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Sorafenib

CAS No. : 284461-73-0

MCE 站：Sorafenib

产品活性：Sorafenib (Bay 43-9006) 是一种有效的口服活性 Raf 抑制剂，对 Raf-1 和 B-Raf 的 IC₅₀ 分别为 6 nM 和 20 nM。Sorafenib 是一种多激酶抑制剂，对 VEGFR2，VEGFR3，PDGFRβ，FLT3 和 c-Kit 的 IC₅₀ 分别为 90 nM，15 nM，20 nM，57 nM 和 58 nM。Sorafenib 诱导细胞自噬 (autophagy) 和凋亡 (apoptosis)，并具有抗肿瘤活性。Sorafenib 也是一种 ferroptosis 激动剂。

研究领域：MAPK/ERK Pathway  |  Protein Tyrosine Kinase/RTK  |  Autophagy  |  Apoptosis

作用靶点：Raf  |  VEGFR  |  FLT3  |  Autophagy  |  Apoptosis  |  Ferroptosis

In Vitro: Sorafenib (BAY 43-9006) also inhibits BRAF^wt (IC₅₀=22 nM), BRAF^V599E (IC₅₀=38 nM), VEGFR-2 (IC₅₀=90 nM), VEGFR-3 (IC₅₀=20 nM), PDGFR-β (IC₅₀=57 nM), c-KIT (IC₅₀=68 nM), and Flt3 (IC₅₀=58 nM) in biochemical assays. In MDA-MB-231 breast cancer cells, Sorafenib completely blocks activation of the MAPK pathway. Cells are preincubated with Sorafenib (0.01 to 3 μM), and dose-dependent inhibition of basal MEK 1/2 and ERK 1/2 phosphorylation (IC₅₀, 40 and 100 nM, respectively).

In Vivo: Sorafenib demonstrates broad oral antitumor efficacy in panel of human tumor xenograft models. Sorafenib is given orally at 7.5 to 60 mg/kg. There is no lethality and no increase in weight loss in any treated group relative to the corresponding control group. Daily oral administration of Sorafenib (30 to 60 mg/kg) produces complete tumor stasis during treatment in five of the six models. The survival rate is 73.3 % in Diethyl nitrosamine (DENA) group and 83.3 % in Sorafenib group compared to 100 % in the normal control group. DENA group shows a significant increase in liver index (1.51-fold increase, p<0.05) compared to normal control group, while treatment with Sorafenib shows significant decrease (p<0.05) in liver index when compared to DENA group. The liver index in Sorafenib group significantly decreases to lower than its value in the normal control.

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