Volixibat
Volixibat Uses, Dosage, Side Effects, Food Interaction and all others data.
Volixibat, also known as SHP626 or LUM002, is an investigational drug that will potentially be used for the treatment of Non-Alcoholic Steatohepatitis (NASH). If approved for use, it will be the first available agent for the treatment of NASH.
Volixibat is a selective inhibitor of the apical sodium-dependent bile acid transporter (ASBT), a transmembrane protein primarily expressed by enterocytes of the ileum. Also known as the ileal bile acid transporter (IBAT), ASBT is primarily responsible for the enterohepatic recirculation of bile acids and ultimately for hepatic lipid and glucose metabolism . Inhibiting this enzyme results in a decrease of bile acids returning to the liver, which is helpful for the treatment of NASH as abnormal cholesterol metabolism and accumulation of free cholesterol in the liver have been implicated in its pathogenesis.
According to Shire, the pharmaceutical manufacturer of Volixibat, it has been granted fast track status by the Food and Drug Administration due to promising initial results and a need for therapeutic treatments for NASH.
Trade Name | Volixibat |
Generic | Volixibat |
Volixibat Other Names | Volixibat |
Type | |
Formula | C38H51N3O12S2 |
Weight | Average: 805.96 Monoisotopic: 805.291416442 |
Groups | Experimental, Investigational |
Therapeutic Class | |
Manufacturer | |
Available Country | |
Last Updated: | September 19, 2023 at 7:00 am |
Uses
Volixibat is an investigational drug that has not been approved for use in any conditions.
How Volixibat works
Volixibat is a selective inhibitor of the apical sodium-dependent bile acid transporter (ASBT), a transmembrane protein primarily expressed by enterocytes of the ileum. ASBT is primarily responsible for the recirculation of bile acids and therefore for hepatic lipid and glucose metabolism. Inhibiting this enzyme results in a decrease of bile acids returning to the liver, which is helpful for the treatment of NASH as abnormal cholesterol metabolism and accumulation of free cholesterol in the liver have been implicated in its pathogenesis.
Innovators Monograph
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