Nintedanib esylate | BIBF 1120 esylate;BIBF 1120 (esylate);Nintedanib;BIBF 1120;Intedanib;Nintedanib Ethanesulfonate Salt | 尼达尼布乙磺酸盐 | VEGFR | PDGFR | FGFR

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Nintedanib esylate/乙磺酸尼达尼布 {[allProObj[0].p_purity_real_show]}

货号：A160216 同义名： 尼达尼布乙磺酸盐 / BIBF 1120 esylate; BIBF 1120 (esylate)

Nintedanib esylate (BIBF 1120 esylate) (BIBF 1120 esylate) 是一种有效的三重血管激酶抑制剂，对VEGFR1/2/3、FGFR1/2/3和PDGFRα/β的IC50值分别为34 nM/13 nM/13 nM、69 nM/37 nM/108 nM和59 nM/65 nM。

Nintedanib esylate/乙磺酸尼达尼布化学结构
CAS号：656247-18-6

Nintedanib esylate/乙磺酸尼达尼布 3D分子结构
CAS号：656247-18-6

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Nintedanib esylate/乙磺酸尼达尼布纯度/质量文件产品仅供科研

货号：A160216 标准纯度： {[allProObj[0].p_purity_real_show]} 产品说明书

批次查询：批次纯度: COA SDS NMR HPLC CNMR LC-MS

全球学术期刊中引用的产品: • Nature, 2025, 645, 793-800. Ambeed. [ A201204 , A444152 , A344107 , A952055 ]; • Cell, 2025. Ambeed. [ A122167 ]; • Science, 2025, 387(6729): eadp5637. Ambeed. [ A875019 ]; • Sig. Transduct. Target. Ther., 2025, 10, 257. Ambeed. [ A104916 ]; • Nat. Nanotechnol., 2025. Ambeed. [ A243018 , A1216705 , A522597 , A125401 , A1355641 ]; 更多 >

