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Status:
US Previously Marketed
Source:
CHOLOXIN by ABBVIE
(1967)
Source URL:
First approved in 1967
Source:
CHOLOXIN by ABBVIE
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Dextrothyroxine is the dextrorotary isomer of the synthetic thyroxine. It is an antihyperlipidemic agent. The mechanism of action is not completely understood, but dextrothyroxine apparently acts in the liver to stimulate formation of low-density lipoprotein (LDL) and, to a much greater extent, to increase catabolism of LDL. This leads to increased excretion of cholesterol and bile acids via the biliary route into the feces, with a resulting reduction in serum cholesterol and LDL. Dextrothyroxine has no significant effect on high-density lipoproteins (HDL). Inherently, it will also bind to thyroid receptors and as it is a prohormone, it will bind as a substrate to iodide peroxidase.
Status:
US Previously Marketed
Source:
CHOLOXIN by ABBVIE
(1967)
Source URL:
First approved in 1967
Source:
CHOLOXIN by ABBVIE
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Dextrothyroxine is the dextrorotary isomer of the synthetic thyroxine. It is an antihyperlipidemic agent. The mechanism of action is not completely understood, but dextrothyroxine apparently acts in the liver to stimulate formation of low-density lipoprotein (LDL) and, to a much greater extent, to increase catabolism of LDL. This leads to increased excretion of cholesterol and bile acids via the biliary route into the feces, with a resulting reduction in serum cholesterol and LDL. Dextrothyroxine has no significant effect on high-density lipoproteins (HDL). Inherently, it will also bind to thyroid receptors and as it is a prohormone, it will bind as a substrate to iodide peroxidase.
Status:
US Previously Marketed
Source:
CLOFIBRATE by USL PHARMA
(1986)
Source URL:
First approved in 1967
Source:
ATROMID-S by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clofibrate is a fibric acid derivative used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent medical problems caused by such substances clogging the blood vessels. However, this treatment was discontinued in 2002 due to adverse effects. Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, and increased lipoprotein lipase activity. Clofibrate increased the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis, inhibited the synthesis, and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. In addition, clofibrate was investigated as a novel therapy agent in multiple myeloma and it shown the promising results.
Status:
US Previously Marketed
Source:
CLOFIBRATE by USL PHARMA
(1986)
Source URL:
First approved in 1967
Source:
ATROMID-S by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clofibrate is a fibric acid derivative used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent medical problems caused by such substances clogging the blood vessels. However, this treatment was discontinued in 2002 due to adverse effects. Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, and increased lipoprotein lipase activity. Clofibrate increased the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis, inhibited the synthesis, and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. In addition, clofibrate was investigated as a novel therapy agent in multiple myeloma and it shown the promising results.
Status:
US Previously Marketed
Source:
CLOFIBRATE by USL PHARMA
(1986)
Source URL:
First approved in 1967
Source:
ATROMID-S by WYETH AYERST
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Clofibrate is a fibric acid derivative used to lower cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent medical problems caused by such substances clogging the blood vessels. However, this treatment was discontinued in 2002 due to adverse effects. Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, and increased lipoprotein lipase activity. Clofibrate increased the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis, inhibited the synthesis, and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. In addition, clofibrate was investigated as a novel therapy agent in multiple myeloma and it shown the promising results.
Status:
First approved in 1966
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Betahistine is an orally administered, centrally acting histamine H1 receptor agonist with partial H3 antagonistic activity. It is proposed that betahistine may reduce peripherally the asymmetric functioning of the sensory vestibular organs in addition to increasing vestibulocochlear blood flow by antagonising local H3 heteroreceptors. Betahistine acts centrally by enhancing histamine synthesis within tuberomammillary nuclei of the posterior hypothalamus and histamine release within vestibular nuclei through antagonism of H3 autoreceptors. This mechanism, together with less specific effects of betahistine on alertness regulation through cerebral H1 receptors, should promote and facilitate central vestibular compensation. Betahistine is used to treat the symptoms associated with Ménière's disease, a condition of the inner ear which causes, vertigo (dizziness), tinnitus (ringing in the ears), hearing loss.
Status:
First approved in 1966
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Betahistine is an orally administered, centrally acting histamine H1 receptor agonist with partial H3 antagonistic activity. It is proposed that betahistine may reduce peripherally the asymmetric functioning of the sensory vestibular organs in addition to increasing vestibulocochlear blood flow by antagonising local H3 heteroreceptors. Betahistine acts centrally by enhancing histamine synthesis within tuberomammillary nuclei of the posterior hypothalamus and histamine release within vestibular nuclei through antagonism of H3 autoreceptors. This mechanism, together with less specific effects of betahistine on alertness regulation through cerebral H1 receptors, should promote and facilitate central vestibular compensation. Betahistine is used to treat the symptoms associated with Ménière's disease, a condition of the inner ear which causes, vertigo (dizziness), tinnitus (ringing in the ears), hearing loss.
Status:
First approved in 1966
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Betahistine is an orally administered, centrally acting histamine H1 receptor agonist with partial H3 antagonistic activity. It is proposed that betahistine may reduce peripherally the asymmetric functioning of the sensory vestibular organs in addition to increasing vestibulocochlear blood flow by antagonising local H3 heteroreceptors. Betahistine acts centrally by enhancing histamine synthesis within tuberomammillary nuclei of the posterior hypothalamus and histamine release within vestibular nuclei through antagonism of H3 autoreceptors. This mechanism, together with less specific effects of betahistine on alertness regulation through cerebral H1 receptors, should promote and facilitate central vestibular compensation. Betahistine is used to treat the symptoms associated with Ménière's disease, a condition of the inner ear which causes, vertigo (dizziness), tinnitus (ringing in the ears), hearing loss.
Status:
First approved in 1966
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Betahistine is an orally administered, centrally acting histamine H1 receptor agonist with partial H3 antagonistic activity. It is proposed that betahistine may reduce peripherally the asymmetric functioning of the sensory vestibular organs in addition to increasing vestibulocochlear blood flow by antagonising local H3 heteroreceptors. Betahistine acts centrally by enhancing histamine synthesis within tuberomammillary nuclei of the posterior hypothalamus and histamine release within vestibular nuclei through antagonism of H3 autoreceptors. This mechanism, together with less specific effects of betahistine on alertness regulation through cerebral H1 receptors, should promote and facilitate central vestibular compensation. Betahistine is used to treat the symptoms associated with Ménière's disease, a condition of the inner ear which causes, vertigo (dizziness), tinnitus (ringing in the ears), hearing loss.
Status:
US Previously Marketed
Source:
Stop-Zit by Nelson Baker & Company
(1962)
Source URL:
First approved in 1962
Source:
Stop-Zit by Nelson Baker & Company
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Denatonium, usually available as denatonium benzoate (trade names Bitrex) is the most bitter chemical compound known, with bitterness thresholds of 0.05 ppm for the benzoate and 0.01 ppm for the saccharide. Scientists at Macfarlan Smith, Ltd. of Edinburgh, Scotland discovered Bitrex during research on derivatives of the anesthetic lidocaine. The extremely bitter taste proved effective in reducing ingestion by humans and animals. Denatonium is commonly included in placebo medications used in clinical trials to match the bitter taste of certain medications. Denatonium activates bitter taste receptor, mainly, TAS2R4, TAS2R8, TAS2R10, TAS2R13 on many cell types and plays important roles in chemical release, ciliary beating and smooth muscle relaxation through intracellular Ca(2+)-dependent pathways.