Sorafenib是一种多靶点激酶抑制剂,能够抑制 Raf-1 和 B-RAF(IC50 分别为 6 和 22 µM),以及受体酪氨酸激酶 VEGFR2、VEGFR3、PDGFRβ、FLT3 和 c-Kit(IC50 分别为 90、15、20、57 和 58 nM)。
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| Limited Quantity | USD 15-60 |
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| 产品名称 | c-Kit ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Tyrphostin AG1296 |
+
c-Kit (Swiss 3T3), IC50: 1.8 μM |
PDGFR | 99%+ | ||||||||||||||||
| Masitinib |
+
Kit, IC50: 200 nM |
99%+ | |||||||||||||||||
| Motesanib Diphosphate |
+++
Kit, IC50: 8 nM |
97% | |||||||||||||||||
| Ki8751 |
++
c-Kit, IC50: 40 nM |
99% | |||||||||||||||||
| Tivozanib |
++
c-Kit, IC50: 78 nM |
99%+ | |||||||||||||||||
| Pazopanib |
+
c-Kit, IC50: 140 nM |
99% | |||||||||||||||||
| Sitravatinib |
+++
Kit, IC50: 6 nM |
99%+ | |||||||||||||||||
| Pexidartinib |
+++
Kit, IC50: 10 nM |
99%+ | |||||||||||||||||
| Lactate |
++++
c-Kit, IC50: 2 nM |
FLT3 | 85% | ||||||||||||||||
| Amuvatinib |
+++
c-Kit (D816H), IC50: 10 nM |
99%+ | |||||||||||||||||
| Imatinib Mesylate |
+
c-Kit, IC50: 100 nM |
PDGFR | 99% | ||||||||||||||||
| AZD2932 |
+++
c-Kit, IC50: 9 nM |
99% | |||||||||||||||||
| Axitinib |
++++
Kit, IC50: 1.7 nM |
98% | |||||||||||||||||
| Dovitinib |
++++
c-Kit, IC50: 2 nM |
FLT3 | 99%+ | ||||||||||||||||
| Sunitinib | ✔ | FLT3 | 98% | ||||||||||||||||
| OSI-930 |
+
Kit, IC50: 80 nM |
99%+ | |||||||||||||||||
| Telatinib |
++++
c-Kit, IC50: 1 nM |
99%+ | |||||||||||||||||
| Dasatinib monohydrate |
++
c-Kit (wt), IC50: 79 nM c-Kit (D816V), IC50: 37 nM |
Src | 98% | ||||||||||||||||
| Dasatinib |
++
c-Kit (wt), IC50: 79 nM c-Kit (D816V), IC50: 37 nM |
Src | 98% | ||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | PDGFR ↓ ↑ | PDGFRα ↓ ↑ | PDGFRβ ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Tyrphostin A9 |
+
PDGFR, IC50: 0.5 μM |
EGFR | 98% | ||||||||||||||||
| Tyrphostin AG1296 | 99%+ | ||||||||||||||||||
| Motesanib Diphosphate |
++
PDGFR, IC50: 84 nM |
97% | |||||||||||||||||
| Pazopanib |
++
PDGFR, IC50: 84 nM |
99% | |||||||||||||||||
| Imatinib |
+
PDGFR, IC50: 100 nM |
c-Kit | 98% | ||||||||||||||||
| Imatinib Mesylate |
+
PDGFR, IC50: 100 nM |
c-Kit | 99% | ||||||||||||||||
| Sennoside B | ✔ | 99%+ | |||||||||||||||||
| PP121 |
++++
PDGFR, IC50: 2 nM |
VEGFR,mTOR | 99%+ | ||||||||||||||||
| Crenolanib |
++++
PDGFRα, Kd: 2.1 nM |
++++
PDGFRβ, Kd: 3.2 nM |
99%+ | ||||||||||||||||
| Masitinib |
+
PDGFRα, IC50: 540 nM |
+
PDGFRβ, IC50: 800 nM |
99%+ | ||||||||||||||||
| Ki8751 |
++
PDGFRα, IC50: 67 nM |
c-Kit | 99% | ||||||||||||||||
| Tivozanib |
++
PDGFRα, IC50: 40 nM |
++
PDGFRβ, IC50: 49 nM |
99%+ | ||||||||||||||||
| Ponatinib |
++++
PDGFRα, IC50: 1.1 nM |
98% | |||||||||||||||||
| Amuvatinib |
++
PDGFRα (V561D), IC50: 40 nM |
99%+ | |||||||||||||||||
| Axitinib |
+++
PDGFRα, IC50: 5.0 nM |
++++
PDGFRβ, IC50: 1.6 nM |
98% | ||||||||||||||||
| CP-673451 |
+++
PDGFRα, IC50: 10 nM |
++++
PDGFRβ, IC50: 1 nM |
