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Status:
US Previously Marketed
Source:
ZURAMPIC by IRONWOOD PHARMS INC
(2015)
Source URL:
First approved in 2015
Source:
ZURAMPIC by IRONWOOD PHARMS INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Lesinurad (brand name Zurampic) is a urate transporter inhibitor for treating hyperuricemia associated with gout in patients who have not achieved target serum uric acid levels with a xanthine oxidase inhibitor alone. In gout patients, Lesinurad lowered serum uric acid levels and increased renal clearance and fractional excretion of uric acid. Following single and multiple oral doses of Lesinurad to gout patients, dose-dependent decreases in serum uric acid levels and increases in urinary uric acid excretion were observed. Lesinurad reduces serum uric acid levels by inhibiting the function of transporter proteins involved in uric acid reabsorption in the kidney. Lesinurad inhibited the function of two apical transporters responsible for uric acid reabsorption, uric acid transporter 1 (URAT1) and organic anion transporter 4 (OAT4), with IC50 values of 7.3 and 3.7 µM, respectively. URAT1 is responsible for the majority of the reabsorption of filtered uric acid from the renal tubular lumen. OAT4 is a uric acid transporter associated with diuretic-induced hyperuricemia. Lesinurad does not interact with the uric acid reabsorption transporter SLC2A9 (Glut9), located on the basolateral membrane of the proximal tubule cell. Based on in vitro studies, lesinurad is an inhibitor of OATP1B1, OCT1, OAT1, and OAT3; however, lesinurad is not an in vivo inhibitor of these transporters. In vivo drug interaction studies indicate that lesinurad does not decrease the renal clearance of furosemide (substrate of OAT1/3), or affect the exposure of atorvastatin (substrate of OATP1B1) or metformin (substrate of OCT1). Based on in vitro studies, lesinurad has no relevant effect on P-glycoprotein.
Status:
US Previously Marketed
Source:
ZURAMPIC by IRONWOOD PHARMS INC
(2015)
Source URL:
First approved in 2015
Source:
ZURAMPIC by IRONWOOD PHARMS INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Lesinurad (brand name Zurampic) is a urate transporter inhibitor for treating hyperuricemia associated with gout in patients who have not achieved target serum uric acid levels with a xanthine oxidase inhibitor alone. In gout patients, Lesinurad lowered serum uric acid levels and increased renal clearance and fractional excretion of uric acid. Following single and multiple oral doses of Lesinurad to gout patients, dose-dependent decreases in serum uric acid levels and increases in urinary uric acid excretion were observed. Lesinurad reduces serum uric acid levels by inhibiting the function of transporter proteins involved in uric acid reabsorption in the kidney. Lesinurad inhibited the function of two apical transporters responsible for uric acid reabsorption, uric acid transporter 1 (URAT1) and organic anion transporter 4 (OAT4), with IC50 values of 7.3 and 3.7 µM, respectively. URAT1 is responsible for the majority of the reabsorption of filtered uric acid from the renal tubular lumen. OAT4 is a uric acid transporter associated with diuretic-induced hyperuricemia. Lesinurad does not interact with the uric acid reabsorption transporter SLC2A9 (Glut9), located on the basolateral membrane of the proximal tubule cell. Based on in vitro studies, lesinurad is an inhibitor of OATP1B1, OCT1, OAT1, and OAT3; however, lesinurad is not an in vivo inhibitor of these transporters. In vivo drug interaction studies indicate that lesinurad does not decrease the renal clearance of furosemide (substrate of OAT1/3), or affect the exposure of atorvastatin (substrate of OATP1B1) or metformin (substrate of OCT1). Based on in vitro studies, lesinurad has no relevant effect on P-glycoprotein.
