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| Product | Description | |
|---|---|---|
| Adavosertib | Adavosertib (AZD-1775; MK-1775) is a potent Wee1 inhibitor with an IC 50 of 5.2 nM. Uses: Scientific research. Group: Signaling pathways. Alternative Names: AZD1775; MK-1775. CAS No. 955365-80-7. Pack Sizes: 10 mM * 1 mL; 5 mg; 10 mg; 50 mg; 100 mg; 200 mg; 500 mg. Product ID: HY-10993. |  |
| Adavosertib | Adavosertib Inhibitor. Uses: Scientific use. Product Category: T2077. CAS No. 955365-80-7. |  |
| Pomalidomide-C3-adavosertib | Pomalidomide-C3-adavosertib is a rapid and selective PROTAC Wee1 degrader (IC50=3.58 nM). Pomalidomide-C3-adavosertib shows anti-cancer cell proliferation activity, and induces apoptosis[1]. Uses: Scientific research. Group: Signaling pathways. CAS No. 2414418-49-6. Pack Sizes: 1 mg; 5 mg; 10 mg. Product ID: HY-133618. | |
| MK-1775 | MK-1775, also known as AZD-1775, is a WEE1 inhibitor and 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 (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. Unlike normal cells, most p53-deficient or mutated human cancers lack the G1 checkpoint as p53 is the key regulator of the G1 checkpoint and these cells rely on the G2 checkpoint for DNA repair to damaged cells. Annulment of the G2 checkpoint may therefore make p53-deficient tumor cells more vulnerable to antineoplastic agents and enhance their cytotoxic effect. Synonyms: MK-1775; MK1775; MK 1775; AZD1775; AZD-1775; AZD 1775; adavosertib. 1-[6-(2-hydroxypropan-2-yl)pyridin-2-yl]-6-[4-(4-methylpiperazin-1-yl)anilino]-2-prop-2-enylpyrazolo[3,4-d]pyrimidin-3-one. Grades: >98%. CAS No. 955365-80-7. Molecular formula: C27H32N8O2. Mole weight: 500.607. |  |
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