field such as the full face or balding scalp."( Lmax and imiquimod 3.75% in daily clinical practice.
Gupta, G, 2015
)
1.56
"Imiquimod cream appears to be a viable option for primary or adjuvant treatment of LM in older patients who are poor surgical candidates."( Imiquimod 5% cream as primary or adjuvant therapy for melanoma in situ, lentigo maligna type.
Chen, FW; Egbert, BM; Kim, DD; Swetter, SM, 2015
)
3.3
"Imiquimod is a chemotherapeutic agent for many skin-associated diseases, but it has also been associated with inflammatory side effects. "( Probing the effects of fish oil on the delivery and inflammation-inducing potential of imiquimod.
Aluwi, MF; Mohd Amin, MC; Rehman, K; Rullah, K; Wai, LK; Zulfakar, MH, 2015
)
2.08
"Imiquimod is a topical immunomodulator used to treat genital warts and cutaneous malignancies that exerts its effects via induction of proinflammatory cytokines through activation of toll-like receptor (TLR) 7. "( Imiquimod-induced subacute cutaneous lupus erythematosus-like changes.
Berger, TG; Farsani, TT; Maguiness, SM; Zedek, DC, 2015
)
3.3
"Imiquimod is a synthetic imidazoquinolone amine, which has potent immune response modifier activity, when topically used. "( Imiquimod - Its role in the treatment of cutaneous malignancies.
Bubna, AK,
)
3.02
"Imiquimod is a topical immune response modifier (imidazoquinoline) with both antiviral and antitumour activities."( Imiquimod-induced apoptosis of melanoma cells is mediated by ER stress-dependent Noxa induction and enhanced by NF-κB inhibition.
Abd Elmageed, ZY; Brodell, RT; El-Khattouti, A; Haikel, Y; Hannig, M; Hassan, M; Hassan, SY; Kandil, E; Leverkus, M; Megahed, M; Selimovic, D; Taylor, EB, 2016
)
2.6
"Imiquimod is an effective long-term treatment for LM. "( Five-year recurrence rate of lentigo maligna after treatment with imiquimod.
Barlow, R; Coleman, A; Craythorne, EE; Kai, AC; Mallipeddi, R; Richards, T, 2016
)
2.11
"Imiquimod 3.75% is an effective actinic keratosis (AK) treatment that detects and clears clinical and subclinical lesions across an entire sun-exposed field such as the full face or balding scalp."( Efficacy and Safety of Imiquimod 3.75% from Lmax in Actinic Keratosis According to Fitzpatrick Skin Type.
Alomar, A; Aractingi, S; Dakovic, R; Dirschka, T; Gupta, G; Peris, K; Stockfleth, E, 2016
)
2.19
"Imiquimod is a synthetic analogue which seems to activate skin immune cells, acting as a Toll-like receptor 7 agonist."( Imiquimod treatment effectively reduces the percentage of viable cells in a cervical carcinoma cell line but does not affect the expression of HLA-G or OCT-4.
Loutradis, D; Patta, J; Pergialiotis, V; Stefanidi, D; Stefanidis, K, 2015
)
2.58
"Imiquimod is an immune response modifier commercially available as a 3.75 and 5% cream. "( Imiquimod in dermatology: an overview.
Abadi, R; Abbas, O; Hanna, E, 2016
)
3.32
"Imiquimod is an immune response modulator which is used for the treatment of external condylomas and other HPV-related genital neoplasias."( Randomised trial on treatment of vaginal intraepithelial neoplasia-Imiquimod, laser vaporisation and expectant management.
Jakobsson, M; Kalliala, I; Louvanto, K; Nieminen, P; Paavonen, J; Riska, A; Tainio, K, 2016
)
1.39
"Imiquimod is a topical immune response modifier, but the thick stratum corneum of common warts prevents drug permeation through skin."( Fractional Laser-Assisted Topical Imiquimod 5% Cream Treatment for Recalcitrant Common Warts in Children: A Pilot Study.
Kim, BS; Kim, GW; Kim, HS; Kim, MB; Ko, HC; Mun, JH; Park, SM; Song, M, 2016
)
1.43
"Imiquimod is a local immune-response modifier that works by stimulating innate and acquired immunity. "( [Eruptive epidermoid cysts during topical imiquimod treatment].
Al Saïf, F; Carmi, E; Dillies, AS; Fraitag-Spinner, S; Gras-Champel, V, 2017
)
2.16
"Imiquimod is an option for patients unfit for or not willing to undergo surgery or radiotherapy."( A systematic review on the role of imiquimod in lentigo maligna and lentigo maligna melanoma: need for standardization of treatment schedule and outcome measures.
Hoekzema, R; Jansma, EP; Prinsen, CAC; Tio, D; van der Woude, J; van Montfrans, C, 2017
)
1.45
"Imiquimod is a topical immune-response modifier that acts on the immune system."( Topical imiquimod therapy for lentigo maligna.
Joseph, MG; Mahoney, MH; Temple, C, 2008
)
1.5
"Imiquimod 5% cream is an immune response modifier approved for the treatment of superficial basal cell carcinoma (sBCC) once daily, 5 x per week for 6 weeks. "( Recurrence rate of superficial basal cell carcinoma following treatment with imiquimod 5% cream: conclusion of a 5-year long-term follow-up study in Europe.
Barona, CG; Frank, RG; Gollnick, H; Maus, J; Megahed, M; Munzel, U; Ruzicka, T,
)
1.8
"Imiquimod is a 240.3-Da synthetic imidazoquinolinamine (C14H16N4), developed in 1983 and approved in 1997 by the US Food and Drug Administration for the topical treatment of external genital and perianal warts and, more recently, also for actinic keratosis and superficial basal cell carcinomas. "( Peculiar clinical and dermoscopic remission pattern following imiquimod therapy of basal cell carcinoma in seborrhoeic areas of the face.
Campione, E; Chimenti, S; Diluvio, L; Orlandi, A; Paternò, EJ; Terrinoni, A, 2009
)
2.04
"Imiquimod 5% cream is a local immune response modifier that has been used off-label to treat LM."( Videodermatoscopy of lentigo maligna treated with imiquimod.
Lacarrubba, F; Micali, G; Nardone, B; Nasca, MR, 2008
)
1.32
"Imiquimod is a topically used immune response modifier effective in the treatment of genital warts caused by HPV. "( Imiquimod inhibits the differentiation but enhances the maturation of human monocyte-derived dendritic cells.
Cen, JP; Chen, XZ; Cheng, H; Lou, JX; Wang, Q; Xu, Y; Zhang, X; Zhu, KJ, 2009
)
3.24
"Imiquimod is a topical immunomodulator which can generate a local cytotoxic response with potentially antiviral and antitumour effects."( Imiquimod and lentigo maligna: a search for prognostic features in a clinicopathological study with long-term follow-up.
Barlow, RJ; Powell, AM; Robson, AM; Russell-Jones, R, 2009
)
2.52
"Imiquimod is a highly interesting therapeutic modality in the elderly, in whom surgery is often contraindicated."( [Alternative to surgery in basal cell carcinoma in the elderly population: imiquimod 5% cream].
Arias Santiago, SA; Burkhardt Pérez, P; Naranjo Sintes, R; Ruiz Villaverde, R,
)
1.08
"Imiquimod is a topically applied immune-response modifier."( Failure of imiquimod 5% cream to prevent recurrence of surgically excised trunk keloids.
Cação, FM; Messina, MC; Tanaka, V, 2009
)
1.46
"Imiquimod is an immunomodifier recently approved for the treatment of superficial basal cell carcinomas (sBCC). "( Pemphigus-like lesions induced by imiquimod.
Bauza, A; Del Pozo, LJ; Martin, A; Saus, C, 2009
)
2.07
"Imiquimod cream 5% is an immune modifier approved for the treatment of genital warts, actinic keratosis, and basal cell carcinoma. "( A case of imiquimod-induced alopecia.
Balmer, N; Conde, J; Davis, K; Jones, D; McMichael, A; Ntuen, E, 2010
)
2.21
"Imiquimod is a topical immune response modifier and Toll-like receptor 7 (TLR7) agonist that induces the immunological destruction of SCC and other skin cancers."( Imiquimod enhances IFN-gamma production and effector function of T cells infiltrating human squamous cell carcinomas of the skin.
Calarese, AW; Clark, RA; Hijnen, D; Huang, SJ; Kupper, TS; Miller, DM; Mollet, IG; Murphy, GF; Schanbacher, CF; Schmults, CD, 2009
)
2.52
"Imiquimod is a safe, cost-effective, and clinically effective management option in the treatment of pyogenic granuloma."( Pyogenic granuloma in ten children treated with topical imiquimod.
Fischer, G; Smith, S; Tritton, SM; Wong, LC; Zagarella, S,
)
1.1
"Imiquimod 3.75% cream is a topical formulation of imiquimod intended for daily application to treat actinic keratoses of the entire face or balding scalp. "( Pharmacokinetics of imiquimod 3.75% cream applied daily for 3 weeks to actinic keratoses on the face and/or balding scalp.
Adams, M; Fein, MC; Furst, J; Kulp, J; Levy, S; Meng, TC, 2010
)
2.13
"Imiquimod appears to be an effective treatment for a subset of patients with LM. "( Treatment of lentigo maligna with imiquimod cream: a long-term follow-up study of 10 patients.
Kirtschig, G; Van Doorn, R; Van Meurs, T, 2010
)
2.08
"Imiquimod cream is an effective and safe therapeutic agent for both primary and recurring vulvar Paget disease."( Treatment of recurrent vulvar Paget disease with imiquimod cream: a case report and review of the literature.
Güngor, T; Ozat, M; Sahin, I; Sirvan, L; Tonguc, E; Var, T, 2011
)
2.07
"imiquimod 3.75% is an interesting, safe and well-tolerated treatment option for actinic keratoses of the face or balding scalp especially in respect of compliance, as it is indicated for daily use for a shorter time period (2 times, 2-week cycles) and approved for use on larger areas compared with imiquimod 5%. "( Imiquimod 3.75% cream (Zyclara) for the treatment of actinic keratoses.
Gollnick, HP; Quist, SR, 2011
)
3.25
"Imiquimod (IQ) is an agonist of Toll-like receptor 7 (TLR7) used to treat various infectious skin diseases such as genital warts, keratosis, and basal cell carcinoma."( Analysis of cellular and behavioral responses to imiquimod reveals a unique itch pathway in transient receptor potential vanilloid 1 (TRPV1)-expressing neurons.
Han, SK; Kim, D; Kim, SJ; Lee, CJ; Lee, J; Lee, SJ; Min, H; Park, GH; Simon, MI; Wall, E, 2011
)
1.34
"Imiquimod is an immunomodulator of the imidazoquinoline group which possesses antiviral and antitumour activities. "( Acute renal failure caused by imiquimod 5% cream in a renal transplant patient: review of the literature on side effects of imiquimod.
Coto-Segura, P; Esteve, A; Galache Osuna, C; Gómez, E; Mas-Vidal, A; Salgueiro, E; Santos-Juanes, J, 2011
)
2.1
"Imiquimod is a topically applied immune modulator that has been used to treat superficial cutaneous melanoma, but has not been reported to treat metastatic melanoma."( Regression of internal melanoma metastases following application of topical imiquimod to overlying skin.
Aires, D; Dusing, R; Meggison, A; Miller, AK, 2011
)
1.32
"Imiquimod is an immune response modifier prescribed as a topical medication for a number of viral and neoplastic conditions. "( Evaluation of imiquimod for topical treatment of vaccinia virus cutaneous infections in immunosuppressed hairless mice.
Anderson, BJ; Bailey, KW; Larson, D; Smee, DF; Tarbet, EB; Wong, MH, 2011
)
2.17
"Imiquimod (Aldara) is a topical immune response modifier effective against a variety of cutaneous tumors. "( Lupus erythematosus-like reaction in imiquimod-treated skin: a report of 2 cases.
Chan, MP; Zimarowski, MJ, 2011
)
2.08
"Imiquimod cream is a topical immune response modifier, which has shown antiviral and anti-tumorous properties by inducing the production of cytokines as well as by stimulating dendritic cells and lymphocytes."( Imiquimod and lymphatic field clearance: a new hypothesis based on a remote immune action on skin cancer.
Akkilic-Materna, M; Komericki, P; Massone, C, 2011
)
2.53
"Imiquimod is an immunomodulator whose approved indications include treatment of nonfacial superficial BCC less than 2 cm in diameter."( [Oral acitretin and topical imiquimod as neoadjuvant treatment for giant basal cell carcinoma].
Aguayo, R; Baradad, M; Casanova, JM; Sanmartín, V, 2012
)
1.39
"Imiquimod is a TLR7/8 agonist that has anticancer therapeutic efficacy in the treatment of precancerous skin lesions and certain nonmelanoma skin cancers. "( Imiquimod-induced TLR7 signaling enhances repair of DNA damage induced by ultraviolet light in bone marrow-derived cells.
Fishelevich, R; Gaspari, AA; Lee, J; Liu, H; Meng, TC; Nakazono, A; Tammaro, A; Tuchinda, P; Zhao, Y, 2011
)
3.25
"Imiquimod is a topical biological response modifier that has been shown to be useful in the treatment of several viral and nonviral skin tumours in humans and animals. "( Topical imiquimod in the treatment of two cutaneous melanocytomas in a dog.
Coyner, K; Loeffler, D, 2012
)
2.26
"Imiquimod (IQ) is a synthetic imidazoquinoline amine that locally enhances, through cytokine induction, both innate and acquired immune pathways, resulting in immunomodulating, antiviral and antitumor effects."( Successful treatment and management of large superficial basal cell carcinomas with topical imiquimod 5% cream: a case series and review.
Gurgone, S; Lacarrubba, F; Micali, G; Potenza, MC, 2011
)
1.31
"Imiquimod is a synthetic Toll-like receptor 7 (TLR7) agonist approved for the topical treatment of actinic keratoses, superficial basal cell carcinoma, and genital warts. "( Immunomodulation by imiquimod in patients with high-risk primary melanoma.
Bentow, JJ; Bruhn, KW; Chang, PL; Comin-Anduix, B; Craft, N; Dauphine, C; Economou, JS; Greger, S; Haskell, J; Konishi, T; Lee, DK; Moy, L; Narayan, R; Nguyen, H; Ribas, A; Tsui, S; Vanchinathan, V; Vargas, HI, 2012
)
2.15
"Imiquimod is a topical medication that enhances the immune response to HPV-induced genital warts."( Randomized clinical trial of imiquimod: an adjunct to treating cervical dysplasia.
Barton, DL; Clayton, AC; Gostout, BS; Jefferies, JA; Loprinzi, CL; McGovern, RM; Novotny, PJ; Pachman, DR; Sloan, JA, 2012
)
1.39
"Imiquimod is an effective therapeutic agent for the conservative treatment of vulvar Paget disease."( Conservative management of extramammary paget disease with imiquimod.
Badiglian-Filho, L; Baiocchi, G; Begnami, MD; Costa, FD; Faloppa, CC; Fukazawa, EM; Kumagai, LY; Oliveira, RA; Soares, FA; Surima, WS, 2012
)
2.06
"Imiquimod is an immune response modifier that stimulates the patient's own immune system to release various chemical substances, such as interferon and interleukin-12. "( Imiquimod 5% cream use in dermatology, side effects and recent patents.
Calvieri, S; Cantisani, C; Clerico, R; Lazic, T; Mattozzi, C; Richetta, AG, 2012
)
3.26
"Imiquimod 3.75% cream is a new formulation intended for daily self-application. "( Pharmacokinetics of daily self-application of imiquimod 3.75% cream in adult patients with external anogenital warts.
Adams, MP; Barry, GT; Feldman, R; Kulp, J; Levy, S; Wu, J, 2012
)
2.08
"Imiquimod 5% cream is an immunomodulator with antiangiogenic effects."( Enhanced port-wine stain lightening achieved with combined treatment of selective photothermolysis and imiquimod.
Armstrong, J; Choi, B; Elkeeb, L; Harris, R; Huang, YC; Kelly, KM; Ortiz, A; Tremaine, AM, 2012
)
1.32
"Imiquimod is a TLR agonist that is used as an antitumor agent, mainly against skin tumors. "( Plasmacytoid dendritic cells lead the charge against tumors.
Bhardwaj, N; Jiménez-Baranda, S; Silva, IP, 2012
)
1.82
"Imiquimod is a synthetic compound with antitumor properties; a 5% cream formulation is successfully used to treat skin tumors. "( Imiquimod clears tumors in mice independent of adaptive immunity by converting pDCs into tumor-killing effector cells.
Amberg, N; Colonna, M; Drobits, B; Grundtner, R; Hammer, M; Holcmann, M; Sibilia, M; Swiecki, M, 2012
)
3.26
"Imiquimod cream is a simple and convenient home-nursing medication."( [Clinical application of imiquimod for the treatment of infantile hemangiomas].
Chen, D; Chen, H; Chen, XD; Hu, XJ; Jiang, CH; Jin, YB; Li, W; Lin, XX; Ma, G; Ye, XX, 2011
)
1.39
"Imiquimod is a topically applied immunomodulator without relevant systemic absorption, and may thus represent a promising treatment for cutaneous KS in RTRs."( Topical treatment of cutaneous Kaposi sarcoma with imiquimod 5% in renal-transplant recipients: a clinicopathological observation.
Dummer, R; French, LE; Hofbauer, GF; Kempf, W; Prinz Vavricka, BM, 2012
)
1.35
"Imiquimod 5% cream is a topical immune-response modifier indicated in the treatment of multiple cutaneous conditions including actinic keratoses, superficial basal cell carcinoma, and condylomata acuminata. "( Psoriasiform eruption and oral ulcerations as adverse effects of topical 5% imiquimod treatment in children: a report of four cases.
Holland, KE; Lyon, VB; Siegel, D; Smith, WA,
)
1.8
"Imiquimod is an effective treatment for LM that provides patients with a cosmetically favorable outcome when standard surgery is not an option."( Topical 5% imiquimod in the treatment of lentigo maligna.
Demers, AA; Musto, G; Toole, JW; Wiseman, MC; Wong, JG,
)
1.96
"Imiquimod 5% cream is an effective treatment option for children with extensive and rapidly progressive perianal warts and is associated with minimal side effects. "( Imiquimod 5% cream treatment for rapidly progressive genital condyloma in a 3-year-old girl.
Black, A; Fleming, N; Leclair, E, 2012
)
3.26
"Imiquimod is a topical immune response modifier used to treat anogenital warts. "( Local and systemic adverse effects of imiquimod therapy for external anogenital warts in men: report of three cases.
de Campos Guidi, HG; Rosenblatt, A, 2012
)
2.09
"Imiquimod is a topical immune response modifier which is effective through toll-like receptor 7, and it has fewer recurrences of actinic keratoses than the existing treatment."( [Field cancerization and field therapy - the therapy of actinic keratosis by imiquimod].
Idezuki, T, 2013
)
1.34
"Imiquimod 5% cream is an effective therapeutic option for both sBCC and nBCC in patients with basal cell nevus syndrome. "( Topical imiquimod treatment of superficial and nodular basal cell carcinomas in patients affected by basal cell nevus syndrome: a preliminary report.
Caltabiano, R; De Pasquale, R; Impallomeni, R; Lacarrubba, F; Micali, G, 2002
)
2.19
"Imiquimod is a recently developed imidazoquinolin heterocyclic amine that is an immune response modifier."( Successful treatment of perianal warts in a child with 5% imiquimod cream.
Gruber, PC; Wilkinson, J, 2001
)
1.28
"Imiquimod is an immunomodulator with indirect antiproliferative and antiviral properties known to be effective against anogenital warts. "( Anecdotal reports of 3 cases illustrating a spectrum of resistant common warts treated with cryotherapy followed by topical imiquimod and salicylic acid.
Housman, TS; Jorizzo, JL, 2002
)
1.96
"Imiquimod is an immune response modifier, currently approved for the treatment of genital warts. "( Clinical effect of imiquimod 5% cream in the treatment of actinic keratosis.
Cervera, C; Lamba, S; Lebwohl, MG; Lou, W; Persaud, AN; Shamuelova, E; Sherer, D; Singer, G, 2002
)
2.09
"Imiquimod (Aldara) is an immune response modifier used primarily to treat anogenital warts. "( Imiquimod: a review.
Bluhm, R; Browne, M; Gupta, AK,
)
3.02
"Imiquimod is an immune response modifier that has demonstrated a good efficacy and relatively low recurrence rates in comparison to other genital wart treatment modalities. "( Effect of adjuvant imiquimod 5% cream on sustained clearance of anogenital warts following laser treatment.
Eul, A; Hagedorn, M; Hopfenmüller, W; Hoyme, UB; Schindler, AE; Schneede, P; Schorn, K, 2002
)
2.09
"Imiquimod 5% cream is an effective treatment for external genital and perianal warts and provides a significant benefit in comparison with vehicle cream, independent of gender, initial wart size, duration of current outbreak of warts, previous wart treatment, or tobacco use."( Topical imiquimod 5% cream as an effective treatment for external genital and perianal warts in different patient populations.
Fox, TL; Owens, ML; Sauder, DN; Skinner, RB, 2003
)
2.2
"Imiquimod is a topical immune response modifier that binds to Toll-like receptors 7 and 8 and induces alpha-interferon. "( Imiquimod induces complete clearance of a PUVA-resistant plaque in mycosis fungoides.
Burg, G; Dummer, R; Kazakov, D; Kempf, W; Urosevic, M, 2003
)
3.2
"Imiquimod cream is a topical immune response modifier with indirect antiviral and antitumor effects through the stimulation of local cytokine production and cell-mediated immune response."( Bowenoid papulosis of the vulva-immunotherapeutical approach with topical imiquimod.
Dorn, C; Kupka, M; Petrow, W; Richter, ON; Ulrich, U; Wardelmann, E, 2003
)
1.27
"Imiquimod cream is a topically applied immunomodulator."( Medical treatment of nasal squamous papilloma with imiquimod cream.
Aebi, S; Caversaccio, M, 2003
)
1.29
"Imiquimod is a local immune response modifier that has demonstrated potent antiviral and antitumor activity. "( Mechanisms underlying imiquimod-induced regression of basal cell carcinoma in vivo.
Benninghoff, B; Burg, G; Dummer, R; Maier, T; Slade, H; Urosevic, M, 2003
)
2.08
"Imiquimod is a member of a novel class of immune response modifiers (IRM), which works by using the toll-like receptor (TLR)-7."( The use of Toll-like receptor-7 agonist in the treatment of basal cell carcinoma: an overview.
Garcia-Bartels, C; Schmook, T; Sterry, W; Stockfleth, E; Trefzer, U; Wegner, T, 2003
)
1.04
"Imiquimod is a topical immune response modifier that binds to Toll-like receptor-7 and -8, inducing interferon-alpha. "( Imiquimod in basal cell carcinoma: how does it work?
Burg, G; Dummer, R; Hafner, J; Hoek, K; Kempf, W; Urosevic, M, 2003
)
3.2
"Imiquimod is a new immunomodulating drug that is registered for genital HPV infection but has also shown good efficacy in several cutaneous malignancies."( Two cases of squamous cell carcinoma treated with topical imiquimod 5%.
Oster-Schmidt, C, 2004
)
1.29
"Imiquimod is an immune-response modifier that has the potential to be useful in many dermatological indications (Table 1). "( Imiquimod as a possible treatment for keratoacanthoma.
Bhatia, N,
)
3.02
"Imiquimod is an immune response modifier that is a Toll-like receptor 7 agonist that induces interferon and other cytokines through the innate immune system and stimulates cell-mediated immunity through T cells. "( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, randomized, vehicle-controlled studies.
Caro, I; Geisse, J; Golitz, L; Lindholm, J; Owens, M; Stampone, P, 2004
)
3.21
"Imiquimod 5% cream is a patient-applied therapy that directly enhances the immune response to HPV and is safe and effective for the treatment of GW."( Using imiquimod for genital warts in female patients.
Cox, JT; Petry, KU; Roy, M; Rylander, E, 2004
)
1.53
"Imiquimod cream is an immune response modifier and induces a predominantly T-helper 1 type response."( A pilot study of treatment of lentigo maligna with 5% imiquimod cream.
Bryden, AM; Dawe, RS; Evans, A; Fleming, CJ; Ibbotson, SH, 2004
)
1.29
"Imiquimod is an immune-response modifier that has been shown to be effective in the treatment of superficial and nodular basal cell carcinoma (BCC). "( Open study of the efficacy and mechanism of action of topical imiquimod in basal cell carcinoma.
Alomar, A; Matías-Guiu, X; Vidal, D, 2004
)
2.01
"Imiquimod is a novel synthetic compound that is a member of the imidazoquinolone family of drugs. "( Imiquimod 5 percent cream and the treatment of cutaneous malignancy.
Huntley, A; Navi, D, 2004
)
3.21
"Imiquimod is a modifier of the immune response that has been proven to be an effective treatment for basal cell carcinoma (BCC). "( Efficacy of imiquimod for the expression of Bcl-2, Ki67, p53 and basal cell carcinoma apoptosis.
Alomar, A; Matías-Guiu, X; Vidal, D, 2004
)
2.15
"Imiquimod 5% cream is a topically applied medicament that should be considered as an effective and reliable medical option in the treatment of anogenital warts."( Topical imiquimod 5% cream in external anogenital warts: a randomized, double-blind, placebo-controlled study.
Arican, O; Bilgic, K; Guneri, F; Karaoglu, A, 2004
)
1.48
"Imiquimod is an immune response modifier that up-regulates cytokines and has been shown in clinical studies to reduce or clear basal cell carcinoma tumors when applied topically."( 5% imiquimod cream and reflectance-mode confocal microscopy as adjunct modalities to Mohs micrographic surgery for treatment of basal cell carcinoma.
Berkes, B; González, S; Marra, D; Morgan, B; Niemeyer, A; Owens, M; Schanbacher, C; Torres, A, 2004
)
2.39
"Imiquimod is a topically applied immunomodulator. "( Imiquimod for the treatment of skin cancer.
Brown, MD; Burns, CA, 2005
)
3.21
"Imiquimod is a potent inducer of antiviral cytokine activity which has shown significant efficacy in the treatment of genital warts."( Imiquimod cream 5% for recalcitrant cutaneous warts in immunosuppressed individuals.
Brown, VL; Harwood, CA; Leigh, IM; McGregor, JM; Perrett, CM; Proby, CM, 2005
)
2.49
"Imiquimod (Aldara) is an immune response modifier approved for the topical treatment of external genital and perianal warts which can mediate regression of several cutaneous malignancies [basal cell carcinoma (BCC), Bowen's disease, actinic keratosis, and metastasis of malignant melanoma]. "( Enhanced type I interferon signaling and recruitment of chemokine receptor CXCR3-expressing lymphocytes into the skin following treatment with the TLR7-agonist imiquimod.
Bieber, T; Haller, O; Tueting, T; Uerlich, M; Wenzel, J, 2005
)
1.97
"Thus imiquimod appears to be an original antiviral compound, because it does not act directly on the virus itself."( [Mechanisms of imiquimod indirect antiviral activity].
Ajram, L; Chehadeh, W; Dewilde, A; Goffard, A; Hober, D; Lazrek, M; Wattré, P,
)
0.94
"Imiquimod is an immune response modifier shown to be effective in basal cell carcinoma (BCC)."( Imiquimod treatment of superficial and nodular basal cell carcinoma: 12-week open-label trial.
Campione, E; Chimenti, S; Fargnoli, MC; Marulli, GC; Micantonio, T; Peris, K, 2005
)
3.21
"Imiquimod is a topical immunomodulator that is indicated for the treatment of external genital and perianal warts. "( Viral and nonviral uses of imiquimod: a review.
Cherman, AM; Gupta, AK; Tyring, SK,
)
1.87
"Imiquimod is an immune response modifier that acts through toll-like receptor 7 to induce cytokine production and a subsequent innate and adaptive cell-mediated immune response. "( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from a randomized vehicle-controlled phase III study in Europe.
Cribier, B; Ferrándiz, C; Garcia Diez, A; McRae, S; Reifenberger, J; Requena, L; Schulze, HJ; Tebbs, V, 2005
)
3.21
"Imiquimod is a new and novel treatment option for cutaneous malignancies. "( Eruptive epidermoid cysts resulting from treatment with imiquimod.
Marty, CL; Randle, HW; Walsh, JS, 2005
)
2.02
"Imiquimod is an immune response modifier that acts through Toll-like receptor 7 to induce innate and cell-mediated immune responses. "( Recurrence rate of superficial basal cell carcinoma following successful treatment with imiquimod 5% cream: interim 2-year results from an ongoing 5-year follow-up study in Europe.
Barona, CG; Frank, RG; Gollnick, H; Megahed, M; Owens, M; Ruzicka, T; Stampone, P; Tebbs, V,
)
1.8
"Imiquimod is a topical immune response modifier that has proved efficacious in the treatment of the superficial variant of basal cell carcinoma. "( A preliminary study of imiquimod treatment in variants of basal cell carcinoma.
Germolic, D; Hamann, MS; Kotwall, C; McCutcheon, B; Rebolloso, Y; Stiles, A; White, K, 2005
)
2.08
"Imiquimod is an immune system-modifying drug that switches the immune system to a Th1 response, enabling it to defeat virus-infected and neoplastic cells. "( [Imiquimod treatment of lentigo maligna to dermoscopic and histologic clearance].
Lorentzen, HF; Weismann, K, 2005
)
2.68
"Imiquimod is an imidazoquinolone immune response modifier that has been shown to have indirect antiviral and antitumor effects with few adverse effects."( [Treatment of Bowen's disease of the penis with imiquimod 5% cream].
de Diego Rodríguez, E; Gómez Ortega, JM; Hernández Castrillo, A; Villanueva Peña, A, 2005
)
1.31
"Imiquimod 5% cream is a topically applied immune response modifier that has been shown to give effective treatment of actinic keratosis (AK). "( Imiquimod-induced regression of actinic keratosis is associated with infiltration by T lymphocytes and dendritic cells: a randomized controlled trial.
Barnetson, RS; Halliday, GM; Lee, JH; McKane, S; Ooi, T; Slade, HB; Zhuang, L, 2006
)
3.22
"Imiquimod appears to be a therapeutic alternative for perianal Bowen's disease, which seems to have a particular tendency to recur in this location where surgery may also be complicated."( [Perianal Bowen's disease treated with imiquimod].
Alfaro-Rubio, A; Botella, R; Guillén, C; Hueso, L; Llombart, B; Nagore, E; Requena, C; Sanmartín, O; Serra, C, 2005
)
1.32
"Imiquimod is a topical immunomodulator that stimulates both acquired and innate immunity."( [Lentigo maligna treated with 5% imiquimod cream].
Martín, T; Martínez, S; Ojeda, A; Vera, A, 2005
)
1.33
"Imiquimod is a topical immunomodulator with antiviral and antineoplastic action."( [Topical treatment of melanoma skin metastases with imiquimod].
Casado, M; González-Beato, M; Mayor, M; Miralles, L; Pizarro, A; Sigüenza, M; Vidaurrázaga, C, 2005
)
1.3
"Imiquimod is an imidazoquinoline, which class of compounds are known to have antiviral and antitumoural properties. "( Treatment of allergic airway inflammation and hyperresponsiveness by imiquimod modulating transcription factors T-bet and GATA-3.
Bian, T; De, W; Hu, JJ; Jin, SX; Ma, XQ; Yin, KS; Zhang, XL; Zhou, JY, 2006
)
2.01
"Imiquimod is a synthetic imidazoquinoline heterocyclic amine of 240.3 Da (C14H16N4). "( Topical imiquimod: mechanism of action and clinical applications.
Vidal, D, 2006
)
2.21
"Imiquimod is an immune response modifier with potent antiviral and antitumour activity. "( Efficacy of imiquimod 5% cream in the treatment of equine sarcoids: a pilot study.
Diaz, SF; Gilbert, S; Jessen, C; Malone, ED; Nogueira, SA; Torres, SM, 2006
)
2.16
"Imiquimod (IQ) is a member of immune response modifiers."( Topical treatment of molluscum contagiosum with imiquimod 5% cream in Turkish children.
Arican, O, 2006
)
1.31
"Imiquimod is an immune response-modifying agent with potent antiviral and antitumor activity effective in the treatment of various skin disorders, including in situ carcinoma of the skin (Bowen's disease). "( Erythroplasia of Queyrat treated with imiquimod 5% cream.
De Pasquale, R; Micali, G; Nasca, MR, 2006
)
2.05
"Imiquimod appears to be a safe and effective treatment option for AIN in HIV-positive MSM. "( Imiquimod treatment of anal intraepithelial neoplasia in HIV-positive men.
Altmeyer, P; Brockmeyer, NH; Hochdorfer, B; Kreuter, A; Pfister, H; Stücker, M; Swoboda, J; Weissenborn, SJ; Wieland, U, 2006
)
3.22
"Imiquimod is a Toll-like receptor-7 agonist capable of inducing complete clearance of basal cell carcinoma (BCC) and other cutaneous malignancies. "( Sequential gene profiling of basal cell carcinomas treated with imiquimod in a placebo-controlled study defines the requirements for tissue rejection.
Abati, A; Aricó, E; Astry, C; Fetsch, P; Filie, A; Marincola, FM; Norwood, C; Panelli, MC; Selleri, S; Slade, HB; Smith, K; Stashower, ME; Walters, SA; Wang, E; Zhao, Y, 2007
)
2.02
"Imiquimod appears to be a useful adjuvant to experimental laser tattoo removal in guinea pigs."( Topical imiquimod as an adjuvant to laser removal of mature tattoos in an animal model.
Colome-Grimmer, M; Diven, D; Magee, N; Motamedi, M; Oliveira, G; Ramirez, M; Uchida, T; Wagner, RF; Zamora, JG, 2007
)
2.22
"5% Imiquimod cream is a topical immune response modifier that has been used off-label to treat malignant melanocytic proliferations such as lentigo maligna. "( Treatment of atypical nevi with imiquimod 5% cream.
Crawford, RI; Dutz, JP; Martinka, M; Rivers, JK; Somani, N, 2007
)
1.24
"Imiquimod is a small molecule with adjuvant pro-inflammatory effects that can be topically delivered as a cream."( Imiquimod enhances the systemic immunity attained by local cryosurgery destruction of melanoma lesions.
Bendandi, M; del Olmo, J; Inoges, S; López-Diaz de Cerio, A; Marquina, M; Melero, I; Redondo, P, 2007
)
2.5
"Imiquimod cream 5% is an immunomodulatory agent that previously has been reported to successfully eradicate LM."( Lentigo maligna (melanoma in situ) treated with imiquimod cream 5%: 12 case reports.
Beltrani, V; Brennick, JB; Chapman, MS; Perry, AE; Spenny, ML; Storm, CA; Walford, J; Werchniak, AE, 2007
)
1.32
"Imiquimod cream 5% is a topical immune response modifier that targets the toll-like receptors 7 and 8 and up-regulates inflammatory pathways targeting diseased tissue."( Topical imiquimod therapy for basal and squamous cell carcinomas: a clinical experience.
Carroll, MT; Tillman, DK, 2007
)
1.5
"Imiquimod 5% cream is a promising, well-tolerated therapy for warts, AK and BP in transplant recipients."( 5% topical imiquimod tolerance in transplant recipients.
Ben M'barek, L; Euvrard, S; Frances, C; Lebbe, C; Legendre, C; Mebazaa, A; Menasché, S; Morel, P; Thervet, E, 2007
)
2.17
"Imiquimod is an immune response modifier approved by the FDA for the treatment of AK and superficial BCC lesions and its use is gradually expanded to various off-label precancerous and cancerous skin lesions."( Imiquimod: an immune response modifier in the treatment of precancerous skin lesions and skin cancer.
Falagas, ME; Papadavid, E; Stratigos, AJ, 2007
)
2.5
"Imiquimod 5% cream is an effective option for the treatment of AK, but the safety of topical immune stimulation in immunocompromised patients has not been widely evaluated."( Topical immunomodulation under systemic immunosuppression: results of a multicentre, randomized, placebo-controlled safety and efficacy study of imiquimod 5% cream for the treatment of actinic keratoses in kidney, heart, and liver transplant patients.
Amerio, P; Bichel, J; Euvrard, S; Guidi, B; Proby, CM; Rønnevig, J; Slade, HB; Stockfleth, E; Ulrich, C; van de Kerkhof, PC, 2007
)
1.26
"Imiquimod appears to be a safe alternative for the treatment of multiple actinic keratoses in patients with solid organ transplants. "( Topical immunomodulation under systemic immunosuppression: results of a multicentre, randomized, placebo-controlled safety and efficacy study of imiquimod 5% cream for the treatment of actinic keratoses in kidney, heart, and liver transplant patients.
Amerio, P; Bichel, J; Euvrard, S; Guidi, B; Proby, CM; Rønnevig, J; Slade, HB; Stockfleth, E; Ulrich, C; van de Kerkhof, PC, 2007
)
1.98
"Imiquimod appears to be an effective adjunctive treatment for LM but does not qualify as a replacement therapy for surgery."( Treatment of lentigo maligna with imiquimod before staged excision.
Bowen, GM; Cotter, MA; McKenna, JK, 2008
)
2.07
"Imiquimod is an immune response modifier currently used as a topical treatment of genital warts, basal cell carcinoma, cutaneous metastasis of malignant melanoma, and vascular tumors. "( EAPB0203, a member of the imidazoquinoxaline family, inhibits growth and induces caspase-dependent apoptosis in T-cell lymphomas and HTLV-I-associated adult T-cell leukemia/lymphoma.
Bazarbachi, A; Bonnet, PA; Deleuze-Masquéfa, C; El-Hajj, H; El-Sabban, ME; Hermine, O; Kfoury, Y; Lepelletier, Y; Moarbess, G, 2008
)
1.79
"Imiquimod is a TLR agonist, with immune response modifying properties that also stimulates antiangiogenic cytokines, downregulates the expression of proangiogenic factors, upregulates the expression of endogenous inhibitors, and induces endothelial cell apoptosis."( Antiangiogenesis in the treatment of skin cancer.
Li, VW; Li, WW, 2008
)
1.07
"Imiquimod is a topical immune response modifier and stimulator used in humans to treat a number of cutaneous neoplasms. "( Apparent clinical resolution of pinnal actinic keratoses and squamous cell carcinoma in a cat using topical imiquimod 5% cream.
Miller, WH; Peters-Kennedy, J; Scott, DW, 2008
)
2
"Imiquimod is a topically active imidazoquinoline immunomodulator agent. "( Imiquimod in mycosis fungoides.
Del Pozo, J; Fonseca, E; Martínez-González, MC; Mazaira, M; Verea-Hernando, MM; Yebra-Pimentel, MT,
)
3.02
"Imiquimod 5% cream is a novel alternative topical treatment that may have a potential role in management of these patients."( Involution of infantile haemangiomas after imiquimod 5% cream.
Barry, RB; Cook, LJ; Hughes, BR, 2008
)
1.33
"Imiquimod is a class of non-nucleoside imidazoquinolinamines which promotes local cytokine release from antigen-presenting cells inducing a T-h1 dominant cell-mediated response against virus-infected cells. "( Successful treatment of intranasal papillomata with imiquimod cream in a human immunodeficiency virus positive patient.
Amat, M; Fernández-Casado, A; Gallardo, F; Pujol, RM, 2009
)
2.05
"Imiquimod is an orally active interferon inducer with anti-tumour activity in experimental animals. "( A phase I clinical trial of imiquimod, an oral interferon inducer, administered daily.
Gore, ME; Horton, V; Moore, J; Owens, M; Savage, P; Witt, P, 1996
)
2.03
"Imiquimod is a novel immune-response modifier capable of inducing a variety of cytokines, including interferon alfa, tumor necrosis factor-alpha, as well as interleukins 1, 6, and 8."( Treatment of genital warts with an immune-response modifier (imiquimod).
Beutner, KR; Douglas, JM; Fox, TL; Hougham, AJ; Owens, ML; Spruance, SL, 1998
)
1.26
"Imiquimod is a new agent, an immune-response modifier, that has been demonstrated to have potent in vivo antiviral and antitumor effects in animal models."( Imiquimod, a patient-applied immune-response modifier for treatment of external genital warts.
Beutner, KR; Douglas, JM; Fox, TL; Hougham, AJ; Owens, ML; Schmitt, KA; Spruance, S; Trofatter, KF; Tyring, SK, 1998
)
2.46
"Imiquimod is an oral inducer of interferon (IFN) and several other proinflammatory cytokines and has been successfully used topically as an antiviral agent for the treatment of genital warts. "( The immune response modifier imiquimod requires STAT-1 for induction of interferon, interferon-stimulated genes, and interleukin-6.
Bottrel, RL; Levy, DE; Reis, LF; Tomai, M; Yang, YL, 1999
)
2.04
"Imiquimod 5% cream is a new compound which modifies the immune response by stimulating the production of interferon alpha and other cytokines. "( Imiqimod in clinical practice.
Trofatter, KF,
)
1.57
"Imiquimod is a topically active immunomodulatory agent that is formulated as a 5% cream for application by the patient. "( Topical imiquimod: a review of its use in genital warts.
Lamb, HM; Perry, CM, 1999
)
2.18
"Imiquimod 5% cream is a new therapeutic option for patients with genital warts. "( Topical imiquimod: a review of its use in genital warts.
Lamb, HM; Perry, CM, 1999
)
2.18
"Imiquimod is a cytokine and interferon inducer."( Therapeutic response of basal cell carcinoma to the immune response modifier imiquimod 5% cream.
Beutner, KR; Fox, TL; Geisse, JK; Ginkel, A; Helman, D; Owens, ML, 1999
)
1.25
"Imiquimod is a unique topical therapeutic agent useful in the treatment of external genital and perianal warts (condyloma acuminata) in adults. "( Topical imiquimod for recalcitrant facial flat warts.
Elston, DM; Schwab, RA, 2000
)
2.18
"Imiquimod is a recently developed imidazoquinolin heterocyclic amine that is an immune response modifier. "( Treatment of facial verrucae with topical imiquimod cream in a patient with human immunodeficiency virus.
Cutler, K; Don, PC; Kagen, MH; McAleer, P; Weinberg, JM,
)
1.84
"Imiquimod 5% cream is a novel topical immunomodulator that has been used successfully in the treatment of genital and common warts."( Treatment of recalcitrant plantar warts with imiquimod.
Parslew, RA; Yesudian, PD, 2002
)
1.3
"Imiquimod (Aldara, 3M) is an immune response modifier used for the treatment of anogenital warts. "( Successful treatment of anogenital Bowen's disease with the immunomodulator imiquimod, and monitoring of therapy by DNA image cytometry.
Brodersen, JP; Gutzmer, R; Kapp, A; Kaspari, M; Kiehl, P; Vogelbruch, M; Werfel, T, 2002
)
1.99
"Imiquimod is an oral IFN-alpha inducer with antitumor effectiveness for transplantable murine tumors."( Inhibition of murine tumor growth by an interferon-inducing imidazoquinolinamine.
Borden, EC; Bryan, GT; Hatcher, JF; Reiter, MJ; Sidky, YA; Weeks, CE, 1992
)
1

