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BC 11-38
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
BC 11-38图片
CAS NO:686770-80-9
包装:5mg
市场价:1440元

产品介绍
BC 11-38 是一种有效的、选择性的、具有生物活性的 PDE11 抑制剂,对 PDE11 和 PDE1-10 的 IC50 分别为 0.28 μM 和 \u003e100 μM。
Cas No.686770-80-9
化学名3-phenyl-2-(propylthio)-6,7-dihydrothieno[3,2-d]pyrimidin-4(3H)-one
Canonical SMILESO=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 tipsFor obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.
Shipping ConditionEvaluation 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:
[1].  Cichero E, D'Ursi P, Moscatelli M, et al. Homology modeling, docking studies and molecular dynamic simulations using graphical processing unit architecture to probe the type-11 phosphodiesterase catalytic site: a computational approach for the rational design of selective inhibitors. Chemical biology & drug design, 2013, 82(6): 718-731.
[2].  Ceyhan O, Birsoy K, Hoffman CS. Identification of biologically active PDE11-selective inhibitors using a yeast-based high-throughput screen. Chemistry & biology, 2012, 19(1): 155-163.
[3].  Lu JY, Sewer MB. p54nrb/NONO Regulates Cyclic AMP-Dependent Glucocorticoid Production by Modulating Phosphodiesterase mRNA Splicing and Degradation. Molecular and cellular biology, 2015, 35(7): 1223-1237.
[4].  Hoffman CS, Ceyhan O. Inhibitors of phosphodiesterase 11 (PDE11): U.S. Patent 9,173,884[P]. 2015-11-3.