IHCH-8110
IHCH-8110 is a peripherally restricted, non-brain-penetrant 5-HT2AR and 5-HT2CR agonist (Ki=47.86 nM) that antagonizes 5-HT2BR. IHCH-8110 induces CXCL10 and IL-18 expression by activating 5-HT2AR on enteric glial cells, thereby promoting CD8+ T cell recruitment and effector polarization, and avoids the risk of cardiac valvulopathy associated with 5-HT2BR activation. IHCH-8110 exhibits a low risk of hERG channel inhibition (IC50=5.96 μM) and is well tolerated, sensitizing immunologically cold colorectal cancer to PD-1 blockade therapy, making it suitable for research related to colorectal cancer.
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- CAS No.: 3078735-55-1
- Formule: C21H35N3O2
- Masse moléculaire:361.52
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Activité biologique
Description
IC50 & Target
[1]|
5-HT2A Receptor 47.86 nM (Ki) |
5-HT2B Receptor |
5-HT2C Receptor |
In Vitro
IHCH-8110 exhibits high binding affinity for the 5-HT2AR with a Ki of 47.86 nM[1].
IHCH-8110 (2-8 μM; 24 h) does not directly enhance CD8+ T cell migration or cytotoxicity in vitro[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
IHCH-8110 (10 mg/kg; i.p.; daily; 10 days) suppresses colorectal cancer progression via activating 5-HT2AR on enteric glial cells to enhance CD8+ T cell recruitment and cytotoxicity[1].
IHCH-8110 (10 mg/kg; i.p.; daily) in combination with anti-PD-1 suppresses primary tumor growth and liver metastasis in the aggressive AKPS CRC model[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (mixed-sex, 6-10 weeks)[1]
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Dosage:1 mg/kg; 10 mg/kg
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Administration:i.p.; daily; 10 days
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Result:Inhibited MC38 tumor growth, reducing tumor volume and tumor weight at 10 mg/kg.
Increased the ratio and number of tumor-infiltrating T cells, specifically CD8+ T cells.
Enhanced tumor infiltration of cytotoxic CD8+ T cell subsets (IFN-γ+, TNF-α+, GZMB+, PD-1+).
Inhibited tumor growth in the MC38-OVA model with an increased ratio of OVA-specific CD8+ T cells.
Completely abolished antitumor effects upon CD8+ T cell depletion.
In combination with anti-PD-1, led to complete tumor rejection in most mice by day 10.
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Animal Model:C57BL/6J (mixed-sex, 6-10 weeks; Htr2a^flox/flox and Htr2a^ΔEGC)[1]
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Dosage:10 mg/kg
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Administration:i.p.; daily; 10 days
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Result:Reduced tumor volume and tumor weight in Htr2a^flox/flox mice.
Increased tumor-infiltrating CD8+ T cells (IFN-γ+, TNF-α+, GZMB+, PD-1+) in Htr2a^flox/flox mice.
Failed to suppress tumor progression and did not increase CD8+ T cells in Htr2a^ΔEGC mice.
Antitumor effects were largely abrogated in Cxcl10^ΔEGC mice.
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Animal Model:C57BL/6J (mixed-sex, 6-10 weeks; Htr2a^flox/flox and Htr2a^ΔEGC)[1]
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Dosage:1 mg/kg; 10 mg/kg
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Administration:i.p.; daily; 10 days
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Result:Markedly reduced tumor volume and tumor weight in AKP tumors.
Substantially increased the proportion and number of tumor-infiltrating CD8+ T cells.
Reduced tumor volume and weight and increased CD8+ T cells in Htr2a^flox/flox mice.
Failed to suppress tumor progression and did not increase CD8+ T cells in Htr2a^ΔEGC mice.
In combination with anti-PD-1, synergistically enhanced the antitumor effect, leading to maximal inhibition of AKP tumor growth.
Chemical Information
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CAS No. 3078735-55-1
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Masse moléculaire 361.52
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Formule C21H35N3O2
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SMILES
CCCCCCOC1=CC=C(C=C1)CNC(N([C@@H]2CC[C@H](CC2)N)C)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
IHCH-8110 Related Classifications
HY-189235 Related Classifications
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