FGFR 亚型比较
PDGFR 亚型比较
VEGFR 亚型比较

产品名称	FGFR ↓ ↑	FGFR1 ↓ ↑	FGFR2 ↓ ↑	FGFR3 ↓ ↑	FGFR4 ↓ ↑	其他靶点	纯度
Tyrphostin AG1296	+ FGFR (Swiss 3T3), IC50: 12.3 μM					PDGFR	99%+
Pazopanib	+ FGFR, IC50: 140 nM						99%
Erdafitinib	✔					RET	99%+
Gambogenic acid	✔						98+%
Sulfatinib		+++ FGFR1, IC50: 15 nM					99+%
Nintedanib esylate		+ FGFR1, IC50: 69 nM	++ FGFR2, IC50: 37 nM	+ FGFR3, IC50: 108 nM			98%
Zoligratinib		+++ FGFR1, IC50: 9.3 nM	+++ FGFR2, IC50: 7.6 nM	++ FGFR3, IC50: 22 nM	+ FGFR4, IC50: 290 nM		99%+
MK-2461		+ FGFR1, IC50: 65 nM	++ FGFR2, IC50: 39 nM	++ FGFR3, IC50: 50 nM			98%+
SU 5402		++ FGFR1, IC50: 30 nM					98%
Brivanib		+ FGFR1, IC50: 148 nM					99%+
Lucitanib		++ FGFR1, IC50: 17.5 nM	+ FGFR2, IC50: 82.5 nM				99%+
Ponatinib		++++ FGFR1, IC50: 2.2 nM					98%
PD-166866		+ FGFR1, IC50: 52.4 nM					99%
Narazaciclib		++ FGFR1, IC50: 26 nM				RET	99%+
Lactate		+++ FGFR1, IC50: 8 nM		+++ FGFR3, IC50: 9 nM		c-Kit,FLT3	85%
Lenvatinib mesylate		++ FGFR1, IC50: 46 nM				c-RET	99%
LY2874455		++++ FGFR1, IC50: 2.8 nM	++++ FGFR2, IC50: 2.6 nM	+++ FGFR3, IC50: 6.4 nM	+++ FGFR4, IC50: 6 nM		99%+
FIIN-2		+++ FGFR1, IC50: 3.09 nM	+++ FGFR2, IC50: 4.3 nM	++ FGFR3, IC50: 27 nM	++ FGFR4, IC50: 45.3 nM		99%
FIIN-3		+++ FGFR1, IC50: 13.1 nM	++ FGFR2, IC50: 21 nM	++ FGFR3, IC50: 31.4 nM	++ FGFR4, IC50: 35.3 nM		98%
Infigratinib		++++ FGFR1, IC50: 0.9 nM	++++ FGFR2, IC50: 1.4 nM	++++ FGFR3, IC50: 1.0 nM FGFR3 (K650E), IC50: 4.9 nM	+ FGFR4, IC50: 60 nM		99%+
Danusertib		++ FGFR1, IC50: 47 nM				RET	99%+
R1530		++ FGFR1, IC50: 28 nM					98%
ENMD-2076		+ FGFR1, IC50: 92.7 nM	+ FGFR2, IC50: 70.8 nM			RET,FLT3	98%
Dovitinib		+++ FGFR1, IC50: 8 nM		+++ FGFR3, IC50: 9 nM		c-Kit,FLT3	99%+
Sorafenib		+ FGFR1, IC50: 580 nM					99%
SSR128129E		+ FGFR1, IC50: 1.9 μM					99%+
AZD-4547		++++ FGFR1, IC50: 0.2 nM	++++ FGFR2, IC50: 2.5 nM	++++ FGFR3, IC50: 1.8 nM			98%
Lenvatinib		++ FGFR1, IC50: 46 nM				RET	98%
PD173074		++ FGFR1, IC50: ~25 nM					99%+
S49076		++ FGFR1, IC50: 18 nM	+++ FGFR2, IC50: 17 nM	+++ FGFR3, IC50: 15 nM			98%
Futibatinib		++++ FGFR1, IC50: 1.8 nM	++++ FGFR2, IC50: 1.4 nM	++++ FGFR3, IC50: 1.6 nM	+++ FGFR4, IC50: 3.7 nM		99%+
Ferulic Acid		+ FGFR1, IC50: 3.78 μM	+ FGFR2, IC50: 12.5 μM				98%
Nintedanib		+ FGFR1, IC50: 69 nM	++ FGFR2, IC50: 37 nM	+ FGFR3, IC50: 108 nM	+ FGFR4, IC50: 610 nM		99+%
ASP5878		++++ FGFR1, IC50: 0.47 nM	++++ FGFR2, IC50: 0.6 nM	++++ FGFR3, IC50: 0.74 nM	+++ FGFR4, IC50: 3.5 nM		99%
PRN1371		++++ FGFR1, IC50: 0.6 nM	++++ FGFR2, IC50: 1.3 nM	+++ FGFR3, IC50: 4.1 nM	++ FGFR4, IC50: 19.3 nM		99%
Derazantinib		+++ FGFR1, IC50: 4.5 nM	++++ FGFR2, IC50: 1.8 nM	+++ FGFR3, IC50: 4.5 nM	++ FGFR4, IC50: 34 nM	RET	99%+
ODM-203		+++ FGFR1, IC50: 11 nM	+++ FGFR2, IC50: 16 nM	+++ FGFR3, IC50: 6 nM	++ FGFR4, IC50: 35 nM		99%+
Pemigatinib		++++ FGFR1, IC50: 0.4 nM	++++ FGFR2, IC50: 0.5 nM	++++ FGFR3, IC50: 1.2 nM	++ FGFR4, IC50: 30 nM		99%+
SKLB 610			✔			PDGFR	99%+
Alofanib			✔				99%+
Lirafugratinib			✔				99%
Masitinib mesylate				✔		FAK	99%+
BLU9931				+ FGFR3, IC50: 150 nM	+++ FGFR4, IC50: 3 nM		99%+
BO-264				✔			99%+
Fisogatinib					+++ FGFR4, IC50: 5 nM		99%+
H3B-6527					++++ FGFR4, IC50: <1.2 nM		99%+
Roblitinib					++++ FGFR4, IC50: 1.9 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	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			mTOR,VEGFR	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	c-Kit,FLT3	85%
Linifanib			++ PDGFRβ, IC50: 66 nM		99%+
AZD2932			+++ PDGFRβ, IC50: 4 nM	c-Kit	99%
Dovitinib			+++ PDGFRβ, IC50: 27 nM	c-Kit,FLT3	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	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,PDGFR,FGFR	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	c-Kit,FLT3	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/Flk1, IC50: 270 nM VEGFR2/KDR, IC50: 37 nM	+ VEGFR3/FLT4, IC50: 660 nM	c-Kit,c-Fms/CSF1R	99%+
Axitinib	++++ VEGFR1/FLT1, IC50: 0.1 nM	++++ VEGFR2/Flk1, IC50: 0.18 nM VEGFR2/KDR, IC50: 0.2 nM			98%
Dovitinib	+++ VEGFR1/FLT1, IC50: 10 nM	+++ VEGFR2/Flk1, IC50: 13 nM	+++ VEGFR3/FLT4, IC50: 8 nM	c-Kit,FLT3	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	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。

