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[求助]
麻烦翻译几句医药方面的东西，谢谢啦
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PARP inhibitor program: SC10914 has single digit nanomolar inhibitory IC50 for PARP-1 enzyme and strong inhibition of VC8 cell proliferation. It also demonstrates the superior PK profiles in rat and efficacy in VC8 (BRCA2 deficient) mice zenograft model compared to Olaparib. In addition, SC10914 has low potential for drug-drug interaction with all six major cytochrome P450 IC50>10uM, low potential for cardiac liabilities with hERG IC50>30uM, and low potential for mutagenicity by showing negative in Ames test. FMS-like receptor tyrosine kinase-3(Flt3), a member of class III tyrosine kinase receptor family, is predominantly expressed in hematopoietic progenitor cells and plays an important role in the pathogenesis of acute myeloid leukemia (AML). Flt3 is expressed in blast cells of most patients with AML including wild-type and two forms of Flt3 mutations. These two mutations identified in the AML patients are internal tandem duplication (ITD) mutations in the juxtamembrane domain and point mutations (TKD) in the activation loop of the TKD. The relapse rates in the Flt3/ITD mutation AML patients are significantly increased and the overall survival rates decreased compared with the AML patients without the Flt3 mutation. So development of a drug inhibited both wide type and mutant Flt3 kinase could provide an effective way to treat AML. Flt3 inhibitor program: SC110219 is a highly potent Flt3 inhibitor both in Flt3 enzyme (IC50 = 5nM) and MV4-11(IC50 = 0.5nM) assays. It also demonstrates very strong antitumor effects in subcutaneous MV4-11 AML Xenograft model in NOD/SCID mice at as low as 3mg/kg dose level. Other biological profiling is under progress. |
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wangpei838
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4楼2012-01-28 20:50:11
wangpei838
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2楼2012-01-28 20:46:38
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3楼2012-01-28 20:47:55
kno3
捐助贵宾 (著名写手)
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爱与雨下(金币+1): 2012-01-29 19:42:37
sltmac(金币+40): 2012-02-13 08:41:04
sltmac(金币+40): 欢迎常来本版交流 2012-02-13 08:41:11
爱与雨下(金币+1): 2012-01-29 19:42:37
sltmac(金币+40): 2012-02-13 08:41:04
sltmac(金币+40): 欢迎常来本版交流 2012-02-13 08:41:11
| FMS酪氨酸激酶样受体-3(Fit3)是酪氨酸激酶受体家族III类受体，主要表达在造血祖细胞上，在急性髓细胞性白血病(AML)发病机制中起重要作用。Fit3在大部分AML患者的胚细胞上表达，这些患者的基因型包括野生型和两种Fit3突变型。经鉴定，这两种AML患者的基因突变是近膜域的内部串联重复(ITD)突变和TKD激活环的点突变(TKD)。AML患者中，与Fit3野生型患者相比，Fit3/ITD突变患者呈现复发率高和整体存活率低的特点。因此，开发能共同抑制Fit3激酶野生型和突变型的药物是治疗AML的有效方式。 |
5楼2012-01-28 21:57:34
