Pelcitoclax (APG-1252, BM-1252)

Chemical Structure : Pelcitoclax

加入收藏

货号: PC-49798Not For Human Use, Lab Use Only.

Pelcitoclax (APG-1252, BM-1252) is a potent dual specific Bcl-2/Bcl-xL inhibitor with Ki of < 1 nM, shows potent antitumor effects with minimal platelet toxicity.

规格	价格	库存	数量
10 mg		Get quote
25 mg		Get quote
50 mg		Get quote
100 mg		Get quote

获取报价单

* 请选择数量再加入购物车

or Bulk Inquiry

大包装，大折扣！

E-mail: sales@probechem.com

Tech Support: tech@probechem.com

生物&药学活性

Pelcitoclax (APG-1252, BM-1252) is a potent dual specific Bcl-2/Bcl-xL inhibitor with Ki of < 1 nM, shows potent antitumor effects with minimal platelet toxicity.
Pelcitoclax (APG-1252, BM-1252) changes to its reactive metabolite, named APG-1252-M1, in vivo can disrupt the anti-apoptotic function of these proteins with potent antitumor effects.
APG-1252 is >10- times less active than APG-1252-M1 in cell growth assay in a panel of small cell lung cancer (SCLC) cell lines.
APG-1252-M1 induces Bax/Bak-dependent apoptosis in MEF/MCL1−/− model cell line.
APG-1252 is >30-times less effective in platelet killing than BM-1252-M1 in animals. APG-1252-M1 exerts nanomolar single agent activity in a small subset of colorectal cancer (CRC) cell lines and synergizes with MEK inhibitor trametinib in a large subset of CRC cell lines.
APG-1252 plus gemcitabine exhibited even remarkable antitumor activity in vivo, has synergistic anticancer activities against advanced nasopharyngeal carcinoma (NPC).

物理化学性质&存储条件

分子量	1281.84
分子式	C57H66ClF4N6O11PS4
外观性状	Solid
CAS No.
储存条件	固体粉末 -20°C 12 个月; 4°C 6 个月	配置液 -80°C 6 个月; -20°C 6 个月
Shipping
Solubility	10 mM in DMSO
Chemical Name/SMILES	3-Phosphonopropyl 1-[(3R)-3-[[4-[[[4-[4-[3-[2-(4-chlorophenyl)-5-methyl-1-(1-methylethyl)-4-(methylsulfonyl)-1H-pyrrol-3-yl]-5-fluorophenyl]-1-piperazinyl]phenyl]amino]sulfonyl]-2-[(trifluoromethyl)sulfonyl]phenyl]amino]-4-(phenylthio)butyl]-4-piperidinecarboxylate

参考文献

1. Yi H, et al. Cancer Med. 2020 Jun;9(12):4197-4206.

2. Luo F, et al. Cell Death Dis. 2021 Aug 5;12(8):772.

3. Bai L, et al. Eur J Cancer. 2014;50:109–10.