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抑制剂/激动剂
细胞生物学 肿瘤
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细胞培养
血管生成 蛋白质酪氨酸激酶 肿瘤生长增殖和凋亡 肿瘤干细胞 胃癌 肝癌 结直肠癌
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类器官培养添加剂
c-Met/HGFR Tie-2 FLT3 VEGFR c-Kit
/ Cabozantinib/卡博替尼

Cabozantinib/卡博替尼 {[allProObj[0].p_purity_real_show]}

货号：A200488 同义名： XL184; BMS-907351

Cabozantinib是一种强效和口服活性的 VEGFR2 和 MET 抑制剂，IC50 值分别为 0.035 和 1.3 nM。它还强效抑制 KIT、RET、AXL、TIE2 和 FLT3，IC50 值分别为 4.6、5.2、7、14.3 和 11.3 nM。Cabozantinib 显示出抗血管生成活性，破坏肿瘤血管结构，并促进肿瘤和内皮细胞凋亡。

Cabozantinib/卡博替尼 化学结构 CAS号：849217-68-1
Cabozantinib/卡博替尼 化学结构
CAS号：849217-68-1
Cabozantinib/卡博替尼 3D分子结构
CAS号：849217-68-1
Cabozantinib/卡博替尼 化学结构 CAS号：849217-68-1
Cabozantinib/卡博替尼 3D分子结构 CAS号：849217-68-1
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Cabozantinib/卡博替尼 纯度/质量文件 产品仅供科研

货号：A200488 标准纯度： {[allProObj[0].p_purity_real_show]}
批次查询： 批次纯度:

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产品名称 Tie-2 ↓ 其他靶点 纯度
Tie2 kinase inhibitor 1 ++

Tie-2, IC50: 0.25 μM

 		99%+
MGCD-265 analog +++

Tie-2, IC50: 7 nM

 		99%+
Pexmetinib ✔ p38 MAPK 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 (ITD), IC50: 1.1 nM

FLT3 (WT), IC50: 4.2 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 (D835Y), IC50: 0.4 nM

FLT3, 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 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。
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。

Cabozantinib/卡博替尼 生物活性

靶点

  • VEGFR2

    VEGFR2/KDR, IC50:0.035 nM
描述 The inhibition of VEGF/VEGFR, as well as HGF/c-Met pathway contributes to tumor growth, angiogenesis, invasiveness and metastasis in preclinical studies. Cabozantinib is a potent VEGFR2 inhibitor with IC50 value of 0.035nM, as well as shows inhibitory effect on c-Met, Ret, Kit, Flt-1/3/4, Tie2, and AXL with IC50 values of 1.3nM, 4nM, 4.6nM, 12nM/11.3nM/6nM, 14.3nM and 7nM (measured by kinase activity), respectively[1]. Treatment with Cabozantinib dose-dependently inhibited HGF-induced p-Met at concentration>0.05μM and its downstream p-AKT at concentration>0.1μM in MPNST724 cells, as well as at concentration of 1μM in HUVECs, 0.5μM in ST88 and STS26T cells. The inhibition of VEGFR-2 by Cabozantinib can be observed, as decreased p-VEGFR2, at concentration>0.5μM in HUVECs. Cabozantinib inhibited HGF-induced MPNST cell migration and invasion at 0.5μM for 4h. As prediction by inhibition of Cabozantinib on VEGFR2 and c-Met, Cabozantinib showed potent anti-angiogenesis effect in vivo. The in vivo gel-foam suggested that angiogenesis induced by HGF, VEGF or both decreased (measured based on CD31) by administration of 30mg/kg Cabozantinib for 10 days[2]. Oral treatment with Cabozantinib for 7 days reduced tumor vascularity by 67% at 3mg/kg and by 83% at 30mg/kg in RIP-Tag2 tumors[1].

