Targeted Drug Inhibitors Mk-1775 CAS 955365-80-7 for Treat Ovarian Cancer
Basic Info.
Model NO.: 955365-80-7
Suitable for: Adult
Purity: >99%
Product Name: Mk-1775
Delivery: Safe & Timely, Around 7days After Payment.
Specification: 1kg foil bag or as require
Powder: Yes
State: Solid
Assay: 99%
Description: Yellow Powder
Alias: Mk1775
Transport Package: Discreet Package for Delivery Guarantee
COA
Product Name
|
MK-1775
|
CAS
|
955365-80-7
|
MF
|
C27H32N8O2
|
MW
|
500.59538
|
Appearance
|
yellow powder
|
Package
|
50G/foil bag
|
Standard
|
enterprise standard
|
Assay
|
99%
|
Grade
|
medical grade
|
MK-1775 Description:
MK-1775 is a small molecule inhibitor of the tyrosine kinase WEE1 with potential antineoplastic sensitizing activity. MK-1775 selectively targets and inhibits WEE1, a tyrosine kinase that phosphorylates cyclin-dependent kinase 1 (CDK1, CDC2) to inactivate the CDC2/cyclin B complex. Inhibition of WEE1 activity prevents the phosphorylation of CDC2 and impairs the G2 DNA damage checkpoint. This may lead to apoptosis upon treatment with DNA damaging chemotherapeutic agents. MK-1775 is a type of biological therapy. It is a cancer growth blocker. It stops signals that cancer cells use to divide and grow. MK-1775 has been used in trials studying the treatment of LYMPHOMA, Neoplasms, Ovarian Cancer, Tongue Carcinoma, and Adult Glioblastoma, among others.
MK-1775 Applicaiton:
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, and >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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