Nintedanib esylate/乙磺酸尼达尼布生物活性

靶点

FGFR2

FGFR2, IC50:37 nM
FGFR3

FGFR3, IC50:108 nM
FGFR1

FGFR1, IC50:69 nM

描述

VEGF/VEGFR (vascular endothelial growth factor/vascular endothelial growth factor receptor) pathway plays a key role in tumor angiogenesis by promotion of vascular and lymphatic endothelial, as well as survival, and invasion, thus resulting in neovascularization, tumor growth and metastasis. In addition, blockade of additional proangiogenic receptor tyrosine kinases, including PDGFR and FGFR, may improve long-term clinical outcomes. BIBF 1120 Esylate is the esylate form of BIBF 1120. BIBF 1120 is a multi-RTKs inhibitor with IC50 values of 13nM, 13nM , 16nM , 26nM , 34nM , 37nM , 59nM , 65nM , 69nM , 108nM for VEGFR2, VEGFR3, LCK, FLT3, VEGFR1, FGFR2, PDGFRα, PDGFRβ, FGFR1, FGFR3 (measured by enzymatic assays), less potent to Src, Lyn and FGFR4 with IC50 values of 156nM , 195nM and 610nM, respectively. Treatment with BIBF 1120 resulted in cell proliferation and apoptosis (EC50<10nM) in HUVECs, HSMECs, as well as the downstream p-MAPK and p-AKT (0.1-1μM). Daily oral treatment with BIBF 1120 at dose of 100mg/kg for 5 days reduced vessel density by 76% in FaDu xenografts, as well as markedly reduced both Meca 32–positive and PDGFRβ-positive cells predominantly in the intratumoral compartment. Once daily oral administration of BIBF 1120 at dose of 50mg/kg and 100mg/kg inhibited tumor growth both in a model of human head and neck small cell carcinoma (FaDu cells) and in a human renal cancer model (Caki-1 cells).

