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
- 화학식: C21H35N3O2
- 분자량:361.52
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
All 5-HT Receptor Isoforms
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Biological Activity
제품 설명
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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분자량 361.52
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화학식 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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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
IHCH-8110 Related Classifications
HY-189235 Related Classifications
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