Status:
US Previously Marketed
Source:
ZURAMPIC by IRONWOOD PHARMS INC
(2015)
Source URL:
First approved in 2015
Source:
ZURAMPIC by IRONWOOD PHARMS INC
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Lesinurad (brand name Zurampic) is a urate transporter inhibitor for treating hyperuricemia associated with gout in patients who have not achieved target serum uric acid levels with a xanthine oxidase inhibitor alone. In gout patients, Lesinurad lowered serum uric acid levels and increased renal clearance and fractional excretion of uric acid. Following single and multiple oral doses of Lesinurad to gout patients, dose-dependent decreases in serum uric acid levels and increases in urinary uric acid excretion were observed. Lesinurad reduces serum uric acid levels by inhibiting the function of transporter proteins involved in uric acid reabsorption in the kidney. Lesinurad inhibited the function of two apical transporters responsible for uric acid reabsorption, uric acid transporter 1 (URAT1) and organic anion transporter 4 (OAT4), with IC50 values of 7.3 and 3.7 µM, respectively. URAT1 is responsible for the majority of the reabsorption of filtered uric acid from the renal tubular lumen. OAT4 is a uric acid transporter associated with diuretic-induced hyperuricemia. Lesinurad does not interact with the uric acid reabsorption transporter SLC2A9 (Glut9), located on the basolateral membrane of the proximal tubule cell. Based on in vitro studies, lesinurad is an inhibitor of OATP1B1, OCT1, OAT1, and OAT3; however, lesinurad is not an in vivo inhibitor of these transporters. In vivo drug interaction studies indicate that lesinurad does not decrease the renal clearance of furosemide (substrate of OAT1/3), or affect the exposure of atorvastatin (substrate of OATP1B1) or metformin (substrate of OCT1). Based on in vitro studies, lesinurad has no relevant effect on P-glycoprotein.
Status:
US Previously Marketed
Source:
NICLOCIDE by BAYER PHARMS
(1982)
Source URL:
First approved in 1982
Source:
NICLOCIDE by BAYER PHARMS
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Niclosamide is an antihelminth used against tapeworm infections. It may act by the uncoupling of the electron transport chain to ATP synthase. The disturbance of this crucial metabolic pathway prevents creation of adenosine tri-phosphate (ATP), an essential molecule that supplies energy for metabolism. Niclosamide works by killing tapeworms on contact. Adult worms (but not ova) are rapidly killed, presumably due to uncoupling of oxidative phosphorylation or stimulation of ATPase activity. The killed worms are then passed in the stool or sometimes destroyed in the intestine. Niclosamide may work as a molluscicide by binding to and damaging DNA. Niclosamide is used for the treatment of tapeworm and intestinal fluke infections: Taenia saginata (Beef Tapeworm), Taenia solium (Pork Tapeworm), Diphyllobothrium latum (Fish Tapeworm), Fasciolopsis buski (large intestinal fluke). Niclosamide is also used as a molluscicide in the control of schistosomiasis. Niclosamide was marketed under the trade name Niclocide, now discontinued.
Status:
First approved in 1953
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
STANOLONE, also known as dihydrotestosterone, is a potent androgenic metabolite of testosterone and anabolic agent for systemic use. It may be used as a replacement of male sex steroids in men who have androgen deficiency, for example as a result of the loss of both testes, and also the treatment of certain rare forms of aplastic anemia which are or may be responsive to anabolic androgens.
Status:
First approved in 1953
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
STANOLONE, also known as dihydrotestosterone, is a potent androgenic metabolite of testosterone and anabolic agent for systemic use. It may be used as a replacement of male sex steroids in men who have androgen deficiency, for example as a result of the loss of both testes, and also the treatment of certain rare forms of aplastic anemia which are or may be responsive to anabolic androgens.
Status:
First approved in 1953
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
STANOLONE, also known as dihydrotestosterone, is a potent androgenic metabolite of testosterone and anabolic agent for systemic use. It may be used as a replacement of male sex steroids in men who have androgen deficiency, for example as a result of the loss of both testes, and also the treatment of certain rare forms of aplastic anemia which are or may be responsive to anabolic androgens.
Status:
US Previously Marketed
Source:
Ammoniated Glycyrrhizin U.S.P.
(1921)
Source URL:
First marketed in 1921
Source:
Ammoniated Glycyrrhizin U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the
potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate
is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1,
1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.
Status:
US Previously Marketed
Source:
Ammoniated Glycyrrhizin U.S.P.
(1921)
Source URL:
First marketed in 1921
Source:
Ammoniated Glycyrrhizin U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the
potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate
is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1,
1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.
Status:
US Previously Marketed
Source:
Ammoniated Glycyrrhizin U.S.P.
(1921)
Source URL:
First marketed in 1921
Source:
Ammoniated Glycyrrhizin U.S.P.
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Potassium Glycyrrhetinate (CAS no. 85985-61-1) is the
potassium salt of Glycyrrhetinic Acid. Potassium Glycyrrhetinate
is also known as Olean-12-En-29-Oic Acid, 3-Hydroxy-1,
1-Oxo-, Monopotassium Salt. Potassium Glycyrrhetinate functions as a flavoring agent and skin-conditioning agent—miscellaneous in cosmetic products.