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Sorafenib/索拉非尼 {[allProObj[0].p_purity_real_show]}

货号:A316727 同义名: Bay 43-9006

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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Sorafenib/索拉非尼 化学结构 CAS号:284461-73-0
Sorafenib/索拉非尼 化学结构
CAS号:284461-73-0
Sorafenib/索拉非尼 3D分子结构
CAS号:284461-73-0
Sorafenib/索拉非尼 化学结构 CAS号:284461-73-0
Sorafenib/索拉非尼 3D分子结构 CAS号:284461-73-0
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Sorafenib/索拉非尼 纯度/质量文件 产品仅供科研

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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。

Sorafenib/索拉非尼 生物活性

靶点
  • VEGFR2

    VEGFR2, IC50:90 nM

    VEGFR2/Flk1, IC50:90 nM

  • PDGFRβ

    mPDGFRβ, IC50:57 nM

    PDGFRβ, IC50:57 nM

  • FGFR1

    FGFR1, IC50:580 nM

  • B-Raf

    B-Raf (V599E), IC50:38 nM

    B-Raf, IC50:22 nM

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]

Sorafenib/索拉非尼 细胞实验

Cell Line
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.

Sorafenib/索拉非尼 动物实验

Species
Animal Model
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

Sorafenib/索拉非尼 动物研究

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
Animal Mice[6] Rats[6] Dogs[6]
Dose 5 mg/kg (i.v. or p.o.) 5.63 mg/kg (i.v.)
4.85 mg/kg (p.o.)
5.77 mg/kg (i.v.)
5.65 mg/kg (p.o.)
Administration i.v.
p.o.
i.v.
p.o.
i.v.
p.o.
F 78.6% (p.o.) 79.1% (p.o.) 59.9% (p.o.)
AUC0→inf 33.30 mg·h/l (i.v.)
19.54 mg·h/l (p.o.)
T1/2 6.53 h (i.v.)
5.77 h (p.o.)
9.33 h (i.v.)
8.86 h (p.o.)
4.33 h (i.v.)
3.59 h (p.o.)
Tmax 1.0 (p.o.) 1.74 (p.o.) 1.59 (p.o.)
MRT 4.55 h (i.v.)
14.72 h (p.o.)
14.87 h (i.v.)
16.08 h (p.o.)
5.83 h (i.v.)
5.5 h (p.o.)
Vz/F 1.59 L/kg (p.o.) 0.71 L/kg (p.o.)
Cmax 13.17 mg/l (i.v.)
1.15 mg/l (p.o.)
8.35 mg/l (i.v.)
3.65 mg/l (p.o.)
CL 0.15 L/h/kg (i.v.)
0.19 L/h/kg (p.o.)
0.04 L/h/kg (i.v.)
0.06 L/h/kg (p.o.)
0.13 L/h/kg (i.v.)
0.21 L/h/kg (p.o.)
Vz/f 1.09 L/kg (p.o.)
Vss 0.68 L/kg (i.v.) 0.65 L/kg (i.v.) 0.74 L/kg (i.v.)
AUC 24.33 mg·h/l (i.v.)
19.13 mg·h/l (p.o.)
94.16 mg·h/l (i.v.)
64.26 mg·h/l (p.o.)

Sorafenib/索拉非尼 临床研究

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 <<

Sorafenib/索拉非尼 参考文献

[1]Wilhelm SM, Carter C, et al. BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res. 2004 Oct 1;64(19):7099-109.

[2]Huynh H, Ngo VC, et al. Sorafenib and rapamycin induce growth suppression in mouse models of hepatocellular carcinoma. J Cell Mol Med. 2009;13(8B):2673-83.

[3]El-Ashmawy NE, Khedr EG, et al. Sorafenib effect on liver neoplastic changes in rats: more than a kinase inhibitor. Clin Exp Med. 2017;17(2):185-191.

[4]Kuczynski EA, Lee CR, et al. Effects of Sorafenib Dose on Acquired Reversible Resistance and Toxicity in Hepatocellular Carcinoma. Cancer Res. 2015 Jun 15;75(12):2510-9.

[5]Iyer RV, Maguire O, et al. Dose-Dependent Sorafenib-Induced Immunosuppression Is Associated with Aberrant NFAT Activation and Expression of PD-1 in T Cells. Cancers (Basel). 2019 May 16;11(5). pii: E681.

[6]Nexavar

Sorafenib/索拉非尼 实验方案

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

Sorafenib/索拉非尼 技术信息

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

请根据您的动物给药指南选择适当的溶解方案。
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
方案 一
方案 二
方案 三
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