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Search results for folic root_names_stdName in Standardized Name (approximate match)
Status:
Possibly Marketed Outside US
Source:
21 CFR 333E
(2011)
Source URL:
First approved in 2011
Source:
21 CFR 333E
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
21 CFR 352
(2012)
Source URL:
First approved in 2011
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
Possibly Marketed Outside US
Source:
NCT01833624: Phase 4 Interventional Unknown status Traumatic and/or Non-traumatic Brain Injury
(2012)
Source URL:
First approved in 2011
Source:
Corvita by Trigen Laboratories, LLC
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
SELENATE ION is a compound containing an oxoanion with selenium in its highest oxidation state of VI. Selenates are analogous to sulfates and have similar chemistry, but unlike sulfate, selenate is a good oxidizer. Selenate is the form required by organisms that need selenium as a micronutrient. These organisms have the ability to acquire, metabolize and excrete selenium. The level at which selenium becomes toxic varies from species to species and is related to other environmental factors like pH and alkalinity that influence the concentration of selenite over selenate. Selenate and other forms of selenium are highest in areas where ancient seas have evaporated. These areas are enriched in selenium and over millennia, biologic adaptation has occurred.
Status:
Possibly Marketed Outside US
Source:
COBAN by Eli Lilly|Indiana University School of Medicine
Source URL:
First approved in 2011
Source:
NADA038878
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Monensin is an antibiotic produced as a byproduct of fermentation by Streptomyces cinnamonensis and belongs to a family of drugs known as polyether antibiotics or ionophores. The drug was approved by FDA for the prevention of coccidiosis in turkeys, chickens, quail, cattle, goats, calves (Coban, Rumensin). The exact mechanism of monesin action is unknown, however there are several hypotesis, which includes the inhibition of K+ transport, the inhibition of the transport of carbohydrates across the host cell membrane, the interruption host cell invasion by sporozoites, etc.
Status:
Possibly Marketed Outside US
Source:
21 CFR 333E
(2011)
Source URL:
First approved in 2011
Source:
21 CFR 333E
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
Regency Pre-Milking Teat Dip by ABS Corporation
(2011)
Source URL:
First approved in 2011
Source:
Regency Pre-Milking Teat Dip by ABS Corporation
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
Possibly Marketed Outside US
Source:
NCT02469337: Phase 4 Interventional Unknown status Insulin Resistance
(2012)
Source URL:
First approved in 2011
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Dichloroacetic acid, often abbreviated DCA (dichloroacetate), is an acid analog of acetic acid in which two of the three hydrogen atoms of the methyl group have been replaced by chlorine atoms. The salts and esters of dichloroacetic acid are called dichloroacetates. Salts of DCA are used as drugs since they inhibit the enzyme pyruvate dehydrogenase kinase. Early reports of its activity against brain cancer cells led patients to treat themselves with DCA, which is commercially available in non-pharmaceutical grade. A phase 1 study in 5 patients concluded that DCA was safe, but wasn't designed to establish effectiveness.
DCA was approved for use in Canada in 1989 (as a topical formulation for the treatment of warts and for cauterization and removal of a wide variety of skin and tissue lesions), but was cancelled post market. DCA is a noncompetitive inhibitor of the endoplasmic reticulum enzyme HMG CoA reductase, which catalyzes the rate limiting step in cholesterol biosynthesis. DCA has been researched in adults, children, animals, and cells as a monotherapy as well as in
combination with other therapies for the treatment of severe metabolic disorders including diabetes and hypercholesterolemia, lactic acidosis, certain heart conditions, and cancer. DCA has been prescribed to reduce tumour size and tumour markers, prevent angiogenesis, reduce
cancer related symptoms, manage pain, and aid in palliation.
Status:
Possibly Marketed Outside US
First approved in 2010
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Behenic acid is a saturated fatty acid that is derived from the oil extracts of plants and used as a component of conditioning agents. Behenic acid is also a part of a novel complex of lipophilic ingredients developed for the treatment of dry skin. The properties of behenic acid were studied in comparison to others fatty acids and it was found that behenic acid does not inhibit the UDP-glucuronosyltransferase (UGT) 1A1 enzyme. The high levels of behenic acid in patients with low-grade glial tumors is an important indicator of the persistence of tissue integrity and tissue resistance. Therefore, behenic acid levels can be a prognostic factor in glial tumors.
Status:
Possibly Marketed Outside US
Source:
21 CFR 358
(2010)
Source URL:
First approved in 2010
Source:
21 CFR 358
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Status:
Possibly Marketed Outside US
Source:
SAFYRAL
Source URL:
First approved in 2010
Source:
Zatean-Pn DHA by Trigen Laboratories, LLC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
For people with MTHFR gene variations, supplementing with the already activated form of folate (5-MTHF/5- METHYLTETRAHYDROFOLATE/LEVOMEFOLIC ACID) is far more effective in providing this form of folate than introducing the pre-converted form to the body through typical folate supplements. L-Methylfolate (5-MTHF) supplements provide the active form of folate naturally present in the body and available for biological action. 5-MTHF—the “active” form of folate that is able to pass the blood brain barrier. However, without a properly functioning methylenetetrahydrofolate reductase, MTHFR this conversion cannot take place and folate is not converted to forms that can cross the blood brain barrier. That is where 5-MTHF supplements come in. Levomefolate calcium is structurally identical to L-5-methyltetrahydrofolate (L-5-methyl-THF), a metabolite of vitamin B9. Mean baseline concentrations of about 15 nmol/L are reached in populations without folate food fortification under normal nutritional conditions. Orally administered levomefolate calcium is absorbed and is incorporated into the body folate pool. Peak plasma concentrations of about 50 nmol/L above baseline are reached within 0.5 – 1.5 hours after single oral administration of 0.451 mg levomefolate calcium. Steady state conditions for total folate in plasma after intake of 0.451 mg levomefolate calcium. In red blood cells, achievement of steady state is delayed due to the long lifespan of red blood cells of about 120 days. Levomefolate calcium is a part of contraceptive tablets: SAFYRA. Safyral is an estrogen/progestin COC (Combined Oral Contraceptive) containing a folate, indicated for use by women to: prevent pregnancy and raise folate levels in women who choose to use an oral contraceptive for contraception. COCs lower the risk of becoming pregnant primarily by suppressing ovulation. Other possible mechanisms may include cervical mucus changes that inhibit sperm penetration and endometrial changes that reduce the likelihood of implantation.