99%+ | ||||||||||||||||
| Telatinib |
+++
PDGFRα, IC50: 15 nM |
c-Kit | 99%+ | ||||||||||||||||
| Nintedanib |
++
PDGFRα, IC50: 59 nM |
++
PDGFRβ, IC50: 65 nM |
99+% | ||||||||||||||||
| Avapritinib |
++++
PDGFRα (D842V), IC50: 0.5 nM |
99%+ | |||||||||||||||||
| MK-2461 |
+++
PDGFRβ, IC50: 22 nM |
98%+ | |||||||||||||||||
| Lactate |
+++
PDGFRβ, IC50: 27 nM |
FLT3,c-Kit | 85% | ||||||||||||||||
| Linifanib |
++
PDGFRβ, IC50: 66 nM |
99%+ | |||||||||||||||||
| AZD2932 |
+++
PDGFRβ, IC50: 4 nM |
c-Kit | 99% | ||||||||||||||||
| Dovitinib |
+++
PDGFRβ, IC50: 27 nM |
FLT3,c-Kit | 99%+ | ||||||||||||||||
| Sorafenib |
++
mPDGFRβ, IC50: 57 nM PDGFRβ, IC50: 57 nM |
99% | |||||||||||||||||
| Sunitinib |
++++
PDGFRβ , IC50: 2 nM |
FLT3 | 98% | ||||||||||||||||
| Orantinib |
+++
PDGFRβ, Ki: 8 nM |
99%+ | |||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | FLT3 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| R406 | ✔ | Syk | 98% | ||||||||||||||||
| Go6976 | ✔ | 99%+ | |||||||||||||||||
| Quizartinib |
+++
FLT3 (WT), IC50: 4.2 nM FLT3 (ITD), IC50: 1.1 nM |
98% | |||||||||||||||||
| Gilteritinib |
++++
FLT3, IC50: 0.29 nM |
99%+ | |||||||||||||||||
| Amuvatinib |
+
FLT3 (D835Y), IC50: 81 nM |
99%+ | |||||||||||||||||
| Pacritinib |
++
FLT3, IC50: 22 nM FLT3 (D835Y), IC50: 6 nM |
97% | |||||||||||||||||
| Dovitinib |
++++
FLT3, IC50: 1 nM |
c-Kit | 99%+ | ||||||||||||||||
| Denfivontinib |
++++
FLT3, IC50: 0.4 nM FLT3 (D835Y), IC50: 0.4 nM |
RET | 99%+ | ||||||||||||||||
| TAK-659 HCl |
++
FLT3, IC50: 4.6 nM |
Syk | 99%+ | ||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | A-raf ↓ ↑ | B-Raf ↓ ↑ | C-Raf/Raf-1 ↓ ↑ | Raf ↓ ↑ | 其他靶点 | 纯度 | |||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Encorafenib | ✔ | 99%+ | |||||||||||||||||
| GDC-0879 |
++++
B-Raf, IC50: 0.13 nM |
99%+ | |||||||||||||||||
| SB-590885 |
++++
B-Raf, Ki: 0.16 nM |
99%+ | |||||||||||||||||
| RAF265 | 99%+ | ||||||||||||||||||
| Dabrafenib |
++++
B-Raf, IC50: 5.2 nM B-Raf (V600E), IC50: 0.7 nM |
+++
C-Raf, IC50: 6.3 nM |
98% | ||||||||||||||||
| Lifirafenib |
++++
WT A-RAF, IC50: 1 nM |
++
BRAF WT, IC50: 32 nM BRAF(V600E), IC50: 23 nM |
+++
C-RAF (Y340/341D), IC50: 7 nM |
EGFR | 98% | ||||||||||||||
| ZM 336372 |
+
C-Raf, IC50: 70 nM |
99%+ | |||||||||||||||||
| NVP-BHG 712 |
+
C-Raf, IC50: 0.395 μM |
99%+ | |||||||||||||||||
| CCT196969 |
+
BRAF, IC50: 0.1 μM |
++
CRAF, IC50: 0.01 μM |
Src | 98% | |||||||||||||||
| Vemurafenib |
++
B-Raf, IC50: 100 nM B-Raf (V600E), IC50: 31 nM |
+
C-Raf, IC50: 48 nM |
98+% | ||||||||||||||||
| PLX4720 |
++
B-Raf, IC50: 160 nM B-Raf (V600E), IC50: 13 nM |
+++
C-Raf-1 (Y340D/Y341D), IC50: 6.7 nM |
BRK | 99+% | |||||||||||||||
| GW 5074 |
+++
C-Raf, IC50: 9 nM |
99%+ | |||||||||||||||||
| Avutometinib |
+++
BRAF, IC50: 19 nM BRAF V600E, IC50: 8.2 nM |
+
CRAF, IC50: 56 nM |
98% | ||||||||||||||||
| LY3009120 |
++++
BRAF WT, IC50: 15 nM BRAF(V600E), IC50: 5.8 nM |
++++
