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HY-10192

CAS:761439-42-3

 (Synonyms  TAE684; NVP TAE684)
761439-42-3  Technical Data: Price and Availability of  Cas No:761439-42-3

Cas : 761439-42-3 M.Wt: 614.2
Cas : 761439-42-3 Formula: C30H40ClN7O3S
Cas : 761439-42-3 Purity: >98 %
Cas : 761439-42-3 Storage: at 20℃ 2 years
Cas : 761439-42-3 Solubility: 10 mM in DMSO
Cas : 761439-42-3 Name: NVP-TAE 684
USD
5mg/$80 In-stock
10mg/$120 In-stock
50mg/$320 In-stock
100mg/$450 In-stock
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761439-42-3  Data Sheet:
 
Introduction of 761439-42-3 :
NVP-TAE684(TAE684) is a highly potent and selective small-molecule ALK inhibitor, which blocked the growth of ALCL-derived and ALK-dependent cell lines with IC50 values between 2 and 10 nM. IC50 value: 2-10 nM [1] Target: ALK in vitro: TAE684 does not exhibit significant cross-reactivity against other kinases. TAE684 potently inhibits the proliferation of Ba/F3 NPM-ALK cells with IC50 of 3 nM, without affecting the survival of Ba/F3 cells even at 1 μM. TAE684 also inhibits proliferation of NPM-ALK-expressing human ALCL cell lines including Karpas-299 and SU-DHL-1 with IC50 of 2–5 nM. Molecular modeling reveals that L258 may be one of the major kinase-selectivity determinants for TAE684. TAE684 treatment results in a rapid and sustained inhibition of phosphorylation of NPM-ALK. TAE684 induces apoptosis and G1 phase arrest in NPM-ALK-expressing Ba/F3 cells and ALCL patient cell lines [1]. TAE684 markedly overcomes Crizotinib-resistance in H3122 CR cells, harboring the fusion oncogene EML4-ALK, decreasing cell growth, suppressing ALK phosphorylation and inducing apoptosis [2]. Neurite outgrowth induced by expression of the mALK R1279Q mutant could be completely inhibited by TAE684 at 30 nM [3]. in vivo: After 4 weeks of treatment with TAE684 at 3 and 10 mg/kg, there is a significant delay in lymphoma development and 100- to 1,000-fold reduction in luminescence signal, without any signs of compound- or disease-related toxicity in Karpas-299 lymphoma model. TAE684 treatment also induces disease regression in established Karpas-299 lymphomas and down-regulates CD30 expression [1]. TAE684 also shows impressive antitumor activity against H3122 CR xenograft tumors [2]. treatment with TAE684 improves the rough eye phenotype of both ALK mutants, especially that seen with ALKR1275Q, whereas Crizotinib has little effect on either phenotype [3].
 
References on 761439-42-3 :
 

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