| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | H1299 cells |
Preparation Method | H1299 cells were treated for 1 h with 200 nM MK-1775, irradiated with 7.5 Gy, incubated for an additional 18 h in MK-1775, and harvested for assessment of apoptosis at 24, 48, and 72 h post-irradiation. |
Reaction Conditions | 200 nM, 1 h |
Applications | The dose of 7.5 Gy induced levels of apoptosis of only about 5% above control at any time point and these levels of apoptosis were not significantly enhanced by MK-1775. |
Animal models | 6-week-old female nu/nu athymic mice |
Preparation Method | When tumors reached a volume of ~200 mm3, mice were individually identified and randomly assigned to treatment groups, with 5–6 mice (8–10 evaluable tumors) in each group: 1) control; 2) MK-1775 (30 mg/kg. p.o., once daily for 4 weeks; 3) GEM (100 mg/kg, i.p., twice weekly on days 1 and 4) for 4 weeks; 4) GEM followed 24 h later by MK-1775 in the above mentioned dose. |
Dosage form | 30 mg/kg. p.o., |
Applications | Single agent MK-1775 treatment produced greater than 50% inhibition of tumor growth in two xenografts (PANC286 and PANC198). |
| 产品描述 | MK-1775 is a potent and selective small-molecule inhibitor of Wee1 kinase with an IC50value of 5.2 nM. MK-1775 is 2- to 3-fold less potent against Yes with an IC50of 14 nM.[1]. In vitro efficacy test it shown that MK-1775 inhibited phosphorylation of CDC2 at Tyr15 with an EC50 value of 85 nM in cells pretreated with gemcitabine. MK-1775 treatment induced pHH3 in a dose-dependent manner with an EC50 value of 81 nM.[1]In vitro efficacy test it indicated that treatment with 10 nM panobinostat in combination with 250 nM or 500 nM MK-1775 in U937 cells, the combination index (CI) values were 0.95 and 0.73, while U937 cells treated with 20 nM panobinostat in combination with 250 nM or 500 nM MK-1775 were 0.39 and 0.40, respectively.[3]In vitro, treatment with 0.1, 0.3, 1 μM of MK-1775 for 48 h in LSCC cells and TU212 and KB-3-1 cells dose-dependently induced early apoptosis (Annexin V+/PI-) and late apoptosis (Annexin V+/PI+) . Moreover, after MK-1775 treatment, the protein levels of apoptosis marker cleaved-PARP was increased in a dose-depend manner[5]. In vivo, treatment with 60 mg/kg MK-1775 orally enhances H1299 xenograft tumor response to fractionated radiotherapy in nude mice.[2]In vivo experiment it indicated that treatment with either MK-1775 (20 mg/kg) or panobinostat (10 mg/kg) alone in mice bearing BxPC-3 xenograft tumors had modest delay of externally measurable tumor growth (30.9% and 37.8% on day 20, respectively). However, combination the MK-1775 (20 mg/kg) with panobinostat (10 mg/kg) can marked delay the tumor growth with 58.7% tumor growth inhibition on day 20.[4]In vivo, Nude Mice were treated with 50 mg/kg orally MK-1775, MK-1775 inhibited the growth of KB-3-1 xenografts with the inhibition ratio of 30.04% by reducing the tumor volumes and weights. And MK-1775 also can cause toxicity in mice at the indicated dose.[6]. References: |
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