Effects

Imiquimod has a relatively low cost compared to other therapeutic options. Can be delivered via ambulatory care to patients with surgery contraindications. Side effects are tolerable.

Imiquimod has been shown to clear cases of melanoma in situ, but its role in the treatment of invasive cutaneous melanomas is unknown. The drug has a relatively low cost compared to other therapeutic options.

ExcerptReferenceRelevance
"Imiquimod 3.75% has an acceptable tolerability profile."( Lmax and imiquimod 3.75%: the new standard in AK management.
Stockfleth, E, 2015
)
1.56
"Imiquimod has a relatively low cost compared to other therapeutic options and can be delivered via ambulatory care to patients with surgery contraindications, and its side effects are tolerable."( Treatment of cutaneous tumors with topical 5% imiquimod cream.
Alessi, SS; Festa Neto, C; Messina, MC; Oliveira, WR; Pimentel, ER; Sanches, JA, 2009
)
1.33
"Imiquimod therapy has high effectiveness and safety in curing HHS."( Therapeutic outcomes and prognostic factors in patients with hypertrophic herpes simplex infection treated with imiquimod: A systematic review and meta-analysis of individual patient data from case reports and case series.
Leeyaphan, C; Nanchaipruek, Y; Phinyo, P, 2022
)
1.65
"Imiquimod has been long suggested as a treatment option for solar dermatitis, but this is the first known case report detailing its efficacy in dogs."( Topical Imiquimod Therapy for Localized Solar Dermatitis in a Dog.
Banovic, F; McHale, B,
)
1.29
"Imiquimod has also been used off-label in various other skin conditions (eg, Bowen's disease, lentigo maligna, vulvar intraepithelial neoplasia)."( Mucosal side effects in patients treated with topical imiquimod-A scoping review of the literature.
Gantenbein, L; Hammerl, V; Mueller, SM; Navarini, A; Parlar, B; Väth, H, 2021
)
1.59
"Imiquimod has been proposed as a treatment for LM."( Change in lentigo maligna score assessed by in vivo reflectance confocal microscopy after 1 month of imiquimod treatment for lentigo maligna management.
Bossard, C; Denis Musquer, M; Dréno, B; Khammari, A; Nguyen, JM; Soenen, A; Vergier, B; Vourc'h, M, 2022
)
1.66
"Imiquimod cream has been used off-label as monotherapy in the treatment of LM and may be used in the neoadjuvant setting prior to staged excision as a strategy to reduce the size of the surgical margins required to confirm negative histologic margins."( Rate of Recurrence of Lentigo Maligna Treated With Off-Label Neoadjuvant Topical Imiquimod, 5%, Cream Prior to Conservatively Staged Excision.
Bowen, GM; Bowling, M; Donigan, JM; Goldgar, DE; Hadley, ML; Hyde, MA, 2018
)
1.43
"Imiquimod has higher efficacy than single-cycle PDT but more adverse effects."( Conventional and combination topical photodynamic therapy for basal cell carcinoma: systematic review and meta-analysis.
Collier, NJ; Exton, LS; Green, AC; Haylett, AK; Ibbotson, SH; Mallipeddi, R; McKenna, KE; Mohd Mustapa, MF; Morton, CA; Moseley, H; Rhodes, LE; Seukeran, D; Ward, KA; Wong, TH, 2018
)
1.2
"Imiquimod therapy has been shown to be a less invasive and cheaper option than many other treatment modalities."( A Review on Imiquimod Therapy and Discussion on Optimal Management of Basal Cell Carcinomas.
Arora, H; Darwin, E; Kamath, P; Nouri, K, 2018
)
1.58
"Imiquimod has been recommended as an alternative treatment in lentigo maligna (LM) when surgical excision is not the treatment of choice."( Confocal Microscopy and Lentigo Maligna: An in vivo Pilot Study for the Assessment of Response to Imiquimod Therapy.
Brand, FL; Hunger, RE; Seyed Jafari, SM, 2019
)
1.45
"Imiquimod has been used for treating lentigo maligna (LM) in selected cases when surgery is not an appropriate option because of functional or aesthetic impairment. "( In vivo reflectance confocal microscopy to monitor the response of lentigo maligna to imiquimod.
Alarcon, I; Alos, L; Carrera, C; Malvehy, J; Palou, J; Puig, S, 2014
)
2.07
"Imiquimod 3.75% has an acceptable tolerability profile."( Lmax and imiquimod 3.75%: the new standard in AK management.
Stockfleth, E, 2015
)
1.56
"Imiquimod has revolutionized the treatment of field cancerization and has been approved for the treatment of superficial basal cell carcinoma with the recommendation of a 6-week treatment strategy, offering an alternative to surgery or other destructive treatment strategies."( Topical treatment of basal cell carcinoma with the immune response modifier imiquimod.
Papakostas, D; Stockfleth, E, 2015
)
1.37
"Imiquimod has been shown to clear cases of melanoma in situ, but its role in the treatment of invasive cutaneous melanomas is unknown."( Topical imiquimod clears invasive melanoma.
Grady, BE; Spencer, JM, 2016
)
1.59
"Imiquimod has a relatively low cost compared to other therapeutic options and can be delivered via ambulatory care to patients with surgery contraindications, and its side effects are tolerable."( Treatment of cutaneous tumors with topical 5% imiquimod cream.
Alessi, SS; Festa Neto, C; Messina, MC; Oliveira, WR; Pimentel, ER; Sanches, JA, 2009
)
1.33
"Imiquimod has immune-stimulant properties that can precipitate autoimmune conditions like eczema, psoriasis and lichenoid conditions. "( Imiquimod use in the genital area and development of lichen sclerosus and lichen planus.
O'Mahony, C; Stanley, M; Yesudian, PD, 2010
)
3.25
"Imiquimod has been shown to be an effective treatment for usual type vulvar intraepithelial neoplasia (uVIN). "( Nonsteroidal anti-inflammatory drugs do not interfere with imiquimod treatment for usual type vulvar intraepithelial neoplasia.
Beckmann, I; Blok, LJ; Heijmans-Antonissen, C; Helmerhorst, TJ; Kleinjan, A; Santegoets, LA; Terlou, A; van Beurden, M; van Seters, M, 2011
)
2.06
"Imiquimod has been reported to be efficacious in the topical treatment of uncomplicated infantile hemangiomas (IH). "( A prospective self-controlled phase II study of imiquimod 5% cream in the treatment of infantile hemangioma.
Chen, D; Chen, H; Chen, X; Hu, X; Jiang, C; Jin, Y; Lin, X; Ma, G,
)
1.83
"Imiquimod cream, 5%, has limited efficacy in the treatment of LM when determined by histopathologic assessment of the entire treated area. "( Efficacy of imiquimod cream, 5%, for lentigo maligna after complete excision: a study of 43 patients.
Byrne, M; Chamberlain, A; Curr, N; Dowling, JP; Haskett, M; Kelly, JW; Ly, L; O'Keefe, R; Sutton, T; Swain, S; Wolfe, R, 2011
)
2.19
"Imiquimod 3.75% cream has recently been approved by both the U.S. "( The role of imiquimod 3.75% cream in the treatment of external genital warts.
Berman, B; Wolf, J, 2012
)
2.2
"Imiquimod has the ability to clear melanoma in situ, but its effect on invasive melanoma is unknown."( Clearance of invasive melanoma with topical imiquimod.
Moon, SD; Spencer, JM, 2013
)
1.37
"Imiquimod 5% cream has been shown to be effective in the treatment of superficial basal cell carcinomas (sBCCs)."( Topical imiquimod treatment of superficial and nodular basal cell carcinomas in patients affected by basal cell nevus syndrome: a preliminary report.
Caltabiano, R; De Pasquale, R; Impallomeni, R; Lacarrubba, F; Micali, G, 2002
)
2.19
"Imiquimod 5% cream has been investigated for non-surgical treatment of superficial and nodular basal cell carcinoma (BCC) tumours."( Imiquimod 5% cream for the treatment of superficial and nodular basal cell carcinoma: randomized studies comparing low-frequency dosing with and without occlusion.
Andres, K; Bichel, J; Ding, L; Herrera, E; Ruzicka, T; Sterry, W; Takwale, A; Thissen, MR, 2002
)
3.2
"Imiquimod has been shown to be significantly more effective than placebo in clearing genital warts, and mechanism of action studies indicate that this is related to the ability to generate proinflammatory cytokines and a Th1 response."( Imiquimod and the imidazoquinolones: mechanism of action and therapeutic potential.
Stanley, MA, 2002
)
2.48
"Imiquimod has the potential to induce apoptosis in skin cancer cells, possibly by circumventing mechanisms developed by malignant tumors to resist apoptotic signals."( Tumor-selective induction of apoptosis and the small-molecule immune response modifier imiquimod.
Benninghoff, B; Bong, AB; Drewniok, C; Geilen, CC; Gollnick, H; Herz, J; Reifenberger, J; Schön, M; Schön, MP; Slade, HB, 2003
)
1.98
"Imiquimod has no efficacy in controlling C. "( Imiquimod does not affect shedding of viable chlamydiae in a murine model of Chlamydia trachomatis genital tract infection.
Ault, KA; Cohoon, KP; Ramsey, KH; Shaba, N, 2003
)
3.2
"Imiquimod has been used for basal cell carcinomas (BCCs). "( Topical imiquimod treatment for nodular basal cell carcinomas: an open-label series.
Amonette, RA; Haque, R; Huber, A; Huber, JD; Kuwahara, RT; Skinner, RB, 2004
)
2.2
"Imiquimod has been shown to be efficacious as a topical treatment for basal cell carcinoma (BCC)."( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, randomized, vehicle-controlled studies.
Caro, I; Geisse, J; Golitz, L; Lindholm, J; Owens, M; Stampone, P, 2004
)
2.49
"Imiquimod has been shown to stimulate the cutaneous immune response and be effective for the treatment of nonmelanoma skin cancers."( Imiquimod 5% cream for the treatment of actinic keratosis: results from two phase III, randomized, double-blind, parallel group, vehicle-controlled trials.
Dinehart, S; Fox, TL; Jorizzo, J; Lebwohl, M; Lee, JH; Lee, PK; Tawfik, N; Whiting, D, 2004
)
2.49
"Imiquimod 5% cream has proven to be effective in superficial and nodular basal cell carcinomas in nonimmunosuppressed patients and treating squamous cell carcinomas in situ in transplant patients. "( Efficacy of imiquimod 5% cream for basal cell carcinoma in transplant patients.
Alomar, A; Vidal, D, 2004
)
2.15
"Imiquimod has been shown to be a safe and effective treatment for a variety of skin conditions."( Viral and nonviral uses of imiquimod: a review.
Cherman, AM; Gupta, AK; Tyring, SK,
)
1.87
"Imiquimod has also been found to be effective for other virus-associated dermatologic lesions, including common and flat warts, molluscum contagiosum, and herpes simplex virus type-2 as well as for some cases of cutaneous leishmaniasis."( Successful treatment of antifungal- and cryotherapy-resistant subcutaneous hyalohyphomycosis in an immunocompetent case with topical 5% imiquimod cream.
Erbagci, Z; Erkilic, S; Tuncel, AA; Zer, Y, 2005
)
1.25
"Imiquimod 5% cream has proven to be an effective treatment for external genital warts, superficial basal cell carcinoma, and actinic keratosis."( Topical imiquimod: mechanism of action and clinical applications.
Vidal, D, 2006
)
1.49
"Imiquimod has been successfully used for treatment of various epithelial cutaneous neoplasms."( Imiquimod 5% cream in the treatment of Bowen's disease and invasive squamous cell carcinoma.
Chimenti, S; Fargnoli, MC; Lozzi, GP; Micantonio, T; Peris, K, 2006
)
3.22
"Imiquimod has been investigated as a safe and effective therapeutic option for the treatment of actinic keratosis (AK)."( Vehicle-controlled, randomized, double-blind study to assess safety and efficacy of imiquimod 5% cream applied once daily 3 days per week in one or two courses of treatment of actinic keratoses on the head.
Alomar, A; Bichel, J; McRae, S, 2007
)
2.01
"Imiquimod 5% cream has been found to be effective and safe in preventing recurrence of keloids on earlobes after excision. "( Imiquimod 5% cream for the prevention of recurrence after excision of presternal keloids.
Gupta, S; Khaitan, BK; Malhotra, AK; Sharma, VK, 2007
)
3.23
"Imiquimod 5% cream has demonstrated effectiveness in the treatment of lentigo maligna (LM) in several small studies. "( Treatment of lentigo maligna with imiquimod before staged excision.
Bowen, GM; Cotter, MA; McKenna, JK, 2008
)
2.07
"Imiquimod has been identified as a potent antiviral and antitumor agent in animal models. "( Cytokine induction in mice by the immunomodulator imiquimod.
Miller, RL; Reiter, MJ; Testerman, TL; Tomai, MA; Weeks, CE, 1994
)
1.98
"Imiquimod has been reported to induce interferon-alpha and other cytokines in animals and humans, but its precise role as an immunomodulator at skin sites has not been determined."( Effects of a novel topical immunomodulator, imiquimod, on keratinocyte cytokine gene expression.
Kondo, S; Kono, T; McKenzie, RC; Pastore, S; Sauder, DN; Shivji, GM; Tomai, MA, 1994
)
1.27
"Imiquimod 5% cream has been formulated for the treatment of external genital and perianal warts (condylomata acuminata) in male and female patients."( Immune response modification: imiquimod.
Tyring, S, 1998
)
1.31
"Imiquimod has no direct antiviral activity but demonstrates efficacy in several animal models of virus infection."( Treatment of primary herpes simplex virus infection in guinea pigs by imiquimod.
Gerster, JF; Imbertson, LM; Miller, RL; Reiter, MJ, 1999
)
1.26
"Imiquimod has anti-viral and anti-tumor effects in animal models and has been approved for the topical treatment of external genital and perianal warts in humans."( Imiquimod, a topical immune response modifier, induces migration of Langerhans cells.
Amerio, P; Miller, RL; Sauder, DN; Shivji, GM; Suzuki, H; Tomai, MA; Toto, P; Wang, B, 2000
)
2.47
"Imiquimod 5% cream has been used effectively to treat superficial basal cell carcinomas (BCCs)."( The use of imiquimod 5% cream for the treatment of superficial basal cell carcinomas in a basal cell nevus syndrome patient.
Amonette, R; Kagy, MK, 2000
)
2.14
"Imiquimod (IQ) has been successfully used in treatment of genital warts. "( Correlation between pretreatment levels of interferon response genes and clinical responses to an immune response modifier (Imiquimod) in genital warts.
Arany, I; Brysk, MM; McDermott, DJ; Miller, RL; Slade, HB; Smith, MH; Stanley, MA; Tomai, MA; Tyring, SK, 2000
)
1.96
"Imiquimod 5% cream has been shown to have activity in treating various cutaneous malignancies."( Therapeutic response of a brother and sister with xeroderma pigmentosum to imiquimod 5% cream.
Varghese, M; Weisberg, NK, 2002
)
1.27

Actions

Imiquimod is at least as cost-effective as podophyllotoxin the treatment of external genital warts. It promotes local immune activation, which results in resolution of viral lesions such as anogenital warts and HSV disease.

ExcerptReferenceRelevance
"Imiquimod plays an important role in the management of condyloma and premalignant lesions. "( Imiquimod induced vitiligo-like lesions-A consequence of modified melanocyte function.
Cen, J; Cheng, H; Lin, X; Seifert, O; Yu, H, 2022
)
3.61
"Imiquimod did not cause the expected psoriasis-like skin changes. "( Imiquimod does not elicit inflammatory responses in the skin of the naked mole rat (Heterocephalus glaber).
Abelson, KSP; Kanui, TI; Kisipan, ML; Ojoo, RO, 2020
)
3.44
"Imiquimod promotes local immune activation, which results in resolution of viral lesions such as anogenital warts and HSV disease."( Topical imiquimod treatment of aciclovir-resistant herpes simplex disease: case series and literature review.
Nisbet, M; Perkins, N; Thomas, M, 2011
)
1.52
"Imiquimod, because of its greater initial efficacy, is at least as cost-effective as podophyllotoxin the treatment of external genital warts."( [A model-based comparison of cost effectiveness of imiquimod versus podophyllotoxin for the treatment of external anogenital warts in France].
Lafuma, A; Monsonego, J; Moyal-Barracco, M; Pribil, C,
)
1.83
"Imiquimod was found to increase the number and maturation status of dendritic cells in draining lymph nodes, and to enhance antigen-specific CD4(+) and CD8(+) T cell responses, as assessed by analyses of clonal expansion, and the quantity and kinetics of cytokine production from these cells in lymph nodes and spleens collected after vaccination."( Imiquimod and resiquimod in a mouse model: adjuvants for DNA vaccination by particle-mediated immunotherapeutic delivery.
Brett, SJ; Daly, MG; Thomsen, LL; Tite, JP; Topley, P, 2004
)
2.49
"Imiquimod does not inhibit viruses directly, nor does it cause direct, non-specific cytolytic destruction [1]."( Cytokine induction and modifying the immune response to human papilloma virus with imiquimod.
Slade, HB,
)
1.08
"Imiquimod's ability to inhibit primary lesion development in the guinea pig model of Herpes simplex virus (HSV) intravaginal infection was studied."( Treatment of primary herpes simplex virus infection in guinea pigs by imiquimod.
Gerster, JF; Imbertson, LM; Miller, RL; Reiter, MJ, 1999
)
1.26
"Imiquimod, however, did enhance Langerhans cell migration from skin to draining lymph nodes."( Imiquimod, a topical immune response modifier, induces migration of Langerhans cells.
Amerio, P; Miller, RL; Sauder, DN; Shivji, GM; Suzuki, H; Tomai, MA; Toto, P; Wang, B, 2000
)
2.47

Treatment

Imiquimod was used as a treatment for HHS by several studies, but the therapeutic outcomes varied. In imiquimods-treated HPV-KER keratinocytes, PARP inhibition recapitulated the in vivo findings, namely keratinocyte hyperproliferation. ImiquimOD treatment of those IL-17 signaling-deficient mice maintained high monocytic infiltration but failed to attract neutrophils into the skin.

