货号:A177150
同义名:
瑞格非尼
/ BAY 73-4506; Fluoro-Sorafenib
Regorafenib(BAY 73-4506)是一种口服活性和高效的多靶点受体酪氨酸激酶抑制剂,对VEGFR1/2/3、PDGFRβ、Kit、RET和Raf-1的IC50值分别为13/4.2/46、22、7、1.5和2.5 nM。Regorafenib显示出强大的抗肿瘤和抗血管生成活性。


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| 产品名称 | c-RET ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Regorafenib |
+++
RET, IC50: 1.5 nM |
98% | |||||||||||||||||
| TG101209 |
++
RET, IC50: 17 nM |
FLT3 | 99%+ | ||||||||||||||||
| Danusertib |
+
RET, IC50: 31 nM |
99%+ | |||||||||||||||||
| AD80 |
++++
RET wt, IC50: 1.3 nM RET V804M, IC50: 0.6 nM |
Raf,Src | 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/Flk1, IC50: 3 nM VEGFR2, 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 |
c-Kit,FGFR,PDGFR | 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/Flk1, IC50: 90 nM VEGFR2, 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 |
FLT3,RET | 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 | Regorafenib strongly prevents VEGFR2 autophosphorylation in NIH-3T3/VEGFR2 cells with IC50 of 3 nM. In HAoSMCs, regorafenib suppress PDGFR-β autophosphorylation after stimulation with PDGF-BB, with an IC50 of 90 nM. Regorafenib also inhibits FGFR signaling in MCF-7 breast cancer (BC) cells stimulated with FGF10. Regorafenib very potently inhibited the mutant receptors KIT and RET, with IC50 of approximately 20 nM and 10 nM, respectively. Regorafenib inhibits the proliferation of VEGF-stimulated HUVECs, with an IC50 of approximately 3 nM. Regorafenib prevents the proliferation of FGF2-stimulated HUVECs and of PDGF-BB-stimulated HAoSMCs with IC50 of 127 nM and 146 nM, respectively. Regorafenib targets both tumor cell proliferation and tumor vasculature through inhibition of receptors of tyrosine kinases (VEGFR, KIT, RET, FGFR, and PDGFR) and serine/threonine kinases (Raf and p38MAPK). Regorafenib suppresses growth of human Hep3B, PLC/PRF/5 and HepG2 cells in a concentration- and time-dependent manner. |
| Concentration | Treated Time | Description | References | |
| SKMEL239 Parental (PAR) cells | 2 μM | 1 h | inhibit MAPK signaling | Cancer Discov. 2021 Jul;11(7):1716-1735. |
| C3 cells | 2 μM | 1 h | inhibit MAPK signaling | Cancer Discov. 2021 Jul;11(7):1716-1735. |
| PC9 cells | 2 μM | 1 h | inhibit MAPK signaling | Cancer Discov. 2021 Jul;11(7):1716-1735. |
| HCT116 cells | 40 µM | 48 h | Analysis of Regorafenib-induced apoptosis showed that FBW7 wild-type cells were more prone to apoptosis compared to FBW7 mutant cells. | Oncogene. 2017 Feb 9;36(6):787-796. |
| HCT116 cells | 5 µM | Analysis of the effect of Regorafenib on Mcl-1 protein levels showed that Mcl-1 was significantly reduced in FBW7 wild-type cells but not in FBW7 mutant cells. | Oncogene. 2017 Feb 9;36(6):787-796. | |
| Hep3B | 1 μM, 2.5 μM, 5 μM, 7.5 μM, 10 μM | 72 or 96 h | Regorafenib inhibited the growth of Hep3B cells in a concentration- and time-dependent manner, with an IC50 of 5 μM. | J Cell Physiol. 2013 Feb;228(2):292-7. |
| PLC/PRF/5 | 1 μM, 2.5 μM, 5 μM, 7.5 μM, 10 μM | 72 or 96 h | PLC/PRF/5 cells responded similarly to Hep3B cells. | J Cell Physiol. 2013 Feb;228(2):292-7. |
| HepG2 | 1 μM, 2.5 μM, 5 μM, 7.5 μM, 10 μM | 72 or 96 h | HepG2 cells were more sensitive to Regorafenib, with an approximate IC50 of 1 μM. | J Cell Physiol. 2013 Feb;228(2):292-7. |
| RIL-175 cells | 1 µM | 36 h | To study the effect of Regorafenib on CXCL10 secretion by RIL-175 cells, results showed that Regorafenib significantly increased CXCL10 secretion | J Immunother Cancer. 2020 Nov;8(2):e001435. |
| HCA1 cells | 1 µM | 36 h | To study the effect of Regorafenib on CXCL10 secretion by HCA1 cells, results showed that Regorafenib increased CXCL10 secretion to a lesser extent | J Immunother Cancer. 2020 Nov;8(2):e001435. |
| T24R1 cells | 1, 6.25, 12.5, 25, 50 µM | 12, 24, 48 h | Regorafenib significantly decreased the viability of T24R1 cells and inhibited the expression of stemness and EMT markers. | Int J Mol Sci. 2023 Dec 18;24(24):17610. |
| T24R2 cells | 1, 6.25, 12.5, 25, 50 µM | 12, 24, 48 h | Regorafenib significantly decreased the viability of T24R2 cells and inhibited the expression of stemness and EMT markers. | Int J Mol Sci. 2023 Dec 18;24(24):17610. |
