AZD1775 SARMS Raw Powder C27H32N8O2 Mk 1775 CAS 955365-80-7

AZD1775 Sarms Anabolic Steroids Mk 1775 For Bodybuilding CAS 955365-80-7

Product Name: MK-1775
CAS No: 955365-80-7
Chemical Formula: C27H32N8O2
Exact Mass: 500.26482
Molecular Weight: 500.59538
Elemental Analysis: C, 64.78; H, 6.44; N, 22.38; O, 6.39

Soluble in 0.1N HCl(aq) and DMSO

Appearance: Yellow solid

Purity: 99.3%

Quality: As stated in COA/HPLC/MSDS report

Min order: 1Grams

Delivery: Within 3-5 days

Shipping: By Express TNT /DHL with tracking number provide

MK-1775 Application:

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. However, 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, 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.

General Comments

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