C-Raf, IC50: 4.3 nM |
99%+ | ||||||||||||||||
| Agerafenib |
++
B-Raf, Kd: 36 nM B-Raf (V600E), Kd: 14 nM |
+
C-Raf, Kd: 39 nM |
RET | 99%+ | |||||||||||||||
| TAK-632 |
+++
B-Raf, IC50: 8.3 nM |
++++
C-Raf, IC50: 1.4 nM |
99%+ | ||||||||||||||||
| AZ 628 |
+
B-Raf, IC50: 105 nM B-Raf (V600E), IC50: 34 nM |
++
C-Raf-1, IC50: 29 nM |
98% | ||||||||||||||||
| PLX7904 | ✔ | 98+% | |||||||||||||||||
| Sorafenib |
++
B-Raf (V599E), IC50: 38 nM B-Raf, IC50: 22 nM |
++++
Raf-1, IC50: 6 nM |
++++
Raf-1, IC50: 6 nM |
99% | |||||||||||||||
| Tovorafenib | ✔ | 99%+ | |||||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 产品名称 | VEGFR1 ↓ ↑ | VEGFR2 ↓ ↑ | VEGFR3 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Motesanib Diphosphate |
++++
VEGFR1, IC50: 2 nM |
++++
VEGFR2, IC50: 3 nM VEGFR2/Flk1, IC50: 3 nM |
+++
VEGFR3, IC50: 6 nM |
RET,PDGFR | 97% | ||||||||||||||
| Tivozanib |
++
VEGFR1, IC50: 30 nM |
+++
VEGFR2, IC50: 6.5 nM |
++
VEGFR3, IC50: 15 nM |
99%+ | |||||||||||||||
| Brivanib |
+
VEGFR1, IC50: 380 nM |
++
Flk1, IC50: 25 nM VEGFR2, IC50: 25 nM |
99%+ | ||||||||||||||||
| Regorafenib |
+++
VEGFR1, IC50: 13 nM |
+++
VEGFR2, IC50: 4.2 nM |
+
VEGFR3, IC50: 46 nM |
RET | 98% | ||||||||||||||
| Pazopanib |
+++
VEGFR1, IC50: 10 nM |
++
VEGFR2, IC50: 30 nM |
+
VEGFR3, IC50: 47 nM |
FGFR,PDGFR,c-Kit | 99% | ||||||||||||||
| Sitravatinib |
+++
VEGFR1 (FLT1), IC50: 6 nM |
+++
VEGFR2 (KDR), IC50: 5 nM |
++++
VEGFR3 (FLT4), IC50: 2 nM |
99%+ | |||||||||||||||
| Foretinib |
+++
VEGFR1/FLT1, IC50: 6.8 nM |
++++
KDR, IC50: 0.86 nM |
++++
VEGFR3/FLT4, IC50: 2.8 nM |
Tie-2 | 99%+ | ||||||||||||||
| MGCD-265 analog |
++++
VEGFR1, IC50: 3 nM |
++++
VEGFR2, IC50: 3 nM |
++++
VEGFR3, IC50: 4 nM |
Tie-2 | 99%+ | ||||||||||||||
| Lactate |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
FLT3,c-Kit | 85% | ||||||||||||||
| AEE788 |
+
FLT1, IC50: 59 nM |
+
KDR, IC50: 77 nM |
EGFR | 98+% | |||||||||||||||
| Linifanib |
++++
VEGFR1/FLT1, IC50: 3 nM |
++++
VEGFR2/KDR, IC50: 4 nM |
+
VEGFR3/FLT4, IC50: 190 nM |
FLT3 | 99%+ | ||||||||||||||
| Vatalanib 2HCl |
+
VEGFR1/FLT1, IC50: 77 nM |
++
VEGFR2/KDR, IC50: 37 nM VEGFR2/Flk1, IC50: 270 nM |
+
VEGFR3/FLT4, IC50: 660 nM |
c-Fms/CSF1R,c-Kit | 99%+ | ||||||||||||||
| Axitinib |
++++
VEGFR1/FLT1, IC50: 0.1 nM |
++++
VEGFR2/KDR, IC50: 0.2 nM VEGFR2/Flk1, IC50: 0.18 nM |
98% | ||||||||||||||||
| Dovitinib |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
FLT3,c-Kit | 99%+ | ||||||||||||||
| ZM 306416 |
+
VEGFR1, IC50: 0.33 μM |
Src | 99%+ | ||||||||||||||||
| KRN-633 |
+
VEGFR1, IC50: 170 nM |
+
VEGFR2, IC50: 160 nM |
+
VEGFR3, IC50: 125 nM |
BTK,c-Kit | 98% | ||||||||||||||
| OSI-930 |
+++
FLT1, IC50: 8 nM |
+++
KDR, IC50: 9 nM |
99%+ | ||||||||||||||||
| Lenvatinib |
++
VEGFR1/FLT1, IC50: 22 nM |
++++
VEGFR2/KDR, IC50: 4.0 nM |
+++
VEGFR3/FLT4, IC50: 5.2 nM |
98% | |||||||||||||||
| NVP-BAW2881 |
+
hVEGFR1, IC50: 820 nM |
+++
hVEGFR2, IC50: 9 nM mVEGF2, IC50: 165 nM |
