产品
编 号：F272756
分子式：C48H55N11O10
分子量：946.02
分子式：C48H55N11O10
分子量：946.02
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
结构图
CAS No: 2140289-17-2
产品详情
生物活性：
BETd-246 is a second-generation and PROTAC-based BET bromodomain (BRD) inhibitor connected by ligands for Cereblon and BET, exhibiting superior selectivity, potency and antitumor activity.
体内研究：
BETd-246 (5 mg/kg, IV, 3 times per week for 3 weeks) treatment effectively inhibits WHIM24 tumor growth, similar to the antitumor activity of BETi-211 with higher dosage and more frequently administration. The treatment of 10 mg/kg induces partial tumor regression during treatment without apparent toxicity. BETd-246 has very limited drug exposure in the xenograft tumor tissue in MDA-M-231and MDA-MB-468 models.Animal Model:“Washington Human in Mouse (WHIM)” (PDX) model developed from a patient with treatment-resistant breast cancer (ESRE380Q, PR- and HER2-)).
Dosage:5, 10 mg/kg
Administration:IV, 3 times per week for 3 weeks.
Result:Effectively inhibited WHIM24 tumor growth.
体外研究：
BETd-246 treatment (0-100 nM, 1-3 h) causes a dose-dependent depletion of BRD2, BRD3 and BRD4 in representative TNBC cell lines with 30-100 nM for 1 h or with 10-30 nM for 3 h incubation. BETd-246 (100 nM, 24/48 hours) displays strong growth inhibition and apoptosis induction activity in MDA-MB-468 cell lines. BETd-246 induces a rapid and time-dependent downregulation of MCL1 protein in all the TNBC cell lines evaluated. BETd-246 induces much stronger apoptosis than BETi-211.BETd-246 (100 nM, 24 hours) induces pronounced cell cycle arrest and apoptosis in TNBC cell lines.
BETd-246 is a second-generation and PROTAC-based BET bromodomain (BRD) inhibitor connected by ligands for Cereblon and BET, exhibiting superior selectivity, potency and antitumor activity.
体内研究：
BETd-246 (5 mg/kg, IV, 3 times per week for 3 weeks) treatment effectively inhibits WHIM24 tumor growth, similar to the antitumor activity of BETi-211 with higher dosage and more frequently administration. The treatment of 10 mg/kg induces partial tumor regression during treatment without apparent toxicity. BETd-246 has very limited drug exposure in the xenograft tumor tissue in MDA-M-231and MDA-MB-468 models.Animal Model:“Washington Human in Mouse (WHIM)” (PDX) model developed from a patient with treatment-resistant breast cancer (ESRE380Q, PR- and HER2-)).
Dosage:5, 10 mg/kg
Administration:IV, 3 times per week for 3 weeks.
Result:Effectively inhibited WHIM24 tumor growth.
体外研究：
BETd-246 treatment (0-100 nM, 1-3 h) causes a dose-dependent depletion of BRD2, BRD3 and BRD4 in representative TNBC cell lines with 30-100 nM for 1 h or with 10-30 nM for 3 h incubation. BETd-246 (100 nM, 24/48 hours) displays strong growth inhibition and apoptosis induction activity in MDA-MB-468 cell lines. BETd-246 induces a rapid and time-dependent downregulation of MCL1 protein in all the TNBC cell lines evaluated. BETd-246 induces much stronger apoptosis than BETi-211.BETd-246 (100 nM, 24 hours) induces pronounced cell cycle arrest and apoptosis in TNBC cell lines.
产品资料
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