Nintedanib esylate/乙磺酸尼达尼布细胞实验

Cell Line Neonatal rat cardiac fibroblasts (CFs) Neonatal rat cardiac fibroblasts (CFs) Human dermal fibroblasts (HDFs) Human ADPKD renal cyst epithelial cells Primary human T cells Human neutrophils HUVECs cells B16-F10 cells 4T1 cells LLC cells MC38 cells Neonatal rat cardiac fibroblasts (CFs) BEAS-2B cells MLE-12 cells Human ADPKD renal cyst epithelial cells CD8+ T cells CD4+ T cells PAN-T cells Peripheral blood mononuclear cells (PBMCs) NIH-3T3 cells GIST-T1-T670I GIST-5R GIST-882 GIST-T1 BaF3-KIT-T670I Human pulmonary fibroblasts (HPFs) Neonatal rat cardiomyocytes (CMs) MRC-5 cells L929 cells NRK-49F rat renal fibroblasts Human ADPKD renal myofibroblasts HuCCT1 and RBE Murine 3D-LTCs Primary murine alveolar epithelial type II cells (pmATII) Human precision-cut lung slices (PCLS) from patients with pulmonary fibrosis Bleomycin-treated rat precision-cut lung slices (PCLS) Human Pulmonary Microvascular Endothelial Cells (HPMECs) Mouse splenocytes CAF1 and CAF2 B16-F10 cells Human 3D-LTCs Human ADPKD renal myofibroblasts	Concentration	Treated Time	Description	References
Neonatal rat cardiac fibroblasts (CFs)	0.5 µM	1 hour	NTB pretreatment prevented bFGF-induced ERK and AKT activation.	Pharmacol Res. 2021 Jul;169:105605.
Neonatal rat cardiac fibroblasts (CFs)	0.5 µM	1 hour	NTB pretreatment prevented TGF-β1-mediated SMAD3 phosphorylation but had no effect on TGF-β1-induced p38 activation. NTB exerts its anti-fibrotic effect via the canonical TGF-β1-SMAD3 pathway in a MAPK p38-independent manner.	Pharmacol Res. 2021 Jul;169:105605.
Human dermal fibroblasts (HDFs)	0.5, 1, 2, 5, 10 µM	1, 2, 3 days	To evaluate the cytotoxicity of Nintedanib on senescent and nonsenescent HDFs. Results showed that Nintedanib exhibited greater cytotoxicity in senescent HDFs, with a difference in cell viability of more than 40% at 5 or 10 μM.	Cell Death Dis. 2022 Sep 2;13(9):760.
Human ADPKD renal cyst epithelial cells	1.5 µM	12 days	To test the effect of Nintedanib on cyst growth, results showed Nintedanib significantly inhibited cyst growth	Cell Death Dis. 2021 Oct 14;12(10):947.
Primary human T cells	10, 30, 100 nM	15 minutes	Nintedanib blocked the activation of T cells (stimulated by anti-CD3/anti-CD28) through the inhibition of Lck-Y394 phosphorylation in a concentration-dependent manner.	Drug Des Devel Ther. 2021 Mar 8;15:997-1011.
Human neutrophils	400 µMol	2 hours	To investigate the effects of nintedanib on human neutrophil migration, results showed that nintedanib reduced neutrophil migration stimulated by MIP-2 or LPS.	Int J Mol Sci. 2021 Sep 13;22(18):9898.
HUVECs cells	≤1 µM	24 hours	No obvious cytotoxicity	Theranostics. 2022 Jan 1;12(2):747-766.
B16-F10 cells	1 µM	24 hours	Promoted STAT3 phosphorylation, upregulated PD-L1 and β2M expression	Theranostics. 2022 Jan 1;12(2):747-766.
4T1 cells	1 µM	24 hours	Promoted STAT3 phosphorylation, upregulated PD-L1 and β2M expression	Theranostics. 2022 Jan 1;12(2):747-766.
LLC cells	1 µM	24 hours	Promoted STAT3 phosphorylation, upregulated PD-L1 and β2M expression	Theranostics. 2022 Jan 1;12(2):747-766.
MC38 cells	1 µM	24 hours	Promoted STAT3 phosphorylation, upregulated PD-L1 and β2M expression	Theranostics. 2022 Jan 1;12(2):747-766.
Neonatal rat cardiac fibroblasts (CFs)	0.5 µM	24 hours	NTB treatment inhibited TGF-β1-induced production of fibrogenic proteins (α-SMA and fibronectin) and prevented agonist-induced cell migration.	Pharmacol Res. 2021 Jul;169:105605.
BEAS-2B cells	1 µM	24 hours	Inhibited radiation-induced activation of PI3K/AKT and MAPK signaling pathways, reduced expression of inflammatory factors COX-2, TGF-β1, IL-1β, and IL-6	Int J Biol Sci. 2024 Jun 11;20(9):3353-3371.
