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Restrict the search for
alpha-tocopherol acetate
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There is one exact (name or code) match for alpha-tocopherol acetate
Status:
US Approved Rx
(2001)
Source:
NDA021265
(2001)
Source URL:
First approved in 1940
Class:
MIXTURE
Targets:
Conditions:
It is known that Vitamin E, traditionally known as α¬ tocopherol, is a mixture of eight different compounds, four tocopherols and four tocotrienols, each one being designated as α, β, γ and δ forms. The two groups differ in the hydrophobic tridecyl side chain which is saturated (phytyl) in tocopherols and unsaturated having three double bonds (geranyl) in tocotrienols. During the last few years, it has been found that all the eight forms are biologically active and perform specific functions. Clinical research has shown that mixture of tocotrienols and tocopherols offer synergistic protective action against heart ailments and cancer that is not exclusively offered by α¬tocopherol. The other advantage of mixed tocopherols and tocotrienols is their role in slowing down aging. Diseases like diabetes 1 and 2, autoimmune diseases, bacterial and viral infections, Alzheimer disease, fungal (Candida) infections are prevented by these compounds. It helps in the maintenance of bones, muscles, eyes (vision), memory, sleep, lungs, infertility, skin and wrinkles. Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity. Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 that lowers the adhesion of blood components to the endothelium. Its antioxidant effects explain the neuroprotective effects of vitamin E. The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity. The mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.
Status:
US Approved Rx
(2001)
Source:
NDA021265
(2001)
Source URL:
First approved in 1940
Class:
MIXTURE
Targets:
Conditions:
It is known that Vitamin E, traditionally known as α¬ tocopherol, is a mixture of eight different compounds, four tocopherols and four tocotrienols, each one being designated as α, β, γ and δ forms. The two groups differ in the hydrophobic tridecyl side chain which is saturated (phytyl) in tocopherols and unsaturated having three double bonds (geranyl) in tocotrienols. During the last few years, it has been found that all the eight forms are biologically active and perform specific functions. Clinical research has shown that mixture of tocotrienols and tocopherols offer synergistic protective action against heart ailments and cancer that is not exclusively offered by α¬tocopherol. The other advantage of mixed tocopherols and tocotrienols is their role in slowing down aging. Diseases like diabetes 1 and 2, autoimmune diseases, bacterial and viral infections, Alzheimer disease, fungal (Candida) infections are prevented by these compounds. It helps in the maintenance of bones, muscles, eyes (vision), memory, sleep, lungs, infertility, skin and wrinkles. Although all forms of Vitamin E exhibit antioxidant activity, it is known that the antioxidant activity of vitamin E is not sufficient to explain the vitamin's biological activity. Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 that lowers the adhesion of blood components to the endothelium. Its antioxidant effects explain the neuroprotective effects of vitamin E. The immunomodulatory effects of Vitamin E have been demonstrated in vitro, where alpha-tocopherol increases mitogenic response of T lymphocytes from aged mice. The mechanism of this response by vitamin E is not well understood, however it has been suggested that vitamin E itself may have mitogenic activity independent of its antioxidant activity. The mechanism of action of vitamin E's antiviral effects (primarily against HIV-1) involves its antioxidant activity. Vitamin E reduces oxidative stress, which is thought to contribute to HIV-1 pathogenesis, as well as to the pathogenesis of other viral infections. Vitamin E also affects membrane integrity and fluidity and, since HIV-1 is a membraned virus, altering membrane fluidity of HIV-1 may interfere with its ability to bind to cell-receptor sites, thus decreasing its infectivity.
Status:
US Approved Rx
(2025)
Source:
NDA219209
(2025)
Source URL:
First approved in 2025
Source:
NDA219209
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(2024)
Source:
NDA213972
(2024)
Source URL:
First approved in 2024
Source:
NDA213972
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Sulopenem is a thiolanylthiopenem derivative patented by American multinational pharmaceutical corporation Pfizer Inc as an antibiotic with broad-spectrum antibacterial activity against most gram-positive and gram-negative bacteria. Sulopenem showed concentration-dependent bactericidal activities against Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter calcoaceticus. Morphological observation using a phase-contrast microscope revealed that sulopenem induced spherical cell formation with E. coli and K. pneumoniae at lower concentrations and bacteriolysis at higher concentrations. Therapeutic efficacies of sulopenem against systemic infections in mice were almost equal to those of imipenem against Streptococcus pneumoniae.