ExcerptReferenceRelevance
"Imiquimod treatment was successful in 60% of women who completed imiquimod treatment and 95% of women treated with LLETZ."( Topical Imiquimod Treatment of High-grade Cervical Intraepithelial Neoplasia (TOPIC-3): A Nonrandomized Multicenter Study.
de Vos Van Steenwijk, PJ; Hendriks, N; Hoosemans, L; Koeneman, MM; Kooreman, LFS; Kruitwagen, RFPM; Kruse, AJ; Nijman, HW; Penders, CGJ; Piek, JMJ; Sep, SJS; Slangen, BFM; van Beekhuizen, HJ; van de Sande, AJM; van Kuijk, SMJ, 2022
)
1.88
"Imiquimod was used as a treatment for HHS by several studies, but the therapeutic outcomes varied."( Therapeutic outcomes and prognostic factors in patients with hypertrophic herpes simplex infection treated with imiquimod: A systematic review and meta-analysis of individual patient data from case reports and case series.
Leeyaphan, C; Nanchaipruek, Y; Phinyo, P, 2022
)
1.65
"In imiquimod-treated HPV-KER keratinocytes, PARP inhibition recapitulated the in vivo findings, namely keratinocyte hyperproliferation; furthermore, the mRNA expression of psoriasis-associated cytokines (IL6, IL1β, IL8, IL17 and IL23A) was also induced."( Poly(ADP-ribose) polymerase-1 depletion enhances the severity of inflammation in an imiquimod-induced model of psoriasis.
Antal, D; Bai, P; Hegedűs, C; Kiss, B; Márton, J; Méhes, G; Szántó, M; Szegedi, A; Szödényi, A; Virág, L, 2020
)
1.3
"The imiquimod treated group and the unstimulated group had a higher immune response to VHSV compared to the poly (I:C) treated group."( Poly (I:C) and imiquimod induced immune responses and their effects on the survival of olive flounder (Paralichthys olivaceus) from viral haemorrhagic septicaemia.
Avunje, S; Jung, SJ, 2017
)
1.29
"Imiquimod treatment resulted in spontaneous scratching, which was significantly inhibited by tofacitinib treatment."( Antipruritic Effects of Janus Kinase Inhibitor Tofacitinib in a Mouse Model of Psoriasis.
Akiyama, T; Hashimoto, T; Sakai, K; Sanders, KM; Yosipovitch, G, 2019
)
1.24
"Imiquimod treatment of those IL-17 signaling-deficient mice maintained high monocytic infiltration but failed to attract neutrophils into the skin."( Imiquimod-Induced Psoriasis in Mice Depends on the IL-17 Signaling of Keratinocytes.
Kurschus, FC; Mohebiany, AN; Moos, S; Waisman, A, 2019
)
2.68
"Imiquimod treatment also resulted in a significant reduction in pro-inflammatory neutrophil chemotactic cytokines and prevented the increase in viral-induced lung dysfunction."( Intranasal and epicutaneous administration of Toll-like receptor 7 (TLR7) agonists provides protection against influenza A virus-induced morbidity in mice.
Bozinovski, S; Brooks, DA; Erlich, J; Liong, F; Liong, S; Luong, R; O'Leary, JJ; Selemidis, S; Seow, HJ; To, EE; Vlahos, R, 2019
)
1.24
"Imiquimod 5% cream treatment has no clinically relevant HRQoL impact in AK and sBCC patients according to the Skindex-17 and SCI. "( Patient Perception of Imiquimod Treatment for Actinic Keratosis and Superficial Basal Cell Carcinoma in 202 Patients.
Gaastra, MT; Hollestein, LM; Holterhues, C; Kuijpers, DI; Nijsten, TE; Schuttelaar, ML; van Hattem, S; Waalboer-Spuij, R, 2015
)
2.17
"Imiquimod treatment induced a psoriasis-like skin inflammation. "( Resveratrol ameliorates imiquimod-induced psoriasis-like skin inflammation in mice.
Jessen, N; Kjær, TN; Pedersen, SB; Stenderup, K; Thorsen, K, 2015
)
2.17
"In imiquimod-treated mice PD-L1-Fc reduced psoriatic inflammation when given alone and enhanced the therapeutic effect of anti-p40 when given in combination."( Programmed cell death ligand 1 alleviates psoriatic inflammation by suppressing IL-17A production from programmed cell death 1-high T cells.
Ban, CY; Choi, YJ; Kim, HP; Kim, J; Kim, JH; Kim, SC; Kim, SE; Kim, TG; Lee, BH; Park, J; Park, SH; Shin, EC; Song, MY; Sung, YC, 2016
)
0.95
"Imiquimod treatment promoted the clearance of EcPV in 71.4% of the treated ears."( Imiquimod treatment for Equus caballus papillomavirus infection in equine aural plaques.
Araujo, JP; Basso, RM; Borges, AS; Herman, M; Mira, J; Oliveira-Filho, JP; Olivo, G; Zakia, LS, 2016
)
2.6
"Imiquimod-treated mice exhibited a significant increase in spontaneous scratching behavior directed to the treated area as well as touch-evoked scratching (alloknesis)."( Mouse model of imiquimod-induced psoriatic itch.
Akiyama, T; Jensen, L; Sakai, K; Sanders, KM; Yanushefski, KM; Yosipovitch, G; Youssef, MR, 2016
)
1.51
"Most imiquimod treatment failures occurred in year 1."( Surgery Versus 5% Imiquimod for Nodular and Superficial Basal Cell Carcinoma: 5-Year Results of the SINS Randomized Controlled Trial.
Armstrong, SJ; Bath-Hextall, F; Colver, GB; Miller, PSJ; Ozolins, M; Perkins, W; Williams, HC, 2017
)
1.24
"If Imiquimod was the treatment selected, alternative therapeutic approaches should be advised if no response is seen after the fourth week of treatment."( [Localization and size as prognostic factors of response to treatment with 5% imiquimod cream in non circumcised males with penile condyloma acuminata].
Cortés-González, JR; Gómez-Guerra, LS; Maqueo, JA,
)
0.87
"Imiquimod-treated tumors contained a decreased percentage of T reg cells, and these cells produced less FOXP3, interleukin (IL)-10, and transforming growth factor (TGF)-beta."( Human squamous cell carcinomas evade the immune response by down-regulation of vascular E-selectin and recruitment of regulatory T cells.
Clark, RA; Edwards, V; Hijnen, D; Huang, SJ; Kim, JE; Kupper, TS; Lambert, J; Miller, DM; Mollet, IG; Murphy, GF; Muthukuru, M; Schanbacher, CF, 2008
)
1.07
"Imiquimod use in the treatment of basal cell carcinoma (BCC) has proven to be successful in a large percentage of cases, inducing tumor regression; however, the exact cellular mechanism has not been fully clarified."( In vivo characterization of the inflammatory infiltrate and apoptotic status in imiquimod-treated basal cell carcinoma.
Carli, P; Chiarugi, A; De Giorgi, V; Maio, V; Massi, D; Nicoletti, P; Paglierani, M; Salvini, C; Santucci, M, 2009
)
2.02
"Imiquimod treatment induced a significant increase in the mononuclear inflammatory response. "( In vivo characterization of the inflammatory infiltrate and apoptotic status in imiquimod-treated basal cell carcinoma.
Carli, P; Chiarugi, A; De Giorgi, V; Maio, V; Massi, D; Nicoletti, P; Paglierani, M; Salvini, C; Santucci, M, 2009
)
2.02
"Imiquimod treatment and office-based excision with immediate repair of the surgical defect have similar total average costs of $959 (BCC cheek) and $931 (SCC arm) and $1006 (BCC cheek) and $907 (SCC arm), respectively."( A relative value unit-based cost comparison of treatment modalities for nonmelanoma skin cancer: effect of the loss of the Mohs multiple surgery reduction exemption.
Coldiron, BM; Rogers, HW, 2009
)
1.07
"Imiquimod treatment induced apoptosis of melanocytes, which was observed by TUNEL assay and Hoechst 33258 staining."( Imiquimod induces apoptosis of human melanocytes.
Ahn, JH; Hwang, HS; Kang, HY; Kang, SU; Kim, CH; Lee, MH; Pyun, JH, 2010
)
2.52
"Imiquimod treatment induced the activation and proliferation of T-helper and cytotoxic T-cells, B-cells and T-regulatory cells."( Long-term remission of recurrent herpes labialis following topical imiquimod application on distant healthy skin: a clinical and immunological study.
Monastirli, A; Mouzaki, A; Papadaki, H; Pasmatzi, E; Rodi, M; Tsambaos, D, 2011
)
1.33
"Imiquimod treatments to both CD11c+ and intestinal epithelial cells significantly increased expression of antimicrobial peptides (AMPs) and reduced survival of intracellular S."( Toll-like receptor-7 ligand Imiquimod induces type I interferon and antimicrobial peptides to ameliorate dextran sodium sulfate-induced acute colitis.
Aden, K; Anant, S; Bishnupuri, KS; Dieckgraefe, BK; Houchen, CW; Luo, Q; Sainathan, SK, 2012
)
1.39
"Imiquimod treatment also appeared to delay the time to recurrence of HSV lesions."( Successful treatment of aciclovir and foscarnet resistant Herpes simplex virus lesions with topical imiquimod in patients infected with human immunodeficiency virus type 1.
Agut, H; Caumes, E; Challine, D; Deback, C; Lascaux, AS; Lévy, Y; Melica, G, 2012
)
1.32
"Imiquimod-treated macrophages activated nuclear factor-κB (NF-κB) and released pro-inflammatory cytokines and chemokines."( Toll-like receptor 7 stimulation by imiquimod induces macrophage autophagy and inflammation in atherosclerotic plaques.
Bult, H; De Meyer, GR; De Meyer, I; Martinet, W; Schrijvers, DM; Timmermans, JP, 2012
)
1.38
"Imiquimod treatment 4 or 15 h before fear conditioning significantly enhanced context-dependent freezing behavior."( Toll-like receptor 7-mediated enhancement of contextual fear memory in mice.
Hiraide, S; Kobayashi, M; Kubo, Y; Matsumoto, M; Togashi, H; Yanagawa, Y, 2012
)
1.1
"Imiquimod treatment was well tolerated, with only grade 1 to 2 transient local and systemic side effects consistent with imiquimod's immunomodulatory effects."( Topical TLR7 agonist imiquimod can induce immune-mediated rejection of skin metastases in patients with breast cancer.
Adams, S; Axelrod, D; Bhardwaj, N; Chiriboga, L; Demaria, S; Formenti, SC; Goldberg, JD; Hochman, T; Kozhaya, L; Liebes, L; Martiniuk, F; Meng, TC; Novik, Y; Shuman, N; Speyer, J; Tiersten, A; Unutmaz, D, 2012
)
1.42
"The imiquimod treatment played a direct effect on SCC, demonstrated by the increased number of S-100(+) dendritic cells, which could suggest an important role of immune surveillance against neoplastic proliferation."( Effects of imiquimod and low-intensity laser (λ660 nm) in chemically induced oral carcinomas in hamster buccal pouch mucosa.
de C Monteiro, JS; de Oliveira, SC; de Souza, SC; dos Santos, JN; Gurgel, CA; Pinheiro, AL; Reis Júnior, JA, 2013
)
1.26
"Imiquimod treatment induced a massive increase in macrophage peritumoral and intratumoral infiltration."( Mechanisms underlying imiquimod-induced regression of basal cell carcinoma in vivo.
Benninghoff, B; Burg, G; Dummer, R; Maier, T; Slade, H; Urosevic, M, 2003
)
1.35
"Imiquimod treatment resulted in clinical and histological eradication of EMPD, with no recurrence observed during 6 months of follow-up."( Successful treatment of extramammary Paget's disease of the scrotum with imiquimod 5% cream.
Berman, B; Elgart, G; Poochareon, V; Spencer, J; Villa, A, 2003
)
1.27
"Imiquimod-treated tumors showed decreased tumor cell proliferation, increased tumor apoptosis, and increased expression of tissue inhibitor of matrix metalloproteinase-1 with decreased activity of matrix metalloproteinase-9."( Topically applied imiquimod inhibits vascular tumor growth in vivo.
Gugneja, S; Miller, R; Neuschler, E; Neuschler, N; Paller, AS; Puscasiu, E; Sidbury, R; Sun, P; Tomai, M; Wang, XQ, 2003
)
1.37
"Imiquimod-treated BCCs stained more strongly for caspase-3 and to a lesser degree p53 as compared with vehicle-treated BCCs."( Evaluation of superficial basal cell carcinomas after treatment with imiquimod 5% cream or vehicle for apoptosis and lymphocyte phenotyping.
Berman, B; Dearaujo, T; Sullivan, TP; Vincek, V, 2003
)
1.27
"Imiquimod treatment leads either to complete regression or to a significant reduction of the tumors."( Identification and characterization of pDC-like cells in normal mouse skin and melanomas treated with imiquimod.
Holcmann, M; Lührs, P; Meindl, S; Palamara, F; Sibilia, M; Stingl, G, 2004
)
1.26
"Two imiquimod-treated sBCC patients who did not mount an inflammatory response to imiquimod and whose lesions lacked the IFN-alpha signature after treatment had fewer PDCs in treated lesions compared with other treated patients with such a response."( Disease-independent skin recruitment and activation of plasmacytoid predendritic cells following imiquimod treatment.
Beyeler, M; Burg, G; Conrad, C; Dummer, R; Gilliet, M; Laine, E; Urosevic, M, 2005
)
1.03
"Imiquimod-treated, UV-irradiated XS52 triggered a more vigorous IFN-gamma production than did either imiquimod-treated XS52 or UV-irradiated XS52, again suggesting a synergy between the two treatments."( Topical imiquimod treatment prevents UV-light induced loss of contact hypersensitivity and immune tolerance.
Fishelevich, R; Gaspari, AA; Luzina, I; Miller, RL; Thatcher, TH; Tomai, MA, 2006
)
1.49
"Imiquimod treatment inhibits OVA induced airway inflammation by modulating key master switches GATA-3 and T-bet that result in committing T helper cells to a Th1 phenotype."( Treatment of allergic airway inflammation and hyperresponsiveness by imiquimod modulating transcription factors T-bet and GATA-3.
Bian, T; De, W; Hu, JJ; Jin, SX; Ma, XQ; Yin, KS; Zhang, XL; Zhou, JY, 2006
)
2.01
"Imiquimod treatment of AK resulted in superior sustained clearance and cosmetic outcomes compared with cryosurgery and 5-FU. "( A randomised study of topical 5% imiquimod vs. topical 5-fluorouracil vs. cryosurgery in immunocompetent patients with actinic keratoses: a comparison of clinical and histological outcomes including 1-year follow-up.
Krawtchenko, N; Mann, I; Roewert-Huber, J; Sterry, W; Stockfleth, E; Ulrich, M, 2007
)
2.06
"Imiquimod treatment of primary genital herpes simplex virus (HSV) infection in guinea pigs reduces the level of genital disease by 90%."( Posttherapy suppression of genital herpes simplex virus (HSV) recurrences and enhancement of HSV-specific T-cell memory by imiquimod in guinea pigs.
Bernstein, DI; Harrison, CJ; Miller, RL, 1994
)
1.22
"Of imiquimod-treated patients whose warts cleared completely and who finished the 10-week follow-up period, 19% (3 of 16) experienced recurrences of warts."( Treatment of genital warts with an immune-response modifier (imiquimod).
Beutner, KR; Douglas, JM; Fox, TL; Hougham, AJ; Owens, ML; Spruance, SL, 1998
)
1.06
"All imiquimod-treated patients had a > or =75% reduction in total wart area while only one of three placebo-treated patients had a similar reduction."( Enhancement of the innate and cellular immune response in patients with genital warts treated with topical imiquimod cream 5%.
Arany, I; McDermott, DJ; Miller, RL; Slade, HB; Smith, MH; Stanley, MA; Tomai, MA; Tyring, SK, 1999
)
1
"Imiquimod treatment inhibited lesion development and/or virus shedding in guinea pigs inoculated with HSV-1, HSV-2 or virus isolates resistant to acyclovir."( Treatment of primary herpes simplex virus infection in guinea pigs by imiquimod.
Gerster, JF; Imbertson, LM; Miller, RL; Reiter, MJ, 1999
)
1.26
"An imiquimod treatment protocol, previously used in a study of this drug for the treatment of external genital warts, was followed."( Self-administered topical imiquimod treatment of vulvar intraepithelial neoplasia. A report of four cases.
Davis, G; Richard, J; Wentworth, J, 2000
)
1.12
"Treatment with imiquimod was self-administered in a slowly escalating dosage scheme up to three times per week for a period of 4-6 months."( Topical imiquimod versus surgery for vulvar intraepithelial neoplasia: a multicentre, randomised, phase 3, non-inferiority trial.
Boandl, A; Bogner, G; Ciresa-König, A; Holter, M; Jan, Z; Joura, EA; Kalteis, MS; Regauer, S; Reich, O; Schauer, C; Tamussino, K; Trutnovsky, G; Widschwendter, A, 2022
)
1.5
"Treatment of imiquimod-challenged mice with an NRTN-neutralizing antibody significantly reduced nonpeptidergic nerve density as well as spontaneous scratching."( Role of neurturin in spontaneous itch and increased nonpeptidergic intraepidermal fiber density in a mouse model of psoriasis.
Akiyama, T; Jensen, LE; Sakai, K; Sanders, KM; Yanushefski, KM; Yosipovitch, G; Youssef, MR, 2017
)
0.81
"NTP treatment in imiquimod-induced psoriasis-like mouse skin inhibited increases in epithelial cell thickness and expression of pro-inflammatory molecules compared to ones without the NTP treatment."( Non-thermal atmospheric plasma ameliorates imiquimod-induced psoriasis-like skin inflammation in mice through inhibition of immune responses and up-regulation of PD-L1 expression.
Kim, CH; Kim, HJ; Lee, MH; Lee, YS; Won, HR, 2017
)
1.05
"Treatment with imiquimod induced cell cycle arrest at the G2/M phase in TRMPA-C2 cells, confirmed by the changes of G2/M checkpoint regulators such as reduction of cyclin B1 expression and increase of phospho-CDC2 and p21 in TRAMP-C2 cells treated with imiquimod."( In vitro and in vivo growth inhibition of prostate cancer by the small molecule imiquimod.
Cho, SD; Choi, ES; Han, JH; Jeon, SJ; Kim, BY; Kim, DJ; Lee, J; Park, JH, 2013
)
0.96
"Mice treated with imiquimod plus PRL, but not those treated with imiquimod plus phosphate-buffered saline, showed significantly increased mRNA levels of TNF-α, IFN-γ, IL-12p35 and CXCL2 compared with controls."( Prolactin induces the production of Th17 and Th1 cytokines/chemokines in murine Imiquimod-induced psoriasiform skin.
Hau, CS; Kanda, N; Sato, S; Shibata, S; Tada, Y; Watanabe, S, 2014
)
0.95
"Mice treated with Imiquimod (IMQ) to induce psoriasis can be used to evaluate the pathogenesis of psoriasis, and this model has become one of the most important in vivo research tools for research on the disease."( A PPARδ-selective antagonist ameliorates IMQ-induced psoriasis-like inflammation in mice.
Chen, Y; Hao, Y; Hu, J; Sun, J; Wang, L; Wang, X, 2016
)
0.76
"Treatment with imiquimod was less painful than cryotherapy (P = 0.034)."( Comparison of cryotherapy to imiquimod 5% in the treatment of anogenital warts.
Antoniou, C; Anyfantakis, V; Bethimoutis, G; Eustathios, R; Hadjivassiliou, M; Hagjivassiliou, M; Katsambas, A; Katzouranis, I; Lagogianni, E; Nicolaidou, E; Panagiotopoulos, A; Rallis, E; Stefanaki, C, 2008
)
0.98
"Treatment with Imiquimod 5% cream 3 times per week was given and follow up was at the first and second week and afterwards every second week."( [Localization and size as prognostic factors of response to treatment with 5% imiquimod cream in non circumcised males with penile condyloma acuminata].
Cortés-González, JR; Gómez-Guerra, LS; Maqueo, JA,
)
0.7
"Treatment with imiquimod cream showed a total clearance of external genital or perianal warts in about 50% of immunocompetent subjects."( Imiquimod 5% cream for external genital or perianal warts in human immunodeficiency virus-positive patients treated with highly active antiretroviral therapy: an open-label, noncomparative study.
Aquilina, C; Bauhofer, A; Bouscarat, F; Dupin, N; Mougin, C; Ortonne, JP; Saiag, P, 2009
)
2.14
"SCC treated with imiquimod before excision contained dense T-cell infiltrates associated with tumor cell apoptosis and histological evidence of tumor regression."( Imiquimod enhances IFN-gamma production and effector function of T cells infiltrating human squamous cell carcinomas of the skin.
Calarese, AW; Clark, RA; Hijnen, D; Huang, SJ; Kupper, TS; Miller, DM; Mollet, IG; Murphy, GF; Schanbacher, CF; Schmults, CD, 2009
)
2.12
"Treatment with imiquimod applied at home by patient gives excellent cosmetic results."( [New perspective in immunotherapy: local imiquimod treatment].
Kemény, L; Nagy, N, 2010
)
0.97
"Treatment with imiquimod significantly inhibited tumor growth, an effect that was associated with increased tumor infiltration by CD11c(+), CD4(+), and CD8(+) cells, and abolished by depletion of CD8(+) cells. "( Synergy of topical toll-like receptor 7 agonist with radiation and low-dose cyclophosphamide in a mouse model of cutaneous breast cancer.
Adams, S; Babb, JS; Demaria, S; Dewan, MZ; DiNapoli, S; Formenti, SC; Kawashima, N; Vanpouille-Box, C, 2012
)
0.73
"Treatment with imiquimod anal tampons was well tolerated. "( Application of imiquimod by suppositories (anal tampons) efficiently prevents recurrences after ablation of anal canal condyloma.
Brodersen, JP; Gutzmer, R; Kapp, A; Kaspari, M; Kaspari, T, 2002
)
1.02
"Treatment with imiquimod cream 5% (Aldara), a topical immune response modifier applied once a day and left for 12 h, led to significant partial tumor regression and clear demarcation of the tumor."( Treatment of verrucous carcinoma with imiquimod and CO2 laser ablation.
Hafner, J; Heinzerling, LM; Kamarashev, J; Kempf, W; Nestle, FO, 2003
)
0.93
"Treatment with imiquimod 5% cream, capable of inducing interferon (IFN)-alpha, effectively cures basal cell carcinoma (BCC), both clinically and histologically. "( Expression of Fas-receptor on basal cell carcinomas after treatment with imiquimod 5% cream or vehicle.
Berman, B; De Araujo, T; Nadji, M; Sullivan, T, 2003
)
0.9
"Treatment with imiquimod 5% cream for 8-10 weeks was effective in both cases with no clinical evidence of relapse at 4 and 6 months."( Topical treatment of intraepithelial penile carcinoma with imiquimod.
Micali, G; Nasca, MR; Tedeschi, A, 2003
)
0.9
"Treatment with imiquimod 5% cream was effective when applied once a day for 3 consecutive days followed by 4 days without treatment, over a period of 5 weeks."( Treatment of Bowen's disease of the penis with imiquimod 5% cream.
Danielsen, AG; Sand, C; Weismann, K, 2003
)
0.92
"Treatment with imiquimod increased the apoptotic index (P < 0.05), reduced Bcl-2 expression (P < 0.05), and increased the number of CD3+, CD8+, CD20+, CD68+, granzyme B+, and S-100+ cells in the inflammatory infiltrate of the BCC (P < 0.05)."( Open study of the efficacy and mechanism of action of topical imiquimod in basal cell carcinoma.
Alomar, A; Matías-Guiu, X; Vidal, D, 2004
)
0.9
"Treatment with imiquimod was initiated, because the patient suffered tremendously from the disease."( [Imiquimod for the topical treatment of focal epithelial hyperplasia (Heck disease) in a child].
Brauns, TC; Goos, M; Maschke, J, 2004
)
1.57
"Treatment with imiquimod was effective, probably due to the area of application, where large hydrated skin folds are found, which helps penetration of the drug on the stratum corneum."( Porokeratosis of Mibelli of the axillae: treatment with topical imiquimod.
García-Ramírez, V; Montes-De-Oca-Sánchez, G; Tirado-Sánchez, A, 2006
)
0.91
"treatment with imiquimod 5% cream vs."( Randomized, comparative trial on the sustained efficacy of topical imiquimod 5% cream versus conventional ablative methods in external anogenital warts.
Eul, A; Henke, U; Lenz, T; Schöfer, H; Van Ophoven, A,
)
0.71
"Treatment with imiquimod, an immune response modifier, stimulated significant increases in mRNA for interferon (IFN)-alpha, IFN-gamma and 2',5' oligoadenylate synthetase (2',5'-AS) as well as a tendency towards increases in tumor necrosis factor (TNF)-alpha and interleukin-12 p40."( Enhancement of the innate and cellular immune response in patients with genital warts treated with topical imiquimod cream 5%.
Arany, I; McDermott, DJ; Miller, RL; Slade, HB; Smith, MH; Stanley, MA; Tomai, MA; Tyring, SK, 1999
)
0.86
"Treatment with imiquimod also inhibited the growth of RIF-1 sarcoma and Lewis lung carcinoma but was ineffective for P388 leukemia."( Inhibition of murine tumor growth by an interferon-inducing imidazoquinolinamine.
Borden, EC; Bryan, GT; Hatcher, JF; Reiter, MJ; Sidky, YA; Weeks, CE, 1992
)
0.62

Toxicity

Imiquimod 5% seems to be an effective and safe method for treating condylomata acuminata of the vulva. Adverse events of grade 3 or higher were reported in 31 (37%) of 84 patients allocated cidofovir.

ExcerptReferenceRelevance
" All completed the dose-escalation phase of weekly dosing at 100-mg increments and received at least one maintenance dose, 100 mg below the patient's toxic dose, for 12 weeks."( Administration of imiquimod, an interferon inducer, in asymptomatic human immunodeficiency virus-infected persons to determine safety and biologic response modification.
Cooper, DA; Couldwell, D; Cunningham, P; Goldstein, D; Hertzog, P; McCarville, S; Newell, M; Owens, M; Parrish, S; Tomkinson, E, 1998
)
0.63
"Safety was assessed through the incidence and severity of local skin reactions and other adverse events, and through clinical laboratory tests."( A randomized, controlled, safety study using imiquimod for the topical treatment of anogenital warts in HIV-infected patients. Imiquimod Study Group.
Conant, MA; Friedman-Kien, AE; Gilson, RJ; Nayagam, AT; Owens, ML; Pietig, DC; Shupack, JL; Smith, MH; Swann, RV; Weber, JN, 1999
)
0.56
"7%, respectively) and the incidence of patients reporting at least one adverse event was 69."( A randomized, controlled, safety study using imiquimod for the topical treatment of anogenital warts in HIV-infected patients. Imiquimod Study Group.
Conant, MA; Friedman-Kien, AE; Gilson, RJ; Nayagam, AT; Owens, ML; Pietig, DC; Shupack, JL; Smith, MH; Swann, RV; Weber, JN, 1999
)
0.56
"Most local skin reactions were mild and no adverse effects on HIV disease were observed."( A randomized, controlled, safety study using imiquimod for the topical treatment of anogenital warts in HIV-infected patients. Imiquimod Study Group.
Conant, MA; Friedman-Kien, AE; Gilson, RJ; Nayagam, AT; Owens, ML; Pietig, DC; Shupack, JL; Smith, MH; Swann, RV; Weber, JN, 1999
)
0.56
" Imiquimod 5% cream was safe in both treatment groups."( Safety and efficacy of imiquimod 5% cream in the treatment of penile genital warts in uncircumcised men when applied three times weekly or once per day.
Barasso, R; Carey-Yard, M; Eul, A; Gollnick, H; Jappe, U; Milde, K; Ward, K, 2001
)
1.53
" A visual analog scale was used to assess any adverse local skin reactions, and for the presence of systemic side effects characteristic of interferon (IFN)."( An open label safety study of topical imiquimod 5% cream in the treatment of Molluscum contagiosum in children.
Barba, AR; Berman, B; Kapoor, S, 2001
)
0.58
" The 25 patients in the treatment group tolerated these adverse effects well."( Is imiquimod effective and safe for actinic keratosis?
Koenig, C; Walker, JK, 2003
)
0.94
" There were no serious adverse events encountered with mild erythema being the commonest."( Safety and efficacy of locally applied imiquimod cream 5% for the treatment of condylomata acuminata of the vulva.
Diakomanolis, E; Elsheikh, A; Haidopoulos, D; Michalas, S; Rodolakis, A; Vlachos, G, 2004
)
0.59
"Imiquimod cream 5% seems to be an effective and safe method for treating condylomata acuminata of the vulva resulting possibly in lower recurrence rates than other current therapies."( Safety and efficacy of locally applied imiquimod cream 5% for the treatment of condylomata acuminata of the vulva.
Diakomanolis, E; Elsheikh, A; Haidopoulos, D; Michalas, S; Rodolakis, A; Vlachos, G, 2004
)
2.04
" Local application site reactions were the most common adverse event, reported by approximately 50% of the subjects in each treatment group."( Pharmacokinetics and safety of imiquimod 5% cream in the treatment of actinic keratoses of the face, scalp, or hands and arms.
Greene, RJ; Harrison, LI; Kurup, S; Marbury, TC; McKane, S; Owens, ML; Skinner, SL, 2004
)
0.61
"Topical 5% imiquimod cream seems to be safe on skin areas up to 60 cm2 in renal transplant recipients."( Safety and efficacy of 5% imiquimod cream for the treatment of skin dysplasia in high-risk renal transplant recipients: randomized, double-blind, placebo-controlled trial.
Atkins, CL; Brown, VL; Cerio, R; Ghali, L; Harwood, CA; Proby, CM, 2005
)
1.02
"Imiquimod has been investigated as a safe and effective therapeutic option for the treatment of actinic keratosis (AK)."( Vehicle-controlled, randomized, double-blind study to assess safety and efficacy of imiquimod 5% cream applied once daily 3 days per week in one or two courses of treatment of actinic keratoses on the head.
Alomar, A; Bichel, J; McRae, S, 2007
)
2.01
"A 4-week course of treatment with three times weekly dosing of imiquimod 5% cream, with a repeated course of treatment for those patients who fail to clear after the first course of treatment, is a safe and effective treatment for AK."( Vehicle-controlled, randomized, double-blind study to assess safety and efficacy of imiquimod 5% cream applied once daily 3 days per week in one or two courses of treatment of actinic keratoses on the head.
Alomar, A; Bichel, J; McRae, S, 2007
)
0.8
" Adverse events were reported in 92% of the patients and were mainly classified as minor or moderate local inflammation."( A phase III, randomized, open label study to evaluate the safety and efficacy of imiquimod 5% cream applied thrice weekly for 8 and 12 weeks in the treatment of low-risk nodular basal cell carcinoma.
Breuninger, H; Caroli, UM; Eigentler, TK; Garbe, C; Kamin, A; Möhrle, M; Radny, P; Weide, BM, 2007
)
0.57
" Patients were assessed for safety variables that included adverse events, local skin reactions, laboratory results, vital signs, dosage of immunosuppressive medication and indication of graft rejection."( Topical immunomodulation under systemic immunosuppression: results of a multicentre, randomized, placebo-controlled safety and efficacy study of imiquimod 5% cream for the treatment of actinic keratoses in kidney, heart, and liver transplant patients.
Amerio, P; Bichel, J; Euvrard, S; Guidi, B; Proby, CM; Rønnevig, J; Slade, HB; Stockfleth, E; Ulrich, C; van de Kerkhof, PC, 2007
)
0.54
"Imiquimod appears to be a safe alternative for the treatment of multiple actinic keratoses in patients with solid organ transplants."( Topical immunomodulation under systemic immunosuppression: results of a multicentre, randomized, placebo-controlled safety and efficacy study of imiquimod 5% cream for the treatment of actinic keratoses in kidney, heart, and liver transplant patients.
Amerio, P; Bichel, J; Euvrard, S; Guidi, B; Proby, CM; Rønnevig, J; Slade, HB; Stockfleth, E; Ulrich, C; van de Kerkhof, PC, 2007
)
1.98
"Imiquimod cycle therapy may be a safe and effective treatment option for AK lesions."( Open-label study to assess the safety and efficacy of imiquimod 5% cream applied once daily three times per week in cycles for treatment of actinic keratoses on the head.
Bissonnette, R; Provost, N; Rivers, JK; Rosoph, L,
)
1.82
" Some rare adverse events are easily explained based upon its mechanism of action (such as induction of vitiligo and worsening of psoriasis)."( Vasodilatory adverse events associated with topical imiquimod 5 percent cream.
Jacobs, AA; Markus, J; Rosen, T; Snavely, N, 2008
)
0.6
" Two participants discontinued treatment early, one for an adverse event (crying upon application), the other because of the lack of compliance."( A phase II, open-label study of the efficacy and safety of imiquimod in the treatment of superficial and mixed infantile hemangioma.
Auger, I; Belleville, C; David, M; Dubois, J; Gendron, R; Jafarian, F; McCuaig, CC; Powell, J; Rousseau, E,
)
0.37
"3% withdrew for local skin reactions or adverse events in the combined placebo, and in the imiquimod 2, 3, 5 or 7 times per week groups, respectively."( Effect of dosing frequency on the safety and efficacy of imiquimod 5% cream for treatment of actinic keratosis on the forearms and hands: a phase II, randomized placebo-controlled trial.
Cowen, PS; Gebauer, K; Shumack, S, 2009
)
0.82
" Several randomized controlled trials have demonstrated that imiquimod 5% cream is a safe and efficacious treatment."( Safety, efficacy & recurrence rates of imiquimod cream 5% for treatment of anogenital warts.
Bartlett, BL; Diamantis, ML; Tyring, SK, 2009
)
0.86
" Immunization with IC41 was generally safe in this study."( Immunogenicity and safety of different injection routes and schedules of IC41, a Hepatitis C virus (HCV) peptide vaccine.
Boehm, T; Buerger, V; Firbas, C; Jilma, B; Klade, CS; Sabarth, N; Schuller, E, 2010
)
0.36
" Only one subject discontinued for a treatment-related adverse event (cryosurgery/3."( A randomized, double-blinded, placebo-controlled, multicenter, efficacy and safety study of 3.75% imiquimod cream following cryosurgery for the treatment of actinic keratoses.
Bourcier, M; Jorizzo, JL; Kulp, J; Lebwohl, MG; Levy, S; Markowitz, O; Meng, TC, 2010
)
0.58
" Both substances constitute effective and safe treatments of untreated anogenital warts in immunocompetent individuals."( Efficacy and safety of imiquimod versus podophyllotoxin in the treatment of anogenital warts.
Aberer, W; Akkilic-Materna, M; Komericki, P; Strimitzer, T, 2011
)
0.68
" Although its mechanism of action has not been entirely elucidated yet, imiquimod 5% cream has been shown to be an efficient, long-lasting and safe therapy for multiple actinic keratoses in non-immunosuppressed patients and in transplant recipients."( Acute renal failure caused by imiquimod 5% cream in a renal transplant patient: review of the literature on side effects of imiquimod.
Coto-Segura, P; Esteve, A; Galache Osuna, C; Gómez, E; Mas-Vidal, A; Salgueiro, E; Santos-Juanes, J, 2011
)
0.89
" Although considered a safe drug, mild to moderate local and systemic side-effects may occasionally occur."( Local and systemic adverse effects of imiquimod therapy for external anogenital warts in men: report of three cases.
de Campos Guidi, HG; Rosenblatt, A, 2012
)
0.65
"The Toll-like receptor 7 (TLR7) activator imiquimod (IMQ) is safe and effective in treating actinic keratosis; however, an intermittent treatment regimen is necessary because of excessive local reactions."( Inhibition of keratinocyte proliferation by phospholipid-conjugates of a TLR7 ligand in a Myc-induced hyperplastic actinic keratosis model in the absence of systemic side effects.
Barberis, A; Carson, DA; Cottam, HB; Crain, B; Hayashi, T; Holldack, J; Kang, M; Keophilaone, V; Maj, R; Mura, E; Ochoa, R; Passini, N; Promessi, V; Yao, S,
)
0.4
"TMX-202 is safe and efficacious without causing excessive adverse effects, suggesting that it may be an alternative to Aldara for the treatment of proliferative skin conditions."( Inhibition of keratinocyte proliferation by phospholipid-conjugates of a TLR7 ligand in a Myc-induced hyperplastic actinic keratosis model in the absence of systemic side effects.
Barberis, A; Carson, DA; Cottam, HB; Crain, B; Hayashi, T; Holldack, J; Kang, M; Keophilaone, V; Maj, R; Mura, E; Ochoa, R; Passini, N; Promessi, V; Yao, S,
)
0.13
" Secondary outcomes were toxic effects (to assess safety) and adherence to treatment (to assess feasibility)."( Activity, safety, and feasibility of cidofovir and imiquimod for treatment of vulval intraepithelial neoplasia (RT³VIN): a multicentre, open-label, randomised, phase 2 trial.
Dutton, P; Fiander, A; Griffiths, G; Hibbitts, S; Hurt, CN; Jones, S; Madden, T; Man, S; Naik, R; Nordin, AJ; Powell, N; Tristram, A, 2014
)
0.65
" Adverse events of grade 3 or higher were reported in 31 (37%) of 84 patients allocated cidofovir and 39 (46%) of 84 patients assigned imiquimod; the most frequent grade 3 and 4 events were pain in the vulva, pruritus, fatigue, and headache."( Activity, safety, and feasibility of cidofovir and imiquimod for treatment of vulval intraepithelial neoplasia (RT³VIN): a multicentre, open-label, randomised, phase 2 trial.
Dutton, P; Fiander, A; Griffiths, G; Hibbitts, S; Hurt, CN; Jones, S; Madden, T; Man, S; Naik, R; Nordin, AJ; Powell, N; Tristram, A, 2014
)
0.86
"There is currently a lack of evidence-based therapies that are safe and effective for plaque-type morphea."( Evaluation of the efficacy and safety of topical imiquimod 5% for plaque-type morphea: a multicenter, prospective, vehicle-controlled trial.
Ackerman, T; Cheung-Lee, M; Dytoc, M; Fiorillo, L; Sawyer, D; Wat, H,
)
0.39
" Adverse effects were minimal and well tolerated."( Evaluation of the efficacy and safety of topical imiquimod 5% for plaque-type morphea: a multicenter, prospective, vehicle-controlled trial.
Ackerman, T; Cheung-Lee, M; Dytoc, M; Fiorillo, L; Sawyer, D; Wat, H,
)
0.39
" Complete lesion response (CLR), complete lesion clearance (CLC), cumulative recurrence probabilities (CRP), and adverse effects (AEs) were considered as outcomes and displayed as odds ratios (ORs) and 95% credible intervals (CrI)."( A Network Meta-Analysis of Non-Melanoma Skin Cancer (NMSC) Treatments: Efficacy and Safety Assessment.
Lv, R; Sun, Q, 2017
)
0.46
"The main outcome measures included histological and composite clearance rates, success rates, complete response rates, tumour-free survival and adverse events."( 'Efficacy and safety of imiquimod 5% cream for basal cell carcinoma: a meta-analysis of randomized controlled trial': a critical appraisal.
Olabi, B; Tasker, F; Williams, HC, 2020
)
0.87
" Pooled analyses comparing imiquimod with all or any of the listed comparators, including vehicle, demonstrated higher histological clearance rates [risk ratio (RR) 9·28, 95% confidence interval (CI) 5·56-15·5; P < 0·001], higher composite clearance rates (RR 34·2, 95% CI 21·3, 55·1; P = 0·001), no significant difference in success rates (RR 0·98, 95% CI 0·89-1·08; P = 0·73), higher complete response rates (RR 3·15, 95% CI 1·55-6·38; P = 0·001), no significant difference in tumour-free survival (RR 1·15, 95% CI 0·98-1·35; P = 0·088) and increased incidence of adverse events (RR 2·00, 95% CI 1·39-2·88; P < 0·001)."( 'Efficacy and safety of imiquimod 5% cream for basal cell carcinoma: a meta-analysis of randomized controlled trial': a critical appraisal.
Olabi, B; Tasker, F; Williams, HC, 2020
)
1.16
" Adverse reactions (ARs) were more common with cryotherapy (9."( Real-World Effectiveness and Safety of Field- and Lesion-Directed Treatments for Actinic Keratosis.
Dunkelly-Allen, N; Feldman, SR; Hansen, JB; Larsson, T; Veverka, KA, 2020
)
0.56
" In addition to imiquimod-associated adverse effects at non-application sites such as fever, vertigo or myalgia there have been anecdotal reports of distant inflammatory mucosal reactions-a side effect not declared in the medicinal product information."( Mucosal side effects in patients treated with topical imiquimod-A scoping review of the literature.
Gantenbein, L; Hammerl, V; Mueller, SM; Navarini, A; Parlar, B; Väth, H, 2021
)
1.22
" Fifty percent of patients reported Common Terminology Criteria for Adverse Events v5."( Topical chemotherapy for penile carcinoma in situ: Contemporary outcomes and reported toxicity.
Aydin, AM; Chahoud, J; Cheryian, SK; Hajiran, A; Pow-Sang, JM; Spiess, PE; Zemp, L, 2021
)
0.62
" It provides a promising long-term relief with a tolerable side-effect profile."( Long-term efficacy and safety of imiquimod 5% and fluorouracil 1% creams in medical monotherapy of complex eyelid basal cell carcinomas.
Gupta, P; Kaur, M; Mehta Grewal, A; Sharma, M; Singh, H; Singh, M; Zadeng, Z, 2022
)
1
" No serious adverse events or systemic adverse events were determined to be due to topical therapies for AK."( INDIVIDUAL ARTICLE: Safety and Tolerability of Topical Agents for Actinic Keratosis: A Systematic Review of Phase 3 Clinical Trials.
Armstrong, AW; Kircik, LH; Rajkumar, JR, 2021
)
0.62
"To investigate the relationship between SCC and topical AK medications including ingenol mebutate in the FDA Adverse Event Reporting System (FAERS)."( Ingenol Mebutate Is Associated With Increased Reporting Odds for Squamous Cell Carcinoma in Actinic Keratosis Patients, a Pharmacovigilance Study of the FDA Adverse Event Reporting System (FAERS).
Jedlowski, PM,
)
0.13
" No serious systemic adverse events were reported in all the treatment arms."( Safety and efficacy of the combination of cryotherapy and photodynamic modalities with imiquimod in patients with actinic keratosis: a systematic review and meta-analysis.
El-Qushayri, AE; Ghozy, S; Sakr, S; Salem, ML; Salman, S; Sarsik, SM, 2023
)
1.13

Pharmacokinetics

Oral imiquimod was absorbed in both fasted and non-fasted states with an absorption half-life of approximately 1 hour.

