imiquimod

Imiquimod (R 837) is an immune response modifier and a toll-like receptor 7 (TLR7) agonist with antiviral and antitumor effects. It is used in the study of external genital warts, perianal warts, cancer, and COVID-19, and is commonly employed to induce psoriasis models.

Imiquimod 2HCl is a toll-like receptor 7 (TLR7) agonist and immune modulator with antiviral and antitumor activities. It can be used to establish psoriasis-like mouse models and for the study of periorbital skin cancer, pemphigus foliaceus, and COVID-19.

Imiquimod hydrochloride (R 837 hydrochloride) is a selective toll-like receptor 7 (TLR7) agonist and immune response modulator with antiviral and antitumor activities. It is used in the study of external genital warts, perianal warts, cancer, COVID-19, pemphigus foliaceus, skin cancer, and psoriasis, and is commonly employed to establish psoriasis models.

Imiquimod maleate (R 837 maleate) is a toll-like receptor 7 (TLR7) agonist and immune response modifier with antiviral and antitumor activities. It is used in the study of external genital warts, perianal warts, cancer, and COVID-19, and can induce psoriasis-like skin lesions in mice, commonly used to establish psoriasis models.

Imiquimod Related Compound A is a useful organic compound for research related to life sciences. The catalog number is T67035 and the CAS number is 99010-24-9.

Imiquimod-D9 is the deuterated form of Imiquimod. Imiquimod (T0134) (R 837) functions as a toll-like receptor 7 (TLR7) agonist, serving as an immune response modifier. It demonstrates antiviral and antitumor effects in vivo and is applicable in research related to external genital and perianal warts, cancer, and COVID-19.

Imiquimod (Standard) is the standard substance of Imiquimod, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Imiquimod (R 837) is an immune response modifier and a toll-like receptor 7 (TLR7) agonist with antiviral and antitumor effects. It is used in the study of external genital warts, perianal warts, cancer, and COVID-19, and is commonly employed to induce psoriasis models.

Protectin D1 (Neuroprotectin D1) is a neuroprotectin produced by neuronal cells and is a potential cardioprotective agent.Protectin D1 attenuates myocardial ischemia/reperfusion injury and inhibits imiquimod-induced psoriasis-like skin inflammation by modulating the PI3K/AKT signaling pathway.

NLRP3-IN-NBC6 is a potent, selective NLRP3 inflammasome inhibitor with an IC50 of 574 nM. It acts independently of Ca 2+ and inhibits Nigericin-induced inflammasome activation in THP-1 cells, as well as Imiquimod-induced IL-1β release from LPS-primed bone marrow-derived macrophages (BMDMs) [1].

12R-LOX-IN-2 is an inhibitor of 12R-lipoxygenase (12R-LOX).12R-LOX-IN-2 inhibits imiquimod (IMQ)-induced hyperproliferation of psoriatic keratinocytes and inhibits colony formation.12R-LOX-IN-2 also decreases the protein level of Ki67 and the mRNA expression of IL-17A in IMQ-induced cells. 12R-LOX-IN-2 may be useful in the study of psoriasis and other skin-associated inflammatory diseases.

BMS-509744 is a selective, ATP-competitive Itk inhibitor with an IC50 of 19 nM. It inhibits IL-8 expression and HIV infection, ameliorates pulmonary inflammation in allergic asthma mouse models, and reduces Imiquimod-induced skin inflammation in mice.

STAT3-IN-34 (Compound 15E) acts as a STAT3 inhibitor, blocking both the nuclear translocation and the transcriptional regulator activity of STAT3. It effectively inhibits HaCaT cell proliferation with an IC50 value of 0.008 μM. Additionally, STAT3-IN-34 reduces IL-17A expression and mitigates Imiquimod-induced psoriasis in mouse models.

JAK/HDAC-IN-4 (compound 11 i) is a dual inhibitor targeting both JAK2 and HDAC6, with IC50 values of 0.49 nM and 12 nM respectively. It inhibits cell proliferation and the production of nitric oxide. In a mouse model induced by Imiquimod, JAK/HDAC-IN-4 ameliorates psoriasiform skin lesions with low toxicity.

PDE4-IN-22 (Compound 2e) is a phosphodiesterase 4 (PDE4) inhibitor with an IC50 value of 2.4 nM. It exhibits anti-inflammatory properties and demonstrates significant anti-psoriatic effects in an Imiquimod-induced psoriasis mouse model.