Status:
US Approved Rx
(2024)
Source:
NDA219249
(2024)
Source URL:
First approved in 2024
Source:
NDA219249
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Status:
US Approved Rx
(2024)
Source:
NDA217785
(2024)
Source URL:
First approved in 2024
Source:
NDA217785
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
MGL-3196 is a first-in-class, orally administered, small-molecule, liver-directed, THR β-selective agonist. Preclinical, toxicology and Phase 1 clinical data suggest MGL-3196 has an attractive, differentiated profile as a potential treatment for non-alcoholic steatohepatitis (NASH) and dyslipidemias. THR-β selectivity also enhances the safety profile of MGL-3196, compared to non-selective agents. MGL-3196 has shown no suppression of the central thyroid axis, no THR-α effects on heart rate or bone, and no elevation of liver enzymes. These characteristics make MGL-3196 among the most promising molecules in development in this therapeutic area. MGL-3196 is in a Phase 2 clinical trial for the treatment of non-alcoholic steatohepatitis (NASH).
Status:
US Approved Rx
(2024)
Source:
NDA218860
(2024)
Source URL:
First approved in 2024
Source:
NDA218860
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Elafibranor (GFT505) is an agonist of the peroxisome proliferator-activated receptor-α and peroxisome proliferator-activated receptor-δ. GFT505 has an active
metabolite, GFT1007, and both have potent agonist activity
for PPAR-a and to a lesser extent for PPAR-d. Elafibranor improves insulin sensitivity, glucose homeostasis, and lipid metabolism and reduces inflammation. Elafibranor (GFT505) reverses nonalcoholic steatohepatitis (NASH) to prevent fibrosis progression. With an outstanding safety and tolerance profile, elafibranor provides NASH patients with needed cardio-protective benefits. Elafibranor is currently being evaluated in the clinical Phase 3 study RESOLVE-IT. The safety profile of GFT505 from the completed clinical
trials appears satisfactory with no indication of PPAR-g agonist
effects such as edema or body weight gain.
Status:
US Approved Rx
(2024)
Source:
NDA217899
(2024)
Source URL:
First approved in 2024
Source:
NDA217899
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
MBX-8025 (Seladelpar) is an agonist of peroxisome proliferator-activated receptor delta. MBX-8025 improves insulin sensitivity and reverses dyslipidemia and hepatic storage of lipotoxic lipids to improve nonalcoholic steatohepatitis pathology in atherogenic diet-fed obese diabetic mice. MBX-8025 improves lipoprotein subfractions associated with atherogenic dyslipidemia. CymaBay Therapeutics is developing MBX-8025 for the treatment of patients with the autoimmune liver disease, primary biliary cholangitis and nonalcoholic steatohepatitis.
Status:
US Approved Rx
(2023)
Source:
NDA218197
(2023)
Source URL:
First approved in 2023
Source:
NDA218197
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
AZD-5363, a novel pyrrolopyrimidine-derived compound, inhibits all AKT isoforms with a potency of <10nM, and inhibited phosphorylation of AKT substrates in cells with a potency of ~0.3 to 0.8µM. AZD5363 monotherapy inhibited the proliferation of 41/182 solid and hematologic tumour cell lines with a potency of <3µM and 25/182 with a potency of <1µM. By targeting AKT, the key node in the PIK3/AKT signaling network, AZD-5363 may be used as monotherapy or combination therapy for a variety of human cancers. There is significant relationship between the presence of PIK3CA and/or PTEN mutations and sensitivity to AZD-5363, and between RAS mutations and resistance. In xenograft studies in vivo AZD-5363 significantly reduced phosphorylation of PRAS40, GSK3β and S6. Chronic oral dosing of AZD-5363 causes dose-dependent inhibition of the growth of xenografts derived from various tumor types and AZD-5363 also significantly enhanced the antitumor activity of docetaxel, lapatinib and trastuzumab in breast cancer xenografts. Dose-response at oral doses of 50 to 150mg/kg twice daily continuous dosing and intermittent dosing in the range of 100 to 200mg/kg twice daily, 4 days on, 3 days off have led to efficacy. AZD-5363 is in phase II clinical studies for the treatment of breast cancer; gastric cancer; non-small cell lung cancer.
Status:
US Approved Rx
(2023)
Source:
NDA216834
(2023)
Source URL:
First approved in 2023
Source:
NDA216834
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(2023)
Source:
NDA216993
(2023)
Source URL:
First approved in 2023
Source:
NDA216993
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Quizartinib (AC220) is an orally bioavailable, small molecule receptor tyrosine kinase inhibitor that is being developed by Daiichi Sankyo Company (previously Ambit Biosciences) and Astellas Pharma as a treatment for acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL) and advanced solid tumours. The highest affinity target identified for Quizartinib was FLT3. The only other kinases with binding constants within 10-fold that for FLT3 were the closely related receptor tyrosine kinases KIT, PDGFRA, PDGFRB, RET, and CSF1R. Kinase inhibition of (mutant) KIT, PDGFR and FLT3 isoforms by quizartinib leads to potent inhibition of cellular proliferation and induction of apoptosis in in vitro leukemia models as well as in native leukemia blasts treated ex vivo.