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Restrict the search for
beta carotene
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There is one exact (name or code) match for beta carotene
Status:
US Previously Marketed
Source:
SOLATENE by ROCHE
(1975)
Source URL:
First approved in 1964
Source:
UDDER BALM by H. W. Naylor Company Inc.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Beta-carotene is found in many foods and is sold as a dietary supplement. Beta-carotene is a carotenoid, weak antioxidant; precursor of vitamin A, which is essential for vision and growth. Used to reduce the severity of photosensitivity reactions in patients with erythropoietic protoporphyria (EPP). Has been used in high-dose antioxidant supplements containing ascorbic acid and vitamin E with zinc in high-risk patients with age-related macular degeneration. Beta-carotene is also used to decrease asthma symptoms caused by exercise; to prevent certain cancers, heart disease, cataracts; and to treat AIDS, alcoholism, Alzheimer’s disease, depression, epilepsy, headache, heartburn, high blood pressure, infertility, Parkinson’s disease, rheumatoid arthritis, schizophrenia, and skin disorders including psoriasis and vitiligo.
Status:
US Previously Marketed
Source:
SOLATENE by ROCHE
(1975)
Source URL:
First approved in 1964
Source:
UDDER BALM by H. W. Naylor Company Inc.
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Beta-carotene is found in many foods and is sold as a dietary supplement. Beta-carotene is a carotenoid, weak antioxidant; precursor of vitamin A, which is essential for vision and growth. Used to reduce the severity of photosensitivity reactions in patients with erythropoietic protoporphyria (EPP). Has been used in high-dose antioxidant supplements containing ascorbic acid and vitamin E with zinc in high-risk patients with age-related macular degeneration. Beta-carotene is also used to decrease asthma symptoms caused by exercise; to prevent certain cancers, heart disease, cataracts; and to treat AIDS, alcoholism, Alzheimer’s disease, depression, epilepsy, headache, heartburn, high blood pressure, infertility, Parkinson’s disease, rheumatoid arthritis, schizophrenia, and skin disorders including psoriasis and vitiligo.
Status:
US Approved Rx
(2024)
Source:
NDA216165
(2024)
Source URL:
First approved in 2024
Source:
NDA216165
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(2023)
Source:
NDA217369
(2023)
Source URL:
First approved in 2023
Source:
NDA217369
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
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:
NDA216203
(2023)
Source URL:
First approved in 2023
Source:
NDA216203
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Sotagliflozin (LX4211) is an orally-delivered small molecule compound that is currently in development for the treatment of type 1 and type 2 diabetes mellitus. Sotagliflozin (LX4211) inhibits both sodium-glucose cotransporter type 2, or SGLT2, a transporter responsible for most of the glucose reabsorption performed by the kidney, and sodium-glucose cotransporter type 1, or SGLT1, a transporter responsible for glucose and galactose absorption in the gastrointestinal tract, and to a lesser extent than SGLT2, glucose reabsorption in the kidney. Combining SGLT1 and SGLT2 inhibition in a single molecule would provide complementary insulin-independent mechanisms to treat diabetes.
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.
Status:
US Approved Rx
(2022)
Source:
NDA215888
(2022)
Source URL:
First approved in 2022
Source:
NDA215888
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Otesaconazole (previously known as VT-1161), an antifungal agent, is an oral inhibitor of fungal lanosterol demethylase (CYP51) but did not inhibit human CYP51. Inhibition of CYP51 results in the accumulation of chemicals known to be toxic to the fungus. CYP51 is the molecular target of the class of drugs referred to as 'azole antifungals'. Mycovia pharmaceuticals initiate enrolment in a phase III trial for the treatment of patients with recurrent vaginal candidiasis (yeast infection). In vitro and in vivo pharmacology studies have demonstrated that the drug is highly active against dermatophytes that cause onychomycosis. Viamet successfully completed phase II clinical trials were was studied the efficacy and safety of oral otesaconazole in patients with onychomycosis of the toenail. In addition, Viamet has completed phase II clinical trial, where was studied the efficacy and safety of otesaconazole in patients with moderate-severe interdigital tinea pedis.
Status:
US Approved Rx
(2022)
Source:
NDA215904
(2022)
Source URL:
First approved in 2022
Source:
NDA215904
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Ganaxolone (3alpha-hydroxy-3beta-methyl-5alpha-pregnan-20-one) (GNX) is the 3beta-methylated synthetic analog of allopregnanolone; it belongs to a class of compounds referred to as neurosteroids. GNX is an allosteric modulator of GABA(A) receptors acting through binding sites which are distinct from the benzodiazepine binding site. It has activity in a broad range of animal models of epilepsy. GNX has been shown to be well tolerated in adults and children. In early phase II studies, GNX has been shown to have activity in adult patients with partial-onset seizures and epileptic children with history of infantile spasms. It is currently undergoing further development in infants with newly diagnosed infantile spasms, in women with catamenial epilepsy, and in adults with refractory partial-onset seizures. Ganaxolone is a CNS-selective GABAA modulator being developed in three different dose forms (IV, capsule, and liquid) intended to maximize therapeutic reach to adult and pediatric patients in both acute and chronic care settings.Ganaxolone is a synthetic analog of endogenous allopregnanolone, which has been shown to be an effective anticonvulsant by restoring electrical balance to the seizing brain. While allopregnanolone’s anticonvulsant and anti-anxiety activities are well documented, allopregnanolone has the potential to convert back to its metabolic precursor progesterone, which could lead to hormonal side effects. Ganaxolone has been designed with an added methyl group that prevents back conversion to an active steroid which unlocks ganaxolone’s potential for chronic use. In preclinical studies, ganaxolone exhibited potency and efficacy comparable to allopregnanolone. Both ganaxolone and allopregnanolone bind to GABAA at the synaptic and extrasynaptic binding sites. Activity with extrasynaptic GABAA receptors are of particular importance for treating patients who developed tolerance to benzodiazepines and barbiturates. Ganaxolone binds to the GABAA receptors, which opens the pore to allow chloride ions to move into the postsynaptic neuron, leading to the inhibition of neurotransmission.
Status:
US Approved Rx
(2022)
Source:
NDA216660
(2022)
Source URL:
First approved in 2022
Source:
NDA216660
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Tauroursodeoxycholic acid (TUDCA) is an endogenous hydrophilic bile acid used clinically to treat certain liver diseases. It is approved in Italy and Turkey for the treatment of cholesterol gallstones and is an investigational drug in China, Unites States, and Italy. Tauroursodeoxycholic acid is being investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis. Tauroursodeoxycholate (TUDC) promote choleresis by triggering the insertion of transport proteins for bile acids into the canalicular and basolateral membranes of hepatocytes. In addition, Tauroursodeoxycholate exerts hepatoprotective and anti-apoptotic effects, can counteract the action of toxic bile acids and reduce endoplasmic reticulum stress. Tauroursodeoxycholate can also initiate the differentiation of multipotent mesenchymal stem cells (MSC) including hepatic stellate cells and promote their development into hepatocyte-like cells. Although the hepatoprotective and choleretic action of TUDC is empirically used in clinical medicine since decades, the underlying molecular mechanisms remained largely unclear.