(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate

(Z)-2-(Oleoyloxy) propane-1,3-diyl dipalmitate (1,3-Dipalmitoyl-2-oleoylglycerol) is an orally effective PTP1B inhibitor with an IC₅₀ of 31.01 μM and a K_i of 16.36 μM. (Z)-2-(Oleoyloxy) propane-1,3-diyl dipalmitate also inhibits α-glucosidase with an IC₅₀ of 163.31 μM. It inhibits phosphorylation of p38 MAPK, activates the PI3K/Akt/CREB pathway, and exhibits antioxidant, anti-apoptosis and anti-inflammatory activities, as well as inhibits peroxynitrite-mediated albumin nitration. (Z)-2-(Oleoyloxy) propane-1,3-diyl dipalmitate can be used in studies related to cerebral ischemia-reperfusion injury and diabetes^[1][2][3]. In Vitro:(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate (1,3-Dipalmitoyl-2-oleoylglycerol) exhibits neuroprotective activity against NMDA-mediated excitotoxicity in cultured cortical neurons^[1].
(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate (4.81-120.19 μM) potently inhibits purified PTP1B with an IC₅₀ of 31.01 μM via mixed-type inhibition^[2].
(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate inhibits purified α-glucosidase with an IC₅₀ of 163.31 μM^[2].
(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate binds to the active pocket of PTP1B (PDB ID: 1NNY) with a docking score of −7.4 kcal/mol via multiple hydrogen bonding and hydrophobic interactions^[2].
(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate binds to the active pocket of α-glucosidase (PDB ID: 3A4A) with a docking score of −7.1 kcal/mol via multiple hydrogen bonding and hydrophobic interactions^[2].
(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate (12.5-100 μM; 30 min) at 100 μM moderately inhibits ONOO⁻-mediated bovine serum albumin nitration in vitro^[2].
(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate forms a complex with α-glucosidase that has adaptive flexibility, with collective motions supporting stable ligand binding^[2]. In Vivo:(Z)-2-(Oleoyloxy)propane-1,3-diyl dipalmitate (1,3-Dipalmitoyl-2-oleoylglycerol) (POP) (1-5 mg/kg; p.o.; administered 0.5 h before MCAO, 1 h after MCAO, and 1 h after reperfusion) exerts dose-dependent neuroprotective effects against MCAO/R-induced ischemic stroke in rats, with the 5 mg/kg dose producing the most significant reductions in infarct volume, edema volume, and neurological deficits via inhibition of p38 MAPK and activation of the PI3K/Akt/CREB pathway, alongside anti-oxidant, anti-apoptotic, and anti-inflammatory actions^[1].