EAPB-0202, the demethylated metabolite of EAPB0203, demonstrates significant in vitro activity against A375 cells when compared to the reference drugs fotemustine and imiquimod.

EAPB-0503, an imidazoquinoxaline derivative and an analog of Imiquimod, selectively reduces HDM2 expression and activates the p53 pathway in cells expressing NPM1c, thereby inducing apoptosis.

M351-0056 is an agonist of the immune checkpoint protein VISTA, diminishing cytokine secretion induced by VISTA, enhancing VISTA-induced T cell proliferation, and exhibiting immunomodulatory activity. Additionally, M351-0056 has been shown to improve psoriasis-like dermatitis induced by Imiquimod in mouse models.

Paeoniflorin-6′-O-benzene sulfonate (CP-25) acts as an inhibitor of G protein-coupled receptor kinase 2 (GRK2), preventing its translocation to the cell membrane and inhibiting the JAK1/STAT3 signaling pathway. It suppresses HaCaT cell proliferation induced by IL-17A/CXCL2. In mouse models, CP-25 reduces the levels of inflammatory cytokines and chemokines such as IL-17A, IL-17F, IFN-γ, TNF-α, IL-22, IL-23, CXCL2, CXCL3, and CXCL9, thereby alleviating psoriasis induced by Imiquimod.

WB518 is a potent STAT3 inhibitor. It effectively suppresses STAT3 activity and the expression of keratin 17. By inhibiting STAT3 phosphorylation and keratin 17, WB518 can significantly alleviate imiquimod and TPA-induced psoriasis in animal models.

PROTACIRAK4 degrader-13 (Degrader 1) is a selective IRAK4 PROTAC degrader, demonstrating DC50 values of 0.86 nM and 1.1 nM in monocytes and lymphocytes within PBMCs, respectively. It significantly induces TIR signaling activation and inhibits the expression of circulating pro-inflammatory cytokines in a psoriasis mouse model induced by Imiquimod. PROTACIRAK4 degrader-13 is applicable in the study of neutrophilic inflammatory diseases driven by TLR and IL-1R, such as hidradenitis suppurativa (HS) and atopic dermatitis (AD).

SMU-R39 is a TLR7 and TLR8 antagonist with IC50 values of 3.22 μM and 0.24 μM, respectively. It binds to recombinant mTLR7 protein (KD= 2.36 μM) and recombinant hTLR8 protein (KD= 105 nM). SMU-R39 inhibits downstream NF-κB and MAPK signaling pathways, reducing the secretion and transcription of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in PBMCs and THP-1 cells. In an Imiquimod (IMQ)-induced psoriasis mouse model, SMU-R39 exhibits anti-inflammatory activity and may be used for researching autoimmune diseases such as psoriasis.

TLR7antagonist-1 (Compound 44#) is an orally bioavailable and selective TLR7 antagonist with an IC50 value of 0.3 nM for TLR7. It specifically binds to TLR7, inhibiting its activation and downregulating the c-Rel signaling pathway. TLR7antagonist-1 also reduces the mRNA levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α and alleviates psoriasiform lesions induced by Imiquimod. This compound is applicable for psoriasis-related research.

BMS-986251 is a potent and specific RORγt inverse agonist that exerts its action via oral administration. It shows an EC 50 of 12 nM for RORγt GAL4. In human whole blood assay, BMS-986251 effectively inhibits IL-17 with an EC 50 of 24 nM. Furthermore, BMS-986251 exhibits strong therapeutic effects in mouse acanthosis and Imiquimod-induced models, which are commonly used preclinical models for psoriasis.

ODN 2088 is an effective Toll-like receptor inhibitor exhibiting significant inhibitory activity against TLR3, TLR7, and TLR9 without cytotoxicity. It reduces IFN-α and IL-6 release by blocking associated innate immune signaling pathways. In vitro experiments demonstrated that ODN 2088 (0.01–10 μM, 48 hours) showed minimal inhibition of IL-6 release induced by CpG-ODN 2006 (100 nM), but markedly suppressed IL-6 secretion from human peripheral blood mononuclear cells stimulated by imiquimod (5 μg/mL). This demonstrates its differential regulatory potential across distinct TLR activation pathways.