| Description | TPPB is a kinase C activator of cell-permeable benzolactam-derived protein (Ki: 11.9 nM). |
| In vitro | TPPB inhibits the activation of caspase-3 induced by Aβ25-35. TPPB could increase the phosphorylation of Akt, PKC, MARCKS, and MAPK, which are inhibited by Aβ25-35 treatment. TPPB at a concentration of 1 μM could antagonize Aβ25-35 induced cell damage. By the use of a cell line derived from an Alzheimer’s disease patient, significant enhancement of sAPPα secretion is achieved at 1 μM concentration for TPPB. TPPB has a role against Aβ25-35-induced neurotoxicity in PC12 cells [1][2]. |
| In vivo | TPPB is evaluated for the induction of hyperplasia displays a modest response at 300 μg after topical application to the shaved backs of outbred Sencar mice and [1]. |
| Target activity | PKC:11.9 nM (ki) |
| molecular weight | 501.54 |
| Molecular formula | C27H30F3N3O3 |
| CAS | 497259-23-1 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| Solubility | DMSO: 125 mg/mL (249.23 mM), Sonication is recommended. |
| References | 1. Kozikowski AP, et al. New amide-bearing benzolactam-based protein kinase C modulators induce enhanced secretion of the amyloid precursor protein metabolite sAPPalpha. J Med Chem. 2003 Jan 30;46(3):364-73. 2. Yang HQ, et al. Neuroprotective effects of new protein kinase C activator TPPB against Aβ25-35 induced neurotoxicity in PC12 cells. Neurochem Res. 2012 Oct;37(10):2213-21. |
| Citations | 1. Ma R, Bi H, Wang Y, et al.Low concentrations of saracatinib promote definitive endoderm differentiation through inhibition of FAK-YAP signaling axis.Cell Communication and Signaling.2024, 22(1): 1-18. |