| Description | IC-87114 is a specific PI3Kδ inhibitor(IC50=0.5 μM). |
| In vitro | 在有炎症反应的鼠模型中,IC87114阻断TNF1α刺激产生蛋白酶的胞外分泌. |
| In vivo | 在人类中性粒细胞中,IC87114（5 μM）能够地抑制N-甲酰 - 甲硫氨酰 - 亮氨酰 - 苯丙氨酸（fMLP） - 刺激的磷脂酰肌醇三磷酸（PIP3）的生物合成和趋化性。在人类急性骨髓性白血病（AML）原始细胞如骨髓单个核细胞（BMMCs）中,IC87114（10 μM）抑制组成型和Flt-3刺激的Akt磷酸化和细胞增殖。在抗CD3刺激的小鼠CD62L +（幼稚）和CD62L-（效应/记忆）CD4 + T细胞中,IC87114抑制增殖和干扰素-γ（IFN-γ）产生。 |
| Cell experiments | For AML cell proliferation assay, BMMCs are isolated and cultured in α-medium with 5% fetal calf serum (FCS) with or without FLT-3 ligand (10 ng/mL) for 48 hours and with or without IC87114. [3H]-thymidine (1 μCi [37 kBq]) is added for a final 6 hours and the amount of radioactivity incorporated is determined by trichloracetic acid precipitation. CD34+ cells from cord blood are cultured in stem cell factor (SCF; 20 ng/mL), FLT-3 ligand (10 ng/mL), and Tpo (20 nM) for 48 hours with or without 10 μM IC87114 and pulsed for 12 hours with [3H]-thymidine. (Only for Reference) |
| Target activity | PI3Kγ:29 μM, PI3Kδ:0.5 μM |
| Synonyms | IC 87114 |
| molecular weight | 397.43 |
| Molecular formula | C22H19N7O |
| CAS | 371242-69-2 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| Solubility | DMSO: 8 mg/mL (20.13 mM), Sonication is recommended. |
| References | 1. Sadhu C, et al. J Immunol, 2003, 170(5), 2647-2654. 2. Sujobert P, et al. Blood, 2005, 106(3), 1063-1066. 3. Ali K, et al. Nature, 2004, 431(7011), 1007-1011. 4. Soond DR, et al. Blood, 2010, 115(11), 2203-2213. 5. Wen PJ, et al. Nat Commun, 2011, doi:10.1038/ncomms1500. 6. Zheng L, et al. Inactivation of PI3Kδ induces vascular injury and promotes aneurysm development by upregulating the AP-1/MMP-12 pathway in macrophages. Arterioscler Thromb Vasc Biol. 2015 Feb;35(2):368-77. 7. El-Hashim AZ, et al. Src-dependent EGFR transactivation regulates lung inflammation via downstream signaling involving ERK1/2, PI3Kδ/Akt and NFκB induction in a murine asthma model. Sci Rep. 2017 Aug 30;7(1):9919. |