MLE-12 cells	1 µM	24 hours	Inhibited radiation-induced activation of PI3K/AKT and MAPK signaling pathways, reduced expression of inflammatory factors COX-2, TGF-β1, IL-1β, and IL-6	Int J Biol Sci. 2024 Jun 11;20(9):3353-3371.
Human ADPKD renal cyst epithelial cells	1.5 µM	24 hours	To test the effect of Nintedanib on epithelial cell proliferation, results showed Nintedanib significantly inhibited cell proliferation	Cell Death Dis. 2021 Oct 14;12(10):947.
CD8+ T cells	0.1–1000 nM	24 hours	Nintedanib attenuated the release of anti-CD3- or anti-CD3/CD28-stimulated IL-2 in a concentration-dependent manner, with IC50 values ranging from 23 to 83 nmol/L. Due to low cell numbers, other cytokines were not evaluated.	Drug Des Devel Ther. 2021 Mar 8;15:997-1011.
CD4+ T cells	0.1–1000 nM	24 hours	Nintedanib attenuated the release of anti-CD3- or anti-CD3/CD28-stimulated IL-2 in a concentration-dependent manner, with IC50 values ranging from 23 to 83 nmol/L. Due to low cell numbers, other cytokines were not evaluated.	Drug Des Devel Ther. 2021 Mar 8;15:997-1011.
PAN-T cells	0.1–1000 nM	24 hours	Nintedanib blocked the release of anti-CD3- or anti-CD3/CD28-stimulated IFN-γ, IL-2, IL-4, IL-5, IL-10 and IL-13 in a concentration-dependent manner, with IC50 values ranging from 5 to 77 nmol/L. Anti-CD3-stimulated IL-12p70 was below the detection limit.	Drug Des Devel Ther. 2021 Mar 8;15:997-1011.
Peripheral blood mononuclear cells (PBMCs)	0.1–1000 nM	24 hours	Nintedanib blocked the release of anti-CD3- or anti-CD3/CD28-stimulated IFN-γ, IL-2, IL-4, IL-5, IL-10, IL-12p70 and IL-13 in a concentration-dependent manner, with IC50 values ranging from 17 to 59 nmol/L.	Drug Des Devel Ther. 2021 Mar 8;15:997-1011.
NIH-3T3 cells	0.5 or 1 µM	24, 48 or 72 hours	To assess the antifibrotic activity of Nintedanib on TGF-β1-stimulated NIH-3T3 cells, results showed that Nintedanib inhibited the proliferation and activation of NIH-3T3 cells.	Br J Cancer. 2021 Mar;124(5):914-924.
GIST-T1-T670I	7.7 nM (GI50)	3 days	Evaluate the antiproliferative effect of Nintedanib on GIST-T1-T670I cells, results showed Nintedanib was more effective than sunitinib.	Mol Oncol. 2022 Apr;16(8):1761-1774.
GIST-5R	2.7 nM (GI50)	3 days	Evaluate the antiproliferative effect of Nintedanib on GIST-5R cells, results showed Nintedanib was more effective than sunitinib.	Mol Oncol. 2022 Apr;16(8):1761-1774.
GIST-882	3.5 nM (GI50)	3 days	Evaluate the antiproliferative effect of Nintedanib on GIST-882 cells, results showed Nintedanib had similar potency to sunitinib but was more potent than imatinib.	Mol Oncol. 2022 Apr;16(8):1761-1774.
GIST-T1	1.7 nM (GI50)	3 days	Evaluate the antiproliferative effect of Nintedanib on GIST-T1 cells, results showed Nintedanib was more potent than imatinib and sunitinib.	Mol Oncol. 2022 Apr;16(8):1761-1774.
BaF3-KIT-T670I	0.0003 µM	3 days	Evaluate the antiproliferative effect of Nintedanib on KIT T670I mutant cells, results showed Nintedanib was more potent than sunitinib, avapritinib and ripretinib.	Mol Oncol. 2022 Apr;16(8):1761-1774.
Human pulmonary fibroblasts (HPFs)	10 µM	3 days	To evaluate the cytotoxicity of Nintedanib on bleomycin-induced senescent HPFs. Results showed that Nintedanib at 10 μM exhibited a senolytic effect, inducing cleavage of caspase-9 and caspase-7, and suppressing p16 expression.	Cell Death Dis. 2022 Sep 2;13(9):760.
Neonatal rat cardiomyocytes (CMs)	1 µM	48 hours	NTB treatment had no significant effect on agonist-induced hypertrophic response but significantly altered key signaling pathways.	Pharmacol Res. 2021 Jul;169:105605.