ExcerptReferenceRelevance
"The present study, the first clinical pharmacokinetic report of the immune response modifier imiquimod, was conducted to assess the effect of food on the oral absorption of imiquimod, to characterize its pharmacokinetics, and to estimate its oral bioavailability."( Effect of food on the pharmacokinetics and bioavailability of oral imiquimod relative to a subcutaneous dose.
Ellefson, P; Horton, V; McCarville, S; Myhre, P; Owens, M; Schmitt, K; Soria, I, 2000
)
0.76
" Oral imiquimod was absorbed in both fasted and non-fasted states with an absorption half-life of approximately 1 hour."( Effect of food on the pharmacokinetics and bioavailability of oral imiquimod relative to a subcutaneous dose.
Ellefson, P; Horton, V; McCarville, S; Myhre, P; Owens, M; Schmitt, K; Soria, I, 2000
)
1.02
" Steady state was achieved by day 14, and the observed half-life of approximately 29 h supports daily dosing of the product."( Pharmacokinetics of imiquimod 3.75% cream applied daily for 3 weeks to actinic keratoses on the face and/or balding scalp.
Adams, M; Fein, MC; Furst, J; Kulp, J; Levy, S; Meng, TC, 2010
)
0.68
"• To study the pharmacokinetic and toxicity profile of intravesically administered TMX-101, with its active ingredient R-837, a synthetic Toll-like receptor (TLR)-7 agonist, in a pig model."( Pharmacokinetics and toxicity of intravesical TMX-101: a preclinical study in pigs.
Arentsen, HC; Hulsbergen-Van de Kaa, CA; Jansen, CF; Leoni, LM; Maj, R; Oosterwijk, E; Witjes, JA, 2011
)
0.37
" • Pharmacokinetic analysis was performed on plasma."( Pharmacokinetics and toxicity of intravesical TMX-101: a preclinical study in pigs.
Arentsen, HC; Hulsbergen-Van de Kaa, CA; Jansen, CF; Leoni, LM; Maj, R; Oosterwijk, E; Witjes, JA, 2011
)
0.37
" Furthermore, pharmacokinetic and pharmacodynamic characteristics and adverse events were evaluated."( Pharmacokinetic, Pharmacodynamic, and Activity Evaluation of TMX-101 in a Multicenter Phase 1 Study in Patients With Papillary Non-Muscle-Invasive Bladder Cancer.
Arends, TJ; Eisenhardt, A; Falke, J; Lammers, RJ; Pozzi, R; Ravic, M; Rustighini, I; van der Heijden, AG; Vergunst, H; Witjes, JA, 2015
)
0.42
" In the pharmacodynamic analysis, urinary interleukin 1 receptor agonist (IL-1ra) represents the most sensitive and uniform response after TMX-101 instillation."( Pharmacokinetic, Pharmacodynamic, and Activity Evaluation of TMX-101 in a Multicenter Phase 1 Study in Patients With Papillary Non-Muscle-Invasive Bladder Cancer.
Arends, TJ; Eisenhardt, A; Falke, J; Lammers, RJ; Pozzi, R; Ravic, M; Rustighini, I; van der Heijden, AG; Vergunst, H; Witjes, JA, 2015
)
0.42

Compound-Compound Interactions

Imiquimod (5-10 microg/ml) combined with either paromomycin or methylbenzethonium chloride (0.2 ml) intralesional interleukin 2 (IL-2) could be considered an effective antimelanoma therapy.

ExcerptReferenceRelevance
"The aim of this study is to evaluate the effects of an immune modulator, imiquimod, given alone or in combination with an HSV vaccine on HSV immune responses and as immunotherapy of a genital recurrence model."( Reduction of recurrent HSV disease using imiquimod alone or combined with a glycoprotein vaccine.
Bernstein, DI; Harrison, CJ; Miller, RL, 2001
)
0.81
"To determine the efficacy and safety of imiquimod in combination with meglumine antimoniate in treating cutaneous leishmaniasis."( Imiquimod in combination with meglumine antimoniate for cutaneous leishmaniasis: a randomized assessor-blind controlled trial.
Dowlati, Y; Eskandari, SE; Firooz, A; Ghoorchi, MH; Gorouhi, F; Hooshmand, B; Khamesipour, A; Khatami, A; Nassiri-Kashani, M; Rashighi-Firoozabadi, M, 2006
)
2.04
" Imiquimod (5-10 microg/ml) combined with either paromomycin (25, 50 and 100 microg/ml) or methylbenzethonium chloride (0."( Leishmania major: in vitro and in vivo anti-leishmanial activity of paromomycin ointment (Leshcutan) combined with the immunomodulator Imiquimod.
Bazarsky, E; El-On, J; Sneir, R, 2007
)
1.45
" We evaluated if pentavalent antimony (an anti-parasitic drug) combined with imiquimod (an immunomodulator) was more effective than pentavalent antimony alone in patients who had not previously been treated."( First-line therapy for human cutaneous leishmaniasis in Peru using the TLR7 agonist imiquimod in combination with pentavalent antimony.
Calderon, W; Cruz, M; Gyorkos, TW; Llanos-Cuentas, A; Matlashewski, G; Miranda-Verastegui, C; Rahme, E; Tulliano, G; Ward, B, 2009
)
0.81
"2 ml) intralesional interleukin 2 (IL-2) in combination with topical imiquimod and a retinoid cream."( Complete regression of subcutaneous and cutaneous metastatic melanoma with high-dose intralesional interleukin 2 in combination with topical imiquimod and retinoid cream.
Chen, SL; Fung, MA; Garcia, MS; Goodarzi, H; Martinez, SR; Maverakis, E; Miyamura, Y; Ono, Y; Phan, T; Wehrli, LN, 2011
)
0.81
" We investigated whether imiquimod, a synthetic TLR7 agonist, can expedite the immune response against influenza virus infection when combined with influenza vaccine."( Toll-like receptor 7 agonist imiquimod in combination with influenza vaccine expedites and augments humoral immune responses against influenza A(H1N1)pdm09 virus infection in BALB/c mice.
Chan, JF; Hung, IF; Lee, AC; Li, C; Li, CG; To, KK; Yuen, KY; Zhang, AJ; Zhu, HS, 2014
)
1
" The aims of our study were to investigate the therapeutic efficacy of Glu in combination with low-dose CsA on imiquimod (IMQ)-induced psoriasis-like dermatitis in mice and to determine its immunomodulatory mechanism."( Therapeutic and immunomodulatory effects of glucosamine in combination with low-dose cyclosporine a in a murine model of imiquimod-induced psoriasis.
Kim, CH; Kim, JY; Lee, AY, 2015
)
0.84
"Imiquimod 5% cream as a monotherapy or in combination with SA can be used safely in children with warts and is equally effective and more effective than cryotherapy in plantar warts."( Cryotherapy versus imiquimod 5% cream combined with a keratolytic lotion in cutaneous warts in children: A randomized study.
Antoniou, C; Katsarou, A; Kontochristopoulos, G; Kouris, A; Lagogiani, I; Stefanaki, C, 2016
)
2.21
" More significantly, PDT with UCNP-Ce6-R837 in combination with the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) checkpoint blockade not only shows excellent efficacy in eliminating tumors exposed to the NIR laser but also results in strong antitumor immunities to inhibit the growth of distant tumors left behind after PDT treatment."( Near-Infrared-Triggered Photodynamic Therapy with Multitasking Upconversion Nanoparticles in Combination with Checkpoint Blockade for Immunotherapy of Colorectal Cancer.
Dong, Z; Han, X; Liu, Z; Peng, R; Wang, C; Xu, J; Xu, L; Yang, R; Zhu, W; Zhuang, Q, 2017
)
0.46
" We tried less invasive therapy, immunocryosurgery, as a single treatment for LM or combined with surgery for LMM, with better aesthetic results."( Immunocryosurgery as monotherapy for lentigo maligna or combined with surgical excision for lentigo maligna melanoma.
Casanova, JM; García-de-la-Fuente, MR; Gatius, S; Huerva, V; Martí, RM; Matas-Nadal, C; Ortega, E; Sòria, X; Vilardell, F, 2018
)
0.48
"B16F1 melanoma-bearing mice were daily treated with topical imiquimod in combination with one intratumoral injection of attenuated Salmonella enterica serovar Typhimurium LVR01."( TLR7 agonist in combination with Salmonella as an effective antimelanoma immunotherapy.
Agorio, CI; Bascuas, T; Chabalgoity, JA; Mónaco, A; Moreno, M; Rimsky, G; Vola, M, 2018
)
0.72
"Salmonella LVR01 immunotherapy in combination with imiquimod is a novel approach that could be considered as an effective antimelanoma therapy."( TLR7 agonist in combination with Salmonella as an effective antimelanoma immunotherapy.
Agorio, CI; Bascuas, T; Chabalgoity, JA; Mónaco, A; Moreno, M; Rimsky, G; Vola, M, 2018
)
0.73
"To investigate the therapeutic effect of Toll-like receptor 7( TLR7) agonist imiquimod combined with dendritic cell( DC)-based tumor vaccine on melanoma in mice and the potential mechanism."( [Imiquimod combined with dendritic cell vaccine decreases Treg proportion and enhances anti-tumor responses in mice bearing melanoma].
Li, P; Li, Y; Lu, C; Ren, S; Wang, Q; Zhang, Y, 2017
)
1.59
"15% cream or imiquimod 5% cream, in combination with a three-dose regimen of qHPV or control vaccination."( Human papillomavirus infection: protocol for a randomised controlled trial of imiquimod cream (5%) versus podophyllotoxin cream (0.15%), in combination with quadrivalent human papillomavirus or control vaccination in the treatment and prevention of recurr
Bennett, K; Copas, AJ; Doré, CJ; Gilson, R; Haddow, LJ; Jit, M; Lacey, C; Meadows, J; Murray, ML; Nathan, M; Soldan, K; Tetlow, M, 2018
)
1.08
"Topical imiquimod administration combined with ID MIV A/H5N1 was safe but did not result in improved serologic responses to the vaccine."( Topical Imiquimod Does Not Provide an Adjuvant Effect When Administered With Inactivated Influenza A/H5N1 Vaccine in Healthy Young Adults.
Atmar, RL; El Sahly, HM; Keitel, WA; Sendra, E; Wegel, A, 2021
)
1.49
"Twelve melanoma peptides plus a tetanus helper peptide were combined with granulocyte macrophage colony stimulating factor (GM-CSF) and were administered topically on days 1, 8, and 15, to 28 patients randomized to one of four adjuvant preparations: (1) incomplete Freund's adjuvant (IFA); (2) IFA plus a TLR7 agonist (imiquimod) administered on days 0, 7, 14; (3) dimethyl sulfoxide (DMSO) or (4) DMSO+ imiquimod administered on day 0, 7, 14."( Immunogenicity in humans of a transdermal multipeptide melanoma vaccine administered with or without a TLR7 agonist.
Chianese-Bullock, KA; Deacon, D; Grosh, WW; Lynch, KT; Meneveau, MO; Olson, WC; Patterson, JW; Petroni, GR; Salerno, EP; Slingluff, CL; Smolkin, M; Woodson, E, 2021
)
0.79

Bioavailability

1.03 mg/kg was approximately 100-fold more potent than that of Imiquimod, and showed an excellent oral bioavailability (F=40%) which was 10-fold improved over 5, a lead compound. Food does not have a major effect on the rate, extent of absorption or bioavailability of oral imiquinod.

ExcerptReferenceRelevance
"The oral bioavailability of imiquimod was on average 47%, and independent of whether imiquimod was administered with or without food."( Effect of food on the pharmacokinetics and bioavailability of oral imiquimod relative to a subcutaneous dose.
Ellefson, P; Horton, V; McCarville, S; Myhre, P; Owens, M; Schmitt, K; Soria, I, 2000
)
0.84
"This study suggests that food does not have a major effect on the rate, extent of absorption or bioavailability of oral imiquimod, and thus, it is suitable to administer imiquimod orally in either the fasted or non-fasted states."( Effect of food on the pharmacokinetics and bioavailability of oral imiquimod relative to a subcutaneous dose.
Ellefson, P; Horton, V; McCarville, S; Myhre, P; Owens, M; Schmitt, K; Soria, I, 2000
)
0.75
"1 mg/kg, which was 30-fold potent than that of Imiquimod, and showed a good oral bioavailability (F=81%)."( Synthesis and structure-activity relationships of 2-amino-8-hydroxyadenines as orally active interferon inducing agents.
Hirota, K; Ichii, S; Isobe, Y; Kawakami, H; Kurimoto, A; Ogino, T; Ogita, H; Sajiki, H; Takaku, H; Tobe, M, 2003
)
0.58
"03 mg/kg, which was approximately 100-fold more potent than that of Imiquimod, and showed an excellent oral bioavailability (F=40%) which was 10-fold improved over 5, a lead compound (F=4%)."( Synthesis and evaluation of 2-substituted 8-hydroxyadenines as potent interferon inducers with improved oral bioavailabilities.
Hirota, K; Ichii, S; Isobe, Y; Kawakami, H; Kurimoto, A; Ogino, T; Ogita, H; Sajiki, H; Takaku, H; Tobe, M, 2004
)
0.56
" After intraperitoneal administration the absolute bioavailability remains limited (22."( Pharmacology of EAPB0203, a novel imidazo[1,2-a]quinoxaline derivative with anti-tumoral activity on melanoma.
Bonnet, PA; Bressolle, FM; Cooper, JF; Deleuze-Masquéfa, C; Gattacceca, F; Khier, S; Margout, D; Moarbess, G; Pinguet, F; Solassol, I, 2010
)
0.36
" Further, the dermatokinetic studies also confirmed better permeation and enhanced skin bioavailability of SA to epidermis as well as dermis vis-à-vis the CGF."( Lanolin-based organogel of salicylic acid: evidences of better dermatokinetic profile in imiquimod-induced keratolytic therapy in BALB/c mice model.
Devi, N; Jain, A; Katare, OP; Sharma, G; Thakur, K, 2018
)
0.7
" However, bioavailability issues have restricted the development of EGCG for the treatment of psoriasis."( Chitosan-based nanoformulated (-)-epigallocatechin-3-gallate (EGCG) modulates human keratinocyte-induced responses and alleviates imiquimod-induced murine psoriasiform dermatitis.
Adame, S; Adhami, VM; Babatunde, AS; Bharali, DJ; Chamcheu, JC; Esnault, S; Longley, BJ; Massey, RJ; Mousa, SA; Mukhtar, H; Siddiqui, IA; Wood, GS, 2018
)
0.69
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
"Methotrexate exhibits poor cutaneous bioavailability and systemic side effects on topical administration, so there is an unmet need for a novel carrier and its optimized therapy."( Methotrexate-Loaded Nanostructured Lipid Carrier Gel Alleviates Imiquimod-Induced Psoriasis by Moderating Inflammation: Formulation, Optimization, Characterization, In-Vitro and In-Vivo Studies.
Agrawal, YO; Mahajan, HS; Mahajan, UB; Ojha, S, 2020
)
0.8

Dosage Studied

Imiquimod can be applied in an efficacious and well-tolerated fashion to treat skin cancer. By titrating its dosing for angiogenesis inhibitory activity and not for gross inflammation,. A number of Phase II trials have demonstrated the efficacy of imquimod for the treatment of BCC.

ExcerptRelevanceReference
" Daily dosing of imiquimod for five consecutive days led to diminished production of IFN in mice as measured after the final dose."( Cytokine induction in mice by the immunomodulator imiquimod.
Miller, RL; Reiter, MJ; Testerman, TL; Tomai, MA; Weeks, CE, 1994
)
0.88
" Further investigation of imiquimod as an interferon-inducing agent in cancer patients is suggested at either the lower dose levels or employing alternative dosing schedules."( A phase I clinical trial of imiquimod, an oral interferon inducer, administered daily.
Gore, ME; Horton, V; Moore, J; Owens, M; Savage, P; Witt, P, 1996
)
0.89
" All completed the dose-escalation phase of weekly dosing at 100-mg increments and received at least one maintenance dose, 100 mg below the patient's toxic dose, for 12 weeks."( Administration of imiquimod, an interferon inducer, in asymptomatic human immunodeficiency virus-infected persons to determine safety and biologic response modification.
Cooper, DA; Couldwell, D; Cunningham, P; Goldstein, D; Hertzog, P; McCarville, S; Newell, M; Owens, M; Parrish, S; Tomkinson, E, 1998
)
0.63
" The dosing regimen found to best balance efficacy, side-effects and practicality is 5% imiquimod cream applied overnight by the patient three times weekly until warts clear, for up to 16 weeks."( Imiquimod in clinical practice.
Edwards, L, 1998
)
1.97
"In this population of 35 patients with BCC, 24 received imiquimod 5% cream and 11 received vehicle cream in 1 of 5 dosing regimens for up to 16 weeks."( Therapeutic response of basal cell carcinoma to the immune response modifier imiquimod 5% cream.
Beutner, KR; Fox, TL; Geisse, JK; Ginkel, A; Helman, D; Owens, ML, 1999
)
0.78
"BCC cleared (on the basis of histologic examination) in all 15 patients (100%) dosed twice daily, once daily, and 3 times weekly; in 3 of 5 (60%) patients dosed twice weekly; 2 of 4 (50%) dosed once weekly; and in 1 of 11 (9%) treated with vehicle."( Therapeutic response of basal cell carcinoma to the immune response modifier imiquimod 5% cream.
Beutner, KR; Fox, TL; Geisse, JK; Ginkel, A; Helman, D; Owens, ML, 1999
)
0.53
" Thus, imiquimod 5% cream administered 3 times/week was the optimal dosing regimen in the treatment of penile warts in uncircumcised men."( Safety and efficacy of imiquimod 5% cream in the treatment of penile genital warts in uncircumcised men when applied three times weekly or once per day.
Barasso, R; Carey-Yard, M; Eul, A; Gollnick, H; Jappe, U; Milde, K; Ward, K, 2001
)
1.08
" The dosing schedule and length of treatment for Bowen's disease require further evaluation."( Imiquimod 5% cream in the treatment of Bowen's disease.
de Launey, J; Kossard, S; Mackenzie-Wood, A; Owens, ML; Wilkinson, B, 2001
)
1.75
"We conducted a multicenter, randomized, open-label dose-response trial of imiquimod 5% cream in the treatment of primary sBCC assessing efficacy and safety of different dose regimens."( Imiquimod 5% cream in the treatment of superficial basal cell carcinoma: results of a multicenter 6-week dose-response trial.
Amies, M; Bryden, J; Fox, TL; Gebauer, K; Marks, R; Owens, ML; Shumack, S, 2001
)
1.98
" There was a significant increase in the incidence and severity of local skin reactions including erythema, vesicle formation, ulceration, and excoriation as the dosing frequency increased from three times a week to three times a day."( Treatment of external genital warts in men using 5% imiquimod cream applied three times a week, once daily, twice daily, or three times a day.
Brown, DR; Douglas, JM; Ferenczy, A; Fife, KH; Owens, ML; Smith, M, 2001
)
0.56
"In this study, the optimal dosage regimen was the approved three times a week regimen."( Treatment of external genital warts in men using 5% imiquimod cream applied three times a week, once daily, twice daily, or three times a day.
Brown, DR; Douglas, JM; Ferenczy, A; Fife, KH; Owens, ML; Smith, M, 2001
)
0.56
"Imiquimod cream at a dosing regimen of three times per week, is effective and has an acceptable safety profile in the treatment of prepuce associated warts and other external anogenital warts in uncircumcised males."( Imiquimod 5% cream is an acceptable treatment option for external anogenital warts in uncircumcised males.
Bowman, CA; Goh, BT; Kinghorn, GR; Maw, RD; Nathan, M; Nayagam, AT, 2002
)
3.2
"The objective of this phase II dose-response study was to explore various dosing regimens using imiquimod 5% cream for sBCC to find the most effective frequency of dosing with tolerable side effects."( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: a double-blind, randomized, vehicle-controlled study.
Andres, K; Geisse, JK; Ginkel, A; Gross, K; Owens, M; Pandya, A; Rich, P, 2002
)
1.98
"Patients (n = 128) were dosed twice daily, once daily, 5 times a week, or 3 times a week in this 12-week, randomized, double-blind, vehicle-controlled study."( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: a double-blind, randomized, vehicle-controlled study.
Andres, K; Geisse, JK; Ginkel, A; Gross, K; Owens, M; Pandya, A; Rich, P, 2002
)
1.76
" Daily or 5 times a week dosing for 12 weeks demonstrated high efficacy results with acceptable safety profiles."( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: a double-blind, randomized, vehicle-controlled study.
Andres, K; Geisse, JK; Ginkel, A; Gross, K; Owens, M; Pandya, A; Rich, P, 2002
)
1.76
"To establish a safe and efficacious dosing regimen for the treatment of primary nodular basal cell carcinoma (BCC) using 5% imiquimod cream."( Efficacy of topical 5% imiquimod cream for the treatment of nodular basal cell carcinoma: comparison of dosing regimens.
Amies, M; Andres, K; Golitz, L; Greenway, H; Kossard, S; Owens, M; Robinson, J; Schroeter, A; Shumack, S, 2002
)
0.83
"Two phase 2 studies were conducted: a 6-week, randomized, open-label, dose-response study evaluating 4 dosing regimens and a 12-week, randomized, vehicle-controlled, double-blind, dose-response study evaluating 4 dosing regimens."( Efficacy of topical 5% imiquimod cream for the treatment of nodular basal cell carcinoma: comparison of dosing regimens.
Amies, M; Andres, K; Golitz, L; Greenway, H; Kossard, S; Owens, M; Robinson, J; Schroeter, A; Shumack, S, 2002
)
0.63
" A trend in increased rates of local adverse events at the application site and a delay in lesion healing with more frequent dosing suggested a pharmacologic effect."( Imiquimod 5-percent cream does not alter the natural history of recurrent herpes genitalis: a phase II, randomized, double-blind, placebo-controlled study.
Conant, M; Schacker, TW; Smith, M; Stanczak, T; Thoming, C; Wang, Z, 2002
)
1.76
"Our aim was to study the potential efficacy of topical 5% imiquimod cream in the treatment of facial or scalp AKs and improve the safety profile by using a novel "cycle" dosing regimen."( Cycle therapy of actinic keratoses of the face and scalp with 5% topical imiquimod cream: An open-label trial.
Levine, N; Morrison, L; Salasche, SJ, 2002
)
0.79
" The identification of a therapeutic interval may prove to be beneficial in formulating individualized dosing regimens."( Cycle therapy of actinic keratoses of the face and scalp with 5% topical imiquimod cream: An open-label trial.
Levine, N; Morrison, L; Salasche, SJ, 2002
)
0.55
"Two studies were conducted to examine the effect of occlusion at low dosing frequencies on the safety and efficacy of topical imiquimod 5% cream for the treatment of superficial and nodular BCC."( Imiquimod 5% cream for the treatment of superficial and nodular basal cell carcinoma: randomized studies comparing low-frequency dosing with and without occlusion.
Andres, K; Bichel, J; Ding, L; Herrera, E; Ruzicka, T; Sterry, W; Takwale, A; Thissen, MR, 2002
)
1.96
" Occlusion did not have a statistically significant effect on response rate at either dosing frequency."( Imiquimod 5% cream for the treatment of superficial and nodular basal cell carcinoma: randomized studies comparing low-frequency dosing with and without occlusion.
Andres, K; Bichel, J; Ding, L; Herrera, E; Ruzicka, T; Sterry, W; Takwale, A; Thissen, MR, 2002
)
1.76
"In the superficial study, the complete response rate of 87% in the 3 days per week with occlusion group was similar to that of daily and 5 days per week dosing without occlusion in a previous 12-week study and one study of daily dosing without occlusion for 6 weeks."( Imiquimod 5% cream for the treatment of superficial and nodular basal cell carcinoma: randomized studies comparing low-frequency dosing with and without occlusion.
Andres, K; Bichel, J; Ding, L; Herrera, E; Ruzicka, T; Sterry, W; Takwale, A; Thissen, MR, 2002
)
1.76
" The dosing schedule and length of treatment requires further evaluation."( Experience in treating molluscum contagiosum in children with imiquimod 5% cream.
Bayerl, C; Feller, G; Goerdt, S, 2003
)
0.56
" A number of Phase II trials have demonstrated the efficacy of imiquimod for the treatment of BCC, although the most appropriate dosing regimen is being confirmed in Phase III studies."( The use of Toll-like receptor-7 agonist in the treatment of basal cell carcinoma: an overview.
Garcia-Bartels, C; Schmook, T; Sterry, W; Stockfleth, E; Trefzer, U; Wegner, T, 2003
)
0.56
" The objective of this clinical study was to describe the pharmacokinetics and safety of topical imiquimod during multiple dosing of AK subjects."( Pharmacokinetics and safety of imiquimod 5% cream in the treatment of actinic keratoses of the face, scalp, or hands and arms.
Greene, RJ; Harrison, LI; Kurup, S; Marbury, TC; McKane, S; Owens, ML; Skinner, SL, 2004
)
0.83
" Subjects with one sBCC were dosed with imiquimod or vehicle cream once daily 5 or 7x/week for 6 weeks in these 2 randomized, double-blind, vehicle-controlled Phase III studies."( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, randomized, vehicle-controlled studies.
Caro, I; Geisse, J; Golitz, L; Lindholm, J; Owens, M; Stampone, P, 2004
)
2.03
" The difference in clearance rates between the two imiquimod dosing groups was not significant."( Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, randomized, vehicle-controlled studies.
Caro, I; Geisse, J; Golitz, L; Lindholm, J; Owens, M; Stampone, P, 2004
)
2.02
" Four groups of BCC (A, B, C, and D) and two dosing regimens were studied: 35 BCCs (groups A, B, and C) were treated with imiquimod three times weekly and 20 BCCs (group D) were treated with imiquimod five times weekly."( Open study of the efficacy and mechanism of action of topical imiquimod in basal cell carcinoma.
Alomar, A; Matías-Guiu, X; Vidal, D, 2004
)
0.77
"Tumors cleared or the target tumor area was reduced in subjects in the 4- and 6-week dosing regimens."( 5% imiquimod cream and reflectance-mode confocal microscopy as adjunct modalities to Mohs micrographic surgery for treatment of basal cell carcinoma.
Berkes, B; González, S; Marra, D; Morgan, B; Niemeyer, A; Owens, M; Schanbacher, C; Torres, A, 2004
)
0.94
"The 5% imiquimod cream dosed 3 times weekly for 16 weeks is safe and effective for the treatment of AK."( Dosing with 5% imiquimod cream 3 times per week for the treatment of actinic keratosis: results of two phase 3, randomized, double-blind, parallel-group, vehicle-controlled trials.
Korman, N; Lee, JH; Ling, M; Matheson, R; McKane, S; Moy, R; Smith, S, 2005
)
1.14
" Patients applied imiquimod or vehicle cream to AK lesions on the face or balding scalp, dosing three times per week or two times per week for 16 weeks."( Long-term clinical outcomes following treatment of actinic keratosis with imiquimod 5% cream.
Andres, KL; Harwell, WB; Lee, JH; Lee, PK; Loven, KH; Phillips, TJ; Whiting, DA, 2005
)
0.89
" Given that patients often apply the cream themselves at home, further dosing variability is expected and, consequently, accurate comparison of the results of different published studies is difficult."( Design and physicochemical characterisation of a bioadhesive patch for dose-controlled topical delivery of imiquimod.
Donnelly, RF; McCarron, PA; Woolfson, AD; Zawislak, AA, 2006
)
0.55
" Future investigation might be aimed at elucidating optimal dosing to minimize adverse events without detriment to efficacy, and evaluating long-term recurrence."( Imiquimod for actinic keratosis: systematic review and meta-analysis.
Derry, S; Hadley, G; Moore, RA, 2006
)
1.78
" However, studies to define the ideal dosing regimen and cost-effectiveness are required before it can be accepted as a recognized therapy."( Imiquimod 5% cream monotherapy for cutaneous squamous cell carcinoma in situ (Bowen's disease): a randomized, double-blind, placebo-controlled trial.
Chawla, M; Finlay, AY; Goodwin, R; Laidler, P; Motley, RJ; Patel, GK; Price, PE, 2006
)
1.78
" However, dosing with masked oral prodrugs of TLR7 agonists, such as ANA-975, limits the adverse events associated with the activation of responsive gastrointestinal immune tissue."( Masked oral prodrugs of toll-like receptor 7 agonists: a new approach for the treatment of infectious disease.
Averett, D; Fletcher, S; Steffy, K, 2006
)
0.33
" Vehicle-controlled, phase III clinical trials show that imiquimod is safe and effective for treating superficial basal cell carcinoma with dosing 5 or 7 times per week for 6 weeks."( Two-year interim results from a 5-year study evaluating clinical recurrence of superficial basal cell carcinoma after treatment with imiquimod 5% cream daily for 6 weeks.
Gebauer, K; Owens, M; Quirk, C; Stampone, P, 2006
)
0.78
" This compound may represent an alternative treatment in patients with erythroplasia of Queyrat, although the dosing schedule and treatment duration require further evaluation."( Erythroplasia of Queyrat treated with imiquimod 5% cream.
De Pasquale, R; Micali, G; Nasca, MR, 2006
)
0.6
"A 4-week course of treatment with three times weekly dosing of imiquimod 5% cream, with a repeated course of treatment for those patients who fail to clear after the first course of treatment, is a safe and effective treatment for AK."( Vehicle-controlled, randomized, double-blind study to assess safety and efficacy of imiquimod 5% cream applied once daily 3 days per week in one or two courses of treatment of actinic keratoses on the head.
Alomar, A; Bichel, J; McRae, S, 2007
)
0.8
"A shorter dosing regimen of imiquimod for the treatment of actinic keratosis may be effective, with long-term clinical benefits."( Vehicle-controlled, double-blind, randomized study of imiquimod 5% cream applied 3 days per week in one or two courses of treatment for actinic keratoses on the head.
Dinehart, S; Fielder, S; Fox, TL; Jorizzo, J; Lee, JH; Ling, M; Matheson, R; McRae, S; Moore, JK, 2007
)
0.88
"This study was designed to compare the safety and efficacy of two cycled dosing regimens of imiquimod 5% cream for treatment of superficial basal cell carcinoma (sBCC)."( A randomized parallel study to assess the safety and efficacy of two different dosing regimens of 5% imiquimod in the treatment of superficial basal cell carcinoma.
Dawe, RS; Ezughah, FI; Fleming, CJ; Ibbotson, SH, 2008
)
0.78
"Patients (n = 32) were randomized to receive one of two treatment regimens: 8 weeks of treatment with once-daily dosing for alternate weeks (R1) and 5 weeks of once-daily dosing with a 1-week interval in the middle of the course (R2)."( A randomized parallel study to assess the safety and efficacy of two different dosing regimens of 5% imiquimod in the treatment of superficial basal cell carcinoma.
Dawe, RS; Ezughah, FI; Fleming, CJ; Ibbotson, SH, 2008
)
0.56
" Dosing continued for 16 weeks regardless of lesion clearance."( Topical immunomodulation under systemic immunosuppression: results of a multicentre, randomized, placebo-controlled safety and efficacy study of imiquimod 5% cream for the treatment of actinic keratoses in kidney, heart, and liver transplant patients.
Amerio, P; Bichel, J; Euvrard, S; Guidi, B; Proby, CM; Rønnevig, J; Slade, HB; Stockfleth, E; Ulrich, C; van de Kerkhof, PC, 2007
)
0.54
" By titrating its dosing for angiogenesis inhibitory activity and not for gross inflammation, imiquimod can be applied in an efficacious and well-tolerated fashion to treat skin cancer."( Antiangiogenesis in the treatment of skin cancer.
Li, VW; Li, WW, 2008
)
0.57
" Peak serum imiquimod concentrations following single and multiple dosing were low (< 10 ng/mL)."( Pharmacokinetics and safety of imiquimod 5% cream in the treatment of molluscum contagiosum in children.
Eichenfield, LF; Fielder, SL; Kolb, VB; Levy, ML; Meng, TC; Myhre, PE,
)
0.8
"Although the effectiveness of daily dosing regimens of 5% imiquimod cream for the treatment of superficial basal cell carcinomas (sBCC) has been documented by recent studies, concerns about long-term outcome remain."( Confirmation of histological clearance of superficial basal cell carcinoma with multiple serial sectioning and Mohs' micrographic surgery following treatment with imiquimod 5% cream.
Affleck, AG; Evans, A; Ezughah, FI; Fleming, CJ; Ibbotson, SH, 2008
)
0.79
"We sought to explore the efficacy and safety of a once weekly for 24 weeks dosing regimen using a left versus right side of head design."( Placebo-controlled, double-blind, randomized pilot study of imiquimod 5% cream applied once per week for 6 months for the treatment of actinic keratoses.
Itenberg, S; Lebwohl, M; Stern, DW; Uliasz, A; Zeichner, JA, 2009
)
0.6
"5 milliseconds pulse duration; spot size 7 mm using a light dosage of 10 J/cm2 with cryogen spray cooling."( Pilot study examining the combined use of pulsed dye laser and topical Imiquimod versus laser alone for treatment of port wine stain birthmarks.
Chang, CJ; Hsiao, YC; Mihm, MC; Nelson, JS, 2008
)
0.58
"Clinical studies in cutaneous conditions other than actinic keratosis (AK) have revealed that the safety and efficacy profile of imiquimod is influenced by dosing frequency."( Effect of dosing frequency on the safety and efficacy of imiquimod 5% cream for treatment of actinic keratosis on the forearms and hands: a phase II, randomized placebo-controlled trial.
Cowen, PS; Gebauer, K; Shumack, S, 2009
)
0.8
"To evaluate dosing frequency response of imiquimod 5% for treatment of AK."( Effect of dosing frequency on the safety and efficacy of imiquimod 5% cream for treatment of actinic keratosis on the forearms and hands: a phase II, randomized placebo-controlled trial.
Cowen, PS; Gebauer, K; Shumack, S, 2009
)
0.86
" No patients discontinued for adverse events; 1 interrupted dosing for an application site ulcer."( Pharmacokinetics of daily self-application of imiquimod 3.75% cream in adult patients with external anogenital warts.
Adams, MP; Barry, GT; Feldman, R; Kulp, J; Levy, S; Wu, J, 2012
)
0.64
" These drugs were incorporated in conventional dosage forms or loaded in lipid nanocarries, which have been used mainly for improved skin delivery and antileishmanial activity."( Drug delivery systems for the topical treatment of cutaneous leishmaniasis.
Aguiar, MG; Carneiro, G; Fernandes, AP; Ferreira, LA, 2012
)
0.38
" Insights into the most promising delivery strategies to improve treatment of CL with PA and AmB using conventional dosage forms, lipid nanocarriers, and combined therapy are presented and discussed."( Drug delivery systems for the topical treatment of cutaneous leishmaniasis.
Aguiar, MG; Carneiro, G; Fernandes, AP; Ferreira, LA, 2012
)
0.38
"Cidofovir cream could be a useful therapeutic alternative, although further studies are required to establish the best dosage and its cost-effectiveness."( [Treatment of anogenital warts with topical cidofovir].
de Troya-Martín, M; Del Boz, J; Fernández-Morano, T; Frieyro-Elichegui, M; Padilla-España, L; Repiso, JB, 2013
)
0.39
"75% is a new agent with fewer side effects and perhaps a better dosing schedule than imquimod 5%, but is not more effective."( Update on the treatment of genital warts.
Scheinfeld, N, 2013
)
0.39
" Although small-molecule microarrays are a promising platform for miniaturized screening, it has been a challenge to use them to obtain quantitative dose-response curves in vitro, especially for lipophilic compounds."( Quantitative dose-response curves from subcellular lipid multilayer microarrays.
Chadwick, BP; Darrow, EM; Davidson, MW; Kusi-Appiah, AE; Lenhert, S; Lowry, TW; Wilson, KA, 2015
)
0.42
" Although upregulation of genes MxA, GRAMD1A and DMXL2 suggested that IMQ treatment did induce skin changes in psoriasis patients, more optimal dosing of IMQ and NB-UVB might be necessary to achieve desired treatment responses."( Does imiquimod pretreatment optimize 308-nm excimer laser (UVB) therapy in psoriasis patients?
Cooper, KD; Groft, S; Honda, K; McCormick, TS; Oyetakin-White, P; Soler, DC; Tacastacas, JD; Young, A, 2017
)
0.97
" A-SAA proteins were dosed by ELISA or immunonephelemetry assay."( Interleukin-17A-induced production of acute serum amyloid A by keratinocytes contributes to psoriasis pathogenesis.
Bernard, FX; Bodet, C; Buffière-Morgado, A; Camus, M; Couderc, E; Favot, L; Garcia, M; Guillet, G; Huguier, V; Jégou, JF; Lacombe, C; Lecron, JC; Levillain, P; Mcheik, J; Morel, F; Paquier, C; Pohin, M; Yssel, H, 2017
)
0.46
" Insufficient dosing regimens or prolonged treatment with TK inhibitors result in the local selection of pre-existing mutant HSV viruses."( [Acyclovir-resistant perineal HSV infection revealing chronic lymphoid leukaemia].
Bulai Livideanu, C; Casassa, EA; Fortenfant, F; Gaudin, C; Konstantinou, MP; Lamant, L; Mengelle, C; Nicol, P; Paul, C; Viraben, R, 2018
)
0.48
" Several dosing regimens have been studied in the literature."( A Review on Imiquimod Therapy and Discussion on Optimal Management of Basal Cell Carcinomas.
Arora, H; Darwin, E; Kamath, P; Nouri, K, 2018
)
0.86
" Results- Low dosage imiquimod significantly attenuated hematoma volume, brain edema, BBB permeability, and neurological deficits after ICH."( TLR7 (Toll-Like Receptor 7) Facilitates Heme Scavenging Through the BTK (Bruton Tyrosine Kinase)-CRT (Calreticulin)-LRP1 (Low-Density Lipoprotein Receptor-Related Protein-1)-Hx (Hemopexin) Pathway in Murine Intracerebral Hemorrhage.
Budbazar, E; Guo, Z; Krafft, PR; Tang, J; Tong, L; Wang, G; Xue, F; Zhang, JH, 2018
)
0.8
"At the beginning of the 20th century, a new immunomodulator molecule, imiquimod, appears in the market for the treatment of actinic keratosis but suffers from the pitfalls of the conventional approach of dosage form preparation including high dose, poor stability and more side effects."( Actinic keratosis and imiquimod: a review of novel carriers and patents.
Katare, OP; Sharma, G; Sharma, M; Singh, B, 2019
)
1.06
" For in vivo studies, we dosed imiquimod (IMQ) -induced mice with Diosgenin and conducted hematoxylin-eosin (HE), TUNEL assay and immunohistochemistry (IHC) to evaluate histological changes, apoptosis and the status of keratinocyte proliferation, epidermal differentiation, vascularity and cutaneous inflammatory cell infiltration respectively."( The potential of Diosgenin in treating psoriasis: Studies from HaCaT keratinocytes and imiquimod-induced murine model.
Huang, C; Le, K; Sun, Y; Wu, S; Xie, M; Xu, M; Zhao, M, 2020
)
1.07
" While oral administration OTX015 in IMQ-treated mice reduced disease severity, ABBV075 equally decreased the symptoms and molecular and cellular severity markers at one-tenth of the minimal dosing required for OTX015."( A monocyte-keratinocyte-derived co-culture assay accurately identifies efficacies of BET inhibitors as therapeutic candidates for psoriasiform dermatitis.
Chong, J; Hsu, DK; Huynh, M; Hwang, ST; Mendoza, L; Shi, Z; Wu, X; Yamada, D, 2020
)
0.56
" In the literature to date, studies evaluating the use of imiquimod to treat LM have utilised varying methodologies and provided short follow-up and these limitations have impaired the development of clear guidelines for dosage and management of side effects."( A practical guide on the use of imiquimod cream to treat lentigo maligna.
Fogarty, GB; Guitera, P; Hong, A; O'Donnell, BA; Paton, E; Pellacani, G; Scolyer, RA; Stretch, JR; Waddell, A, 2021
)
1.15
" Treatment with imiquimod was self-administered in a slowly escalating dosage scheme up to three times per week for a period of 4-6 months."( Topical imiquimod versus surgery for vulvar intraepithelial neoplasia: a multicentre, randomised, phase 3, non-inferiority trial.
Boandl, A; Bogner, G; Ciresa-König, A; Holter, M; Jan, Z; Joura, EA; Kalteis, MS; Regauer, S; Reich, O; Schauer, C; Tamussino, K; Trutnovsky, G; Widschwendter, A, 2022
)
1.5
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
interferon inducerAn agent that promotes the production and release of interferons.
[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 (1)