+
hVEGFR3, IC50: 420 nM |
99% | |||||||||||||||
| Cediranib |
+++
VEGFR1/FLT1, IC50: 5 nM |
++++
VEGFR2/KDR, IC50: 0.5 nM |
c-Kit | 99%+ | |||||||||||||||
| Nintedanib |
++
VEGFR1, IC50: 34 nM |
+++
VEGFR2, IC50: 13 nM |
+++
VEGFR3, IC50: 13 nM |
FLT3 | 99+% | ||||||||||||||
| BMS-794833 |
++
VEGFR2, IC50: 15 nM |
99%+ | |||||||||||||||||
| SKLB1002 |
++
VEGFR2, IC50: 32 nM |
99% | |||||||||||||||||
| Cabozantinib S-malate |
++++
VEGFR2/KDR, IC50: 0.035 nM |
99+% | |||||||||||||||||
| Ki8751 |
++++
VEGFR2, IC50: 0.9 nM |
c-Kit | 99% | ||||||||||||||||
| SU 5402 |
++
VEGFR2, IC50: 20 nM |
98% | |||||||||||||||||
| Apatinib mesylate |
++++
VEGFR2, IC50: 1 nM |
RET | 98+% | ||||||||||||||||
| Ponatinib |
++++
VEGFR2, IC50: 1.5 nM |
98% | |||||||||||||||||
| LY2874455 |
+++
VEGFR2, IC50: 7 nM |
99%+ | |||||||||||||||||
| ZM323881 HCl |
++++
VEGFR2, IC50: <2 nM |
98% | |||||||||||||||||
| AZD2932 |
+++
VEGFR-2, IC50: 8 nM |
c-Kit | 99% | ||||||||||||||||
| Cabozantinib |
++++
VEGFR2/KDR, IC50: 0.035 nM |
98% | |||||||||||||||||
| Sorafenib |
++
VEGFR2, IC50: 90 nM VEGFR2/Flk1, IC50: 90 nM |
99% | |||||||||||||||||
| CYC-116 |
++
VEGFR2, Ki: 44 nM |
FLT3 | 99%+ | ||||||||||||||||
| Golvatinib |
++
VEGFR2, IC50: 16 nM |
99%+ | |||||||||||||||||
| Sunitinib |
+
VEGFR2 , IC50: 80 nM |
FLT3 | 98% | ||||||||||||||||
| RAF265 |
++
VEGFR2, EC50: 30 nM |
99%+ | |||||||||||||||||
| PD173074 | 99%+ | ||||||||||||||||||
| BFH772 |
++++
VEGFR2, IC50: 3 nM |
98% | |||||||||||||||||
| Semaxinib |
+
VEGFR2/Flk1, IC50: 1.23 μM |
98% | |||||||||||||||||
| Vandetanib |
++
VEGFR2, IC50: 40 nM |
+
VEGFR3, IC50: 110 nM |
EGFR | 99% | |||||||||||||||
| SAR131675 |
++
VEGFR3, IC50: 23 nM |
99%+ | |||||||||||||||||
| ENMD-2076 |
+
VEGFR2/KDR, IC50: 58.2 nM |
++
VEGFR3/FLT4, IC50: 15.9 nM |
RET,FLT3 | 98% | |||||||||||||||
| Telatinib |
+++
VEGFR2, IC50: 6 nM |
++++
VEGFR3, IC50: 4 nM |
c-Kit | 99%+ | |||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 靶点 |
|
| 描述 | The RAS/RAF signaling pathway is an important mediator of tumor cell proliferation and angiogenesis. Sorafenib is a multitargeted inhibitor with IC50 values of 6nM, 22nM and 38nM for Raf-1, wt-BRAF and BRAF-V599E mutant, respectively, as well as less potent to mVEGFR2, mVEGFR3, mPDGFRβ, FLT3, c-Kit, VEGFR2 and FGFR1 with IC50 values of 15nM, 20nM, 57nM, 58nM, 68nM, 90nM and 580nM (measured by kinase assays), respectively. Sorafenib inhibited activation of the RAF/MEK/ERK pathway at concentration below 15μM, performing by suppressing p-Erk, in most of cell lines tested (like MDA-MB-231. Mia PaCa 2, HCT 116 and HT-29) independent of which mutation caused aberrant activation of the RAS/RAF pathway. Sorafenib targeted receptor tyrosine kinases and inhibited autophosphorylation of VEGFR-2 and PDGFR-β induced by VEGF165 (30ng/ml) in HUVECs/ NIH 3T3 cells and PDGF BB (10ng/ml) in HAoSMCs, respectively. Oral treatment with Sorafenib, at