This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
This compound is a customized synthesis product. We have a strong synthesis team with excellent synthesis technology and capabilities. However, due to various objective factors, there is a low probability that the synthesis will not be successful. If you need to learn more, please feel free to consult us, we will serve you wholeheartedly.
(Z)-Orantinib
Catalog No. T9684 CAS
210644-62-5
(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive inhibitor of Flk‐1/KDR, PDGFRβ, and FGFR1, with IC 50 s of 2.1, 0.008, and 1.2 μM, respectively. (Z)-Orantinib is a potent antiangiogenic and antitumor agent that induces established tumor regression[1] [2].
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(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive inhibitor of Flk‐1/KDR, PDGFRβ, and FGFR1, with IC 50 s of 2.1, 0.008, and 1.2 μM, respectively. (Z)-Orantinib is a potent antiangiogenic and antitumor agent that induces established tumor regression[1] [2].
In vitro
SU6668 rapidly inhibits Flk-1 trans-phosphorylation (K i =2.1 μM), FGFR1 trans-phosphorylation (K i =1.2 μM), and PDGFR autophosphorylation (K i =0.008 μM) within 5-15 minutes, as well as the VEGF-induced increase in KDR tyrosine phosphorylation in HUVECs at concentrations between 0.03-10 μM after 60 minutes [1]. Additionally, it dose-dependently suppresses HUVEC mitogenesis triggered by VEGF and FGF, with IC 50 values of 0.34 μM and 9.6 μM, respectively [1].
In vivo
SU6668, administered orally (p.o.) at dosages ranging from 4 to 200 mg/kg/day for 21 days, demonstrates a dose-dependent suppression of A431 tumor growth in athymic mice, with the most significant growth inhibition observed at 200 mg/kg/day, achieving a 97% reduction without any mortality across treatment groups. When administered intraperitoneally (i.p.) at 75 mg/kg/day for 22 days, SU6668 markedly inhibits tumor angiogenesis and vascularization. Additionally, oral administration of SU6668 at 200 mg/kg/day for durations between 11 to 27 days results in the significant regression of large established A431 xenografts. The study involved female athymic mice (BALB/c, nu/nu) implanted with A431 tumor cells.
Molecular Weight
310.35
Formula
C18H18N2O3
CAS No.
210644-62-5
Storage
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Dose Conversion
You can also refer to dose conversion for different animals.
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Method for preparing DMSO master liquid: mg
drug pre-dissolved in μL DMSO (Master liquid concentration
mg/mL),
Method for preparing in vivo formulation:Take μL
DMSO master liquid, next add μL PEG300, mix and clarify, next add μL
Tween 80,mix and clarify, next add μL ddH2O, mix and clarify.
Method for preparing in vivo formulation:Take μL
DMSO master liquid, next add μL Corn oil,mix and clarify.
Note:
Be sure to add the solvent(s) in order. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
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Tech Support
Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc.