Adavosertib

Research use only, not for human use.

A potent and selective small-molecule inhibitor of Wee1 kinase with IC50 of 5.2 nM.

A potent and selective small-molecule inhibitor of Wee1 kinase with IC50 of 5.2 nM; exhibits ATP-competitive and highly selective against other serine/threonine or tyrosine kinases; inhibits phosphorylation of CDC2 at Tyr15 in cells; potentiates tumor growth inhibition in vivo.Lung Cancer Phase 2 Clinical(In Vitro):Adavosertib (MK-1775) enhances the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells. Adavosertib (MK-1775) inhibits CDC2 Y15 phosphorylation in cells, abrogates DNA damaged checkpoints induced by 5-FU treatment, and causes premature entry of mitosis determined by induction of Histone H3 phosphorylation. Adavosertib (MK-1775) abrogates the radiation-induced G2 block in p53-defective cells but not in p53 wild-type lines. The combination of NSC 613327 with Adavosertib (MK-1775) produces robust anti-tumor activity and remarkably enhances tumor regression response (4.01 fold) compared to NSC 613327 treatment in p53-deficient tumors.(In Vivo):In vivo, Adavosertib (MK-1775) potentiates the anti-tumor efficacy of 5-FU at tolerable doses. Adavosertib (MK-1775) (60 mg/kg twice daily, p.o.) enhances H1299 xenograft tumor response to fractionated radiotherapy. Adavosertib (MK-1775) (30 mg/kg. p.o.) regresses tumor growth in PANC198, PANC215 and PANC185 as compared to GEM treated mice.

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AZD-1775 | MK-1775

Cell Cycle/DNA Damage

Wee1

Wee1

Cancer

Lung Cancer

955365-80-7

500.5954

C27H32N8O2

>98% (HPLC)

10 mM in DMSO

O=C1N(CC=C)N(C2=NC(C(C)(O)C)=CC=C2)C3=NC(NC4=CC=C(N5CCN(C)CC5)C=C4)=NC=C31

3H-Pyrazolo[3,4-d]pyrimidin-3-one, 1,2-dihydro-1-[6-(1-hydroxy-1-methylethyl)-2-pyridinyl]-6-[[4-(4-methyl-1-piperazinyl)phenyl]amino]-2-(2-propen-1-yl)-

(-20℃)

With Ice Pack

≥ 2 years