| Administration | Dosage | Frequency | Description | References | ||
| Mice | Acute myeloid leukemia (AML) model | Oral | 5 mg/kg | Once daily for 1 month | To evaluate the therapeutic potential of Regorafenib in the AML model, results showed that AML cells in the periphery and spleen were sensitive to treatment, while those in the bone marrow were protected. | J Hematol Oncol. 2017 Oct 6;10(1):162 |
| Nude mice | HCT116 xenograft model | Oral | 30 mg/kg | 10 consecutive days | Evaluation of the antitumor effects of Regorafenib in vivo showed that FBW7 wild-type tumors were more sensitive to Regorafenib, while Mcl-1 degradation was blocked and apoptosis was reduced in FBW7 knockout tumors. | Oncogene. 2017 Feb 9;36(6):787-796. |
| Mice | HCC model with liver damage | Oral | 5, 10, 20 mg/kg | Once daily for 5 days | To study the effect of Regorafenib combined with PD1 blockade on vascular structure and function, antitumor immunity, tumor growth, and survival in HCC mouse models, results showed that 10 mg/kg Regorafenib combined with PD1 blockade significantly improved survival | J Immunother Cancer. 2020 Nov;8(2):e001435. |
| Nude mice | T24R1 and T24R2 xenograft tumor model | Intraperitoneal injection | 20 mg/kg | 20 consecutive days | Regorafenib significantly inhibited the growth of T24R1 and T24R2 xenograft tumors, reduced tumor proliferation and angiogenesis, and promoted tumor cell apoptosis. | Int J Mol Sci. 2023 Dec 18;24(24):17610. |
| Nude mice | BRAF(V600E) CRC tumor models | Oral | 30 mg/kg | Once daily for 40 or 60 days | Suppress tumor growth | Cancer Discov. 2021 Jul;11(7):1716-1735. |
| Mice | HT-29 and HCT116 human colorectal cancer xenograft models | Oral | 30 mg/kg | Once daily for 7 days | To investigate the mechanisms of tumor revascularization after regorafenib withdrawal | J Extracell Vesicles. 2021 May;10(7):e12096 |
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
| NCT02288078 | Rectal Cancer | Phase 2 | Unknown | September 2016 | Japan ... 展开 >> Saiseikai Fukuoka General Hospital Recruiting Fukuoka, Japan, 810-0001 Contact: Yasunori Emi, MD, PhD +81-92-771-8151 emi-y@saiseikai-hp.chuo.fukuoka.jp 收起 << |
| NCT03347292 | Carcinoma, Hepatocellular | Phase 1 | Recruiting | February 17, 2021 | United States, California ... 展开 >> USC Norris Hospital and Clinics Recruiting Los Angeles, California, United States, 90033 United States, Florida H. Lee Moffitt Cancer Center & Research Institute Recruiting Tampa, Florida, United States, 33612 United States, New York Mount Sinai Medical Center Recruiting New York, New York, United States, 10029 United States, Washington Seattle Cancer Care Alliance Recruiting Seattle, Washington, United States, 98109-1023 Germany Universitätsklinikum Köln Not yet recruiting Köln, Nordrhein-Westfalen, Germany, 50937 Universitätsmedizin der Johannes Gutenberg Universität Mainz Not yet recruiting Mainz, Rheinland-Pfalz, Germany, 55131 收起 << |
| NCT01187615 | Small Cell Lung Carcinoma | Phase 1 | Terminated | - | United States, Connecticut ... 展开 >> New Haven, Connecticut, United States, 06519 United States, Nevada Las Vegas, Nevada, United States, 89135-3011 United States, New York New York, New York, United States, 10065 United States, North Carolina Chapel Hill, North Carolina, United States, 27599 收起 << |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
2.07mL 0.41mL 0.21mL |
10.36mL 2.07mL 1.04mL |
20.71mL 4.14mL 2.07mL |
|
| CAS号 | 755037-03-7 |
| 分子式 | C21H15ClF4N4O3 |
| 分子量 | 482.82 |
| SMILES Code | O=C(NC)C1=NC=CC(OC2=CC=C(NC(NC3=CC=C(Cl)C(C(F)(F)F)=C3)=O)C(F)=C2)=C1 |
| MDL No. | MFCD16038047 |
| 别名 | 瑞格非尼 ;BAY 73-4506; Fluoro-Sorafenib |
| 运输 | 蓝冰 |
| InChI Key | FNHKPVJBJVTLMP-UHFFFAOYSA-N |
| Pubchem ID | 11167602 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Sealed in dry, store in freezer, under -20°C |
| 溶解方案 |
DMSO: 120 mg/mL(248.54 mM),配合低频超声助溶,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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