ClassDescription
imidazoquinoline
[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]

Pathways (1)

PathwayProteinsCompounds
Toll-Like Receptor Pathway 2322

Protein Targets (28)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
TDP1 proteinHomo sapiens (human)Potency6.68380.000811.382244.6684AID686978
GLI family zinc finger 3Homo sapiens (human)Potency0.96680.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency13.78250.000221.22318,912.5098AID1259243; AID1259247
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency1.00240.001022.650876.6163AID1224838; AID1224893
EWS/FLI fusion proteinHomo sapiens (human)Potency15.34060.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
pregnane X nuclear receptorHomo sapiens (human)Potency31.62280.005428.02631,258.9301AID1346985
estrogen nuclear receptor alphaHomo sapiens (human)Potency6.13340.000229.305416,493.5996AID743075; AID743079; AID743091
cytochrome P450 2D6Homo sapiens (human)Potency6.00810.00108.379861.1304AID1645840
aryl hydrocarbon receptorHomo sapiens (human)Potency9.43920.000723.06741,258.9301AID743085; AID743122
DNA polymerase betaHomo sapiens (human)Potency100.00000.022421.010289.1251AID485314
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency10.61460.000627.21521,122.0200AID743202; AID743219
urokinase-type plasminogen activator precursorMus musculus (house mouse)Potency1.41250.15855.287912.5893AID540303
plasminogen precursorMus musculus (house mouse)Potency1.41250.15855.287912.5893AID540303
urokinase plasminogen activator surface receptor precursorMus musculus (house mouse)Potency1.41250.15855.287912.5893AID540303
gemininHomo sapiens (human)Potency1.58670.004611.374133.4983AID624296; AID624297
peripheral myelin protein 22Rattus norvegicus (Norway rat)Potency16.13660.005612.367736.1254AID624032
lamin isoform A-delta10Homo sapiens (human)Potency12.58930.891312.067628.1838AID1487
Cellular tumor antigen p53Homo sapiens (human)Potency11.88320.002319.595674.0614AID651631
[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)
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
Bile salt export pumpHomo sapiens (human)IC50 (µMol)133.00000.11007.190310.0000AID1473738
Histamine H2 receptorHomo sapiens (human)IC50 (µMol)1.50600.02202.298710.0000AID625270
Histamine H2 receptorHomo sapiens (human)Ki1.48100.00062.197310.0000AID625270
Alpha-1D adrenergic receptorHomo sapiens (human)IC50 (µMol)2.62100.00020.75688.8970AID625200
Alpha-1D adrenergic receptorHomo sapiens (human)Ki1.28800.00000.360910.0000AID625200
Adenosine receptor A2aHomo sapiens (human)IC50 (µMol)5.32000.00071.559410.0000AID625195
Adenosine receptor A2aHomo sapiens (human)Ki2.98700.00001.06099.7920AID625195
7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)IC50 (µMol)0.64600.05201.20935.6000AID1679179
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
[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)
Toll-like receptor 8Homo sapiens (human)EC50 (µMol)270.00000.48004.26369.0000AID719614
Toll-like receptor 7Homo sapiens (human)EC50 (µMol)8.22000.00721.57446.8000AID1068405; AID1504602; AID1556486; AID1646838; AID484311; AID719613
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (257)

Processvia Protein(s)Taxonomy
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)
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)
gastric acid secretionHistamine H2 receptorHomo sapiens (human)
immune responseHistamine H2 receptorHomo sapiens (human)
positive regulation of vasoconstrictionHistamine H2 receptorHomo sapiens (human)
G protein-coupled serotonin receptor signaling pathwayHistamine H2 receptorHomo sapiens (human)
chemical synaptic transmissionHistamine H2 receptorHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerHistamine H2 receptorHomo 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)
synaptic transmission, dopaminergicAdenosine receptor A2aHomo sapiens (human)
response to amphetamineAdenosine receptor A2aHomo sapiens (human)
regulation of DNA-templated transcriptionAdenosine receptor A2aHomo sapiens (human)
phagocytosisAdenosine receptor A2aHomo sapiens (human)
apoptotic processAdenosine receptor A2aHomo sapiens (human)
inflammatory responseAdenosine receptor A2aHomo sapiens (human)
cellular defense responseAdenosine receptor A2aHomo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayAdenosine receptor A2aHomo sapiens (human)
adenylate cyclase-activating G protein-coupled receptor signaling pathwayAdenosine receptor A2aHomo sapiens (human)
protein kinase C-activating G protein-coupled receptor signaling pathwayAdenosine receptor A2aHomo sapiens (human)
cell-cell signalingAdenosine receptor A2aHomo sapiens (human)
synaptic transmission, cholinergicAdenosine receptor A2aHomo sapiens (human)
central nervous system developmentAdenosine receptor A2aHomo sapiens (human)
blood coagulationAdenosine receptor A2aHomo sapiens (human)
sensory perceptionAdenosine receptor A2aHomo sapiens (human)
locomotory behaviorAdenosine receptor A2aHomo sapiens (human)
blood circulationAdenosine receptor A2aHomo sapiens (human)
negative regulation of cell population proliferationAdenosine receptor A2aHomo sapiens (human)
response to xenobiotic stimulusAdenosine receptor A2aHomo sapiens (human)
response to inorganic substanceAdenosine receptor A2aHomo sapiens (human)
positive regulation of glutamate secretionAdenosine receptor A2aHomo sapiens (human)
positive regulation of acetylcholine secretion, neurotransmissionAdenosine receptor A2aHomo sapiens (human)
regulation of norepinephrine secretionAdenosine receptor A2aHomo sapiens (human)
response to purine-containing compoundAdenosine receptor A2aHomo sapiens (human)
response to caffeineAdenosine receptor A2aHomo sapiens (human)
positive regulation of synaptic transmission, GABAergicAdenosine receptor A2aHomo sapiens (human)
synaptic transmission, glutamatergicAdenosine receptor A2aHomo sapiens (human)
positive regulation of urine volumeAdenosine receptor A2aHomo sapiens (human)
vasodilationAdenosine receptor A2aHomo sapiens (human)
eating behaviorAdenosine receptor A2aHomo sapiens (human)
negative regulation of vascular permeabilityAdenosine receptor A2aHomo sapiens (human)
negative regulation of neuron apoptotic processAdenosine receptor A2aHomo sapiens (human)
positive regulation of circadian sleep/wake cycle, sleepAdenosine receptor A2aHomo sapiens (human)
negative regulation of alpha-beta T cell activationAdenosine receptor A2aHomo sapiens (human)
astrocyte activationAdenosine receptor A2aHomo sapiens (human)
neuron projection morphogenesisAdenosine receptor A2aHomo sapiens (human)
positive regulation of protein secretionAdenosine receptor A2aHomo sapiens (human)
negative regulation of inflammatory responseAdenosine receptor A2aHomo sapiens (human)
regulation of mitochondrial membrane potentialAdenosine receptor A2aHomo sapiens (human)
membrane depolarizationAdenosine receptor A2aHomo sapiens (human)
regulation of calcium ion transportAdenosine receptor A2aHomo sapiens (human)
positive regulation of synaptic transmission, glutamatergicAdenosine receptor A2aHomo sapiens (human)
excitatory postsynaptic potentialAdenosine receptor A2aHomo sapiens (human)
inhibitory postsynaptic potentialAdenosine receptor A2aHomo sapiens (human)
prepulse inhibitionAdenosine receptor A2aHomo sapiens (human)
apoptotic signaling pathwayAdenosine receptor A2aHomo sapiens (human)
presynaptic modulation of chemical synaptic transmissionAdenosine receptor A2aHomo sapiens (human)
positive regulation of long-term synaptic potentiationAdenosine receptor A2aHomo sapiens (human)
positive regulation of apoptotic signaling pathwayAdenosine receptor A2aHomo sapiens (human)
G protein-coupled adenosine receptor signaling pathwayAdenosine receptor A2aHomo sapiens (human)
purine nucleoside catabolic process7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
DNA repair7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
response to oxidative stress7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
male gonad development7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
DNA protection7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
response to cadmium ion7,8-dihydro-8-oxoguanine triphosphataseHomo 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)
regulation of protein phosphorylationToll-like receptor 8Homo sapiens (human)
inflammatory responseToll-like receptor 8Homo sapiens (human)
response to virusToll-like receptor 8Homo sapiens (human)
immunoglobulin mediated immune responseToll-like receptor 8Homo sapiens (human)
negative regulation of interleukin-12 productionToll-like receptor 8Homo sapiens (human)
positive regulation of interferon-alpha productionToll-like receptor 8Homo sapiens (human)
positive regulation of interferon-beta productionToll-like receptor 8Homo sapiens (human)
positive regulation of type II interferon productionToll-like receptor 8Homo sapiens (human)
positive regulation of interleukin-1 beta productionToll-like receptor 8Homo sapiens (human)
positive regulation of interleukin-6 productionToll-like receptor 8Homo sapiens (human)
positive regulation of interleukin-8 productionToll-like receptor 8Homo sapiens (human)
toll-like receptor 8 signaling pathwayToll-like receptor 8Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionToll-like receptor 8Homo sapiens (human)
innate immune responseToll-like receptor 8Homo sapiens (human)
positive regulation of innate immune responseToll-like receptor 8Homo sapiens (human)
defense response to virusToll-like receptor 8Homo sapiens (human)
cellular response to mechanical stimulusToll-like receptor 8Homo sapiens (human)
toll-like receptor signaling pathwayToll-like receptor 8Homo sapiens (human)
canonical NF-kappaB signal transductionToll-like receptor 8Homo sapiens (human)
regulation of protein phosphorylationToll-like receptor 7Homo sapiens (human)
inflammatory responseToll-like receptor 7Homo sapiens (human)
canonical NF-kappaB signal transductionToll-like receptor 7Homo sapiens (human)
I-kappaB phosphorylationToll-like receptor 7Homo sapiens (human)
JNK cascadeToll-like receptor 7Homo sapiens (human)
positive regulation of chemokine productionToll-like receptor 7Homo sapiens (human)
positive regulation of interferon-alpha productionToll-like receptor 7Homo sapiens (human)
positive regulation of interferon-beta productionToll-like receptor 7Homo sapiens (human)
positive regulation of type II interferon productionToll-like receptor 7Homo sapiens (human)
positive regulation of interleukin-8 productionToll-like receptor 7Homo sapiens (human)
toll-like receptor 7 signaling pathwayToll-like receptor 7Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionToll-like receptor 7Homo sapiens (human)
innate immune responseToll-like receptor 7Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIToll-like receptor 7Homo sapiens (human)
positive regulation of inflammatory responseToll-like receptor 7Homo sapiens (human)
defense response to virusToll-like receptor 7Homo sapiens (human)
positive regulation of macrophage cytokine productionToll-like receptor 7Homo sapiens (human)
response to cGMPToll-like receptor 7Homo sapiens (human)
cellular response to mechanical stimulusToll-like receptor 7Homo sapiens (human)
cellular response to virusToll-like receptor 7Homo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transductionToll-like receptor 7Homo sapiens (human)
toll-like receptor signaling pathwayToll-like receptor 7Homo sapiens (human)
positive regulation of interleukin-6 productionToll-like receptor 7Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (85)

Processvia Protein(s)Taxonomy
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)
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)
histamine receptor activityHistamine H2 receptorHomo sapiens (human)
G protein-coupled serotonin receptor activityHistamine H2 receptorHomo sapiens (human)
neurotransmitter receptor activityHistamine H2 receptorHomo 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)
G protein-coupled adenosine receptor activityAdenosine receptor A2aHomo sapiens (human)
protein bindingAdenosine receptor A2aHomo sapiens (human)
calmodulin bindingAdenosine receptor A2aHomo sapiens (human)
lipid bindingAdenosine receptor A2aHomo sapiens (human)
enzyme bindingAdenosine receptor A2aHomo sapiens (human)
type 5 metabotropic glutamate receptor bindingAdenosine receptor A2aHomo sapiens (human)
identical protein bindingAdenosine receptor A2aHomo sapiens (human)
protein-containing complex bindingAdenosine receptor A2aHomo sapiens (human)
alpha-actinin bindingAdenosine receptor A2aHomo sapiens (human)
5'-(N(7)-methylguanosine 5'-triphospho)-[mRNA] hydrolase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
protein binding7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
8-oxo-7,8-dihydroguanosine triphosphate pyrophosphatase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
dATP diphosphatase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
hydrolase activity, acting on acid anhydrides, in phosphorus-containing anhydrides7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
snoRNA binding7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
8-oxo-7,8-dihydrodeoxyguanosine triphosphate pyrophosphatase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
metal ion binding7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
ATP diphosphatase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
2-hydroxy-ATP hydrolase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
2-hydroxy-dATP hydrolase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
N6-methyl-(d)ATP hydrolase activity7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
O6-methyl-dGTP hydrolase activity7,8-dihydro-8-oxoguanine triphosphataseHomo 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)
DNA bindingToll-like receptor 8Homo sapiens (human)
RNA bindingToll-like receptor 8Homo sapiens (human)
double-stranded RNA bindingToll-like receptor 8Homo sapiens (human)
single-stranded RNA bindingToll-like receptor 8Homo sapiens (human)
signaling receptor activityToll-like receptor 8Homo sapiens (human)
pattern recognition receptor activityToll-like receptor 8Homo sapiens (human)
double-stranded RNA bindingToll-like receptor 7Homo sapiens (human)
single-stranded RNA bindingToll-like receptor 7Homo sapiens (human)
protein bindingToll-like receptor 7Homo sapiens (human)
siRNA bindingToll-like receptor 7Homo sapiens (human)
pattern recognition receptor activityToll-like receptor 7Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (55)

Processvia Protein(s)Taxonomy
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)
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 membraneHistamine H2 receptorHomo sapiens (human)
synapseHistamine H2 receptorHomo sapiens (human)
plasma membraneHistamine H2 receptorHomo sapiens (human)
dendriteHistamine H2 receptorHomo sapiens (human)
plasma membraneAlpha-1D adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-1D adrenergic receptorHomo sapiens (human)
plasma membraneAdenosine receptor A2aHomo sapiens (human)
intermediate filamentAdenosine receptor A2aHomo sapiens (human)
plasma membraneAdenosine receptor A2aHomo sapiens (human)
membraneAdenosine receptor A2aHomo sapiens (human)
dendriteAdenosine receptor A2aHomo sapiens (human)
axolemmaAdenosine receptor A2aHomo sapiens (human)
asymmetric synapseAdenosine receptor A2aHomo sapiens (human)
presynaptic membraneAdenosine receptor A2aHomo sapiens (human)
neuronal cell bodyAdenosine receptor A2aHomo sapiens (human)
postsynaptic membraneAdenosine receptor A2aHomo sapiens (human)
presynaptic active zoneAdenosine receptor A2aHomo sapiens (human)
glutamatergic synapseAdenosine receptor A2aHomo sapiens (human)
acrosomal vesicle7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
extracellular space7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
nucleus7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
cytoplasm7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
mitochondrion7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
mitochondrial matrix7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
cytosol7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
nuclear membrane7,8-dihydro-8-oxoguanine triphosphataseHomo sapiens (human)
cytoplasm7,8-dihydro-8-oxoguanine triphosphataseHomo 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)
Golgi membraneToll-like receptor 8Homo sapiens (human)
endoplasmic reticulum membraneToll-like receptor 8Homo sapiens (human)
external side of plasma membraneToll-like receptor 8Homo sapiens (human)
endosome membraneToll-like receptor 8Homo sapiens (human)
endolysosome membraneToll-like receptor 8Homo sapiens (human)
plasma membraneToll-like receptor 8Homo sapiens (human)
Golgi membraneToll-like receptor 7Homo sapiens (human)
cytoplasmToll-like receptor 7Homo sapiens (human)
lysosomeToll-like receptor 7Homo sapiens (human)
endosomeToll-like receptor 7Homo sapiens (human)
endoplasmic reticulumToll-like receptor 7Homo sapiens (human)
endoplasmic reticulum membraneToll-like receptor 7Homo sapiens (human)
plasma membraneToll-like receptor 7Homo sapiens (human)
endosome membraneToll-like receptor 7Homo sapiens (human)
early phagosomeToll-like receptor 7Homo sapiens (human)
endolysosome membraneToll-like receptor 7Homo sapiens (human)
receptor complexToll-like receptor 7Homo sapiens (human)
plasma membraneToll-like receptor 7Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (127)

Assay IDTitleYearJournalArticle
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.
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.
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.
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.
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.
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.
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
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.
AID719613Agonist activity at human TLR7 transfected in HEK cells assessed as NFkappaB induction after 24 hrs by specific secreted alkaline phosphatase gene assay2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
Discovery of Imidazoquinolines with Toll-Like Receptor 7/8 Independent Cytokine Induction.
AID341177Toxic induction of TNFalpha level in human PBMC assessed as drug level causing maximal cytokine induction after 24 hrs relative to control2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
AID1068403Agonist activity at TLR7/TLR8 in C57BL/6 mouse BMDC assessed as induction of TNF-alpha production at 30 uM after 3 days by flow cytometric analysis2014Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2
Structure-activity relationship analysis of imidazoquinolines with Toll-like receptors 7 and 8 selectivity and enhanced cytokine induction.
AID1068400Agonist activity at TLR7/TLR8 in C57BL/6 mouse BMDC assessed as induction of IL-10 production at 30 uM after 3 days by flow cytometric analysis2014Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2
Structure-activity relationship analysis of imidazoquinolines with Toll-like receptors 7 and 8 selectivity and enhanced cytokine induction.
AID433907Cytotoxicity against human A375 cells after 96 hrs by MTT assay2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
New imidazo[1,2-a]quinoxaline derivatives: synthesis and in vitro activity against human melanoma.
AID1646855Solubility of the compound at >100 uM2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID341175Antiviral activity against HCV infected human Huh7 replicon cells treated with 20 uM drug-induced human PBMC supernatants assessed as viral levels in presence of type I IFN receptor antibody by luciferase assay2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
AID341170Antiviral activity against HCV infected human Huh7 replicon cells assessed as viral levels by luciferase assay2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
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).
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.
AID1504615Immunostimulatory activity in human PBMC assessed as increase in TNFalpha levels at 0.39 to 50 uM after 24 hrs by ELISA2017ACS medicinal chemistry letters, Nov-09, Volume: 8, Issue:11
Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.
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.
AID1504605Agonist activity at human TLR8 expressed in HEK cells at 180 uM after 8 to 12 hrs by NFkappaB/SEAP reporter gene assay2017ACS medicinal chemistry letters, Nov-09, Volume: 8, Issue:11
Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.
AID484312Agonist activity at human TLR8 expressed in NF-kappaB-stimulated HEK293 cells assessed as induction of secreted alkaline phosphatase expression by reporter gene assay2010Journal of medicinal chemistry, Jun-10, Volume: 53, Issue:11
Structure-activity relationships in human toll-like receptor 7-active imidazoquinoline analogues.
AID719614Agonist activity at human TLR8 transfected in HEK cells assessed as NFkappaB induction after 24 hrs by specific secreted alkaline phosphatase gene assay2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
Discovery of Imidazoquinolines with Toll-Like Receptor 7/8 Independent Cytokine Induction.
AID341161Toxic induction of IL6 level in human PBMC assessed as drug level causing maximal cytokine induction after 24 hrs relative to control2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
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).
AID1646849Agonist activity at TLR7/8 in dog PBMC assessed as maximal increase in TNFalpha secretion at 20 uM after 30 to 48 hrs by ELISA2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID406725Cytotoxicity against human RPMI7591 cells after 96 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13
In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID1646840Agonist activity at TLR7/8 in dog PBMC assessed as TNFalpha secretion at 20 uM after 29 hrs by ELISA (Rvb = 8 +/- 2 pg/ml)2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
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).
AID1556491Induction of TNFalpha production in human PBMC at 10 ug/ml incubated for 24 hrs by flow cytometry analysis2019European journal of medicinal chemistry, Oct-01, Volume: 179Selective Toll-like receptor 7 agonists with novel chromeno[3,4-d]imidazol-4(1H)-one and 2-(trifluoromethyl)quinoline/ quinazoline-4-amine scaffolds.
AID484311Agonist activity at human TLR7 expressed in NF-kappaB-stimulated HEK293 cells assessed as induction of secreted alkaline phosphatase expression by reporter gene assay2010Journal of medicinal chemistry, Jun-10, Volume: 53, Issue:11
Structure-activity relationships in human toll-like receptor 7-active imidazoquinoline analogues.
AID244777Minimum effective concentration required to induce interferon (IFN) production in human peripheral blood mononuclear cells (hPBMC)2005Journal of medicinal chemistry, May-19, Volume: 48, Issue:10
Synthesis and structure-activity-relationships of 1H-imidazo[4,5-c]quinolines that induce interferon production.
AID1068405Agonist activity at human TLR-7 expressed in HEK293 cells after 24 hrs by SEAP reporter gene assay2014Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2
Structure-activity relationship analysis of imidazoquinolines with Toll-like receptors 7 and 8 selectivity and enhanced cytokine induction.
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).
AID341172Increase in IFNalpha level in human PBMC after 24 hrs relative to control2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
AID406727Cytotoxicity against human LS174T cells after 96 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13
In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID719610Immunomodulatory activity in C57BL/6 mouse BMDC assessed as IL-1beta production at 30 uM after 3 days by FACS flow cytometric analysis (Rvb = 26.2 +/- 3.7 pg/mL)2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
Discovery of Imidazoquinolines with Toll-Like Receptor 7/8 Independent Cytokine Induction.
AID406726Cytotoxicity against human MCF7 cells after 96 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13
In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID406728Cytotoxicity against human Raji cells after 96 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13
In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID1646850Agonist activity at TLR7/8 in dog PBMC assessed as maximal increase in IL-12 secretion at 20 uM after 30 to 48 hrs by ELISA2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID1068401Agonist activity at TLR7/TLR8 in C57BL/6 mouse BMDC assessed as induction of IL-12p40 production at 30 uM after 3 days by flow cytometric analysis2014Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2
Structure-activity relationship analysis of imidazoquinolines with Toll-like receptors 7 and 8 selectivity and enhanced cytokine induction.
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).
AID1646841Agonist activity at TLR7/8 in dog PBMC assessed as IL-12 secretion at 20 uM after 29 hrs by ELISA (Rvb = 18 +/- 8 pg/ml)2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
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.
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).
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).
AID719609Immunomodulatory activity in C57BL/6 mouse BMDC assessed as TNFalpha production at 30 uM after 3 days by FACS flow cytometric analysis (Rvb = 91.3 +/- 34.5 pg/mL)2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
Discovery of Imidazoquinolines with Toll-Like Receptor 7/8 Independent Cytokine Induction.
AID1068404Agonist activity at human TLR-8 expressed in HEK293 cells after 24 hrs by SEAP reporter gene assay2014Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2
Structure-activity relationship analysis of imidazoquinolines with Toll-like receptors 7 and 8 selectivity and enhanced cytokine induction.
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).
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).
AID1646854Agonist activity at TLR7/8 in dog PBMC assessed as increase in IFN-gamma secretion at 20 uM measured over 24 hrs by ELISA2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID1504613Immunostimulatory activity in human PBMC assessed as increase in IL-1beta levels at 0.39 to 50 uM after 24 hrs by ELISA2017ACS medicinal chemistry letters, Nov-09, Volume: 8, Issue:11
Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.
AID1504612Immunostimulatory activity in human PBMC assessed as increase in IL-12p70 levels at 0.39 to 50 uM after 24 hrs by ELISA2017ACS medicinal chemistry letters, Nov-09, Volume: 8, Issue:11
Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.
AID1679178Agonist activity at TLR7 in human PBMC assessed as induction of IN-12 stimulation2016Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6
Potent and Selective Inhibitors of MTH1 Probe Its Role in Cancer Cell Survival.
AID1442705Immunomodulatory activity in human PBMC assessed as induction of IL-6 secretion at 5 uM after 24 hrs by ELISA2017Bioorganic & medicinal chemistry letters, 04-01, Volume: 27, Issue:7
1-ethyl-3-(6-methylphenanthridine-8-il) urea modulates TLR3/9 activation and induces selective pro-inflammatory cytokine expression in vitro.
AID341169Antiviral activity against HCV infected human Huh7 replicon cells treated with drug-induced human PBMC supernatants assessed as viral levels by luciferase assay2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
AID1504614Immunostimulatory activity in human PBMC assessed as increase in IFNgamma levels at 0.39 to 50 uM after 24 hrs by ELISA2017ACS medicinal chemistry letters, Nov-09, Volume: 8, Issue:11
Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.
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.
AID1556486Agonist activity at human TLR7 in HEK293 cells cotransfected with SEAP reporter gene assessed as activity of SEAP incubated for 24 hrs by quanti-blue staining based SEAP reporter gene assay2019European journal of medicinal chemistry, Oct-01, Volume: 179Selective Toll-like receptor 7 agonists with novel chromeno[3,4-d]imidazol-4(1H)-one and 2-(trifluoromethyl)quinoline/ quinazoline-4-amine scaffolds.
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).
AID1646851Agonist activity at TLR7/8 in dog PBMC assessed as maximal increase in IFN-gamma secretion at 20 uM after 30 to 48 hrs by ELISA2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID406723Cytotoxicity against human A375 cells after 96 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13
In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID1646838Agonist activity at human TLR7 expressed in HEK-Blue cells assessed as induction of NFkappaB activation by measuring increase in SEAP level by SEAP reporter gene-based UV-vis absorbance method2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID1646842Agonist activity at TLR7/8 in dog PBMC assessed as IL-6 secretion at 20 uM after 29 hrs by ELISA (Rvb = 310 +/- 90 pg/ml)2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID1068402Agonist activity at TLR7/TLR8 in C57BL/6 mouse BMDC assessed as induction of IL-1beta production at 30 uM after 3 days by flow cytometric analysis2014Journal of medicinal chemistry, Jan-23, Volume: 57, Issue:2
Structure-activity relationship analysis of imidazoquinolines with Toll-like receptors 7 and 8 selectivity and enhanced cytokine induction.
AID719612Immunomodulatory activity in C57BL/6 mouse BMDC assessed as IL-10 production at 30 uM after 3 days by FACS flow cytometric analysis (Rvb = 16.2 +/- 4.7 pg/mL)2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
Discovery of Imidazoquinolines with Toll-Like Receptor 7/8 Independent Cytokine Induction.
AID341160Induction of IFNalpha2a level in human PBMC assessed as drug level causing maximal cytokine induction after 24 hrs relative to control2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
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).
AID1646852Agonist activity at TLR7/8 in dog PBMC assessed as increase in TNFalpha secretion at 20 uM measured over 24 hrs by ELISA2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID1646845Agonist activity at TLR7/8 in dog PBMC assessed as IFNgamma secretion at 20 uM after 29 hrs by ELISA (Rvb = 0.4 +/- 0.7 pg/ml)2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID406724Cytotoxicity against human M4Be cells after 96 hrs by MTT assay2008Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13
In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID133109Minimum effective dose required for more than 100 IU/mL induction of IFN using mice after peroral administration.2002Journal of medicinal chemistry, Dec-05, Volume: 45, Issue:25
Discovery of 8-hydroxyadenines as a novel type of interferon inducer.
AID1556490Induction of IL-12p70 production in human PBMC at 10 ug/ml incubated for 24 hrs by flow cytometry analysis2019European journal of medicinal chemistry, Oct-01, Volume: 179Selective Toll-like receptor 7 agonists with novel chromeno[3,4-d]imidazol-4(1H)-one and 2-(trifluoromethyl)quinoline/ quinazoline-4-amine scaffolds.
AID1556488Induction of IL-8 production in human PBMC at 10 ug/ml incubated for 24 hrs by flow cytometry analysis2019European journal of medicinal chemistry, Oct-01, Volume: 179Selective Toll-like receptor 7 agonists with novel chromeno[3,4-d]imidazol-4(1H)-one and 2-(trifluoromethyl)quinoline/ quinazoline-4-amine scaffolds.
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).
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).
AID341171Increase in 2',5'-oligoadenylate synthase level in human PBMC after 24 hrs by PCR method relative to control2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
AID1646844Agonist activity at TLR7/8 in dog PBMC assessed as IL-2 secretion at 20 uM after 29 hrs by ELISA (Rvb = 47 +/- 20 pg/ml)2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID132946Minimum effective concentration required for more than 1 IU/mL induction of IFN using mice spleen cells2002Journal of medicinal chemistry, Dec-05, Volume: 45, Issue:25
Discovery of 8-hydroxyadenines as a novel type of interferon inducer.
AID1645924Antiviral activity against HCV2019European journal of medicinal chemistry, Feb-15, Volume: 164A review on HCV inhibitors: Significance of non-structural polyproteins.
AID1646843Agonist activity at TLR7/8 in dog PBMC assessed as IL-10 secretion at 20 uM after 29 hrs by ELISA (Rvb = 33 +/- 16 pg/ml)2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID341159Toxic induction of IL1-beta level in human PBMC assessed as drug level causing maximal cytokine induction after 24 hrs relative to control2007Antimicrobial agents and chemotherapy, Aug, Volume: 51, Issue:8
Investigating Toll-like receptor agonists for potential to treat hepatitis C virus infection.
AID719611Immunomodulatory activity in C57BL/6 mouse BMDC assessed as IL-12p40 production at 30 uM after 3 days by FACS flow cytometric analysis (Rvb = 260.6 +/- 11.9 pg/mL)2012ACS medicinal chemistry letters, Jun-14, Volume: 3, Issue:6
Discovery of Imidazoquinolines with Toll-Like Receptor 7/8 Independent Cytokine Induction.
AID1646853Agonist activity at TLR7/8 in dog PBMC assessed as increase in IL-12 secretion at 20 uM measured over 24 hrs by ELISA2020Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2
Further exploration of the structure-activity relationship of imidazoquinolines; identification of potent C7-substituted imidazoquinolines.
AID1679179Inhibition of MTH1 (unknown origin) using 8-oxo-dGTP as substrate preincubated for 15 mins followed by substrate addition and measured after 20 mins by PPiLight detection reagent based luminescence assay2016Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6
Potent and Selective Inhibitors of MTH1 Probe Its Role in Cancer Cell Survival.
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).
AID1504602Agonist activity at human TLR7 expressed in HEK cells after 8 to 12 hrs by NFkappaB/SEAP reporter gene assay2017ACS medicinal chemistry letters, Nov-09, Volume: 8, Issue:11
Design and Synthesis of N1-Modified Imidazoquinoline Agonists for Selective Activation of Toll-like Receptors 7 and 8.
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.
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.
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.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID1745855NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1745854NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (3,052)

TimeframeStudies, This Drug (%)All Drugs %
pre-19903 (0.10)18.7374
1990's57 (1.87)18.2507
2000's907 (29.72)29.6817
2010's1351 (44.27)24.3611
2020's734 (24.05)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 96.93

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

MetricThis Compound (vs All)
Research Demand Index96.93 (24.57)
Research Supply Index8.17 (2.92)
Research Growth Index6.56 (4.65)
Search Engine Demand Index192.70 (26.88)
Search Engine Supply Index2.19 (0.95)

