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编 号：F762441
分子式：C32H72Cl4N6O2
分子量：714.77
分子式：C32H72Cl4N6O2
分子量：714.77
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是否有货
1mg
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询价
5mg
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询价
10mg
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CAS No: 2444815-84-1
产品详情
生物活性：
AMXT-1501 tetrahydrochloride is an orally active polyamine transport inhibitor. AMXT1501 blocks tumor growth in immunocompetent mice but not in athymic nude mice lacking T cells. Combination of DFMO and AMXT‐1501 induces caspase‐3 mediated apoptosis in NB cell lines.
体内研究：
AMXT-1501 tetrahydrochloride (3 mg/kg; subcutaneous injection; every day; 28 days) alone is sufficient to delay EAE onset moderately,but fails to protect animals from reaching the endpoint. However, the combination of DFMO and AMXT-1501 tetrahydrochloride are sufficient to deplete T cell polyamine pool, and consequently suppress T cell proliferation and effector function in vivo.Animal Model:C57BL/6 (WT) and ODC knockout strain (ODC cKO) mice bearing experimental autoimmune encephalomyelitis (EAE) model
Dosage:3 mg/kg
Administration:Subcutaneous injection; every day; 28 days
Result:Displayed a delayed disease onset initially, but eventually proceeded with pathologic development and reached the endpoint.
体外研究：
AMXT-1501 tetrahydrochloride (0.39-50 μM; 48 hours) treatment exhibits cytotoxicity against this panel of NB cell lines (BE(2)-C, SMS-KCNR and SH-SY5Y cells), with IC50 values of 17.72 μM for SMS-KCNR, 17.69?μM for BE(2)-C, and 14.13?μM for SH-SY5Y.BE(2)‐C, SMS‐KCNR and SH‐SY5Y cells are exposed to AMXT-1501 tetrahydrochloride (2.5 μM) and DFMO (2.5 mM) alone or in combination (AMXT-1501 tetrahydrochloride 2.5 μM + DFMO 2.5 mM). After 96 hours exposure to AMXT-1501 tetrahydrochloride or DFMO does not significantly alter the level of noncleaved PARP, cleaved PARP and cleaved caspase 3, whereas cells treated with the combination of AMXT-1501 tetrahydrochloride with DFMO decrease the amount of noncleaved PARP and increase the amount of cleaved PARP and cleaved caspase 3.
AMXT-1501 tetrahydrochloride is an orally active polyamine transport inhibitor. AMXT1501 blocks tumor growth in immunocompetent mice but not in athymic nude mice lacking T cells. Combination of DFMO and AMXT‐1501 induces caspase‐3 mediated apoptosis in NB cell lines.
体内研究：
AMXT-1501 tetrahydrochloride (3 mg/kg; subcutaneous injection; every day; 28 days) alone is sufficient to delay EAE onset moderately,but fails to protect animals from reaching the endpoint. However, the combination of DFMO and AMXT-1501 tetrahydrochloride are sufficient to deplete T cell polyamine pool, and consequently suppress T cell proliferation and effector function in vivo.Animal Model:C57BL/6 (WT) and ODC knockout strain (ODC cKO) mice bearing experimental autoimmune encephalomyelitis (EAE) model
Dosage:3 mg/kg
Administration:Subcutaneous injection; every day; 28 days
Result:Displayed a delayed disease onset initially, but eventually proceeded with pathologic development and reached the endpoint.
体外研究：
AMXT-1501 tetrahydrochloride (0.39-50 μM; 48 hours) treatment exhibits cytotoxicity against this panel of NB cell lines (BE(2)-C, SMS-KCNR and SH-SY5Y cells), with IC50 values of 17.72 μM for SMS-KCNR, 17.69?μM for BE(2)-C, and 14.13?μM for SH-SY5Y.BE(2)‐C, SMS‐KCNR and SH‐SY5Y cells are exposed to AMXT-1501 tetrahydrochloride (2.5 μM) and DFMO (2.5 mM) alone or in combination (AMXT-1501 tetrahydrochloride 2.5 μM + DFMO 2.5 mM). After 96 hours exposure to AMXT-1501 tetrahydrochloride or DFMO does not significantly alter the level of noncleaved PARP, cleaved PARP and cleaved caspase 3, whereas cells treated with the combination of AMXT-1501 tetrahydrochloride with DFMO decrease the amount of noncleaved PARP and increase the amount of cleaved PARP and cleaved caspase 3.
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