MRC-5 cells	1 µM	48 hours	Inhibited radiation-induced activation of TGF-β/Smad and PI3K/AKT/mTOR signaling pathways, reduced expression of fibrosis markers COL1A1, α-SMA, and CTGF	Int J Biol Sci. 2024 Jun 11;20(9):3353-3371.
L929 cells	1 µM	48 hours	Inhibited radiation-induced activation of TGF-β/Smad and PI3K/AKT/mTOR signaling pathways, reduced expression of fibrosis markers COL1A1, α-SMA, and CTGF	Int J Biol Sci. 2024 Jun 11;20(9):3353-3371.
NRK-49F rat renal fibroblasts	1.5 µM	48 hours	To test the effect of Nintedanib on TGFβ-induced fibroblast-to-myofibroblast differentiation, results showed Nintedanib significantly inhibited differentiation	Cell Death Dis. 2021 Oct 14;12(10):947.
Human ADPKD renal myofibroblasts	1 µM	48 hours	To test the effect of Nintedanib on cell viability, results showed Nintedanib significantly reduced cell viability	Cell Death Dis. 2021 Oct 14;12(10):947.
HuCCT1 and RBE	0-10 µM	48 hours	Nintedanib showed suppression effects on ICC cell lines only at high concentrations of 3 or 10 µM.	Br J Cancer. 2020 Mar;122(7):986-994.
Murine 3D-LTCs	0.1 µM, 1 µM, 10 µM	48 hours	Nintedanib significantly downregulated Fn1 and Col1a1 mRNA levels and increased proSP-C protein expression and SP-C secretion.	Respir Res. 2018 Sep 15;19(1):175.
Primary murine alveolar epithelial type II cells (pmATII)	1 µM	48 hours	Nintedanib significantly downregulated Fn1 mRNA levels and restored the expression of Sftpc, Nkx2.1, and Hopx to the level of the PBS control.	Respir Res. 2018 Sep 15;19(1):175.
Human precision-cut lung slices (PCLS) from patients with pulmonary fibrosis	0.01 µM, 0.03 µM, 0.1 µM, 0.3 µM	48 hours	To evaluate the effect of Nintedanib on type III collagen formation and degradation, results showed that 0.3 µM Nintedanib significantly reduced PRO-C3 and C3M levels	Respir Res. 2022 Aug 4;23(1):201.
Bleomycin-treated rat precision-cut lung slices (PCLS)	0.01 µM, 0.03 µM, 0.1 µM, 0.3 µM	48 hours	To evaluate the effect of Nintedanib on type III collagen degradation, results showed that 0.3 µM Nintedanib significantly reduced C3M levels by 40%	Respir Res. 2022 Aug 4;23(1):201.
Human Pulmonary Microvascular Endothelial Cells (HPMECs)	400 mM	6 hours	To investigate the inhibitory effect of Nintedanib on BLM-induced endothelial-mesenchymal transition (EndoMT). Results showed that Nintedanib treatment inhibited BLM-induced transformation of HPMECs into fibroblast-like morphology and reversed the changes in endothelial and mesenchymal markers.	Int J Mol Sci. 2022 Jul 25;23(15):8193.
Mouse splenocytes	100 nM and 500 nM	72 hours	NTB treatment induced an increase in Treg frequency and significantly increased CTLA-4 and PD-1 expressing CD4+ T cells, confirming the immunosuppressive phenotype of these cells.	Pharmacol Res. 2021 Jul;169:105605.
CAF1 and CAF2	0-10 µM	72 hours	Nintedanib significantly suppressed CAF proliferation and α-SMA expression in a concentration-dependent manner.	Br J Cancer. 2020 Mar;122(7):986-994.
B16-F10 cells	up to 1 µM	72 hours	To evaluate the antitumor effect of Nintedanib on B16-F10 cells, results showed that Nintedanib did not exhibit direct cytotoxicity to B16-F10 cells at concentrations up to 1 µM.	Br J Cancer. 2021 Mar;124(5):914-924.
Human 3D-LTCs	1 µM	72 hours	Nintedanib restored epithelial gene expression and increased proSP-C protein expression and SP-C secretion.	Respir Res. 2018 Sep 15;19(1):175.
Human ADPKD renal myofibroblasts	1 µM		To test the effect of Nintedanib on cell migration, results showed Nintedanib significantly inhibited cell migration	Cell Death Dis. 2021 Oct 14;12(10):947.

