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規格	2mg 5mg 10mg 25mg 50mg
CAS	1234356-69-4
別名	N/A
化學名	N/A
分子式	C29H29FN4O
分子量	468.57
溶解度	DMSO : ≥ 100 mg/mL (213.42 mM)
儲存條件	Store at -20°C
General tips	For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping Condition	Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request

產品描述：

Derazantinib (ARQ-087) is an ATP competitive tyrosine kinase inhibitor; exhibits potent activity against FGFR1-3 chondrocytes with IC50s of 4.5, 1.8, and 4.5 nM, respectively.

In cells, inhibition of FGFR2 auto-phosphorylation and other proteins downstream in the FGFR pathway (FRS2α, AKT, ERK) is evident by the response to Derazantinib treatment. Cell proliferation studies demonstrate Derazantinib has anti-proliferative activity in cell lines driven by FGFR dysregulation, including amplifications, fusions, and mutations. Cell cycle studies in cell lines with high levels of FGFR2 protein show a positive relationship between Derazantinib induced G1 cell cycle arrest and subsequent induction of apoptosis[1]. Derazantinib rescues the FGF2-mediated growth arrest with EC50 at about 100 nM, with no significant toxicity detected for up to 500 nM. The concentration range at which Derazantinib significantly suppresses the FGF2 effect is between 70-500 nM. Derazantinib inhibits FGF-mediated loss of extracellular matrix and induction of chondrocyte premature senescence. Derazantinib rescues FGF-mediated inhibition of chondrocyte differentiation in tibia cultures. Derazantinib inhibits FGFR1-4 but no other receptor tyrosine kinases in cell-free kinase assay. Derazantinib inhibits FGFR1 and FGFR2 mutants associated with craniosynostoses. Derazantinib rescues FGFR-mediated bone differentiation in mouse limb bud micromass cultures and ex vivo mouse calvarial organ cultures[2].

Derazantinib is effective at inhibiting tumor growth in FGFR2 altered, SNU-16 and NCI-H716, xenograft tumor models with gene amplifications and fusions[1]. Most of the embryos exhibit abnormal external phenotype (81.3%) in Derazantinib-injected wings, possibly due to inhibition of proliferation of limb bud mesenchyme. The wings are shorter and thinner, with skeletal phenotype typical for FGFR inhibition, where ulna and radius are shorter or smaller in size, or occasionally missing completely[2].

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原創作者：上海莼試生物技術有限公司

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