Cabozantinib/卡博替尼 细胞实验

Cell Line
Concentration Treated Time Description References
HCT116 cells 5 μM 24 h To evaluate the effect of Cabozantinib on autophagy, results showed that Cabozantinib significantly induced autophagy. Mol Cancer Ther. 2018 Oct;17(10):2112-2122.
HT29 cells 5 μM 24 h To evaluate the effect of Cabozantinib on autophagy, results showed that Cabozantinib significantly induced autophagy. Mol Cancer Ther. 2018 Oct;17(10):2112-2122.
2H11 cells 1 μM 20 h To evaluate the effect of Cabozantinib on tube formation in 2H11 cells, results showed that Cabozantinib inhibited tube formation. Cancer Res. 2022 Sep 2;82(17):3158-3171.
H460/MX20 5 μM 72 h Cabozantinib significantly sensitized H460/MX20 cells to ABCG2 substrate drugs (such as mitoxantrone, SN-38, and topotecan), reversing ABCG2-mediated multidrug resistance. Pharmacol Res. 2017 May;119:89-98.
ABCG2-482-R2 5 μM 72 h Cabozantinib significantly sensitized ABCG2-482-R2 cells to ABCG2 substrate drugs (such as mitoxantrone, SN-38, and topotecan), reversing ABCG2-mediated multidrug resistance. Pharmacol Res. 2017 May;119:89-98.
ABCG2-482-G2 5 μM 72 h Cabozantinib significantly sensitized ABCG2-482-G2 cells to ABCG2 substrate drugs (such as mitoxantrone, SN-38, and topotecan), reversing ABCG2-mediated multidrug resistance. Pharmacol Res. 2017 May;119:89-98.
ABCG2-482-T7 5 μM 72 h Cabozantinib significantly sensitized ABCG2-482-T7 cells to ABCG2 substrate drugs (such as mitoxantrone, SN-38, and topotecan), reversing ABCG2-mediated multidrug resistance. Pharmacol Res. 2017 May;119:89-98.
JHH5 cells 3 µM 72 h To evaluate the inhibitory effect of Cabozantinib on JHH5 cells, results showed that Cabozantinib alone only partially interfered with cell viability Cell Death Dis. 2022 Nov 24;13(11):994.
Hep3B cells 3 µM 72 h To evaluate the inhibitory effect of Cabozantinib on Hep3B cells, results showed that Cabozantinib alone only partially interfered with cell viability Cell Death Dis. 2022 Nov 24;13(11):994.
Huh7 cells 3 µM 72 h To evaluate the inhibitory effect of Cabozantinib on Huh7 cells, results showed that Cabozantinib alone only partially interfered with cell viability Cell Death Dis. 2022 Nov 24;13(11):994.
SC1 cells 10 μM 24 h To detect the release of CXCL12 after Cabozantinib treatment, the results showed that Cabozantinib treatment significantly increased the release of CXCL12. Cancer Discov. 2017 Jul;7(7):750-765.
SC1 cells 10 μM 28 h To detect the release of HMGB1 after Cabozantinib treatment, the results showed that Cabozantinib treatment significantly increased the release of HMGB1. Cancer Discov. 2017 Jul;7(7):750-765.
HCT116 cells 5 μM 24 h To evaluate the effect of Cabozantinib on autophagy, results showed that Cabozantinib significantly induced autophagy Mol Cancer Ther. 2018 Oct;17(10):2112-2122.
HT29 cells 5 μM 24 h To evaluate the effect of Cabozantinib on autophagy, results showed that Cabozantinib significantly induced autophagy Mol Cancer Ther. 2018 Oct;17(10):2112-2122.

Cabozantinib/卡博替尼 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
NOD/SCID mice Peritoneal dissemination model Intraperitoneal injection 30 mg/kg 5 times per week for 15 days To evaluate the antitumor efficacy of cabozantinib as monotherapy or in combination with nal-IRI in gastric cancer mouse models. Results showed that cabozantinib monotherapy significantly extended animal survival (24 days, a 33% increase), and its combination with nal-IRI further extended survival (50 days, a 178% increase). Mol Cancer Ther. 2022 Jul 5;21(7):1149-1159.
Nude mice Colorectal cancer patient-derived xenograft model Oral 30 mg/kg Daily for 28 days To evaluate the antitumor effects of Cabozantinib in colorectal cancer xenograft models, results showed that Cabozantinib significantly inhibited tumor growth. Mol Cancer Ther. 2018 Oct;17(10):2112-2122.
Mice CcRCC tumor xenograft model Oral gavage 10mg/kg Daily Cabozantinib significantly reduced the tumor growth of the ccRCC M62 tumor xenografts. Cancer Res. 2019 Nov 15;79(22):5758-5768
Mice PTEN/p53 deficient prostate cancer model Oral 100 mg/kg Once daily for 3 weeks Cabozantinib significantly reduced tumor volume and nearly completely cleared poorly differentiated prostate cancer within 4 days. Cancer Discov. 2017 Jul;7(7):750-765.
Mice Colorectal cancer patient-derived xenograft model Oral 30 mg/kg Once daily for 28 days To evaluate the antitumor effects of Cabozantinib in colorectal cancer xenograft models, results showed that Cabozantinib significantly inhibited tumor growth and reduced tumor vascularity Mol Cancer Ther. 2018 Oct;17(10):2112-2122.