Nintedanib esylate/乙磺酸尼达尼布动物实验

Species Female ICR mice Sprague-Dawley rats C57BL/6 J mice C57BL/6 mice Mice C57BL/6 mice C57BL/6 mice NOD-SCID mice C57BL/6 mice C57BL/6 mice C57BL/6 mice Male C57BL/6 mice BALB/C-nu mice C57BL/6J mice	Animal Model Ovarian hyperstimulation syndrome (OHSS) model Bleomycin-induced pulmonary fibrosis Bleomycin-induced lung fibrosis model Bleomycin-induced pulmonary fibrosis model Pkd1RC/RC mice MC38 and LLC tumor models Radiation-induced pulmonary fibrosis model Xenograft model of HuCCT1 plus CAF cells B16-F10 melanoma syngeneic model Bleomycin (BLM)-induced pulmonary fibrosis model LPS-induced acute lung injury model Bleomycin-induced pulmonary fibrosis model GIST-T1 xenograft model Heart failure model induced by Transverse Aortic Constriction (TAC) surgery	Administration	Dosage	Frequency	Description	References
Female ICR mice	Ovarian hyperstimulation syndrome (OHSS) model	Subcutaneous injection	0.2 mL nintedanib suspension	12 and 24 hours after hCG trigger	Nintedanib significantly alleviated the symptoms of OHSS, including weight change, ovarian weight, and peritoneal exudation level. Further studies showed that nintedanib inhibited corpus luteum development and angiogenesis, reducing the increase in vascular permeability. Additionally, nintedanib treatment did not increase the risk of thrombosis or bleeding.	Drug Des Devel Ther. 2022 Feb 18;16:397-411
Sprague-Dawley rats	Bleomycin-induced pulmonary fibrosis	Intratracheal installation	0.25 mL/kg	Two doses, 2 days apart, sacrificed 14 days after the last dose	To establish a pulmonary fibrosis model for subsequent in vitro experiments	Respir Res. 2022 Aug 4;23(1):201.
C57BL/6 J mice	Bleomycin-induced lung fibrosis model	Intraperitoneal injection	0.5396 mg/kg	Three times per week for 24 days	To evaluate the senolytic effect of Nintedanib in a bleomycin-induced lung fibrosis model. Results showed that Nintedanib significantly reduced the number of SA βG-positive senescent cells, ameliorated collagen deposition, and inhibited STAT3 phosphorylation.	Cell Death Dis. 2022 Sep 2;13(9):760.
C57BL/6 mice	Bleomycin-induced pulmonary fibrosis model	Intratracheal administration	2 U/kg	Single dose, sacrificed after 14 days	Nintedanib was not used in in vivo experiments	Respir Res. 2018 Sep 15;19(1):175.
Mice	Pkd1RC/RC mice	Intraperitoneal injection	20 mg/kg	Every other day from three to five months of age	To test the effect of Nintedanib on renal cyst growth and fibrosis, results showed Nintedanib significantly reduced kidney size, kidney-to-body-weight ratio, cystic index, and fibrosis	Cell Death Dis. 2021 Oct 14;12(10):947.
C57BL/6 mice	MC38 and LLC tumor models	Oral	30 mg/kg	5 days ON, 1 day OFF, total 10 times	Significantly inhibited tumor growth, promoted tumor vessel normalization, increased immune cell infiltration and activation	Theranostics. 2022 Jan 1;12(2):747-766.
C57BL/6 mice	Radiation-induced pulmonary fibrosis model	Oral	30 mg/kg	Once daily for 4 weeks	Alleviated radiation-induced lung pathological changes, suppressed collagen deposition, and improved overall health status of mice; mitigated radiation-induced inflammatory responses in epithelial cells by inhibiting PI3K/AKT and MAPK signaling pathways, and inhibited fibroblast-to-myofibroblast transition by suppressing TGF-β/Smad and PI3K/AKT/mTOR signaling pathways	Int J Biol Sci. 2024 Jun 11;20(9):3353-3371.
NOD-SCID mice	Xenograft model of HuCCT1 plus CAF cells	Oral	30 mg/kg	Five times a week for two weeks	Nintedanib reduced xenografted ICC growth and activated CAFs expressing α-SMA, and combination therapy with gemcitabine showed the strongest inhibition of tumour growth.	Br J Cancer. 2020 Mar;122(7):986-994.
C57BL/6 mice	B16-F10 melanoma syngeneic model	Oral	50 mg/kg	Five times a week for two weeks	To evaluate the antitumor efficacy of Nintedanib in a B16-F10 melanoma syngeneic model, results showed that Nintedanib significantly delayed tumor growth and prolonged survival of the mice without health-related toxicity.	Br J Cancer. 2021 Mar;124(5):914-924.
C57BL/6 mice	Bleomycin (BLM)-induced pulmonary fibrosis model	Oral gavage	50 mg/kg	Once daily, 5 days per week for 3 weeks	To investigate the therapeutic effect of Nintedanib on BLM-induced pulmonary fibrosis. Results showed that Nintedanib treatment significantly alleviated pulmonary injury and fibrosis, suppressed EndoMT, and reduced FAK phosphorylation in murine lung tissues.	Int J Mol Sci. 2022 Jul 25;23(15):8193.
C57BL/6 mice	LPS-induced acute lung injury model	Oral gavage	50 mg/kg	Once 24 hours and 10 minutes before	To assess the effect of nintedanib in attenuating the histopathological changes of LPS-induced ALI, results showed that nintedanib significantly reduced lung injury scores and neutrophil recruitment.	Int J Mol Sci. 2021 Sep 13;22(18):9898.
Male C57BL/6 mice	Bleomycin-induced pulmonary fibrosis model	Oral gavage	50 mg/kg	Daily for five days every week	Nintedanib significantly decreased the histopathological changes and neutrophil recruitment in BLM-induced pulmonary fibrosis. Nintedanib mediated a downregulation of CXCR2 and VLA-4 expression, as well as an upregulation of GRK2 activity in peripheral blood neutrophils in BLM-induced pulmonary fibrosis.	Int J Mol Sci. 2020 Jul 2;21(13):4735
BALB/C-nu mice	GIST-T1 xenograft model	Oral	50 mg/kg and 100 mg/kg	Daily	Evaluate the antitumor effect of Nintedanib on GIST-T1 xenograft models, results showed Nintedanib inhibited tumor growth by 72.3% and 78.2% at doses of 50 mg/kg and 100 mg/kg, respectively.	Mol Oncol. 2022 Apr;16(8):1761-1774.
C57BL/6J mice	Heart failure model induced by Transverse Aortic Constriction (TAC) surgery	Oral gavage	50mg/kg/day	Once daily, continued till 16 weeks post-TAC or till 8 weeks post-TAC followed by washout period	NTB treatment prevented TAC-induced cardiac functional decline and adverse cardiac remodeling, reduced cardiac fibrosis and hypertrophy, and decreased myocardial and systemic inflammation. The cardioprotective effects of NTB were sustained even after interruption of the treatment.	Pharmacol Res. 2021 Jul;169:105605.