dose of 7.5-60mg/kg daily for 9 days, illustrated a spectrum of antitumor efficacy in a representative panel of tumor xenograft models in a dose-dependent manner, including MDA-MB-231, Colo-205, HT-29, DLD-1, NCI-H460 and A549. Sorafenib showed significant tumor angiogenesis activity, performing as daily oral administration of 30 or 60 mg/kg Sorafenib produced 50-80% inhibition of microvessel area and microvessel density compared with vehicle group in HT-29 tumors[1]. |
| 作用机制 | Sorafenib is a multitargeted ATP-competitive inhibitor.[1] |
| Concentration | Treated Time | Description | References | |
| AML12 and BNLCL.2 cells | 2 μM | 5 days | Evaluation of toxicity in untransformed liver cells, showing that compound 40 combined with sorafenib had low toxicity in normal liver cells | J Med Chem. 2025 Apr 10;68(7):7180-7196 |
| Hep3B cells | 1.7 μM | 5 days | Assessment of cell viability, showing that compound 40 combined with sorafenib significantly reduced Hep3B cell viability | J Med Chem. 2025 Apr 10;68(7):7180-7196 |
| L02 hepatocytes | 10 μM | 18 h | To investigate the effects of Sorafenib on lipid accumulation and inflammation, the results showed that Sorafenib significantly reduced lipid accumulation in L02 hepatocytes and suppressed the expression of inflammatory factors. | Cell Metab. 2020 May 5;31(5):892-908.e11. |
| Huh7 | 10 μM | 24 h | To investigate Sorafenib-induced macropinocytosis and its effect on ferroptosis. Results showed that Sorafenib induced macropinocytosis through activation of PI3K-RAC1-PAK1 signaling, replenishing intracellular cysteine and conferring resistance to Sorafenib. | J Exp Clin Cancer Res. 2022 Mar 14;41(1):98. |
| SK-Hep1 | 10 μM | 24 h | To investigate Sorafenib-induced macropinocytosis and its effect on ferroptosis. Results showed that Sorafenib induced macropinocytosis through activation of PI3K-RAC1-PAK1 signaling, replenishing intracellular cysteine and conferring resistance to Sorafenib. | J Exp Clin Cancer Res. 2022 Mar 14;41(1):98. |
| MHCC97L | 10 µM | 24 h | To assess the effect of Sorafenib on cell viability, the results showed that Sorafenib significantly reduced cell viability. | J Exp Clin Cancer Res. 2024 May 14;43(1):143. |
| MHCC97H | 10 µM | 24 h | To assess the effect of Sorafenib on cell viability, the results showed that Sorafenib significantly reduced cell viability. | J Exp Clin Cancer Res. 2024 May 14;43(1):143. |
| MOLM-13 cells | 0.1 μM | 24 h | Sorafenib increased IL-15 production by inhibiting ATF4 expression, thereby activating the IRF7/IL-15 axis. | Nat Med. 2018 Mar;24(3):282-291. |
| MV4-11 cells | 0.1 μM | 24 h | Sorafenib increased IL-15 production by inhibiting ATF4 expression, thereby activating the IRF7/IL-15 axis. | Nat Med. 2018 Mar;24(3):282-291. |
| Ba/F3-ITD cells | 10 nM | 24 h | Sorafenib increased IL-15 production by inhibiting ATF4 expression, thereby activating the IRF7/IL-15 axis. | Nat Med. 2018 Mar;24(3):282-291. |