This Compound (96.93)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials284 (8.70%)5.53%
Reviews454 (13.91%)6.00%
Case Studies744 (22.79%)4.05%
Observational15 (0.46%)0.25%
Other1,767 (54.14%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (167)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Open-label, Single-arm Pilot Study of the Effects of Topical 5% Imiquimod Cream on Preventing Keloid Recurrence After Surgical Keloidectomy [NCT03760250]Phase 26 participants (Actual)Interventional2019-02-05Terminated(stopped due to Investigator decision)
Open Study to Evaluate the Efficacy and Tolerance of Imiquimod 5% Cream for the Treatment of a Large and/or Multiple Superficial Basal Cell Carcinoma. [NCT00189280]Phase 3111 participants (Actual)Interventional2003-05-31Completed
A Phase 1/2 Study of SL-701, a Subcutaneously Injected Multivalent Glioma-Associated Antigen Vaccine, in Adult Patients With Recurrent Glioblastoma Multiforme (GBM) [NCT02078648]Phase 1/Phase 274 participants (Actual)Interventional2014-05-31Completed
Effect of Topical Imiquimod on Lentigo Maligna [NCT01161888]Phase 430 participants (Actual)Interventional2010-06-30Completed
Evaluation of Topical Application of 5% Imiquimod, 0.05% Imiquimod and 0.05% Nanoencapsulated Imiquimod Gel in the Treatment of Actinic Cheilitis: a Randomized Controlled Trial [NCT04219358]Phase 149 participants (Actual)Interventional2019-03-23Terminated(stopped due to Study terminated because of COVID19 pandemics.)
Characterization of the Toll-like Receptor 7-agonist Imiquimod 3.75% as a New Surrogate Model of Itch [NCT03943407]0 participants (Actual)Interventional2019-11-30Withdrawn(stopped due to The Imiquimod 3.75% was ineffective)
An Investigator-Initiated Study to Assess the Safety and Efficacy of Imiquimod 3.75% Cream When Used After Cryotherapy in the Treatment of Hypertrophic Actinic Keratoses (AK) on Dorsal Hands and Forearms [NCT01229319]Phase 420 participants (Anticipated)Interventional2010-10-31Recruiting
Combination Therapy of Topical Imiquimod Plus Multipeptide Vaccination for Cutaneous Metastases of Melanoma [NCT01264731]Phase 14 participants (Actual)Interventional2011-01-31Completed
ITIC2 Trial - Topical Imiquimod Versus Conization to Treat Cervical Intraepithelial Neoplasia: Randomised Controlled, Non-inferiority Trial [NCT01283763]Phase 395 participants (Actual)Interventional2013-05-31Terminated(stopped due to poor recruitment)
Topical Imiquimod in Treating Patients With Grade 2/3 Cervical Intraepithelial Neoplasia [NCT00941252]Phase 2/Phase 360 participants (Anticipated)Interventional2009-07-31Completed
[NCT01567683]Phase 10 participants InterventionalCompleted
Vaccination of Patients With Ovarian Cancer With Dendritic Cell/Tumor Fusions With GM-CSF and Imiquimod [NCT00799110]Phase 223 participants (Anticipated)Interventional2008-08-31Active, not recruiting
Betaglucin 0.2% Gel Versus Imiquimod Cream 5% in the Treatment of Anogenital Warts in 102 Individuals Older Than 18 Years. [NCT03901690]Phase 3102 participants (Anticipated)Interventional2019-08-27Recruiting
An Open-label Study to Evaluate the Safety and Long-Term Clinical Efficacy of Imiquimod 5% Cream Applied Once Daily 7 Days Per Week for 6 Weeks in the Treatment of Superficial Basal Cell Carcinoma [NCT00189306]Phase 3169 participants (Actual)Interventional2001-03-31Completed
Phase I/II Study of Peptide Vaccination Associated With Tumoral Immunomodulation With Proinflammatory Cytokines and Imiquimod in Patients With Advanced Metastatic Melanoma [NCT01191034]Phase 1/Phase 22 participants (Actual)Interventional2010-08-31Terminated(stopped due to Completion after 2 patients then stop due to end of validity of vaccine peptide)
Open-Label Safety and Pharmacokinetic Study of AldaraTM (Imiquimod) Cream, 5% for One, Two, or Three Treatment Cycles to Surface Areas Greater Than 25 cm2 With Actinic Keratosis [NCT00116649]Phase 4551 participants (Actual)Interventional2005-06-30Completed
A Phase I Trial of Dendritic Cell Vaccination for Children and Adults With Sarcoma [NCT01803152]Phase 119 participants (Actual)Interventional2014-01-06Active, not recruiting
Combination Therapy With Imiquimod Cream 5% and Tazarotene Cream 0.1% for the Treatment of Lentigo Maligna [NCT00707174]90 participants (Actual)Interventional2005-03-31Completed
A Randomized, Open-label Study to Evaluate the Safety and Efficacy of GX-188E, a DNA Therapeutic Vaccine Administered Intramuscularly by Electroporation, With GX-I7 Intravaginal Application or Imiquimod Topical Application in HPV16 and/or 18 Positive Pati [NCT03206138]50 participants (Anticipated)Interventional2017-05-30Recruiting
Pilot Study to Evaluate Two Different Non-invasive Techniques to Monitor the Clearance of Actinic Keratosis Lesions (Clinical and Sub-clinical), When Treated With Aldara 5% (Imiquimod) Cream [NCT00294320]Phase 312 participants (Actual)Interventional2006-02-28Completed
A Follow-up Study to Evaluate Actinic Keratosis Recurrence Rates One Year After Completion of the 1487-IMIQ Study [NCT00189254]72 participants Observational2005-04-30Completed
Topical 5% Imiquimod Cream for Vulvar Paget's Disease: Clinical Efficacy, Safety and Immunological Response [NCT02385188]Phase 325 participants (Actual)Interventional2015-05-31Completed
ANCHOR Study: Anal Cancer/HSIL Outcomes Research Study [NCT02135419]Phase 34,446 participants (Actual)Interventional2014-09-24Active, not recruiting
Topical Ingenol Mebutate Versus 5% 5-fluorouracil Versus 5% Imiquimod Versus Photodynamic Therapy in Treatment of Actinic Keratosis: a Multi-centre Randomized Efficacy and Cost-effectiveness Study [NCT02281682]Phase 4624 participants (Actual)Interventional2014-11-30Active, not recruiting
Identification of Novel Biomarkers of Cervicovaginal Mucosal Inflammation [NCT01593124]Phase 220 participants (Actual)Interventional2012-05-31Completed
Feasibility Study to Determine Effectiveness of 3.75% Topical Imiquimod Cream and Topical Vanos (Fluocinonide) Cream 0.1% in the Treatment of Early Stage Cutaneous T-cell Lymphoma [NCT02301494]0 participants (Actual)Interventional2020-04-30Withdrawn(stopped due to No participants were enrolled in the study.)
Effectiveness and Safety of Intra-Dermal Hepatitis B Vaccination After Topical Application of IMIQUIMOD, in Cirrhotics Patients, Who Did Not Respond to the Conventional Vaccine Regimen: a Pilot Study [NCT05028322]Phase 260 participants (Anticipated)Interventional2021-11-01Not yet recruiting
A Phase I Clinical Trial to Evaluate the Safety and Immunogenicity of Inactivated Influenza A/H5N1 Vaccine Administered Intradermally With or Without Topical Aldara(R) in Healthy Young Adults [NCT03472976]Phase 150 participants (Actual)Interventional2018-06-13Completed
A First-in-human Study to Evaluate the Safety, Tolerability and Pharmacokinetics of LFX453, After Multiple Topical Applications in Healthy Volunteers. [NCT02052687]Phase 141 participants (Actual)Interventional2014-01-31Completed
A MultIceNTER Phase I Peptide VaCcine Trial to Exploit NeoePitope-Specific T Cells for the Treatment of H3-Mutated Gliomas - (INTERCEPT-H3) [NCT04808245]Phase 115 participants (Anticipated)Interventional2023-02-15Recruiting
A Feasibility Trial of Alternating Intravaginal Application of 5-Fluorouracil and Imiquimod for Treatment of High-Grade Cervical Squamous Intraepithelial Lesions [NCT03196180]Early Phase 113 participants (Actual)Interventional2019-09-30Active, not recruiting
Treatment of Bolivian Cutaneous Leishmaniasis With a Combination of Oral Miltefosine Plus Topical Imiquimod 5% [NCT01380314]Phase 260 participants (Anticipated)Interventional2008-03-31Completed
Phase I Study of Vaccination With Dendritic Cells Loaded With Brain Tumor Stem Cells for Recurrent or Progressive Malignant Gliomas [NCT01171469]Phase 18 participants (Actual)Interventional2010-09-30Completed
Gene and Protein Expression Profiles After Treatment of Actinic Keratoses [NCT05740969]Phase 248 participants (Anticipated)Interventional2023-02-01Recruiting
A Multicenter, Double-Blind, Randomized, Parallel Group, Vehicle-Controlled Study to Determine the Clinical Equivalence of a Generic Imiquimod Cream, 5% and Aldara™ Cream in Subjects With Actinic Keratosis [NCT00948428]Phase 3462 participants (Actual)Interventional2008-05-31Completed
Prevalence, Genetic Risk Factor and the Use of Intradermally-administered Inactivated Influenza Vaccine With Topical Imiquimod in Influenza Vaccine Non-responsive Children [NCT05315024]72 participants (Anticipated)Interventional2022-04-30Not yet recruiting
A Multicenter, Double-Blind, Vehical-Controlled Study Comparing Imiquimod Cream, 5% (Apotex Inc.) to Aldara™ Cream, 5%(3M Pharmaceutials, U.S.) and Aldara™ Cream, 5%(3M Pharmaceuticals, Canada) in the Treatments of Actinic Keratosis. [NCT00859105]Phase 3497 participants (Actual)Interventional2008-02-29Completed
iVAC-CLL01: Patient-individualized Peptide Vaccination After First Line Therapy of CLL [NCT02802943]Phase 256 participants (Anticipated)Interventional2016-10-05Completed
Vehicle-Controlled, Double-Blind Study to Assess the Safety and Efficacy of Imiquimod 5% Cream Applied Once Daily 3 Days Per Week for the Treatment of Actinic Keratoses in Immunosuppressed Organ Transplant Recipients. [NCT00189267]Phase 245 participants Interventional2002-11-30Completed
Intradermal Trivalent Influenza Vaccine in Young Adults, a Double-blind Randomized Controlled Trial [NCT02103023]Phase 3160 participants (Actual)Interventional2014-03-31Completed
Long-term Effects of Aldara® 5% Cream and Solaraze® 3% Gel in the Treatment of Actinic Keratoses on the Face or Scalp With Respect to the Risk of Progression to In-situ and Invasive Squamous Cell Carcinoma [NCT01453179]Phase 4221 participants (Actual)Interventional2011-10-31Completed
Phase 3 Randomized Controlled Trial of Non-inferiority of Topical Imiquimod vs. LEEP for Women With Carcinoma In-situ of the Cervix [NCT02130323]Phase 2/Phase 322 participants (Actual)Interventional2015-02-28Completed
"Treatment of High-Grade Pre-Neoplastic Cervical Lesions (CIN 2/3) Using a Novel Prime and Pull Strategy" [NCT02864147]Phase 2134 participants (Actual)Interventional2016-07-31Completed
Pilot Study of the Feasibility and Safety of a Personalized Peptide Vaccine in Patients With Advanced Pancreatic Ductal Adenocarcinoma or Colorectal Adenocarcinoma [NCT02600949]Phase 1150 participants (Anticipated)Interventional2016-05-11Recruiting
An Open Monocentric Pilot Study to Investigate the Potential of Imiquimod 5% Cream to Detect Residual and to Prevent Recurrence of Lentigo Maligna After Surgical Excision [NCT01088737]Phase 2/Phase 360 participants (Actual)Interventional2011-01-31Active, not recruiting
Topical Imiquimod 5% Cream in the Treatment of Nodular Basal Cell Carcinoma After Initial Treatment With Curettage [NCT00314756]Phase 415 participants Interventional2005-03-31Completed
A Phase 3b Randomized, Double-blinded, Placebo-controlled, Multicenter, Efficacy and Safety Study of Imiquimod Cream Following Cryosurgery for the Treatment of Actinic Keratoses [NCT00894647]Phase 3247 participants (Actual)Interventional2009-05-31Completed
A Phase I Study With a Personalized NeoAntigen Cancer Vaccine Combined With Anti-PD-1 in Metastatic Melanoma [NCT04072900]Phase 130 participants (Anticipated)Interventional2020-04-21Recruiting
A Randomized, Phase III Study of Intra-anal Imiquimod 2.5% vs. Topical 5-fluorouracil 5% vs. Observation for the Treatment of High-grade Anal Squamous Intraepithelial Lesions in HIV-infected Men and Women [NCT02059499]Phase 391 participants (Actual)Interventional2015-12-28Active, not recruiting
An Investigator-initiated Study to Evaluate Genomic Markers of Immune Infiltration Before and After Treatment of Actinic Keratosis With Imiquimod 3.75% Cream [NCT03914417]Phase 221 participants (Actual)Interventional2013-01-31Completed
A Randomized, Single Blinded Trial to Evaluate the Efficacy of Imiquimod in Women With Residual/Recurrent Cervical Intraepithelial Neoplasia (CIN) After Previous Treatment [NCT02669459]Phase 3433 participants (Anticipated)Interventional2016-05-31Recruiting
An Open Label, Multicenter Phase 1-2 Study to Investigate the Effectiveness, Safety and Immunogenicity of a Monotherapy With Intradermal IMA910 Plus GM-CSF Following Pre-treatment With Low-dose Cyclophosphamide in Advanced Colorectal Carcinoma Patients Wh [NCT00785122]Phase 1/Phase 292 participants (Actual)Interventional2008-06-30Completed
Imiquimod 5% Cream for the Treatment of Periocular Basal Cell Carcinoma [NCT00803907]Phase 420 participants (Anticipated)Interventional2008-12-31Recruiting
A Phase 3, Randomized, Double-blinded, Placebo-controlled, Multicenter, Efficacy and Safety Study of Four Weeks of Treatment With Imiquimod Creams for Actinic Keratoses [NCT00605176]Phase 3479 participants (Actual)Interventional2008-01-31Completed
A Randomized, Open-label, Assessor-blinded, Split-face Study of Imiquimod 5% Cream Applied After Cryotherapy of Actinic Keratoses [NCT00774787]Phase 427 participants (Actual)Interventional2008-10-31Completed
A Randomized, Double-Blind, Parallel-Group, Vehicle-Controlled Therapeutic Equivalence Study of Two Imiquimod Cream 5% Treatments for Patients With Actinic Keratosis [NCT00828568]Phase 1425 participants (Actual)Interventional2008-06-30Completed
An Explorative, Single Center and Controlled Study to Analyze the Immune Escape Mechanisms of HPV-associated Lesions and to Evaluate the Efficiency and Mechanisms of Imiquimod Treatment of Vulvar Intraepithelial Neoplasias 2/3 (VIN) and Anogenital Warts [NCT00941811]Phase 25 participants (Actual)Interventional2008-12-31Completed
Clinical and Histological Analysis of Photoaging Treatment With Imiquimod Cream 5% [NCT01935310]17 participants (Actual)Interventional2010-07-31Completed
Pilot Study of Topical Imiquimod 5% Cream for Treatment of Cutaneous Neurofibromas in Adults With Neurofibromatosis 1 [NCT00865644]Phase 111 participants (Actual)Interventional2009-03-31Completed
A Phase 3, Randomized, Double-blinded, Placebo-controlled, Multicenter, Efficacy and Safety Study of Six Weeks of Treatment With Imiquimod Creams for Actinic Keratoses [NCT00603798]Phase 3490 participants (Actual)Interventional2008-01-31Completed
Combining Topical Imiquimod 5% Cream With a Pulsed Dye Laser to Treat Port Wine Stain Birthmarks [NCT00585247]27 participants (Actual)Interventional2006-11-30Completed
Comparison of Occlusive Dressings, Salicylate Ointment, Cryotherapy, Topical 5-fluoro-uracil and Imiquimod in Immunocompetent Patients Presenting Plantar Warts in Office-based Settings: a Randomized Clinical Trial [NCT01059110]Phase 4358 participants (Actual)Interventional2010-02-28Terminated(stopped due to Difficulty to enrollment patients)
Phase IB Pilot Study of Epicutaneous Cryoimmunotherapy Combined With Pembrolizumab for Cutaneous Metastatic Breast Cancer [NCT03982004]Phase 11 participants (Actual)Interventional2020-09-14Terminated(stopped due to Sponsor decision.)
A Phase I Study of Dendritic Cell Vaccine Therapy With In Situ Maturation for Pediatric Brain Tumors [NCT01902771]Phase 11 participants (Actual)Interventional2013-09-03Terminated(stopped due to Lack of Accrual)
Randomized Phase II Trial of Cyclophosphamide With Allogeneic Non-Small Cell Lung Cancer (NSCLC) DRibble Vaccine Alone or With Granulocyte-Macrophage Colony-Stimulating Factor or Imiquimod for Adjuvant Treatment of Definitively-Treated Stage IIIA or IIIB [NCT01909752]Phase 212 participants (Actual)Interventional2013-07-31Completed
Evaluation of the Efficacy and Safety of Imiquimod 5% Cream in Plaque-type Morphea: A Pilot, Prospective Open-label Study [NCT00230373]Phase 30 participants (Actual)Interventional2005-11-30Withdrawn(stopped due to Study never started.)
Exploratory Clinical Trial of Topical Imiquimod 5% Cream as Window-of-opportunity Monotherapy for Early-stage Oral Cancer [NCT04883645]Early Phase 116 participants (Actual)Interventional2022-04-28Active, not recruiting
Predicting Response In Cervical Intraepithelial Neoplasia to Topical Imiquimod Treatment [NCT05405270]410 participants (Anticipated)Observational [Patient Registry]2022-06-01Recruiting
A Randomized Phase II Trial to Determine Whether the Application of Imiquimod Cream to the Vaccination Site Can Improve the Immune Responsiveness to Influenza Vaccination in Patients With Untreated Chronic Lymphocytic Leukemia [NCT00596336]Phase 224 participants (Actual)Interventional2007-10-31Terminated(stopped due to Recruitment issues)
A Phase II Study of Imiquimod 5 % Cream for the Treatment of Hemangioma in Infancy [NCT00601016]Phase 218 participants (Actual)Interventional2005-03-31Completed
Efficacy of Intradermal Hepatitis B Vaccine in Renal Failure Patients [NCT02621112]Phase 2/Phase 394 participants (Actual)Interventional2016-01-31Completed
Photodynamic Therapy Mediated by Topical Application of 5- ALA for the Treatment of Actinic Keratoses [NCT00814528]0 participants (Actual)Interventional2007-11-30Withdrawn(stopped due to The study never started due to the Principal Investigator leaving the institution)
Safety, Tolerability, and Immunogenicity of CYT004-MelQbG10 Vaccine With or Without Immunostimulating Adjuvant in HLA-A2 Positive Patients With Stage III/IV Malignant Melanoma [NCT00651703]Phase 221 participants (Actual)Interventional2008-04-30Completed
An Exploratory, Open-label Study of Sequential Field-directed Treatment of Actinic Keratoses of the Face With Imiquimod 3.75% Cream Followed by Photodynamic Therapy [NCT01203878]Phase 421 participants (Actual)Interventional2010-09-30Terminated(stopped due to Unable to reach target enrollment of 60 subjects)
A Phase 1, Open-Label Study to Evaluate the Safety, Tolerability, and Immunogenicity of GTL001 Vaccine Adjuvanted With Imiquimod Cream in HPV 16- and/or HPV 18-Infected Women Aged 25 to 65 Years, With Normal Cytology, ASCUS, or LSIL [NCT02689726]Phase 113 participants (Actual)Interventional2015-08-31Terminated(stopped due to Lack of efficacy in European Phase 2 study)
Intra-dermal With Topical Imiquimod Pretreatment Versus Intra-muscular Hepatitis B Vaccination in IBD Patients - a Double-blind Randomized Controlled Trial [NCT04083157]Phase 2/Phase 3104 participants (Actual)Interventional2019-08-12Completed
Imiquimod/BTIC Lysate-Based Vaccine Immunotherapy for Diffuse Intrinsic Pontine Glioma in Children and Young Adults [NCT01400672]Phase 18 participants (Actual)Interventional2012-07-17Terminated(stopped due to Treatment ineffective; Extreme toxicity)
A Phase 1 Trial of Peptide-Based Glioma Vaccine IMA950 in Patients With Glioblastoma (GBM) [NCT01403285]Phase 16 participants (Actual)Interventional2011-08-31Terminated(stopped due to Due to poor accrual. This decision was taken without any safety reasons. Since beginning of the study (June 2011) only six patients were enrolled.)
A Double-blind, Randomized, Placebo-controlled, 2-way Crossover Study to Assess the Potential Effect of Topically Applied Imiquimod Cream on Atrial Ectopy in Patients With Actinic Keratosis [NCT01413763]Phase 450 participants (Anticipated)Interventional2011-07-31Active, not recruiting
Aldara for the Treatment of Extensive Alopecia Areata [NCT00177021]Phase 420 participants Interventional2000-10-31Completed
Randomized Prospective Study Comparing 5% Imiquimod and Photodynamic Therapy for Actinic Cheilitis [NCT00849992]Phase 453 participants (Actual)Interventional2009-03-31Completed
Open-Label Study to Assess Safety and Efficacy of Imiquimod 5% Cream Applied 3 Days Per Week in 1 or 2 Cycles for Treatment of Actinic Keratoses on the Head [NCT00175643]Phase 320 participants Interventional2005-02-28Completed
A Randomized Open Label Study to Evaluate the Safety and Efficacy if Imiquimod 5% Cream Applied 3 Times Per Week for 8 or 12 Weeks in the Treatment of Low Risk Nodular Basal Cell Carcinoma [NCT00204555]Phase 4100 participants (Actual)Interventional2002-01-31Completed
Immunotherapy for Recurrent Ependymomas in Children Using Human Leukocyte Antigen (HLA)-A2 Restricted Tumor Antigen Peptides in Combination With Imiquimod [NCT01795313]Phase 124 participants (Anticipated)Interventional2012-08-31Recruiting
Primary Imiquimod Treatment Versus Surgery for Vulvar Intraepithelial Neoplasia [NCT01861535]Phase 3110 participants (Actual)Interventional2013-06-30Completed
Relevance of Imiquimod as Neo-adjuvant Treatment to Reduce Excision Size and the Risk of Intralesional Excision in Lentigo Malignant of the Face [NCT01720407]Phase 3259 participants (Actual)Interventional2012-12-31Completed
Prospective Phase I/II Study: Patient-individualized Peptide Vaccination Based on Whole Exome Sequencing With Adjuvant GM-CSF (Granulocyte Macrophage Colony-stimulating Factor) in Children and Young Adults With Primary/Relapsed Acute Lymphoblastic Leukemi [NCT03559413]Phase 1/Phase 230 participants (Anticipated)Interventional2016-06-30Completed
Evaluation of Local Hyperthermia for the Treatment of Flat Warts After 4 Months: a Single-center, Single-blind, Randomized Controlled Trial [NCT05146895]60 participants (Anticipated)Interventional2018-10-20Recruiting
TOPical Imiquimod Treatment of High-grade Cervical Intraepithelial Neoplasia, a Multicenter, Open-label, Non-randomized, Controlled Study (TOPIC-3 Study) [NCT02917746]120 participants (Actual)Interventional2016-11-30Active, not recruiting
Pilot Study to Test the Safety and Efficacy of the Combination of Imiquimod and Pembrolizumab for the Treatment of Metastatic Melanoma [NCT03276832]Early Phase 17 participants (Actual)Interventional2017-12-20Active, not recruiting
Dendritic Cell Vaccine For Malignant Glioma and Glioblastoma Multiforme in Adult and Pediatric Subjects [NCT01808820]Phase 120 participants (Actual)Interventional2013-08-21Completed
Surgical Excision Versus Combined Treatment With Curettage and Imiquimod for Nodular Basal Cell Carcinoma: an Open, Non-inferiority, Randomized Controlled Trial [NCT02242929]Phase 3145 participants (Actual)Interventional2016-01-31Active, not recruiting
A Randomized Controlled Trial of Excisional Surgery Versus Imiquimod 5% Cream for Nodular and Superficial Basal Cell Carcinoma [NCT00066872]Phase 3500 participants (Anticipated)Interventional2002-10-31Completed
Randomized Double Blind Clinical Trial of Imiquimod (Aldara) Versus Placebo Used in Combination With Pentavalent Antimony (Glucantime) in Peruvian Cutaneous Leishmaniasis Patients [NCT00257530]Phase 380 participants Interventional2005-12-31Completed
A Randomized, Parallel-Group, Vehicle-Controlled, Double-Blind Study of Topical Imiquimod 5% Cream Used as an Adjunct to Cryotherapy in the Management of Actinic Keratoses, With a Long-Term (1 Year) Follow-Up [NCT00110682]Phase 460 participants Interventional2005-04-30Completed
Safety and Immunogenicity of Seasonal Influenza Vaccine With Topical Imiquimod in Immunocompromised Patients: A Randomized Controlled Pilot Trial [NCT02960815]Phase 270 participants (Actual)Interventional2016-11-30Completed
Combining Topical Imiquimod With Local Radiotherapy for Treatment of Mycosis Fungoides [NCT05838599]Early Phase 125 participants (Anticipated)Interventional2023-07-01Not yet recruiting
A Phase 1, Open-label, Dose-escalation Study to Investigate the Safety, Tolerability, and Pharmacokinetics of UGN-301 (Zalifrelimab) Administered Intravesically as Monotherapy and in Combination With Other Agents in Patients With Recurrent NMIBC [NCT05375903]Phase 160 participants (Anticipated)Interventional2022-06-01Recruiting
Double-Blind, Vehicle-Controlled Study to Evaluate Cellular and Molecular Events During Four Weeks of Treatment for Actinic Keratosis With Aldara (Imiquimod) Cream, 5% [NCT00335179]Phase 217 participants (Actual)Interventional2003-01-31Completed
Phase II Pilot Study With TMX 101 in Patients With Carcinoma In Situ (CIS) Bladder Cancer [NCT01731652]Phase 212 participants (Actual)Interventional2013-02-28Completed
A Phase I Trial of Surgical Resection Followed by Vaccination With Dendritic Cells Pulsed With Tumor Lysate With Imiquimod for Patients With Malignant Glioma [NCT01792505]Phase 171 participants (Actual)Interventional2009-10-31Completed
A Follow-up Study to Evaluate Actinic Keratosis Recurrence Rates One Year After Completion of the 1473-IMIQ Study [NCT00114023]84 participants Observational2005-01-31Completed
Vehicle-Controlled, Double-Blind Study to Assess the Safety and Efficacy of Imiquimod 5% Cream for the Treatment of Actinic Keratosis on the Upper Extremities [NCT00115154]Phase 4270 participants Interventional2005-05-31Completed
Evaluation of Different Adjuvants for the Transdermal Administration of a Peptide-Based Vaccine in Participants With High-Risk Melanoma [NCT00118313]Phase 10 participants Interventional2004-11-04Completed
Evaluation of the Efficacy and Safety of the Imiquimod 5% Topical Cream in Plaque Morphea: A Prospective, Multiple Baseline, Open Label Pilot Study [NCT00147771]Phase 310 participants (Anticipated)Interventional2005-09-30Completed
A Safety and Effectiveness Study of Imiquimod Creams in the Treatment of External Genital Warts [NCT00735462]Phase 3511 participants (Actual)Interventional2008-08-31Completed
Phase II Study of Topical Imiquimod and Weekly Abraxane for the Treatment of Breast Cancer Cutaneous Metastases [NCT00821964]Phase 215 participants (Actual)Interventional2008-12-31Completed
Phase II Evaluation of Imiquimod, a Topical Toll-like Receptor 7 (TLR7) Agonist in Breast Cancer Patients With Chest Wall Recurrence or Skin Metastases [NCT00899574]Phase 210 participants (Actual)Interventional2009-05-31Completed
Phenotype and Cytokine Production Characteristics of T Cells From Alopecia Areata Scalp Skin Before and After Aldara 5% Cream Using Flow Cytometry [NCT00176943]Phase 420 participants Interventional2000-10-31Completed
Intron-A/Aldara Combination Therapy for BCC Excluding the Face and Scalp [NCT00581425]Phase 449 participants (Actual)Interventional2007-12-31Completed
A Pilot Study of the Treatment of Facial Nodular and Nodulocystic Basal Cell Carcinoma With Double Curettage and Cautery Followed by Application of Imiquimod to the Base [NCT00463359]50 participants InterventionalNot yet recruiting
A Phase 1 Study of Peptide Vaccination for the Treatment of Patients With Solid Tumors Moderately Expressing HER2/Neu [NCT02276300]Phase 12 participants (Actual)Interventional2014-12-31Completed
Topical Imiquimod 5% Cream Therapy Versus Photodynamic Therapy With Methyl-aminolaevulinate 16% Cream of Actinic Keratoses in Organ Transplant Recipients [NCT01538901]Phase 410 participants (Actual)Interventional2012-09-30Terminated(stopped due to prolonged recruitment phase)
Phase II Topical Immunomodulatory Therapy With Imiquimod for the Chemoprevention of Recurrent and High-Grade Cervical Intraepithelial Neoplasia (CIN) [NCT00031759]Phase 257 participants (Actual)Interventional1999-06-30Completed
Double-Blind, Vehicle-Controlled Study to Evaluate Apoptosis in Basal Cell Carcinoma Treated With Aldara™ (Imiquimod) Cream, 5% Applied Once or Twice a Day [NCT00079300]Phase 10 participants Interventional2004-01-31Completed
Open-label Study to Evaluate the Use of Imiquimod 5% Cream for Reducing Postsurgical Recurrence or Persistence of Basal Cell Carcinoma Following Excision by Curettage [NCT00129519]Phase 363 participants (Actual)Interventional2004-01-31Completed
NY-ESO-1 Protein Vaccination in Malignant Melanoma Administered With Imiquimod as Adjuvant [NCT00142454]Phase 19 participants (Actual)Interventional2005-08-24Completed
A Pilot Study of Topical Imiquimod Therapy for the Treatment of Recurrent Extramammary Paget's Disease [NCT00504023]8 participants (Actual)Interventional2007-04-30Completed
A Pilot Study to Evaluate the Effects of Imiquimod and Tumor Lysate Vaccine Immunotherapy for Adults With High Risk or Recurrent/Post-Chemotherapy WHO Grade II Gliomas [NCT01678352]Early Phase 119 participants (Actual)Interventional2012-10-31Completed
A Phase 3, Randomized, Double-blind, Placebo-controlled, Multi-center, Efficacy and Safety Study of Imiquimod Creams in the Treatment of External Genital Warts [NCT00674739]Phase 3470 participants (Actual)Interventional2008-05-31Completed
Topical Imiquimod in Conjunction With Nd:YAG Laser for Tattoo Removal [NCT00638651]Phase 13 participants (Actual)Interventional2008-02-29Completed
A Randomised Controlled Multicentre Trial of Imiquimod Versus Radiotherapy for Lentigo Maligna (LM) When Staged Surgical Excision With 5mm Margins is Not Possible, is Refused, or Fails [NCT02394132]Phase 3216 participants (Anticipated)Interventional2015-08-31Active, not recruiting
A Phase I Efficacy and Safety Study of HPV16-specific Therapeutic DNA-vaccinia Vaccination in Combination With Topical Imiquimod, in Patients With HPV16+ High Grade Cervical Dysplasia (CIN3) [NCT00788164]Phase 175 participants (Actual)Interventional2008-11-30Completed
A Phase 1b, Multicenter Study to Determine the Dose, Safety, Efficacy and Pharmacokinetics of TRK-950 When Used in Combinations With Selected Anti-Cancer Treatment Regimens in Patients With Selected Advanced Solid Tumors [NCT03872947]Phase 1169 participants (Anticipated)Interventional2019-04-26Recruiting
Laser and TLR-Agonist Immunotherapy: A Novel Autologous Melanoma Vaccine Study [NCT00453050]Phase 111 participants (Actual)Interventional2006-03-31Completed
A Multicenter, Randomized, Double-Blind, Vehicle-Controlled, Parallel Group Comparison Study to Determine the Therapeutic Equivalence of Generic Imiquimod Cream, 3.75% and Zyclara™ (Imiquimod) Cream, 3.75% in Subjects With Actinic Keratoses [NCT01502020]410 participants (Actual)Interventional2011-02-28Completed
Efficacy and Effectiveness of Intradermal Trivalent Influenza Vaccine With Topical Imiquimod, a Double Blind Randomized Controlled Trial [NCT01508884]93 participants (Actual)Interventional2012-01-31Completed
Anal Dysplasia Study of Men Who Have Sex With Men Living With HIV [NCT01663558]Phase 40 participants (Actual)Interventional2015-05-31Withdrawn(stopped due to funding not available)
A Randomized, Double-Blind, Parallel-Group, Vehicle-Controlled, Multicenter Study Comparing Imiquimod Cream, 3.75% to Zyclara® (Imiquimod) Cream, 3.75% in the Treatment of Actinic Keratosis of the Face or Balding Scalp [NCT01686152]Phase 3589 participants (Actual)Interventional2012-09-30Completed
A Randomized, Double Blind, Placebo Controlled, Parallel Design, Multiple Site, Clinical Study to Evaluate the Bioequivalence of Two Imiquimod Cream 3.75% Formulations in Patients With Actinic Keratosis. [NCT01788007]Phase 1443 participants (Actual)Interventional2013-01-31Completed
Immunologic Profile of Chronically Photodamaged Skin [NCT02889159]Phase 440 participants (Anticipated)Interventional2016-06-06Recruiting
A Randomized, Evaluator-blinded, Vehicle-controlled Study to Explore the Pharmacodynamic Effects of Omiganan and Omiganan in Combination With Imiquimod in Healthy Volunteers [NCT03071679]Phase 116 participants (Actual)Interventional2017-02-06Completed
A Pilot Study of DPV-001 DRibble Vaccine With Imiquimod in Advanced Prostate Cancer [NCT02234921]Phase 13 participants (Actual)Interventional2014-10-24Completed
Earliest Stage Treatment of Aktinic Keratosis With Imiquimod 3.75% Cream [NCT04842422]Phase 448 participants (Actual)Interventional2021-04-16Completed
Intradermal Quadrivalent Influenza Vaccine With Topical Imiquimod in Elderly & Chronic Ill Subjects, a Double-Blind Randomized Controlled Trial [NCT04143451]Phase 34,000 participants (Anticipated)Interventional2019-10-23Recruiting
Phase III Trial of 6 Weeks of Imiquimod for the Treatment of Bowens Disease of the Head and Neck. Outcome is Histologic Clearance at 14 Weeks. [NCT00384124]Phase 2/Phase 350 participants (Anticipated)Interventional2006-11-30Enrolling by invitation
Phase I, Dual Arm, Open-Label, Trial of Intralesional 5-Fluorouracil (5FU) and Intralesional 5FU Combined With Topical Imiquimod in Patients With Squamous Cell Carcinoma (SCC) of the Lower Extremities [NCT03370406]Phase 130 participants (Anticipated)Interventional2018-08-03Recruiting
A Pilot Study of pnGVL4a-CRT/E7 (Detox) for the Treatment of Patients With HPV16+ Cervical Intraepithelial Neoplasia 2/3 (CIN2/3) [NCT00988559]Phase 1132 participants (Actual)Interventional2009-09-30Completed
A Pilot Study to Evaluate Short Term Neoadjuvant Sonidegib Followed by Surgery or Imiquimod in the Management of Basal Cell Carcinomas in Cosmetically Challenging Locations [NCT03534947]Phase 210 participants (Anticipated)Interventional2019-07-23Recruiting
Efficacy of Tazarotene Versus Topical 5-Fluorouracil, and Imiquimod in The Treatment of Verruca Plana [NCT05314127]Phase 280 participants (Anticipated)Interventional2022-04-15Recruiting
[NCT01611480]Phase 20 participants InterventionalCompleted
A Multicenter, Randomized, Double-Blind, Vehicle-Controlled, Parallel Group Comparison Study to Determine the Therapeutic Equivalence of Generic Imiquimod Cream, 2.5% and Zyclara® (Imiquimod) Cream, 2.5% in Subjects With Actinic Keratoses [NCT02120898]Phase 3467 participants (Actual)Interventional2013-10-10Completed
Coadministration of Genetically Attenuated Plasmodium Falciparum ∆mei2 (GA2) Sporozoites With Adjuvants - a Proof of Principle Study [NCT05468606]Early Phase 145 participants (Anticipated)Interventional2023-02-03Recruiting
Comparing Immune Responses to Topical Imiquimod [NCT04809662]110 participants (Anticipated)Observational2021-03-16Active, not recruiting
The Effects of Aldara as an Adjunct to Laser Treatment of Port Wine Stains [NCT00979550]Phase 27 participants (Actual)Interventional2008-10-31Terminated(stopped due to Failure to enroll enough participants)
The Real Life Topical Field Treatment of Actinic Keratosis Study. An Observational Study Focusing on Patient Reported Outcomes [NCT02362152]1,168 participants (Actual)Observational2014-07-31Completed
Long-term Effects of Aldara® 5% Cream and Solaraze® 3% Gel in the Treatment of Actinic Keratoses on the Face or Scalp (LEIDA) [NCT00777127]Phase 4258 participants (Actual)Interventional2008-12-31Completed
Exploratory Evaluation of Imiquimod 5% Cream in the Treatment of External Genital or Perianal Warts in HIV+ Patients Treated With HAART (CD4+ ≥ 200 Cells mm3): An Open Labeled, Non-comparative Study [NCT00761371]Phase 452 participants (Actual)Interventional2002-08-31Completed
An Open-Label Study to Evaluate the Safety and Long-Term Clinical Efficacy of Imiquimod 5% Cream Applied Once Daily 5 Days Per Week for 6 Weeks in the Treatment of Superficial Basal Cell Carcinoma [NCT00189241]Phase 3160 participants Interventional2001-02-28Completed
Prospective Randomized Trial of Peptide-specific Vaccination in HLA-A*02 Positive Prostate Carcinoma Patients With Biochemical Recurrence After Radical Prostatectomy [NCT02452307]Phase 1/Phase 236 participants (Actual)Interventional2004-04-30Active, not recruiting
Comparison of Conservative Treatment of Cervical Intraepithelial Lesions With Imiquimod With Standard Excisional Technique Using LLETZ: a Randomized Controlled Trial [NCT04859361]104 participants (Actual)Interventional2018-11-20Active, not recruiting
Multicenter, Randomised, Double-blind, Vehicle-controlled Study Comparing Recurrence Rate Following Imiquimod 5% Cream or Vehicle 3 Times Per Week for 4 Weeks Prior to Ablative Therapy in Subjects Suffering From External Ano-Genital Warts [NCT00189293]Phase 4128 participants (Actual)Interventional2005-06-30Completed
CTCL Directed Therapy [NCT03116659]Early Phase 18 participants (Anticipated)Interventional2018-02-01Recruiting
TOPical Imiquimod Treatment of High-grade Cervical Intraepithelial Neoplasm: a Randomized Controlled Trial. [NCT02329171]Phase 39 participants (Actual)Interventional2014-12-31Terminated(stopped due to Insufficient number of participants.)
Phase I/II Study of TLR7 Agonist Imiquimod, Cyclophosphamide, and Radiotherapy in Breast Cancer Patients With Chest Wall Recurrence or Skin Metastases [NCT01421017]Phase 1/Phase 231 participants (Actual)Interventional2011-08-19Completed
CSP #2019 - Basal Cell Carcinoma Chemoprevention Trial (B3C) [NCT05212246]Phase 31,630 participants (Anticipated)Interventional2024-01-15Not yet recruiting
Evaluation of the Impact of Adjuvants Accompanying Peptide Immunization in High Risk Melanoma [NCT00273910]Phase 2104 participants (Actual)Interventional2006-01-31Completed
Mechanistically-based Optimization of UV Radiation Therapy in Psoriasis [NCT00470392]9 participants (Actual)Interventional2007-05-31Terminated(stopped due to Recruiting complete and administrative termination)
Ensaio clínico Randomizado Avaliando a eficácia do Tratamento tópico Com Imiquimode em lesões Intraepiteliais Cervicais de Alto Grau [NCT03233412]Phase 290 participants (Actual)Interventional2018-01-01Completed
A Randomized, Open Label, Multi-center, Comparative Trial, to Assess the Efficacy and Safety of Pritelivir for the Treatment of Acyclovir-resistant Mucocutaneous HSV (Herpes Simplex Virus) Infections in Immunocompromised Subjects (PRIOH-1) [NCT03073967]Phase 3153 participants (Anticipated)Interventional2017-05-08Recruiting
A Randomized, Vehicle Controlled, Active Comparator, Parallel Group Study to Evaluate Efficacy, Safety, and Tolerability of Topical LFX453 Formulations in Patients With External Genital Warts (EGWs) [NCT02482428]Phase 288 participants (Actual)Interventional2015-05-12Completed
Intradermal Hepatitis B Vaccination With Imiquimod in Occult Hepatitis B Infection [NCT03307902]Phase 2/Phase 3120 participants (Actual)Interventional2016-10-01Completed
A Phase 4 Trial Comparing the Cumulative Incidence of SCC After Treatment With Ingenol Mebutate and Imiquimod for Multiple Actinic Keratoses on Face and Scalp. A Multi-centre, Randomised, Two-arm, Open Label, Active-controlled, Parallel Group, 36-month Tr [NCT01926496]Phase 4485 participants (Actual)Interventional2013-09-11Completed
Adjuvant Imiquimod Therapy to Reduce Recurrence Rate in Patients After Surgical Therapy of Anal HPV (Human Papilloma Virus)-Lesions [NCT03289260]Phase 3200 participants (Anticipated)Interventional2021-11-15Not yet recruiting
A Window of Opportunity Phase I Study of UGN-201 in Patients With Bladder Cancer Undergoing Radical Cystectomy [NCT05055050]Phase 110 participants (Anticipated)Interventional2022-01-24Recruiting
A Phase 2, Randomized, Open Label, Efficacy Study of VGX-3100 Delivered Intramuscularly Followed by Electroporation With CELLECTRA™ 2000 Alone or in Combination With Imiquimod, for the Treatment of HPV-16 and/or HPV-18 Related High Grade Squamous Intraepi [NCT03180684]Phase 233 participants (Actual)Interventional2017-08-31Completed
Phase I/II Study of Low-Dose Cyclophosphamide, Tumor Associated Peptide Antigen-Pulsed Dendritic Cell Therapy and Imiquimod, in Patients With Progressive and/or Refractory Solid Malignancies [NCT02224599]Phase 1/Phase 23 participants (Actual)Interventional2017-07-28Terminated(stopped due to Sponsor decision to terminate study due to poor accrual)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00116649 (2) [back to overview]Percent Reduction From Baseline to the Final Follow-up in Total Actinic Keratosis Lesion Count
NCT00116649 (2) [back to overview]Number of Participants Who Experienced an Adverse Event
NCT00142454 (3) [back to overview]Number of Patients With Humoral Antibody Response to NY-ESO-1
NCT00142454 (3) [back to overview]Number of Patients With Treatment-emergent Adverse Events (TEAEs)
NCT00142454 (3) [back to overview]Number of Patients With Cellular Antibody Response to NY-ESO-1 at Two or More Post-vaccination Time Points
NCT00189306 (2) [back to overview]Number of Participants Cleared of Superficial Basal Cell Carcinoma at 12 Weeks
NCT00189306 (2) [back to overview]Number of Participants With Sustained Clearance Rate of Superficial Basal Cell Carcinoma (sBCC)
NCT00273910 (2) [back to overview]Immunologic Response Rate
NCT00273910 (2) [back to overview]Number of Participants With Adverse Events
NCT00470392 (3) [back to overview]Number of Subjects With Improvement in Lesional Psoriasis Area and Assessment (PASI) Score After Imiquimod and UVB Treatment
NCT00470392 (3) [back to overview]Number of Subjects With Elevated MyxA
NCT00470392 (3) [back to overview]Number of Subjects With a 1.5 Fold Increase in mRNA Expression of GRAMD1A and DMXL2
NCT00504023 (1) [back to overview]Percentage of Participants With Clinical and Histologic Remission
NCT00585247 (1) [back to overview]Change From Baseline in a* and E at 8 Weeks
NCT00603798 (4) [back to overview]Number of Participants With Complete Clearance of AK Lesions
NCT00603798 (4) [back to overview]Percent Change From Baseline in AK Lesion Count
NCT00603798 (4) [back to overview]Number of Participants With Partial Clearance of AK Lesions
NCT00603798 (4) [back to overview]Local Skin Reactions (LSR)
NCT00605176 (4) [back to overview]Local Skin Reactions
NCT00605176 (4) [back to overview]Number of Participants With Complete Clearance of AK Lesions
NCT00605176 (4) [back to overview]Number of Participants With Partial Clearance of AK Lesions
NCT00605176 (4) [back to overview]Percent Change From Baseline in AK Lesion Count
NCT00638651 (1) [back to overview]Efficacy of Tattoo Removal Using Topical Imiquimod 5% Cream
NCT00674739 (3) [back to overview]Safety Variables Include Adverse Reactions (AEs), Local Skin Reactions (LSRs), and Number of Subjects Who Took Rest Periods During the Treatment Period.
NCT00674739 (3) [back to overview]Treatment Related Adverse Events
NCT00674739 (3) [back to overview]Proportion of Subjects With Complete Clearance of All Warts (Both Presented at Baseline and Newly Emerged Warts) at End of Study
NCT00707174 (1) [back to overview]The Absence of Lentigo Maligna (LM) at the Time of Staged Excisions in Participants
NCT00735462 (2) [back to overview]Proportion of Subjects Achieving Complete Clearance of All Warts (Baseline and New) at the End of Study.
NCT00735462 (2) [back to overview]Number of Subjects With Any Treatment Related Adverse Reactions (AEs), Any Local Skin Reactions (LSRs), and Number of Subjects Who Took Rest Periods During the Treatment Period
NCT00774787 (4) [back to overview]Cosmetic Appearance Score at 4-8 Weeks Post-treatment
NCT00774787 (4) [back to overview]Local Skin Reactions
NCT00774787 (4) [back to overview]Complete Clearance of Actinic Keratoses at 4-8 Weeks Post-treatment
NCT00774787 (4) [back to overview]Change From Baseline in Actinic Keratoses Count at 4-8 Weeks Post-treatment
NCT00821964 (5) [back to overview]Pathologic Response by Immunohistochemical (IHC)as Assessed by Skin Punch Biopsy of the Target Lesion
NCT00821964 (5) [back to overview]Endogenous Immunity to Common Breast Tumor Antigens (HER2, IGFBP-2, Topoisomerase II-alpha, and p53) in Peripheral Blood as Assessed by IFN-gamma and ELISPOT Assay
NCT00821964 (5) [back to overview]Safety and Systemic Toxicity as Assessed by a Review of Medical History, Physical Exam, Systems, Performance Status, and Clinical Labs (CBC and CMP)
NCT00821964 (5) [back to overview]Incidence of Reduction of Serum TGF-beta Levels as Assessed by ELISA and Correlation With Th1 Adaptive Immunity and Clinical Response
NCT00821964 (5) [back to overview]Anti-tumor Effects of Imiquimod as Assessed by Modified World Health Organization (WHO) Criteria
NCT00828568 (3) [back to overview]Patients Reporting at Least One Adverse Event
NCT00828568 (3) [back to overview]Number of Participants With 100% Clearance of Actinic Keratosis Lesions: Comparison of Taro Imiquimod 5% and Aldara-Imiquimod 5%
NCT00828568 (3) [back to overview]Number of Participants in Intention-to-treat (ITT)Population With 100% Clearance of Actinic Keratosis (AK) Lesions Identified at Baseline
NCT00894647 (3) [back to overview]Number of Participants With Any Post-baseline Local Skin Reactions (LSRs)
NCT00894647 (3) [back to overview]Percent of Subjects With Complete Clearance
NCT00894647 (3) [back to overview]Change From Baseline in Percentage of Lesion Count
NCT00899574 (2) [back to overview]Objective Response (Complete Clinical Response+ Partial Response)
NCT00899574 (2) [back to overview]Clinical Benefits
NCT00948428 (3) [back to overview]Percentage of Subjects With at Least a 75% Reduction in the Number of AK Lesions From Baseline to End of Treatment (EOT) Visit (Week 16).
NCT00948428 (3) [back to overview]Percentage of Subjects With at Least a 75% Reduction in the Number of AK Lesions From Baseline to 8 Weeks Post Treatment (Test of Cure Visit).
NCT00948428 (3) [back to overview]Percentage of Subjects in Each Treatment Group With Complete Clearance of AK Lesions at the Test of Cure Visit (Week 24)
NCT00988559 (2) [back to overview]Absence of CIN2/3 Lesion by Week 15
NCT00988559 (2) [back to overview]Number of Participants With Related Serious Adverse Events
NCT01203878 (3) [back to overview]Actinic Keratosis Count
NCT01203878 (3) [back to overview]Complete Clearance
NCT01203878 (3) [back to overview]Cosmetic Appearance
NCT01421017 (2) [back to overview]Systemic Tumor Response Rates (Complete Response+Partial Response)
NCT01421017 (2) [back to overview]Local Skin Tumor Response Rates (Complete Response + Partial Response)
NCT01926496 (5) [back to overview]Number of Participants With Partial Clearance of AK Lesions
NCT01926496 (5) [back to overview]Incidence of SCC
NCT01926496 (5) [back to overview]Incidence of SCC and Other Neoplasia
NCT01926496 (5) [back to overview]Number of Participants With Complete Clearance of AK Lesions After Last Treatment
NCT01926496 (5) [back to overview]Number of Participants With Complete Clearance of AK Lesions at 12 Months
NCT02078648 (4) [back to overview]Complete Response (CR) or Partial Response (PR)
NCT02078648 (4) [back to overview]Objective Response Rate (ORR)
NCT02078648 (4) [back to overview]Overall Survival at 12 Months (OS-12)
NCT02078648 (4) [back to overview]Progression-free Survival at 6 Months (PFS-6)
NCT02120898 (5) [back to overview]Number of Participants With Local Skin Reactions
NCT02120898 (5) [back to overview]Complete Clearance Rate - Percentage of Participants With Treatment Success: Per-Protocol (PP) Population
NCT02120898 (5) [back to overview]Percentage of Drug Compliance
NCT02120898 (5) [back to overview]Number of Participants With Adverse Events (AEs)
NCT02120898 (5) [back to overview]Complete Clearance Rate - Percentage of Participants With Treatment Success: ITT Population
NCT02135419 (3) [back to overview]Change in Physical Symptom Score From Baseline (2-7 Days Post Randomization) Until 4 Weeks Post Randomization
NCT02135419 (3) [back to overview]Anal Cancer Incidence
NCT02135419 (3) [back to overview]Incidence of Adverse Events for Each Treatment
NCT02482428 (3) [back to overview]Number of Participants That Had Partial Clearance Rate of at Least 75 Percent Reduction in External Genital Wart (EGW)s Count at End of Treatment (EOT) Week 12 or 16
NCT02482428 (3) [back to overview]Number of Adverse Events (AE)/Serious Adverse Events (SAE) as a Measure of Safety and Tolerability up to 30 Weeks
NCT02482428 (3) [back to overview]Complete Clearance of Disease at Week 14
NCT03180684 (12) [back to overview]Percent Change From Baseline in the Cumulative Surface Area of the Acetowhite Vulvar Lesion(s)
NCT03180684 (12) [back to overview]Percentage of Participants With Adverse Events (AEs)
NCT03180684 (12) [back to overview]Percentage of Participants With at Least One Local and Systemic Treatment-emergent Adverse Event (TEAE) During 7 Days Following Each Dose
NCT03180684 (12) [back to overview]Percentage of Participants With No Evidence of HPV-16 and/or HPV-18 in Vulvar Tissue Samples
NCT03180684 (12) [back to overview]Percentage of Participants With No Evidence of Vulvar HSIL, No Evidence of Vulvar LSIL (VIN1), and No Evidence of Condyloma on Histology
NCT03180684 (12) [back to overview]Percentage of Participants With No Histologic Evidence of Vulvar HSIL
NCT03180684 (12) [back to overview]Percentage of Participants With No Histologic Evidence of Vulvar HSIL and No Evidence of HPV-16 and/or HPV-18 in Vulvar Tissue Samples
NCT03180684 (12) [back to overview]Percentage of Participants With No Histologic Evidence of Vulvar HSIL or No Evidence of HPV-16/18 in Vulvar Tissue
NCT03180684 (12) [back to overview]Percentage of Participants With No Progression of Vulvar HSIL to Vulvar Cancer
NCT03180684 (12) [back to overview]Change From Baseline in Flow Cytometry Response Magnitude
NCT03180684 (12) [back to overview]Change From Baseline in Interferon-Gamma (IFN-γ) Response Magnitude
NCT03180684 (12) [back to overview]Levels of Serum Anti-HPV-16 and Anti-HPV-18 Antibody Concentrations
NCT03196180 (1) [back to overview]Feasibility of Intravaginal Use 5-FU and Imiquimod on Alternating Weeks in Women With Biopsy Confirmed High Grade Cervical Squamous Intraepithelial Lesions.
NCT03760250 (1) [back to overview]Keloid Recurrence
NCT03914417 (2) [back to overview]Number of Treatment Related Adverse Events
NCT03914417 (2) [back to overview]Number of Responders

