产品
编 号：F290068
分子式：C11H8Br2N2O2
分子量：360.01
分子式：C11H8Br2N2O2
分子量：360.01
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
5mg
询价
询价
10mg
询价
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50mg
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询价
结构图
CAS No: 244240-24-2
产品详情
生物活性：
LFM-A13 is a potent BTK, JAK2, PLK inhibitor, inhibits recombinant BTK, Plx1 and PLK3 with IC50s of 2.5 μM, 10 μM and 61 μM; LFM-A13 shows no effects on JAK1 and JAK3, Src family kinase HCK, EGFR and IRK.
体内研究：
LFM-A13 (25, 50 and 100 mg/kg) shows no apparent toxicity to rats. LFM-A13 (50 mg/kg, three times a week, i.p.) attenuatesmammary tumorigenesis in mice. LFM-A13 alone or in combination with paclitaxel shows marked effect on the breast tumor incidence, mean tumor numbers, average tumor weight, and size in BALB/c mice. LFM-A13 (50 mg/kg, three times a week, i.p.) significantly decreases PLK1, cyclin D1, CDK-4, P53 and Bcl-2 expression, but increases the expression of p21, IκB, Bax and caspase 3 expression in mice. LFM-A13 (200 mg/kg) does not cause hematologic toxicity in rats. LFM-A13 (10 or 50 mg/kg, i.p.) exhibits anti-tumor effects dose dependently in the MMTV/Neu transgenic mouse model of breast cancer.
体外研究：
LFM-A13 significantly inhibits BTK activity with an IC50 of 6.2 ± 0.3 μg/mL (= 17.2 ± 0.8 μM). The calculated Kis of LFM-A13 for BTK, JAK1, JAK3, IRK, EGFR and HCK are 1.4, 110, 148, 31.6, 166 and 214 μM. LFM-A13 (200 μM) markedly increases the chemosensitivity of ALL-1 cells to ceramide-induced apoptosis. LFM-A13 (100 μM) suppresses Epo-induced phosphorylation of EpoR, Jak2, Btk, Stat5 and Erk1/2 in R10 cells. LFM-A13 (100 μM) inhibits auto-phosphorylation of Jak2, Tec and Btk rather than Lyn kinase auto-phosphorylation in COS cells. LFM-A13 potently inhibits Plx1 with IC50 of 10 μM; also inhibits BRK, BMX, FYN and with IC50s of 267, 281, 240 and 215 μM.
LFM-A13 is a potent BTK, JAK2, PLK inhibitor, inhibits recombinant BTK, Plx1 and PLK3 with IC50s of 2.5 μM, 10 μM and 61 μM; LFM-A13 shows no effects on JAK1 and JAK3, Src family kinase HCK, EGFR and IRK.
体内研究：
LFM-A13 (25, 50 and 100 mg/kg) shows no apparent toxicity to rats. LFM-A13 (50 mg/kg, three times a week, i.p.) attenuatesmammary tumorigenesis in mice. LFM-A13 alone or in combination with paclitaxel shows marked effect on the breast tumor incidence, mean tumor numbers, average tumor weight, and size in BALB/c mice. LFM-A13 (50 mg/kg, three times a week, i.p.) significantly decreases PLK1, cyclin D1, CDK-4, P53 and Bcl-2 expression, but increases the expression of p21, IκB, Bax and caspase 3 expression in mice. LFM-A13 (200 mg/kg) does not cause hematologic toxicity in rats. LFM-A13 (10 or 50 mg/kg, i.p.) exhibits anti-tumor effects dose dependently in the MMTV/Neu transgenic mouse model of breast cancer.
体外研究：
LFM-A13 significantly inhibits BTK activity with an IC50 of 6.2 ± 0.3 μg/mL (= 17.2 ± 0.8 μM). The calculated Kis of LFM-A13 for BTK, JAK1, JAK3, IRK, EGFR and HCK are 1.4, 110, 148, 31.6, 166 and 214 μM. LFM-A13 (200 μM) markedly increases the chemosensitivity of ALL-1 cells to ceramide-induced apoptosis. LFM-A13 (100 μM) suppresses Epo-induced phosphorylation of EpoR, Jak2, Btk, Stat5 and Erk1/2 in R10 cells. LFM-A13 (100 μM) inhibits auto-phosphorylation of Jak2, Tec and Btk rather than Lyn kinase auto-phosphorylation in COS cells. LFM-A13 potently inhibits Plx1 with IC50 of 10 μM; also inhibits BRK, BMX, FYN and with IC50s of 267, 281, 240 and 215 μM.
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