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Search results for desoxycorticosterone root_names_stdName in Standardized Name (approximate match)
Desoxycorticosterone glucoside was studied in human in 1950th, where was shown, that intravenous injection of this compound did not narrow arterial-cerebral venous glucose difference. In no instance did cerebral venous blood sugar content surpass or approach arterial levels.
Status:
US Previously Marketed
First approved in 1948
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
First approved in 1939
Source:
DOCA by ORGANON USA INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Desoxycorticosterone pivalate (DOCP) is a mineralocorticoid hormone and an analog of desoxycorticosterone. DOCP is a long-acting ester of desoxycorticosterone acetate (DOCA) which is recognized as having the same qualitative effects as the natural mineralocorticoid hormone aldosterone. It’s used as Percorten-V for replacement therapy for the mineralocorticoid deficit in dogs with primary adrenocortical insufficiency. Percorten-V is only available in the U.S., Canada, Australia and recently, Denmark. Percorten was originally developed for the treatment of Addison's disease in humans but the demand for it decreased significantly once Florinef was available. Unaware that their product was being prescribed “off-label” for the treatment of canine Addison’s Disease and faced with a decreased demand for Percorten, the manufacturer *almost* discontinued production until the veterinary community rose up and voiced their distress. Field trials were run and the FDA approved the use of Percorten-V (the "v" is for veterinary). DOCP like other adrenocorticoid hormones is thought to act by controlling the rate of synthesis of proteins. It reacts with receptor proteins in the cytoplasm to form a steroid-receptor complex. This complex moves into the nucleus, where it binds to chromatin that result in genetic transcription of cellular DNA to messenger RNA. The steroid hormones appear to induce transcription and synthesis of specific proteins, which produce the physiologic effects seen after administration. The most important effect of DOCP is to increase the rate of renal tubular absorption of sodium. This effect is seen most intensely in the thick portion of the ascending limb of the loop of Henle. It also increases sodium absorption in the proximal convoluted tubule but this effect is less important in sodium retention. Chloride follows the sodium out of the renal tubule. Another important effect of DOCP is enhanced renal excretion of potassium. This effect is driven by the resorption of sodium that pulls potassium from the extracellular fluid into the renal tubules, thus promoting potassium excretion.
Status:
Possibly Marketed Outside US
Source:
21 CFR 333D
(2014)
Source URL:
First approved in 2007
Source:
21 CFR 358H
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2012)
Source URL:
First approved in 2000
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Status:
US Approved Rx
(2013)
Source:
ANDA202051
(2013)
Source URL:
First approved in 2002
Source:
HEPSERA by GILEAD
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
The potential antiviral effect of adefovir, an acyclic nucleoside phosphonate analog of 2′-deoxyadenosine monophosphate, was first studied by Holý and De Clercq in 1980s.
Adefovir is an acyclic nucleotide analog of adenosine monophosphate which is phosphorylated to the active metabolite adefovir diphosphate by cellular kinases. Adefovir diphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate and by causing DNA chain termination after its incorporation into viral DNA. Oral adefovir dipivoxil is effective and generally well tolerated in HBeAg-positive and -negative patients chronically infected with wild-type or lamivudine-resistant HBV.