Cyproheptadine
CAS No. : 129-03-3
| Size | Price | Stock |
|---|---|---|
| 5mg | $80 | In-stock |
| 10mg | $130 | In-stock |
| 25mg | $240 | In-stock |
| 50mg | $350 | In-stock |
| 100mg | $520 | In-stock |
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| Cat. No. : | HY-B1622 |
| M.Wt: | 287.40 |
| Formula: | C21H21N |
| Purity: | >98 % |
| Solubility: | DMSO : 3.17 mg/mL (ultrasonic;warming;adjust pH to 3 with HCl;heat to 60°C) |
Cyproheptadine acts as a p38 MAP kinase activator, CHK2 activator, histamine H1 receptor inhibitor and serotonin receptor inhibitor. Cyproheptadine mediates cell cycle arrest via G1 phase arrest, G1/S transition arrest, G0/G1 phase arrest, reduced expression of cyclins D1/D2/D3, upregulated expression of HBP1, p16, p21, p27, and decreased phosphorylation of retinoblastoma protein. Cyproheptadine induces Apoptosis by increasing PARP and cleaved PARP, as well as activating the mitochondrial caspase pathway. Cyproheptadine inhibits tumor growth with extremely low toxicity to normal cells. Cyproheptadine can be used in research related to hepatocellular carcinoma, multiple myeloma and acute myeloid leukemia[1][2].
In Vitro:Cyproheptadine (0-30 μM; 3-24 h) reduces cyclin D1, D2, and D3 protein and mRNA levels in human multiple myeloma (LP-1, KMS11, OCI-MY5, U266, MM1.R, OPM1, KMS12) and leukemia (OCI-AML2, OCI-AML3, HL60, OCI-M2, NB4, Jurkat) cell lines in a time- and concentration-dependent manner[2].
Cyproheptadine (0-20 μM) arrests human multiple myeloma (LP-1, MM1.S, MM1.R, KMS11) and leukemia (OCI-AML2, Jurkat) cell lines in the G0/G1 phase, reduces cellular proliferation, increases p21 expression, and decreases AP2A expression in a time- and concentration-dependent manner[2].
Cyproheptadine (0-30 μM; 24-72 h; 7-14 days) reduces viability and induces apoptosis in human multiple myeloma and leukemia cell lines and primary patient samples, inhibits clonogenic growth of primary AML samples, and exhibits reduced toxicity toward normal human hematopoietic stem cells, with cytotoxic effects occurring in a time- and concentration-dependent manner[2].
Cyproheptadine (0-30 μM; 24-48 h) induces caspase-dependent apoptosis in human multiple myeloma (OCI-MY5, OPM1, U266, LP-1) and leukemia (OCI-AML2, CEM, NB4) cell lines and murine leukemia (MDAY-D2) cells via activation of the mitochondrial pathway of caspase activation[2].
In Vivo:Cyproheptadine (36 mg/kg; i.p.; daily; 7 weeks) reduces tumor volume in a subcutaneous multiple myeloma xenograft model[2].
Cyproheptadine (10 mg/kg; i.p.; once daily; for 10 consecutive days) reduces the expression level of Cyclin D2 protein in a subcutaneous multiple myeloma xenograft model[2].
Cyproheptadine (10 mg/kg; i.p.; once daily; for 5 consecutive days) reduces the protein expression levels of cyclin D2 and cyclin D3 in subcutaneous leukemia xenograft models[2].
Cyproheptadine (40 mg/kg; i.p.; once daily for 7 consecutive days) completely eliminates malignant ascites formation in a mouse intraperitoneal leukemia model[2].
Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.
Cyproheptadine is primarily used to establish a rat model of reversible diabetes-like conditions or β-cell functional inhibition, characterized by non-fasting hyperglycemia, abnormal glucose tolerance, reduced pancreatic insulin levels, and abnormal β-cell morphology[3].
Administration: Cyproheptadine (22.5-90 mg/kg): administered orally once daily for 14 days.
Histology analysis: Vacuolization of islet tissue; vesiculation of the rough endoplasmic reticulum and loss of secretory granules in β-cells.
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