Nintedanib esylate/乙磺酸尼达尼布动物研究

Dose

Mice: 25 mg/kg - 100 mg/kg^[2] (p.o.)
Rat: 8.3 mg/kg– 41.5 mg/kg^[3] (p.o.)

Administration

p.o.

Pharmacokinetics

Animal	Mice^[4]	Rats^[4]	Monkeys^[4]
Dose	50 mg/kg	50 mg/kg (p.o.) 2 mg/kg (i.v.)	40 mg/kg (cynomolgus, p.o.) 5 mg/kg (cynomolgus, i.v.)
Administration	p.o.	p.o. or i.v.	p.o. or i.v.
MRT	5.19 h	3.25 h (i.v.)	3.82 h (i.v.)
F		11.9% (p.o.)	13.2% (p.o.)
T_1/2	5.15 h	3.95 h (i.v.)	5.95 h (i.v.)
AUC	2720 ng·h/ml	375 ng·h/ml (p.o.) 181 ng·h/ml (i.v.)	2390 ng·h/ml (p.o.) 2260 ng·h/ml (i.v.)
CL		202 ml/min/kg (i.v.)	37.5 ml/min/kg (i.v.)
C_max	547 ng/ml	105 ng/ml (p.o.) 124 ng/ml (i.v.)	175 ng/ml (p.o.) 1300 ng/ml (i.v.)
Protein bound (%)			92.9% (p.o.)
Protein binding (free drug %)	97.2	98.5% (p.o.)
Vss		41.2 L/kg (i.v.)	8.64 L/kg (i.v.)

Nintedanib esylate/乙磺酸尼达尼布参考文献

[1]Roth GJ, Heckel A, et al. Design, synthesis, and evaluation of indolinones as triple angiokinase inhibitors and the discovery of a highly specific 6-methoxycarbonyl-substituted indolinone (BIBF 1120). J Med Chem. 2009 Jul 23;52(14):4466-80.

[2]Hilberg F, Roth GJ, et al. BIBF 1120: triple angiokinase inhibitor with sustained receptor blockade and good antitumor efficacy. Cancer Res. 2008 Jun 15;68(12):4774-82.

[3]Nintedanib

[4]Nintedanib

Nintedanib esylate/乙磺酸尼达尼布实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

1.54mL

0.31mL

0.15mL

7.70mL

1.54mL

0.77mL

15.39mL

3.08mL

1.54mL

Nintedanib esylate/乙磺酸尼达尼布技术信息

CAS号	656247-18-6
分子式	C₃₃H₃₉N₅O₇S
分子量	649.76
SMILES Code	O=C1NC2=C(C=CC(C(OC)=O)=C2)/C1=C(NC3=CC=C(N(C(CN4CCN(C)CC4)=O)C)C=C3)\C5=CC=CC=C5.CCS(=O)(O)=O
MDL No.	MFCD26142360

别名	尼达尼布乙磺酸盐 ;BIBF 1120 esylate; BIBF 1120 (esylate); Nintedanib; BIBF 1120; Intedanib; Nintedanib Ethanesulfonate Salt
运输	蓝冰
InChI Key	ZNMRDZZRAFJOKY-UHFFFAOYSA-N
Pubchem ID	135476717

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

细胞实验：

DMSO: 40 mg/mL(61.56 mM)，配合低频超声，并水浴加热至45℃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

H₂O: 15 mg/mL(23.09 mM)，配合低频超声助溶

无水乙醇: 2.5 mg/mL(3.85 mM)，配合低频超声助溶，注意：无水乙醇开封后，易挥发，也会吸收空气中的水分，导致溶解能力下降，请避免使用开封较久的乙醇

动物实验：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

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

方案二

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Nintedanib esylate/乙磺酸尼达尼布动物实验

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FGFR2	FGFR2, IC50:37 nM
FGFR3	FGFR3, IC50:108 nM
FGFR1	FGFR1, IC50:69 nM

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