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MK-1775 CAS:955365-80-7

MK-1775
Alias:MK1775, MK 1775
CAS:955365-80-7
MF:C27H32N8O2
MW:500.59538
Saflık:99.50%
Seviye:Farmasötik Sınıf
Dış görünüş:Yellow Powder
Brand Nmae:HKYC
Standart:USP
Stock:Mass Stock
Storage store at 0-5
Packing Methods designed disguised packing ways, 100% pass custom guarantee
Delivery time within 18 hours after payment confirmed
Payment:T/T, Batı Birliği,Para gram , Bitcoin
Kullanım:MK-1775, kontrol noktası kinaz Wee1'in bir inhibitörüdür

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MK-1775 Nedir??

MK-1775, kontrol noktası kinaz Wee1'in bir inhibitörüdür (IC50 = 5.2 nM).1 Triozin-15'te Cdc2'nin fosforilasyonunu inhibe ettiği gösterilmiştir., bu, G2 DNA hasarı kontrol noktasını ortadan kaldırır.1 DNA hasarı üzerine yalnızca G2 kontrol noktasına dayanan p53 eksikliği olan tümörlerde, MK-1775, DNA'ya zarar veren kemoterapötik ajanlarla kombinasyon halinde, is reported to induce apoptosis in vitro and potentiate the inhibition of tumor growth in vivo.

 

MK-1775 treatment led to the inhibition of Wee1 kinase and reduced inhibitory phosphorylation of its substrate Cdc2. MK-1775, when dosed with gemcitabine, abrogated the checkpoint arrest to promote mitotic entry and facilitated tumor cell death as compared to control and gemcitabine treated tumors. MK-1775 monotherapy did not induce tumor regressions. Yine de, the combination of gemcitabine with MK-1775 produced robust anti-tumor activity and remarkably enhanced tumor regression response (4.01 fold) compared to gemcitabine treatment in p53-deficient tumors. Tumor re-growth curves plotted after the drug treatment period suggest that the effect of the combination therapy is longer-lasting than that of gemcitabine. None of the agents produced tumor regressions in p53-wild type xenografts.

MK-1775 inhibits Wee1 kinase in an ATP-competitive manner. Compared to Wee1, MK-1775 displays 2- to 3-fold less potency against Yes with IC50 of 14 nM, 10-fold less potency against seven other kinases with >80% inhibition at 1 μM, ve >100-fold selectivity over human Myt 1, another kinase that inhibits cyclin-dependent kinase 1 (CDC2) by phosphorylation at an alternative site (Thr14).

By abrogating the DNA damage checkpoint via blockade of Wee1 activity in WiDr cells bearing mutated p53, MK-1775 treatment inhibits the basal phosphorylation of CDC2 at Tyr15 (CDC2Y15) with EC50 of 49 nM, and suppresses gemcitabine-, carboplatin- or cisplatin-induced phosphorylation of CDC2 and cell cycle arrest in a dose-dependent manner, with EC50 of 82 nM and 81 nM, 180 nM and 163 nM, as well as 159 nM and 160 nM, respectively. MK-1775 treatment alone at 30-100 nM has no significant antiproliferative effect in WiDr and H1299 cells, whereas MK-1775 at 300 nM, sufficient to inhibit Wee1 by >80%, displays moderate but significant antiproliferative effects by 34.1% in WiDr cells and 28.4% in H1299 cells.

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