Percent Reduction From Baseline to the Final Follow-up in Total Actinic Keratosis Lesion Count

Percent reduction = (total baseline AK lesion count - total final lesion count)x100/ total baseline AK lesion count (NCT00116649)
Timeframe: At Month 18

Interventionpercent reduction (Mean)
Aldara (Imiquimod) Cream80.2

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Number of Participants Who Experienced an Adverse Event

Adverse events that occurred between the first day of exposure to the study cream and study discharge were summarized. Adverse events - any untoward medical occurrence in a subject that is temporally related to protocol procedures, including the administration of a pharmaceutical product at any dose, but which does not necessarily have a causal relationship with the treatment. (NCT00116649)
Timeframe: from first dose up to 18 months

Interventionparticipants (Number)
Aldara (Imiquimod) Cream472

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Number of Patients With Humoral Antibody Response to NY-ESO-1

Assays to assess NY-ESO-1 specific antibodies were performed at baseline (Cycle 1 Day 1), throughout the vaccination period (Day 1 of Cycles 2 through 4 and Day 10 of each cycle), and at the 2 post-treatment follow-up visits (Weeks 13 and 16) by enzyme-linked immunosorbent assay (ELISA). Samples were diluted serially. The induction and augmentation of immunity were defined as an increase in antibody titer of ≥ 3× over buffer alone or ≥ 4× the pre-vaccination titer, respectively. Sera from the responding patients were tested a second time against a pool of NY-ESO-1 overlapping peptides to confirm NY-ESO-1 specificity; the number of patients in the table reflect the patients with confirmed NY-ESO-1 specificity. (NCT00142454)
Timeframe: Up to 4 months

InterventionParticipants (Count of Participants)
Imiquimod + NY-ESO-14

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Number of Patients With Treatment-emergent Adverse Events (TEAEs)

Toxicity was graded in accordance with the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE), version 3.0, as follows: Grade 1 (mild), Grade 2 (moderate), Grade 3 (severe), Grade 4 (life-threatening), and Grade 5 (fatal). Adverse events (AEs) were reported based on clinical laboratory tests, vital sign and weight measurements, physical examinations, performance status evaluations, and any other medically indicated assessments, including patient interviews, from the time informed consent was signed through the last follow-up visit. AEs were considered to be treatment emergent (TEAE) if they occurred or worsened in severity after the first dose of study treatment. (NCT00142454)
Timeframe: Up to 4 months

InterventionParticipants (Count of Participants)
Any TEAEMaximum TEAE severity Grade 1Serious TEAETEAE leading to discontinuation
Imiquimod + NY-ESO-18800

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Number of Patients With Cellular Antibody Response to NY-ESO-1 at Two or More Post-vaccination Time Points

Assays to assess cluster of differentiation (CD)8+ and CD4+ antigen-specific responses were performed at baseline (Cycle 1 Day 1), throughout the vaccination period (Day 1 of Cycles 2 through 4 and Day 10 of each cycle), and at the 2 post-treatment follow-up visits (Weeks 13 and 16) by enzyme-linked immune absorbent spot (ELISPOT) assay following prior in vitro sensitization. A 3-fold increase in spot-forming cells over baseline defined a positive response. Suitable antigens may have included recombinant viral vectors encoding NY-ESO-1, or NY-ESO-1 overlapping peptides, depending upon availability. (NCT00142454)
Timeframe: Up to 4 months

InterventionParticipants (Count of Participants)
CD4+ T cell responseCD8+ T cell response
Imiquimod + NY-ESO-170

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Number of Participants Cleared of Superficial Basal Cell Carcinoma at 12 Weeks

Number of participants cleared at 12 weeks(the number of subjects with no clinical evidence of superficial basal cell carcinoma at the target tumor site at the 12-week posttreatment visit) (NCT00189306)
Timeframe: 12 week posttreatment visit

Interventionparticipants (Number)
Aldara159

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Number of Participants With Sustained Clearance Rate of Superficial Basal Cell Carcinoma (sBCC)

Number of participants clinically clear of superficial basal cell carcinoma at the treated target tumor site at the 12-week posttreatment visit (ie, initial clearance rate) who remain clear during a 5 year follow-up period. (NCT00189306)
Timeframe: 5 years

Interventionparticipants (Number)
Aldara119

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Immunologic Response Rate

Comparison of six different preparations of the gp100:209-217 (210M) melanoma antigen peptide. The arm with the greater number of immunologic responses will be the one most likely to be selected for future study on the basis of immunization alone. Evidence of immunization consist of at least 10 Elispots/100,000 cells above background. An injection site reaction is not an immune response. (NCT00273910)
Timeframe: 48 months

InterventionParticipants (Number)
Adj-3 A2 gp209(2M) in IFA SQ (Vortex)2
Adj-3 A2 gp209(2M) in IFA SQ + Imiquimod (Vortex)0
Adj-3 A2 gp209(2M) in Saline ID0
Adj-3 A2 gp209(2M) in Saline ID + Imiquimod3
Adj-3 A2 gp209(2M) in IFA SQ (2 Syringe)1
Adj-3 A2 gp209(2M) in IFA SQ + Imiquimod (2 Syringe)0

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Number of Participants With Adverse Events

Here are the number of participants with adverse events. For a detailed list of adverse events see the adverse event module. (NCT00273910)
Timeframe: 48 months

InterventionParticipants (Number)
Adj-3 A2 gp209(2M) in IFA SQ (Vortex)19
Adj-3 A2 gp209(2M) in IFA SQ + Imiquimod (Vortex)19
Adj-3 A2 gp209(2M) in Saline ID18
Adj-3 A2 gp209(2M) in Saline ID + Imiquimod19
Adj-3 A2 gp209(2M) in IFA SQ (2 Syringe)15
Adj-3 A2 gp209(2M) in IFA SQ + Imiquimod (2 Syringe)14

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Number of Subjects With Improvement in Lesional Psoriasis Area and Assessment (PASI) Score After Imiquimod and UVB Treatment

The PASI is a disease burden measure that integrates area, erythema, thickness and scale of each target lesion. The severity score for each region is calculated by adding the scores for redness, thickness and scale (each of which are graded from 0 to 4). The maximum severity score is 12. The higher the PASI, the worse the disease. Thus, an improvement in PASI score is a lower score than the pre-treatment PASI. (NCT00470392)
Timeframe: 2 weeks after Imiquimod and UVB

Interventionparticipants (Number)
Imiquimod4

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Number of Subjects With Elevated MyxA

Lesions were treated with either Imiquimod or Clobetasol cream. Lesions were subsequently treated with UVB and biopsied. From the biopsy samples obtained from the Imiquimod arm, quantitative PCR was performed to measure levels of Myx A, an imiquimod response gene. (NCT00470392)
Timeframe: Biopsy samples for analysis were taken 1 hour post UVB treatment

Interventionparticipants (Number)
Imiquimod1

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Number of Subjects With a 1.5 Fold Increase in mRNA Expression of GRAMD1A and DMXL2

Based upon upregulated mRNA expression of MyxA in 1 out of 7 patients treated with Imiquimod, a list of alternative target genes responsive to Imiquimod was generated. The target mRNAs examined included GRAMD1A, IL2RA, TGHD1, DMXL2. The target gene was consider upregulated if there was a 1.5 fold increase in the mRNA expression of the target gene. (NCT00470392)
Timeframe: Biopsy samples for analysis were taken 1 hour post UVB treatment

Interventionparticipants (Number)
Imiquimod1

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Percentage of Participants With Clinical and Histologic Remission

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00504023)
Timeframe: 12 weeks post treatment

Intervention% of participants (Number)
Imiquimod75

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Change From Baseline in a* and E at 8 Weeks

Change in a* and ΔE is a way to quantify PWS treatment outcome: a* is the erythema of the vascular lesions and varies from +60 for green to -60 for red with a value of +9.28 for Normal Skin. Higher a* values indicates a greater reduction in erythema hence better treatment outcome. ΔE detects all three dimensions of colorspace (L*a*b*) and represents the difference in color between normal and PWS skin. Range of ΔE is 0 to 100. Higher values indicates improved treatment efficacy by greater skin color improvement. (NCT00585247)
Timeframe: 8 weeks baseline

,
Interventionunits on a scale (Mean)
a*ΔE
Imiquimod1.274.08
Placebo0.432.59

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Number of Participants With Complete Clearance of AK Lesions

"Subject status with respect to complete clearance of AK lesions at End of Study (EOS), ie, the Week 17 visit. Complete clearance was defined as the absence of clinically visible or palpable AK lesions in the treatment area. All lesions within the identified treatment area were included in the count, even if the lesion was a new lesion or subclinical lesion that had not been identified at Baseline." (NCT00603798)
Timeframe: End of Study the Week 17 visit

Interventionparticipants (Number)
3.75% Imiquimod Cream55
2.5% Imiquimod Cream41
Placebo Cream9

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Percent Change From Baseline in AK Lesion Count

Percent change from Baseline to end of study (EOS) in investigator counts of AK lesions. A negative percent change is better than a positive percent change. (NCT00603798)
Timeframe: At all visits - Baseline through the Week 17 EOS visit

Interventionpercentage of participants (Median)
3.75% Imiquimod Cream-80.0
2.5% Imiquimod Cream-66.7
Placebo Cream-23.6

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Number of Participants With Partial Clearance of AK Lesions

Subject status with respect to complete clearance of AK lesions at End of Study (EOS), defined as at least a 75% reduction in the number of AK lesions in the treatment area compared with Baseline. (NCT00603798)
Timeframe: End of Study the Week 17 visit

Interventionparticipants (Number)
3.75% Imiquimod Cream87
2.5% Imiquimod Cream70
Placebo Cream21

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Local Skin Reactions (LSR)

Six local skin reaction (LSR) signs were predefined and were assessed for presence and intensity at each visit. These included: Erythema, edema, Weeping/Exudate, Flaking/Scaling/Dryness, Scabbing/Crusting and Erosion/Ulceration. The LSRs were scored as 0=none, 1=mild, 2=moderate, 3=severe. Summary of LSR - area under the curve (AUC) of sum of LSR scores (days). (NCT00603798)
Timeframe: The time period for the AUC extends to 8 weeks after the end of treatment (Week 17)

Interventionunits on a scale * days (Mean)
3.75% Imiquimod Cream413.5
2.5% Imiquimod Cream372.0
Placebo Cream188.6

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Local Skin Reactions

Six local skin reaction (LSR) signs were predefined and were assessed for presence and intensity at each study visit. These included: Erythema, Edema, Weeping/Exudate, Flaking/Scaling/Dryness, Scabbing/Crusting and Erosion/Ulceration. The LSRs were scored as 0=none, 1=mild, 2=moderate, 3=severe. Mean scores were summated over time (14 weeks) to yield a mean LSR AUC (area under the curve) (NCT00605176)
Timeframe: At all visits - from Baseline to End of study (Week 14)

Interventionunits on a scale * days (Mean)
3.75% Imiquimod Cream272.0
2.5% Imiquimod Cream242.5
Placebo Cream139.8

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Number of Participants With Complete Clearance of AK Lesions

Subject status with respect to complete clearance of AK lesions at End of Study (EOS), ie, the Week 14 visit. Complete clearance was defined as the absence of clinically visible or palpable AK lesions in the treatment area. All lesions within the identified treatment area were included in the count, even if the lesion was a new lesion or 'subclinical' lesion that had not been identified at Baseline. (NCT00605176)
Timeframe: End of Study the Week 14 visit

Interventionparticipants (Number)
3.75% Imiquimod Cream57
2.5% Imiquimod Cream49
Placebo Cream10

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Number of Participants With Partial Clearance of AK Lesions

Subject status with respect to partial clearance of AK lesions at end of study (EOS), defined as at least a 75% reduction in the number of AK lesions in the treatment area compared with Baseline. (NCT00605176)
Timeframe: End of Study the Week 14 visit

Interventionparticipants (Number)
3.75% Imiquimod Cream95
2.5% Imiquimod Cream77
Placebo Cream36

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Percent Change From Baseline in AK Lesion Count

Percent change from Baseline to end of study (EOS) in investigator counts of AK lesions. (NCT00605176)
Timeframe: From baseline to End of Study the Week 14 visit

Interventionpercent change (Median)
3.75% Imiquimod Cream-81.8
2.5% Imiquimod Cream-71.8
Placebo Cream-25.0

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Efficacy of Tattoo Removal Using Topical Imiquimod 5% Cream

To evaluate the efficacy of tattoo removal using topical imiquimod, 5% cream (Aldara™, 3M/Graceway Pharmaceuticals, an immune response modifier) in conjunction with the 1064 nm Nd:YAG laser. This procedure for tattoo removal will be compared to laser removal alone. (NCT00638651)
Timeframe: approximately 14 weeks

Interventionpercentage of tattoo pigment removed (Mean)
Laser Treatment With Imiquimod (Group 1)4.3
Laser Treatment With Placebo Cream (Group 2)2.7

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Safety Variables Include Adverse Reactions (AEs), Local Skin Reactions (LSRs), and Number of Subjects Who Took Rest Periods During the Treatment Period.

"Local skin reactions in the treatment and/or immediate surrounding area were clinically identified as: erythema, edema, weeping/exudate, flaking/scaling/dryness, and erosion/ulceration. LSRs were visually assessed by investigator at each visit.~Rest period was a temporary interruption of dosing dur to intolerable LSRs." (NCT00674739)
Timeframe: Up to 16 weeks

,,
Interventionparticipants (Number)
Adverse ReactionsLocal Skin ReactionsNumber of Subjects with Rest Period in Treatment
2.5% Imiquimod Cream2711049
3.75% Imiquimod Cream3014459
Placebo2291

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Proportion of Subjects With Complete Clearance of All Warts (Both Presented at Baseline and Newly Emerged Warts) at End of Study

Proportion of subjects with complete clearance of all warts (both presented at Baseline and newly emerged warts) at End of Study. Primary analysis performed on the Intent to Treat population with imputation (Last Observation Carried Forward)for missing data points. (NCT00674739)
Timeframe: Up to 16 weeks

Interventionparticipants (Number)
2.5% Imiquimod Cream0.191
3.75% Imiquimod Cream0.272
Placebo0.103

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The Absence of Lentigo Maligna (LM) at the Time of Staged Excisions in Participants

Negative histologic margins for the imiquimod plus tazarotene group compared to the imiquimod only group. (NCT00707174)
Timeframe: 24 months

Interventionparticipants (Number)
Imiquimod Only27
Imiquimod and Tazarotene Combined29

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Proportion of Subjects Achieving Complete Clearance of All Warts (Baseline and New) at the End of Study.

