Selective Androgen Inhibitors MK-1775 Oral Anabolic Steroids CAS 955365-80-7 for Bodyhealth
- Manufacturer: Dewael
- Product Assay: 99%+
- Appearance: yellow powder
- Place of Origin: China
- Certification: SGS,ISO9001,GMP
- Minimum Order Quantity: 10g
- Packaging Details: Discreet ways of packing for Customs pass guaranteed
- Delivery Time: Within 12 hours after receiving your payment
- Payment Terms: Western Union, MoneyGram,Bitcoin,Bank Transfer
- Shipping: EMS,DHL,Fedex,UPS,TNT and so on.
- Policy: Re-Shipping Policy
- Supply ability: 500-600kg/month
Selective Androgen Inhibitors MK-1775 Oral Anabolic Steroids CAS 955365-80-7 for Bodyhealth
MK-1775 Basic Info
Product Name | MK-1775 |
Alias | MK1775, MK 1775 |
CAS | 955365-80-7 |
MF | C27H32N8O2 |
MW | 500.59538 |
Purity | 99.50% |
Grade | Pharmaceutical Grade |
Appearance | yellow powder |
Brand Nmae | HKYC |
Standard | 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, Western Union,Money Gram , Bitcoin |
Usage | MK-1775 is an inhibitor of the checkpoint kinase Wee1 |
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 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.
Other Related SARMs:
Name | CAS NO. | Usage |
AICAR | 2627-69-2 | acts by entering nucleoside pools, significantly increasing levels of adenosine during periods of ATP breakdown |
MK2866 | 841205-47-8 | medical prescription for prevention of cachexia, atrophy, and sarcopenia and for Hormone or Testoserone Replacement Therapy. |
MK-677 | 15972-10-0 | A growth hormone secretagogue, treatment of obesity, a promising therapy for the treatment of frailty in the elderly |
LGD-4033 | 1165910-22-4 | pharmacological profile similar to that of enobosarm, Ostarine,MK-2866 |
GW501516 | 317318-70-0 | For obesity, diabetes, dyslipidemia and cardiovascular disease |
Andarine(S4) | 401900-40-0 | partial agonist, intended mainly for treatment of benign prostatic hypertrophy |
SR9009 | 1379686-30-2 | under development at The Scripps Research Institute (TSRI), increases the level of metabolic activity in skeletal muscles of mice |
RAD140 | 1182367-47-0 | New generation for gaining mass and cutting edges |
YK11 | 431579-34-9 | YK11: a SARM and myostatin inhibitor in on |
———————————————————————————————————————————————————————————————————————————————————————-
Contact Now
Reviews
There are no reviews yet.