Ascorbyl palmitate


CAS No. : 137-66-6

(Synonyms: L-Ascorbic acid 6-hexadecanoate; 6-O-Palmitoyl-L-ascorbic acid)

137-66-6
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Cat. No. : HY-B0987
M.Wt: 414.53
Formula: C22H38O7
Purity: >98 %
Solubility: H2O : 1 mg/mL (ultrasonic);DMSO : 100 mg/mL (ultrasonic)
Introduction of 137-66-6 :

Ascorbyl palmitate is an orally active ester formed from ascorbic acid and palmitic acid, used as an antioxidant and food additive. Ascorbyl palmitate in preventing fat and oil oxidation is more efficient than Butylated hydroxyanisole (HY-B1066) and Butylated hydroxytoluene (HY-Y0172). Ascorbyl palmitate mitigates inhibition of collagen synthesis by select calcium and sodium channel blockers. Ascorbyl palmitate induces Apoptosis in human umbilical vein endothelial cells (HUVECs). Ascorbyl palmitate ameliorates inflammatory diseases by inhibition of NLRP3 inflammasome[1][2][3][4]. In Vitro:Ascorbyl palmitate (25-400 μM, 24 h and 48 h) induces cell cytotoxicity and inhibits cell growth in HUVECs in a dose- and time-dependent manner[1].
Ascorbyl palmitate (125 μM, 24 h and 48 h) inhibits proliferation of HUVECs and induces cell death by inducing apoptosis, which decreases Bcl-2 gene expression ratio and increases Caspase-3, 9 activities in HUVECs[1].
Ascorbyl palmitate (1.25-20 μM, 72 h) dependent extracellular matrix (ECM) deposition of collagen type l is significantly reduced in aortic smooth muscle cells, which is inhibited by Nifedipine (HY-B0284) (50 µM, 72 h)[2].
Ascorbyl palmitate (0-20 μM, 1 h) has stronger inhibitory activity against NLRP3 inflammasome through its antioxidant ability than ascorbic acid in LPS (HY-D1056)-primed bone marrow-derived macrophages (BMDMs)[3].
In Vivo:Ascorbyl palmitate (25 mg/kg, i.p., every 2 days for 10 or 14 days) alleviates LPS (HY-D1056)-induced NLRP3 inflammasome activation, dextran sulfate sodium (DSS) (HY-116282C)-induced colitis and experimental autoimmune encephalomyelitis (EAE) in mice[3].

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