Cabozantinib/卡博替尼 动物研究

Animal Administration Mice: min = 30 mg/kg[3], max = 100 mg/kg[4]
Dose Mice: 30 mg/kg[5] (i.p.); 30 mg/kg[6] (p.o.)
Administration i.p., p.o.
Pharmacokinetics
Animal Rats[7] Monkeys[7]
Dose 5 mg/kg 3 mg/kg [formulation: EPW(ethanol:PEG400:water=5:45:50)]
Administration i.v. or p.o. i.v. or p.o.
F 111% (p.o.) 73% (p.o.)
AUC0-inf 259 μM·h (i.v.)
288 μM·h (p.o.)
T1/2 10.9 h (i.v.)
14.1 h (p.o.) 		3.92 h (i.v.)
4.18 h (p.o.)
AUC0→inf 8.65 μM·h (i.v.)
6.33 μM·h (p.o.)
Tmax 0.25 h (i.v.)
4.0 h (p.o.) 		0.08 h (i.v.)
3.0 h (p.o.)
CL 0.038 L/kg/h (i.v.) 0.64 L/kg/h (i.v.)
Cmax 18.7 μM (i.v.)
14.6 μM (p.o.) 		2.51 μM (i.v.)
0.98 μM (p.o.)
Vdss 0.6 L/kg (i.v.) 2.67 L/kg (i.v.)
AUC0→t 196 μM·h (i.v.)
192 μM·h (p.o.) 		8.74 μM·h (i.v.)
6.46 μM·h (p.o.)

Cabozantinib/卡博替尼 参考文献

[1]You WK, Sennino B, et al. VEGF and c-Met blockade amplify angiogenesis inhibition in pancreatic islet cancer. Cancer Res. 2011;71(14):4758-68.

[2]Torres KE, Zhu QS, et al. Activated MET is a molecular prognosticator and potential therapeutic target for malignant peripheral nerve sheath tumors. Clin Cancer Res. 2011;17(12):3943-55.

[3]Nguyen HM, Ruppender N, et al. Cabozantinib inhibits growth of androgen-sensitive and castration-resistant prostate cancer and affects bone remodeling. PLoS One. 2013;8(10):e78881.

[4]Navis AC, Bourgonje A, et al. Effects of dual targeting of tumor cells and stroma in human glioblastoma xenografts with a tyrosine kinase inhibitor against c-MET and VEGFR2. PLoS One. 2013;8(3):e58262.

[5]Haider MT, Hunter KD, et al. Rapid modification of the bone microenvironment following short-term treatment with Cabozantinib in vivo. Bone. 2015 Dec;81:581-592.

[6]Yang S, Zhang X, et al. Cabozantinib induces PUMA-dependent apoptosis in colon cancer cells via AKT/GSK-3β/NF-κB signaling pathway. Cancer Gene Ther. 2019 Jun 11.

[7]XL 184

Cabozantinib/卡博替尼 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

1.99mL

0.40mL

0.20mL

9.97mL

1.99mL

1.00mL

19.94mL

3.99mL

1.99mL

Cabozantinib/卡博替尼 技术信息

CAS号849217-68-1
分子式C28H24FN3O5
分子量 501.51
SMILES Code O=C(C1(C(NC2=CC=C(F)C=C2)=O)CC1)NC3=CC=C(OC4=CC=NC5=CC(OC)=C(OC)C=C45)C=C3
MDL No. MFCD20926324
别名 XL184; BMS-907351
运输蓝冰
InChI Key ONIQOQHATWINJY-UHFFFAOYSA-N
Pubchem ID 25102847
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: 25 mg/mL(49.85 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

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
方案 四
配制的工作液建议现用现配，短期内尽快用完。 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

Tags: Cabozantinib | XL184;BMS-907351 | c-Met/HGFR | FLT3 | VEGFR | c-Kit | Tie-2 | AmBeed-信号通路专用抑制剂 | Cabozantinib/卡博替尼 纯度/质量文件 | Cabozantinib/卡博替尼 亚型比较 | Cabozantinib/卡博替尼 生物活性 | Cabozantinib/卡博替尼 动物研究 | Cabozantinib/卡博替尼 参考文献 | Cabozantinib/卡博替尼 实验方案 | Cabozantinib/卡博替尼 技术信息

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