| HSC-T6 cells | 10 μM | 24 h | To investigate the effect of Sorafenib on ferroptosis in HSC-T6 cells, results showed that Sorafenib significantly inhibited cell growth and induced ferroptosis. | Autophagy. 2020 Aug;16(8):1482-1505. |
| HSC-LX2 cells | 10 μM | 24 h | To investigate the effect of Sorafenib on ferroptosis in HSC-LX2 cells, results showed that Sorafenib significantly inhibited cell growth and induced ferroptosis. | Autophagy. 2020 Aug;16(8):1482-1505. |
| HSC-T6 | 5 μM | 24 h | To evaluate the effect of Sorafenib on HSC-T6 cells, the results showed that Sorafenib induced ferroptosis, which was validated by the inhibition of the ferroptosis inhibitor ferrostatin-1. | Autophagy. 2018;14(12):2083-2103. |
| HSC-LX2 | 5 μM | 24 h | To evaluate the effect of Sorafenib on HSC-LX2 cells, the results showed that Sorafenib induced ferroptosis, which was validated by the inhibition of the ferroptosis inhibitor ferrostatin-1. | Autophagy. 2018;14(12):2083-2103. |
| HT-29 colorectal cancer cells | 6 μM | 24 h | To study the effect of sorafenib on ERK1/2 and CSE1L phosphorylation in HT-29 cells. Results showed that sorafenib treatment inhibited ERK1/2 and CSE1L phosphorylation. | J Transl Med. 2015 Jun 13;13:191. |
| Administration | Dosage | Frequency | Description | References | ||
| Mice | Akt1Myr;MycOE HCC organoids | In vitro culture | 4 μM | 5 days | Assessment of therapeutic efficacy, showing that compound 40 combined with sorafenib exhibited significant therapeutic effects in HCC organoids | J Med Chem. 2025 Apr 10;68(7):7180-7196 |
| Mice | NASH-HCC model | Oral | 15 mg/kg/2 days | Every 2 days for 8 weeks | To evaluate the therapeutic effects of low-dose Sorafenib on the NASH-HCC model, the results showed that Sorafenib significantly reduced tumor incidence and size, and improved major pathological features of NASH, including steatosis, inflammation, and fibrosis. | Cell Metab. 2020 May 5;31(5):892-908.e11. |
| Mice | SK-Hep1 and Huh7 xenograft models | Intraperitoneal injection | 5 mg/kg | Daily for 3 days | To investigate the effect of combined Sorafenib and Amiloride treatment on tumor growth. Results showed that Amiloride enhanced the antitumor effect of Sorafenib by inhibiting macropinocytosis, significantly suppressing tumor growth. | J Exp Clin Cancer Res. 2022 Mar 14;41(1):98. |
| BALB/c nude mice | Subcutaneous tumor model and orthotopic tumor model | Oral | 10 mg/kg | Once daily for two weeks | To evaluate the efficacy of Sorafenib in inhibiting tumor growth, the results showed that Sorafenib significantly inhibited tumor growth. | J Exp Clin Cancer Res. 2024 May 14;43(1):143. |
| Mice | Bile duct ligation-induced liver fibrosis model | Intraperitoneal injection | 10 mg/kg | Once every other day for 2 weeks | To investigate the effect of Sorafenib on liver fibrosis in mice, results showed that Sorafenib significantly alleviated liver fibrosis and induced HSC ferroptosis. | Autophagy. 2020 Aug;16(8):1482-1505. |
