PI3K/Akt/CREB activator 1

PI3K/Akt/CREB activator 1 (compound AE-18) is a potent, orally active PI3K/Akt/CREB activator. PI3K/Akt/CREB activator 1 promotes neuronal proliferation, induced differentiation of Neuro-2a cells into a neuron-like morphology, and accelerated the establishment of axon-dendrite polarization of primary hippocampal neurons through upregulating brain-derived neurotrophic factor via the PI3K/Akt/CREB pathway. PI3K/Akt/CREB activator 1 can be used in research of vascular dementia (VaD)[1].

Signaling Pathways >> PI3K/Akt/mTOR >> PI3K

Signaling Pathways >> PI3K/Akt/mTOR >> Akt

Research Areas >> Neurological Disease

Signaling Pathways >> Epigenetics >> Epigenetic Reader Domain

PI3K/Akt/CREB activator 1 (compound AE-18; 10 and 20 μM; 48 h) induces neurite outgrowth and proliferation through upregulating BDNF via the PI3K/Akt/CREB pathway Neuro-2a cells[1]. PI3K/Akt/CREB activator 1 (10 and 20 μM; neurons) enhances neuronal differentiation and axon-dendrite polarization in cultured hippocampal neurons through the PI3K/AKT signal pathway[1]. Western Blot Analysis[1] Cell Line: Neuro-2a cells Concentration: 10 and 20 μM Incubation Time: 48 hours Result: Increased the expressions of BDNF and the phosphorylated form of AKT (pAKT) and CREB (pCREB).

PI3K/Akt/CREB activator 1 (compound AE-18; 5 and 10 mg/kg; i.g.; male Sprague-Dawley rats with chronic cerebral hypoperfusion (CCH) model) improves cerebral blood flow (CBF) recovery after bilateral common carotid artery occlusion (BCCAO)[1]. PI3K/Akt/CREB activator 1 (5 and 10 mg/kg; i.g.; for 5 d) mitigates impairment of learning and memory in chronic cerebral hypoperfusion (CCH) rat model and alleviates CCH-induced pathological injury in the hippocampus after BCCAO[1]. Animal Model: Male Sprague-Dawley rats (200-220 g) with chronic cerebral hypoperfusion (CCH) model[1] Dosage: 5 and 10 mg/kg Administration: Oral gavage; daily, for 6 weeks Result: Promoted the recovery of CBF after BCCAO. Animal Model: Male Sprague-Dawley rats (200-220 g) with chronic cerebral hypoperfusion (CCH) model[1] Dosage: 5 and 10 mg/kg Administration: Oral gavage; daily, for 5 days Result: Reduced escape latency from day 1 to day 5 of the morris water maze (MWM) test compared with the CCH group. Improved cognitive deficits in CCH rat model.