For research use only. Not for therapeutic Use.
TGX-221 is a potent, selective, and cell membrane permeable inhibitor of the PI3K p110β catalytic subunit, used for cancer treatment.
TGX-221, BL05 and BL05-HA show selective cytotoxicity to LNCaP cells, which may be due to the deficiency of PTEN in this cell line and the accumulation of PIP3 in the cells[1]. TGX-221 (1 μM) does not affect the expression and phosphorylation of AMPK in C2C12 myoblasts[2]. TGX221 (0.1, 1, 10 μM) induces IL-6 release from ASM cells[2]. TGX-221 does not affect neurotensin-stimulated Akt phosphorylation when used alone, but it further suppresses neurotensin-stimulated phosphorylation of Akt when combined with gefitinib. TGX-221 abolishes the neurotensin-stimulated phosphorylation of Akt in Panc-1 cells[3].
TGX-221 (TGX221, 2.5 mg/kg i.v.) abolishes cyclic flow reductions in a Folts-like carotid artery stenosis preparation of thrombosis, without changing bleeding time, heart rate, blood pressure or carotid vascular conductance[4].
| Catalog Number | I004497 |
| CAS Number | 663619-89-4 |
| Synonyms | 9-(1-anilinoethyl)-7-methyl-2-morpholin-4-ylpyrido[1,2-a]pyrimidin-4-one |
| Molecular Formula | C21H24N4O2 |
| Purity | ≥95% |
| InChI | InChI=1S/C21H24N4O2/c1-15-12-18(16(2)22-17-6-4-3-5-7-17)21-23-19(13-20(26)25(21)14-15)24-8-10-27-11-9-24/h3-7,12-14,16,22H,8-11H2,1-2H3 |
| InChIKey | CPRAGQJXBLMUEL-UHFFFAOYSA-N |
| SMILES | CC1=CN2C(=O)C=C(N=C2C(=C1)C(C)NC3=CC=CC=C3)N4CCOCC4 |
| Reference | [1]. Zhao Y, et al. Prodrug strategy for PSMA-targeted delivery of TGX-221 to prostate cancer cells. Mol Pharm. 2012 Jun 4;9(6):1705-16. [2]. Sturgeon SA, et al. Advantages of a selective beta-isoform phosphoinositide 3-kinase antagonist, an anti-thrombotic agent devoid of other cardiovascular actions in the rat. Eur J Pharmacol. 2008 Jun 10;587(1-3):209-15. [3]. Ge Q, et al. The phosphoinositide 3′-kinase p110δ modulates contractile protein production and IL-6 release in human airway smooth muscle. J Cell Physiol. 2012 Aug;227(8):3044-52. [4]. Chaussade C, et al. Evidence for functional redundancy of class IA PI3K isoforms in insulin signalling. Biochem J. 2007 Jun 15;404(3):449-58. [5]. Müller KM, et al. Role of protein kinase C and epidermal growth factor receptor signalling in growth stimulation by neurotensin in colon carcinoma cells. BMC Cancer. 2011 Oct 2;11:421. |