The complete clearance was defined as completely cleared all warts including baseline and newly emerged during the study at all anatomic areas. (NCT00735462)
Timeframe: Up to 16 weeks

Interventionproportion of participants (Number)
2.5% Imiquimod Cream0.248
3.75% Imiquimod Cream0.294
Placebo0.09

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Cosmetic Appearance Score at 4-8 Weeks Post-treatment

Cosmetic appearance score, based recall comparison to appearance at baseline. Seven point scale: +3 = treatment area is much better appearing; +2 = treatment area is moderately better appearing; + 1 = treatment area is slightly better appearing; 0 = treatment area appears same; -1 = treatment area is slightly worse appearing; -2 = treatment area is moderately worse appearing; -3 = treatment area is much worse appearing. Data from one patient, lost to follow-up immediately after cryotherapy, not included in these analyses. (NCT00774787)
Timeframe: 4-8 weeks post-treatment

InterventionScores on a scale (Mean)
Investigator assessed, imiquimod sideInvestigator assessed, observation sidePatient assessed, imiquimod sidePatient assessed, observation side
Cryotherapy Followed by Imiquimod 5% Cream or Observation2.11.62.61.2

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Local Skin Reactions

Mean maximum post-baseline intensity of investigator assessed local skin reactions (erythema, edema, weeping/exudate, flaking/scaling/dryness, scabbing/crusting, erosion/ulceration) by treatment area. 0 = none, 1 = mild, 2 = moderate, 3 = severe. Data from one patient, lost to follow-up immediately after cryotherapy, not included in these analyses. (NCT00774787)
Timeframe: Post baseline to end of study (4-8 weeks post-treatment)

InterventionScores on a scale (Mean)
Erythema, imiquimod sideErythema, observation sideEdema, imiquimod sideEdema, observation sideWeeping/exudate, imiquimod sideWeeping/exudate, observation sideFlaking/scaling/dryness, imiquimod sideFlaking/scaling/dryness, observation sideScabbing/crusting, imiquimod sideScabbing/crusting, observation sideErosion/ulceration, imiquimod sideErosion/ulceration, observation side
Cryotherapy Followed by Imiquimod 5% Cream or Observation1.51.30.20.10.30.01.41.20.90.60.40.1

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Complete Clearance of Actinic Keratoses at 4-8 Weeks Post-treatment

Complete clearance (actinic keratosis count of 0) in each respective area at 4-8 weeks post-treatment. Actinic keratoses at 4-8 weeks post-treatment visit includes all actinic keratoses in each respective treatment area, baseline and new. (NCT00774787)
Timeframe: 4-8 weeks post-treatment

InterventionParticipants (Number)
Completely cleared, imiquimod sideCompletely cleared, observation side
Cryotherapy Followed by Imiquimod 5% Cream or Observation85

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Change From Baseline in Actinic Keratoses Count at 4-8 Weeks Post-treatment

Percent change = [(actinic keratoses count at 4-8 weeks post-treatment)-(actinic keratoses count at baseline)]/(actinic keratoses count at baseline)]*100%. Data from one patient, lost to follow-up immediately after cryotherapy, not included in these analyses. Actinic keratoses at 4-8 weeks post-treatment visit includes all actinic keratoses in each respective treatment area, baseline and new. (NCT00774787)
Timeframe: Baseline, 4-8 weeks post-treatment

InterventionPercent change (Mean)
Change from baseline, imiquimod sideChange from baseline, observation side
Cryotherapy Followed by Imiquimod 5% Cream or Observation-73.2-62.0

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Pathologic Response by Immunohistochemical (IHC)as Assessed by Skin Punch Biopsy of the Target Lesion

This is done by IHC staining reviewed by a pathologist. This is done by comparing the baseline to the post-treatment biopsy tissue. Yes equals absence of residual disease. (NCT00821964)
Timeframe: Pre-and post-treatment

InterventionParticipants (Count of Participants)
Total Number of Evaluable for Pathologic ResponseEvaluable Pts. with Pathologic Response Post TxEvaluable Pts. without Pathologic Response Post Tx
Treatment (Biological Therapy, Chemo)752

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Endogenous Immunity to Common Breast Tumor Antigens (HER2, IGFBP-2, Topoisomerase II-alpha, and p53) in Peripheral Blood as Assessed by IFN-gamma and ELISPOT Assay

Peripheral blood will be obtained at baseline, after cycle 3 (end of study treatment) and at week 24 (end of study) to assess the immune response. A positive antigen-specific T cell immune response will be defined as a T cell precursor frequency more robust than 1:20,000 PBMC if the patients did not have a detectable response prior to treatment. In patients with a pre-existent immune response, the development of an immune response twice baseline will constitute augmentation. (NCT00821964)
Timeframe: Baseline and at weeks 13 and 24

InterventionParticipants (Count of Participants)
HER2 Antigen72239519HER2 Antigen72239520IGFBP-2 Antigen72239519IGFBP-2 Antigen72239520MAGE3 Antigen72239519MAGE3 Antigen72239520TopoII-alpha Antigen72239519TopoII-alpha Antigen72239520
Negative antigen specific T cell immune responsePositive antigen-specific T cell immune response
HER2, IGFBP-2, MAGE3, TopoIIa Antigen - Baseline to Week 130
HER2, IGFBP-2, MAGE3, Topo IIa Antigen - Baseline to Week 240
HER2, IGFBP-2, MAGE3, TopoIIa Antigen - Baseline to Week 138
HER2, IGFBP-2, MAGE3, Topo IIa Antigen - Baseline to Week 243
HER2, IGFBP-2, MAGE3, Topo IIa Antigen - Baseline to Week 242
HER2, IGFBP-2, MAGE3, TopoIIa Antigen - Baseline to Week 135
HER2, IGFBP-2, MAGE3, Topo IIa Antigen - Baseline to Week 241
HER2, IGFBP-2, MAGE3, TopoIIa Antigen - Baseline to Week 133
HER2, IGFBP-2, MAGE3, TopoIIa Antigen - Baseline to Week 132
HER2, IGFBP-2, MAGE3, TopoIIa Antigen - Baseline to Week 136

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Safety and Systemic Toxicity as Assessed by a Review of Medical History, Physical Exam, Systems, Performance Status, and Clinical Labs (CBC and CMP)

"Evaluated according to the Cancer Therapy Evaluation Program (CTEP) Common Terminology Criteria for Adverse Events (CTCAE) v3.0 and monitoring of adverse events will be done per Food and Drug Administration (FDA) and National Cancer Institute (NCI) guidelines for the time frame below.~Number of Participants with at Least 1 Adverse Event as Assessed by a Review of Medical History, Physical Exam, Systems, Performance Status, and Clinical Labs (CBC and CMP) under the following CTCAE categories:~Constitutional (Fatigue) Neurological (Neuropathy (sensory or motor)) Cardiac (Arrhythemia) Pulmonary (Cough, Pharyngitis) GI (Constipation, Diarrhea, Mucositis, Vomiting) Dermatology (Ulceration, Hairloss/alopecia) Pain (Headache, other pain) Syndrome (Flu-like) Visual Changes Hearing/Auditory Edema Other (General)~In addition they were asked the severity of the event so that a clinician could grade the event." (NCT00821964)
Timeframe: Baseline and weeks 5, 9 13, 16, 20, and 24

InterventionParticipants (Count of Participants)
Treatment (Biological Therapy, Chemo)15

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Incidence of Reduction of Serum TGF-beta Levels as Assessed by ELISA and Correlation With Th1 Adaptive Immunity and Clinical Response

Incidence of reduction of serum TGF-beta levels as assessed by ELISA and correlation with Th1 adaptive immunity and clinical response is defined as a reduction of at least 25% from baseline value to the value measured at week 13. (NCT00821964)
Timeframe: Baseline and at weeks 13

InterventionParticipants (Count of Participants)
No incidence of 25% reduction of TGF-beta at week1Incidence of 25% reduction of TGF-beta at week 13
Incidence of Reduction of TGF-beta Levels80

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Anti-tumor Effects of Imiquimod as Assessed by Modified World Health Organization (WHO) Criteria

"Tumor responses will be determined using the sum of the products of the largest perpendicular dimensions. Target lesions will be evaluated by the following response criteria: complete response (CR), partial response (PR), stable disease (SD), or progressive disease (PD).~Evaluation of target lesions per modified WHO response criteria:~Complete response (CR): complete clearance (100%) of target lesion(s)~Partial response (PR): ≥ 50% decrease in target lesion size~Stable disease (SD): < 50% decrease in target lesion size~Progressive (PD): ≥ 25% increase in target lesion size Overall Response Rate (ORR) determined at end of study treatment which was 1 week after cycle #3, unless patient was withdrawn from study. If patient was withdrawn from study, then ORR was determined after their last cycle of treatment received." (NCT00821964)
Timeframe: Baseline and then every 4 weeks until week 24

InterventionParticipants (Count of Participants)
Total Evaluated in this Outcome MeasureComplete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)
Treatment (Biological Therapy, Chemo)145531

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Patients Reporting at Least One Adverse Event

For all patients who received a single dose, adverse events were collected at each follow-up visit. Any patient reporting a single or multiple adverse events at any visit was conisdered to have had at least one adverse event. (NCT00828568)
Timeframe: 24 weeks

InterventionParticipants (Number)
Imiquimod 5% Taro69
Aldara - Imiquimod 5%57
Vehicle15

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Number of Participants With 100% Clearance of Actinic Keratosis Lesions: Comparison of Taro Imiquimod 5% and Aldara-Imiquimod 5%

"Uses per protocol (PP) population.~Each patient is assessed at 24 weeks. Actinic keratosis (AK) lesions that were identified and measured at baseline are reevaluated at the conclusion of the study. If all lesions that were identified at baseline are no longer present and there are no new lesions, the patient is 100% clear of AK lesions." (NCT00828568)
Timeframe: 24 weeks

InterventionParticipants (Number)
Imiquimod 5% Taro63
Aldara - Imiquimod 5%54

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Number of Participants in Intention-to-treat (ITT)Population With 100% Clearance of Actinic Keratosis (AK) Lesions Identified at Baseline

"Uses ITT population. Three patients (1 Imiquimod 5% Taro and 2 Imiquimod Aldara) did not have a follow-up visit after dosing and were excluded from ITT. Three patients (2 Imiquimod 5% Taro and 1 Imiquimod Aldara) were not evaluable at the 24-week visit and were not in the analysis.~Each patient is assessed at 24 weeks. Actinic keratosis (AK) lesions that were identified and measured at baseline are reevaluated at the conclusion of the study. If all lesions that were identified at baseline are no longer present and there are no new lesions, the patient is 100% clear of AK lesions." (NCT00828568)
Timeframe: 24 weeks

InterventionParticipants (Number)
Imiquimod 5% Taro74
Aldara - Imiquimod 5%64
Vehicle6

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Number of Participants With Any Post-baseline Local Skin Reactions (LSRs)

"LSRs were assessed independently from AEs. The frequency and percentage of subjects, as well as the mean (SD) and median score for severity (none=0, mild=1, moderate=2, and severe=3), were summarized by treatment group and by visit for the following LSRs: erythema, edema, weeping/exudates, flaking/ scaling/dryness, and scabbing/crusting. Erosion and ulceration were also evaluated (none=0, erosion=1, and ulceration=2). A score of greater than 0 for the specified LSR was considered a treatment site reaction." (NCT00894647)
Timeframe: Weeks 2, 4, 6, 10, 14, 20, and 26

,
Interventionparticipants (Number)
EdemaErythemaWeeping/ExudateFlaking/Scaling/DrynessScabbing, crustingErosion/Ulceration
Imiquimod Cream931256411411260
Placebo Cream988938122

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Percent of Subjects With Complete Clearance

Proportion of subjects who achieved complete clearance of all AK lesions, cryosurgery-treated AK lesions, and non cryosurgery-treated AK lesions from baseline to Week 26/EOS in the ITT population. (NCT00894647)
Timeframe: Week 26

Interventionpercentage of participants (Number)
Placebo Cream3
Imiquimod Cream30

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Change From Baseline in Percentage of Lesion Count

The primary efficacy endpoint was a comparison between the active and placebo treatment groups of percent change from baseline in the total AK lesion count at Week 26. All AK lesions on the face were included in the analysis-treated and untreated AK lesions at baseline (defined as the AK lesion count just prior to cryosurgery) and new lesions that appeared post-baseline. (NCT00894647)
Timeframe: Week 26

Interventionpercentage of lesion count (Mean)
Placebo Cream-43.3
Imiquimod Cream-77.4

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Objective Response (Complete Clinical Response+ Partial Response)

This is defined as percentage of patients who achieved complete clinical response or partial response at end of cycle 1 of treatment. The tumor size will be measured as lesion surface area (region of interest, ROI). The response to the treatment is then evaluated as a function of post-treatment over pre-treatment ROI, expressed in percentage. Response criteria for this study are based on European Organisation for Research and Treatment of Cancer definitions for chest wall tumors: complete clinical response: absence of any detectable residual disease; partial response: <50% of ROI change. (NCT00899574)
Timeframe: 9 weeks

Interventionpercentage of patients (Number)
Imiquimod20

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Clinical Benefits

This outcome measure is defined as number of patients with improvement of symptoms after 8 weeks of treatment. (NCT00899574)
Timeframe: 9 weeks

Interventionpatients (Number)
Pain improvementPruritus improvementDermatology Life Quality Index (DLQI) improvement
Imiquimod450

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Percentage of Subjects With at Least a 75% Reduction in the Number of AK Lesions From Baseline to End of Treatment (EOT) Visit (Week 16).

(NCT00948428)
Timeframe: Week 16

InterventionParticipants (Count of Participants)
Generic Imiquimod110
Aldara™114
Vehicle Cream14

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Percentage of Subjects With at Least a 75% Reduction in the Number of AK Lesions From Baseline to 8 Weeks Post Treatment (Test of Cure Visit).

(NCT00948428)
Timeframe: Week 24

InterventionParticipants (Count of Participants)
Generic Imiquimod77
Aldara™77
Vehicle Cream7

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Percentage of Subjects in Each Treatment Group With Complete Clearance of AK Lesions at the Test of Cure Visit (Week 24)

(NCT00948428)
Timeframe: Week 24

InterventionParticipants (Count of Participants)
Generic Imiquimod74
Aldara™72
Vehicle Cream7

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Absence of CIN2/3 Lesion by Week 15

Number of participants with no CIN2/3 lesion at the week 15 visit (NCT00988559)
Timeframe: 15 weeks

InterventionParticipants (Count of Participants)
PMED Delivery - Groups 1 and 22
IM Injections - Groups 5 and 63
Intralesional Delivery - Group 3 and 43
Intralesional Delivery + Imiquimod - Group 71

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Actinic Keratosis Count

The percent change in actinic keratosis count as compared to the baseline lesion count (NCT01203878)
Timeframe: Week 18 (4 weeks after randomization visit)

Interventionpercent reduction in baseline count (Mean)
Imiquimod Followed by Photodynamic Therapy81
Imiquimod Followed by Observation83

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Complete Clearance

The proportion of randomized patients with complete clearance of actinic keratoses in the treatment area (entire face). (NCT01203878)
Timeframe: Week 18 (4 weeks after randomization visit)

Interventionparticipants (Number)
Imiquimod Followed by Photodynamic Therapy5
Imiquimod Followed by Observation2

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Cosmetic Appearance

"Change (improvement) in investigator scores of cosmetic appearance of the treatment area (entire face) by objective and subjective assessments:~INVESTIGATOR COSMETIC ASSESSMENT 0 - Facial skin is smooth to the touch, without significant lines or unevenness in pigmentation~1 - Facial skin shows 1 area (cheeks, forehead, or the perioral area) of significant 3 - Facial skin shows 3 areas with significant roughness, dyspigmentation, or fine lines 2 - Facial skin shows 2 areas of significant roughness, dyspigmentation, or fine lines 4 - All are severe in severity" (NCT01203878)
Timeframe: Week 18 (4 weeks after randomization visit)

Interventionunits on a scale (Mean)
Imiquimod Followed by Photodynamic Therapy1.67
Imiquimod Followed by Observation1.25

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Systemic Tumor Response Rates (Complete Response+Partial Response)

The systemic tumor response refers to the response at the time of best overall response. The response criteria are specially adapted from Response Evaluation Criteria in Solid Tumor for Immunotherapies (Wolchok, et al., 2009). (NCT01421017)
Timeframe: 9 weeks from the start of the treatment of RT

Interventionproportion of tumors (Number)
IMQ+RT.25
CTX/IMQ/RT.083
CTX/RT0

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Local Skin Tumor Response Rates (Complete Response + Partial Response)

The response refers to the best overall response, based on European Organization for Research and Treatment of Cancer's definitions for chest wall tumors (Kouloulias, et al., 2002). (NCT01421017)
Timeframe: 9 weeks from the start of the treatment

,
Interventionproportion of tumors (Number)
Local Area A; irradiated areaLocal Area B; non-irradiated area
CTX/IMQ/RT0.75.083
IMQ+RT0.83.33

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Number of Participants With Partial Clearance of AK Lesions

To compare the partial (at least 75%) clearance of AK lesions in the selected treatment area after the last treatment cycle (at Week 8 or 16) (NCT01926496)
Timeframe: 8-16 weeks

InterventionParticipants (Count of Participants)
Ingenol Mebutate195
Imiquimod210

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Incidence of SCC

Cumulative incidence of SCC after treatment with ingenol mebutate gel and imiquimod cream.> The primary response criterion is diagnosis of SCC (defined as invasive SCC i.e. excludes SCC in situ) in the treatment field across the 3-year trial period.> Kaplan-Meier estimate based on time to SCC or censoring. (NCT01926496)
Timeframe: 3 years

Interventionpercentage of subjects (Number)
Ingenol Mebutate3.1
Imiquimod0.4

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Incidence of SCC and Other Neoplasia

Cumulative incidence of SCC and other neoplasia after treatment with ingenol mebutate gel and imiquimod cream.> The secondary response criterion is diagnosis of SCC and other neoplasia in the treatment field across the 3-year trial period.> Kaplan-Meier estimate based on time to SCC and other neoplasia, or censoring. (NCT01926496)
Timeframe: 3 years

Interventionpercentage of subjects (Number)
Ingenol Mebutate6.2
Imiquimod2.3

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Number of Participants With Complete Clearance of AK Lesions After Last Treatment

To compare the complete clearance of AK lesions in the selected treatment area after the last treatment cycle (at Week 8 or 16) (NCT01926496)
Timeframe: 8-16 weeks

InterventionParticipants (Count of Participants)
Ingenol Mebutate168
Imiquimod192

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Number of Participants With Complete Clearance of AK Lesions at 12 Months

To compare the complete clearance of AK lesions at 12 months, defined as no AK lesions in the selected treatment area at any time from the last treatment cycle at Week 8 or 16 through to Month 12. (NCT01926496)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Ingenol Mebutate70
Imiquimod108

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Complete Response (CR) or Partial Response (PR)

Measure the number of subjects with a CR or PR. A CR requires all of the following: complete disappearance of all enhancing measurable and nonmeasurable disease sustained for at least 4 weeks; no new lesions; and stable or improved nonenhancing (T2/FLAIR) lesions. Patients must be off corticosteroids (or on physiologic replacement doses only) and stable or improved clinically. A PR requires all of the following: ≥50% decrease, compared with baseline; the sum of products of perpendicular diameters of all measurable enhancing lesions sustained for at least 4 weeks; no progression of nonmeasurable disease; no new lesions; stable or improved nonenhancing (T2/FLAIR) lesions on the same or a lower dose of corticosteroids compared with baseline scan; and the patient being on a corticosteroid dose not greater than the dose at time of the baseline scan and stable or improved clinically. (NCT02078648)
Timeframe: 3 years

InterventionParticipants (Count of Participants)
SL-701 + GM-CSF + Imiquimod1
SL-701 + Poly-ICLC 1.6 mg + Bevacizumab4

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Objective Response Rate (ORR)

The ORR was the percentage of subjects who had at least 1 overall tumor response of CR or PR documented on 2 consecutive MRIs ≥4 weeks apart by modified Response Assessment in Neuro-Oncology criteria. (NCT02078648)
Timeframe: 3 years

InterventionParticipants (Count of Participants)
SL-701 + GM-CSF + Imiquimod1
SL-701 + Poly-ICLC 1.6 mg + Bevacizumab4

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Overall Survival at 12 Months (OS-12)

OS-12 after the initiation of SL-701, per Kaplan-Meier estimate. (NCT02078648)
Timeframe: up to 12 months

InterventionParticipants (Count of Participants)
SL-701 + GM-CSF + Imiquimod8
SL-701 + Poly-ICLC 1.6 mg + Bevacizumab12

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Progression-free Survival at 6 Months (PFS-6)

Estimate the percent of patients alive and progression-free survival at 6 months (PFS-6) after the initiation of SL-701. (NCT02078648)
Timeframe: Up to 6 months

Interventionpercentage of subjects (Mean)
SL-701 + GM-CSF + Imiquimod26.7
SL-701 + Poly-ICLC 1.6 mg + Bevacizumab46.6

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Number of Participants With Local Skin Reactions

Local skin reactions included erythema, flaking/scaling/dryness, scabbing/crusting, pruritus, erosion/ulceration, pain, edema, and weeping/exudate. A summary of other non-serious AEs and all serious AEs, regardless of causality is located in Reported AE section. (NCT02120898)
Timeframe: Baseline (Day 1) up to Week 14

,,
InterventionParticipants (Count of Participants)
ErythemaFlaking/Scaling/DrynessScabbing/CrustingPruritusErosion/UlcerationPainEdemaWeeping/Exudate
Generic Imiquimod Cream 2.5%333222123221
Vehicle Cream17221141000
Zyclara® (Imiquimod) Cream 2.5%30291352221

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Complete Clearance Rate - Percentage of Participants With Treatment Success: Per-Protocol (PP) Population

Complete clearance rate (treatment success) was defined as the percentage of participants in each treatment group with a count of zero actinic keratosis (AK) lesions in the treatment area at Week 14. All AKs (baseline and new lesions) independent of size within the treatment area were included in the efficacy lesion count. The AK clearance rate for a participant was calculated as follows: {1 - [ (number of AK lesions at Week 14) / (number of AK lesions at Baseline)]} * 100. (NCT02120898)
Timeframe: Week 14

Interventionpercentage of participants (Number)
Generic Imiquimod Cream 2.5%12.4
Zyclara® (Imiquimod) Cream 2.5%13.6
Vehicle Cream4.8

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Percentage of Drug Compliance

The overall drug compliance (%) = (Observed Consumption / Expected Consumption) * 100%. (NCT02120898)
Timeframe: Baseline (Day 1) up to Week 6

Interventionpercentage of drug compliance (Mean)
Generic Imiquimod Cream 2.5%96.55
Zyclara® (Imiquimod) Cream 2.5%97.83
Vehicle Cream97.43

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Number of Participants With Adverse Events (AEs)

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. Mild AEs: awareness of sign or symptom, but easily tolerated. Moderate AEs: discomfort sufficient to cause interference with normal activities. Severe AEs: inability to carry out usual activities. Serious AEs: death, a life-threatening AE, inpatient hospitalization or prolongation of existing hospitalization, persistent or significant disability or incapacity, a congenital anomaly or birth defect, or an important medical event that jeopardized the participant and required medical intervention to prevent 1 of the outcomes listed in this definition. A summary of other non-serious AEs and all serious AEs, regardless of causality is located in Reported AE section. (NCT02120898)
Timeframe: Baseline (Day 1) up to Week 14

,,
InterventionParticipants (Count of Participants)
Any AEsAny AEs in treatment areaSAEsSAEs in treatment areaMild AEsModerate AEsSevere AEs
Generic Imiquimod Cream 2.5%5176031164
Vehicle Cream2252110111
Zyclara® (Imiquimod) Cream 2.5%5054029201

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Complete Clearance Rate - Percentage of Participants With Treatment Success: ITT Population

Complete clearance rate (treatment success) was defined as the percentage of participants in each treatment group with a count of zero AK lesions in the treatment area at Week 14. All AKs (baseline and new lesions) independent of size within the treatment area were included in the efficacy lesion count. The AK clearance rate for a participant was calculated as follows: {1 - [ (number of AK lesions at Week 14) / (number of AK lesions at Baseline)]} * 100. (NCT02120898)
Timeframe: Week 14

Interventionpercentage of participants (Number)
Generic Imiquimod Cream 2.5%12.6
Zyclara® (Imiquimod) Cream 2.5%12.4
Vehicle Cream4.3

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Change in Physical Symptom Score From Baseline (2-7 Days Post Randomization) Until 4 Weeks Post Randomization

The physical symptom score is made up of the sum of responses to whether or not the participant had any of the 9 physical symptoms: anal pain, pain other than anal pain, pain during bowel movements, constipation, bleeding from anus, itching in/around the anus, discharge (wetness) in anal area, burning sensations in the anal area, and urgency for bowel movements. Responses are 0- not at all, 1-a little bit, 2-somewhat, 3-quite a bit, 4-very much. Thus physical symptom score ranges from 0 to 36. (NCT02135419)
Timeframe: 4 weeks post randomization

Interventionscore on a scale (Mean)
Arm I (Treatment)-2.22
Arm II (Active Monitoring) (Closed Since SEP2021)-0.08

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Anal Cancer Incidence

Anal cancer incidence is calculated as the number of anal cancer cases detected per 100,000 person years (NCT02135419)
Timeframe: Time from randomization to diagnosis of anal cancer, assessed up to 5 years post randomization

Interventioncases per 100,000 person years (Number)
Arm I (Treatment)173
Arm II (Active Monitoring) (Closed Since SEP2021)402

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Incidence of Adverse Events for Each Treatment

Participants who had at least one adverse event (serious or non-serious) (NCT02135419)
Timeframe: Up to 5 years after randomization

InterventionParticipants (Count of Participants)
Arm I (Treatment)416
Arm II (Active Monitoring) (Closed Since SEP2021)429

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Number of Participants That Had Partial Clearance Rate of at Least 75 Percent Reduction in External Genital Wart (EGW)s Count at End of Treatment (EOT) Week 12 or 16

Number of Participants that had partial clearance rate of at least 75 percent reduction in External Genital Wart (EGW)s count at end of treatment (EOT) Week 12 or 16 (NCT02482428)
Timeframe: End of Treatment (EOT) Week 12 or Week 16

Interventionparticipants (Number)
LFX453 0.1% NMC2
LFX453 0.15% LCC1
Combined Vehicle0
Aldara3

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Number of Adverse Events (AE)/Serious Adverse Events (SAE) as a Measure of Safety and Tolerability up to 30 Weeks

Number of participants with at least one AE/SAE in the category up to 30 weeks (NCT02482428)
Timeframe: 30 weeks

,,,,
Interventionparticipants (Number)
Adverse Events (AEs)Serious Adverse Events (SAEs)
Aldara100
LFX453 0.1% NMC30
LFX453 0.15% LCC50
Vehicle to LCC20
Vehicle to NMC30

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Complete Clearance of Disease at Week 14

Number of participants achieving complete clearance of genital warts at Week 14 (NCT02482428)
Timeframe: Week 14

Interventionparticipants (Number)
LFX453 0.1% NMC1
LFX453 0.15% LCC0
Combined Vehicle0
Aldara0

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Percent Change From Baseline in the Cumulative Surface Area of the Acetowhite Vulvar Lesion(s)

Lesion(s), defined as areas that stain acetowhite were assessed. Analysis of qualifying lesions was defined as the change in total surface area of only lesions with both baseline and Week 48 measurements. Percent change in the cumulative surface area of the acetowhite vulvar lesion(s) was determined by the quantitative analysis of standardized prebiopsy photographic imaging of qualifying lesion(s) at Week 48 compared to baseline. (NCT03180684)
Timeframe: From baseline to Week 48

Interventionpercent change in surface area (Mean)
VGX-3100 + EP47.7
VGX-3100 + EP + Imiquimod10.5

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Percentage of Participants With Adverse Events (AEs)

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body, or worsening of a pre-existing condition, temporally associated with the use of a product whether or not considered related to the use of the product. (NCT03180684)
Timeframe: From baseline up to Week 100

Interventionpercentage of participants (Number)
VGX-3100 + EP92.0
VGX-3100 + EP + Imiquimod100

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Percentage of Participants With at Least One Local and Systemic Treatment-emergent Adverse Event (TEAE) During 7 Days Following Each Dose

An adverse event (AE) was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body, or worsening of a pre-existing condition, temporally associated with the use of a product whether or not considered related to the use of the product. A TEAE was defined per protocol as any AE with onset after the administration of study medication through the end of the study (i.e., study discharge). (NCT03180684)
Timeframe: 7 days following each dose: Day 0 (Days 0 to 7), Week 4 (Days 22 to 28), Week 12 (Days 78 to 84), Week 24 (Days 162 to 168), and Week 52 (Days 358 to 364)

Interventionpercentage of participants (Number)
VGX-3100 + EP84.0
VGX-3100 + EP + Imiquimod75.0

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Percentage of Participants With No Evidence of HPV-16 and/or HPV-18 in Vulvar Tissue Samples

Participants with no evidence of HPV-16 and/or HPV-18 indicated the clearance of the specific HPV genotypes [16, 18, or both]. All lesions were evaluated for evidence of HPV-16/18 in vulvar tissue. (NCT03180684)
Timeframe: Week 48

Interventionpercentage of participants (Number)
VGX-3100 + EP15.0
VGX-3100 + EP + Imiquimod50.0

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Percentage of Participants With No Evidence of Vulvar HSIL, No Evidence of Vulvar LSIL (VIN1), and No Evidence of Condyloma on Histology

Histologic regression was defined as a participant with no histologic evidence of vulvar HSIL, no evidence of LSIL (VIN1), and no evidence of condyloma. Histologic regression of vulvar HSIL to normal tissue was assessed. (NCT03180684)
Timeframe: Week 48

Interventionpercentage of participants (Number)
VGX-3100 + EP10.0
VGX-3100 + EP + Imiquimod37.5

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Percentage of Participants With No Histologic Evidence of Vulvar HSIL

Participants with no histologic evidence of vulvar HSIL (normal tissue or vulvar LSIL [VIN1] or condyloma) based on histology (i.e. biopsies or excisional treatment) were considered. All lesions were evaluated for histologic evidence of vulvar HSIL. (NCT03180684)
Timeframe: Week 48

Interventionpercentage of participants (Number)
VGX-3100 + EP15.0
VGX-3100 + EP + Imiquimod37.5

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Percentage of Participants With No Histologic Evidence of Vulvar HSIL and No Evidence of HPV-16 and/or HPV-18 in Vulvar Tissue Samples

A treatment responder for the primary endpoint was defined as a participant with no histologic evidence of vulvar HSIL (normal tissue or vulvar low grade squamous intraepithelial lesions (LSIL) [vulval intraepithelial neoplasia 1 (VIN1)] or condyloma) and no evidence of HPV-16 or HPV-18 (i.e., elimination of the specific genotypes [16, 18, or both]) in vulvar tissue at evaluation and who did not receive any non-study related treatment for vulvar HSIL. All lesions were evaluated for histologic evidence of vulvar HSIL or evidence of HPV-16/18 in vulvar tissue. (NCT03180684)
Timeframe: Week 48

Interventionpercentage of participants (Number)
VGX-3100 + EP15.0
VGX-3100 + EP + Imiquimod37.5

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Percentage of Participants With No Histologic Evidence of Vulvar HSIL or No Evidence of HPV-16/18 in Vulvar Tissue

A treatment responder for the endpoint was defined as a participant with no histologic evidence of vulvar HSIL (normal tissue or LSIL [VIN1] or condyloma) based on histology (i.e. biopsies or excisional treatment) or no evidence of HPV-16 or HPV-18 (i.e., elimination of the specific genotypes [16, 18, or both]) in vulvar tissue at evaluation and who did not receive any non-study related treatment for vulvar HSIL. All lesions were evaluated for histologic evidence of vulvar HSIL or evidence of HPV-16/18 in vulvar tissue. (NCT03180684)
Timeframe: Week 48

Interventionpercentage of participants (Number)
VGX-3100 + EP15.0
VGX-3100 + EP + Imiquimod50.0

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Percentage of Participants With No Progression of Vulvar HSIL to Vulvar Cancer

Non-progression of vulvar HSIL to vulvar cancer was evaluated from baseline to Week 48. Progression was defined as advancement to carcinoma by histology. (NCT03180684)
Timeframe: From baseline up to Week 48

Interventionpercentage of participants (Number)
VGX-3100 + EP100.0
VGX-3100 + EP + Imiquimod100.0

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Change From Baseline in Flow Cytometry Response Magnitude

Assessment of cellular immune activity was measured using the application of flow cytometry for the purpose of performing a Lytic Granule Loading Assay. The Lytic Granule Loading Assay examines the following external cellular markers: cluster of differentiation 3 (CD3), CD4, CD8 (T-cell identification), CD137, CD38, and CD69 (T-cell activation markers) as well as PD-1 (exhaustion/activation marker). Here, a change from baseline in CD8+/CD137+ PBMCs expressing Perforin+ was reported. (NCT03180684)
Timeframe: Baseline; Week 27

,
InterventionSFU/10^6 PBMC (Median)
BaselineChange from Baseline at Week 27
VGX-3100 + EP0.1500.000
VGX-3100 + EP + Imiquimod1.2500.000

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Change From Baseline in Interferon-Gamma (IFN-γ) Response Magnitude

Peripheral blood mononuclear cells (PBMCs) were isolated from whole blood samples. Assessment of cellular immune activity was performed by IFN-γ enzyme-linked immunosorbent spot-forming (ELISpot) assay. (NCT03180684)
Timeframe: Baseline; Weeks 15, 27, 48, 74, and 96

,
Interventionspot forming units (SFU) per 10^6 cells (Median)
HPV-16 E6 (Baseline)HPV-16 E6 (Change From Baseline at Week 15)HPV-16 E6 (Change From Baseline at Week 27)HPV-16 E6 (Change From Baseline at Week 48)HPV-16 E6 (Change From Baseline at Week 74)HPV-16 E6 (Change From Baseline at Week 96)HPV-16 E7 (Baseline)HPV-16 E7 (Change From Baseline at Week 15)HPV-16 E7 (Change From Baseline at Week 27)HPV-16 E7 (Change From Baseline at Week 48)HPV-16 E7 (Change From Baseline at Week 74)HPV-16 E7 (Change From Baseline at Week 96)HPV-18 E6 (Baseline)HPV-18 E6 (Change From Baseline at Week 15)HPV-18 E6 (Change From Baseline at Week 27)HPV-18 E6 (Change From Baseline at Week 48)HPV-18 E6 (Change From Baseline at Week 74)HPV-18 E6 (Change From Baseline at Week 96)HPV-18 E7 (Baseline)HPV-18 E7 (Change From Baseline at Week 15)HPV-18 E7 (Change From Baseline at Week 27)HPV-18 E7 (Change From Baseline at Week 48)HPV-18 E7 (Change From Baseline at Week 74)HPV-18 E7 (Change From Baseline at Week 96)
VGX-3100 + EP1.6670.8330.8330.8331.6671.6671.6673.3333.3331.6671.6670.0000.00019.16710.83314.1678.33320.0000.0002.5001.6671.6671.6673.333
VGX-3100 + EP + Imiquimod1.6670.0003.3330.0000.0000.8330.0001.6676.6671.6670.8330.0000.00010.0005.0003.3339.16719.1670.0003.3336.6670.0000.0004.167

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Levels of Serum Anti-HPV-16 and Anti-HPV-18 Antibody Concentrations

A standardized binding enzyme-linked immunosorbent assay (ELISA) was performed to measure the anti-HPV-16/18 antibody response induced by VGX-3100. (NCT03180684)
Timeframe: Weeks 15, 27, 48, 74, and 96

,
Interventionreciprocal endpoint titer (Geometric Mean)
Anti-HPV-16 (Week 15)Anti-HPV-16 (Week 27)Anti-HPV-16 (Week 48)Anti-HPV-16 (Week 74)Anti-HPV-16 (Week 96)Anti-HPV-18 (Week 15)Anti-HPV-18 (Week 27)Anti-HPV-18 (Week 48)Anti-HPV-18 (Week 74)Anti-HPV-18 (Week 96)
VGX-3100 + EP7.39.615.914.537.024.844.769.383.22.9
VGX-3100 + EP + Imiquimod13.115.017.26.111.4133.789.4133.745.02.2

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Feasibility of Intravaginal Use 5-FU and Imiquimod on Alternating Weeks in Women With Biopsy Confirmed High Grade Cervical Squamous Intraepithelial Lesions.

Feasibility is evaluated based on safety and tolerability of the study intervention. For safety, the study assessed the number of participants experiencing the specified adverse events defined as Grade 2 or greater toxicity (or Grade 1 toxicity of any genital lesion (blisters, ulcerations, or pustules)) that is possibly, probably, or definitely related and lasts for more than 5 days. For tolerability, the study assessed the number of participants who were not able to apply at least 50% of the treatment due to the specified adverse events. (NCT03196180)
Timeframe: Up to 22 weeks

InterventionParticipants (Count of Participants)
SafetyTolerability
Treatment (Topical Fluorouracil, Imiquimod)41

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Keloid Recurrence

To assess the efficacy of 5% Imiquimod cream on decreasing keloid recurrence after excision when initiated prior to excision (NCT03760250)
Timeframe: 12 weeks after surgical excision

InterventionParticipants (Count of Participants)
RecurredDid not recur
Imiquimod31

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Number of Responders

The number of participants with reduction in number of AKs on the face and/or scalp after application of imiquimod 3.75%. (NCT03914417)
Timeframe: Day 70

InterventionParticipants (Count of Participants)
Imiquimod 3.75% Cream19

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