| Mice | Bile duct ligation (BDL)-induced liver fibrosis model | Intraperitoneal injection | 10 mg/kg | Once every other day for 2 weeks | To evaluate the effect of Sorafenib on murine liver fibrosis, the results showed that Sorafenib alleviated liver fibrosis by inducing HSC ferroptosis. | Autophagy. 2018;14(12):2083-2103. |
| C57BL/6 mice | Subcutaneous Hepa1-6 liver cancer model | Oral gavage | 10 mg/kg | Daily for 12 days | To evaluate the antitumor effects of low-dose Sorafenib alone or in combination with R848 in a liver cancer model. The results showed that the combination of low-dose Sorafenib with R848 significantly enhanced antitumor activity with no obvious toxic side effects. | Adv Sci (Weinh). 2023 Jun;10(18):e2207650 |
| Nude Balb/c mice | HepG2/SOR tumor model | Intravenous injection | 5 mg/kg | Every two days for a total of four injections, lasting 14 days | To evaluate the anti-tumor effect of CTNP-PMS/SOR in the HepG2/SOR tumor model. Results showed that CTNP-PMS/SOR significantly inhibited tumor growth and prolonged the survival time of mice. | Drug Deliv. 2019 Dec;26(1):1080-1091 |
| Dose | Mice: 30 mg/kg, 60 mg/kg[4] (p.o.), 10 mg/kg - 100 mg/kg[2] (p.o.) Woodchucks: 2.5 mg/kg, 5 mg/kg[5] (p.o.) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Administration | p.o. | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Pharmacokinetics |
|
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
| NCT03565536 | Thyroid Cancer, Anaplastic | Phase 2 | Recruiting | October 30, 2019 | China, Fujian ... 展开 >> Fujian Medical University Union Hospital Recruiting FuZhou, Fujian, China, 350001 Contact: bo wang, md 13705947900 wangbo@fjmu.edu.cn 收起 << |
| NCT00984425 | Solid Tumors | Phase 1 | Completed | - | Italy ... 展开 >> Istituto Clinco Humanitas Rozzano, Milano, Italy, 20089 收起 << |
| NCT01259193 | Hepatocellular Carcinoma | Phase 2 | Unknown | July 2012 | China, Shanghai ... 展开 >> Liver Cancer Institute Recruiting Shanghai, Shanghai, China, 200032 Contact: Zheng-Gang Ren, Ph.D 0086-021-64041990 ext 2137 ren.zhenggang@zs-hospital.sh.cn Contact: Lan Zhang, Master 0086-021-64041990 ext 2171 zhang.lan@zs-hospital.sh.cn Principal Investigator: Zheng-Gang Ren, Ph.D Sub-Investigator: Jubo Zhang, PhD 收起 << |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
2.15mL 0.43mL 0.22mL |
10.76mL 2.15mL 1.08mL |
21.51mL 4.30mL 2.15mL |
|
| CAS号 | 284461-73-0 |
| 分子式 | C21H16ClF3N4O3 |
| 分子量 | 464.83 |
| SMILES Code | O=C(NC)C1=NC=CC(OC2=CC=C(NC(NC3=CC=C(Cl)C(C(F)(F)F)=C3)=O)C=C2)=C1 |
| MDL No. | MFCD06411450 |
| 别名 | Bay 43-9006 |
| 运输 | 蓝冰 |
| InChI Key | MLDQJTXFUGDVEO-UHFFFAOYSA-N |
| Pubchem ID | 216239 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry,2-8°C |
| 溶解方案 |
DMSO: 45 mg/mL(96.81 mM),注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
|
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