| CAS NO: | 686770-80-9 |
| 包装: | 5mg |
| 市场价: | 1440元 |
| Cas No. | 686770-80-9 |
| 化学名 | 3-phenyl-2-(propylthio)-6,7-dihydrothieno[3,2-d]pyrimidin-4(3H)-one |
| Canonical SMILES | O=C1N(C2=CC=CC=C2)C(SCCC)=NC3=C1SCC3 |
| 分子式 | C15H16N2OS2 |
| 分子量 | 304.43 |
| 溶解度 | DMF: 30 mg/mL,DMSO: 30 mg/mL,DMSO:PBS (pH 7.2) (1:2): 0.33 mg/mL,Ethanol: 5 mg/mL |
| 储存条件 | Store at -20℃ |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
| 产品描述 | BC 11-38 is a selective inhibitor of PDE11 with an IC50 value of 0.28 μM [1]. PDE11 is a PDE family. In humans the PDE11A gene encodes four isoforms hydrolyzing both cAMP and cGMP. PDE11A is expressed in skeletal muscle, brain, prostate, testis, kidney, pancreas, liver, lymphoid cells, and pituitary and adrenal glands [2]. In H295R human adenocarcinoma cells, BC11-38 significantly increased cortisol production and cAMP levels, both in the presence and absence of the adenylate cyclase activator forskolin. In H295R cells, BC11-38 elevated ATF-1 phosphorylation in a manner that corresponded with its potency against PDE11. In several lines including MDA-MB-231 and HeLa cells, there were very low levels of PDE11A mRNA. In MDA-MB-231 cells, BC11-38 failed to elevate cAMP levels and CREB phosphorylation. In HeLa cells, BC11-38 did not affect cAMP levels or CREB phosphorylation [2]. In p54nrb/NONOKD cells, combining treatment with BC11-38 and ACTH restored partially the capacity to produce DHEA and cortisol in response to cAMP stimulation and the ability to generate cAMP in response to ACTH stimulation [3]. An invention also relates to the use of compounds such as BC11-38 to elevate cortisol levels in a subject who has adrenal suppression, e.g. where a subject is being administered with a corticosteroid, or on a long-term corticosteroid treatment [4]. References: |
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