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Restrict the search for
valproic acid
to a specific field?
Status:
US Approved Rx
(1998)
Source:
NDA021004
(1998)
Source URL:
First approved in 1995
Source:
NDA020564
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Lamivudine is a reverse transcriptase inhibitor used alone or in combination with other classes of anti-human immunodeficiency virus (HIV) drugs in the treatment of HIV infection. This molecule has two stereo-centers, thus giving rise to four stereoisomers: (+/-)-cis-lamivudine and (+/-)-trans-lamivudine. The latter is considered to be impurity of the pharmaceutically active isomer, (-)-cis-lamivudine.
Status:
US Approved Rx
(2010)
Source:
ANDA090416
(2010)
Source URL:
First approved in 1995
Source:
UNIVASC by UCB INC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Moexipril is a non-sulfhydryl containing the precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. Moexipril hydrochloride is a prodrug for Moexiprilat, which inhibits ACE in humans and animals. The mechanism through which Moexiprilat lowers blood pressure is believed to be primarily inhibition of ACE activity. ACE is a peptidyl dipeptidase that catalyzes the conversion of the inactive decapeptide angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates aldosterone secretion by the adrenal cortex and provides negative feedback on renin secretion. ACE is identical to kininase II, an enzyme that degrades bradykinin, an endothelium-dependent vasodilator. Moexiprilat is about 1000 times as potent as Moexipril in inhibiting ACE and kininase II. Inhibition of ACE results in decreased angiotensin II formation, leading to decreased vasoconstriction, increased plasma renin activity and decreased aldosterone secretion. The latter results in diuresis and natriuresis and a small increase in serum potassium concentration.
Status:
US Approved Rx
(1995)
Source:
NDA020599
(1995)
Source URL:
First approved in 1995
Source:
NDA020599
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Riluzole, a member of the benzothiazole class, is indicated for the treatment of patients with amyotrophic lateral sclerosis. Its pharmacological properties include the following, some of which may be related to its effect: 1) an inhibitory effect on glutamate release (activation of glutamate reuptake), 2) inactivation of voltage-dependent sodium channels, and 3) ability to interfere with intracellular events that follow transmitter binding at excitatory amino acid receptors. Common adverse reactions include headache, abdominal pain, back pain, vomiting, dyspepsia, diarrhea, dizziness. Riluzole-treated patients that take other hepatotoxic drugs may be at increased risk for hepatotoxicity.
Status:
US Approved Rx
(2010)
Source:
ANDA090568
(2010)
Source URL:
First approved in 1995
Source:
NDA020541
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Anastrozole (marketed under the trade name Arimidex by AstraZeneca) is a drug indicated in the treatment of breast cancer in post-menopausal women. It is used both in adjuvant therapy (i.e. following surgery) and in metastatic breast cancer. It decreases the amount of estrogens that the body makes. Anastrozole belongs in the class of drugs known as aromatase inhibitors. It inhibits the enzyme aromatase, which is responsible for converting androgens (produced by women in the adrenal glands) to estrogens. The growth of many cancers of the breast is stimulated or maintained by estrogens. In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, which converts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore be achieved by specifically inhibiting the aromatase enzyme. Anastrozole is a selective non-steroidal aromatase inhibitor. It significantly lowers serum estradiol concentrations and has no detectable effect on formation of adrenal corticosteroids or aldosterone.
Status:
US Approved Rx
(2022)
Source:
NDA216472
(2022)
Source URL:
First approved in 1995
Source:
NDA020597
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Latanoprostene Bunod (LBN) is a topical ophthalmic therapeutic for the reduction of intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension. There is no cure for glaucoma and therapeutic management is predominantly focused on minimizing disease progression and clinical sequelae via the reduction and maintenance of appropriate target IOPs. Latanoprostene Bunod is thought to lower intraocular pressure via a dual mechanism of action since the medication is metabolized into two relevant moieties upon administration: latanoprost acid, and butanediol mononitrate. As a prostaglandin F2-alpha analog, the latanoprost acid moiety operates as a selective PGF2-alpha (FP) receptor agonist. Since FP receptors occur in the ciliary muscle, ciliary epithelium, and sclera the latanoprost acid moiety primarily acts in the uveoscleral pathway where it increases the expression of matrix metalloproteinases (MMPs) like MMP-1, -3, and -9 which promote the degradation of collagen types I, III, and IV in the longitudinal bundles of the ciliary muscle and surrounding sclera. The resultant extracellular matrix remodeling of the ciliary muscle consequently produces reduced outflow resistance via increased permeability and increased aqueous humor outflow through the uveoscleral route. Conversely, the butanediol mononitrate undergoes further metabolism to NO and an inactive 1,4-butanediol moiety. As a gas that can freely diffuse across plasma membranes, it is proposed that the relaxing effect of NO to induce reductions in the cell volume and contractility of vascular smooth muscle-like cells is dependent upon activation of the sGC/cGMP/PKG cascade pathway. NO released from butanediol mononitrate consequently enters the cells of the TM and an inner wall of SC, causing decreases in myosin light chain-2 phosphorylation, increased phosphorylation of large-conductance calcium-activated potassium (BKCa) channels, and a subsequent efflux of potassium ions through such BKCa channels. All of these changes serve to decrease the cell contractility and volume, as well as to rearrange the actin cytoskeleton of the TM and SC cells. These biomechanical changes ultimately allow for enhanced conventional outflow of aqueous humor.
Status:
US Approved Rx
(1995)
Source:
NDA020221
(1995)
Source URL:
First approved in 1995
Source:
NDA020221
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Amifostine is an organic thiophosphate cytoprotective agent known chemically as 2-[(3¬ aminopropyl)amino]ethanethiol dihydrogen phosphate (ester), it’s adjuvant used in cancer chemotherapy and radiotherapy involving DNA-binding chemotherapeutic agents. It is marketed under the trade name Ethyol. Amifostine is a prodrug and is dephosphorylated by alkaline phosphatase in tissues to a pharmacologically active free thiol metabolite. This metabolite is believed to be responsible for the reduction of the cumulative renal toxicity of cisplatin and for the reduction of the toxic effects of radiation on normal oral tissues. The ability of Ethyol to differentially protect normal tissues is attributed to the higher capillary alkaline phosphatase activity, higher pH and better vascularity of normal tissues relative to tumor tissue, which results in a more rapid generation of the active thiol metabolite as well as a higher rate constant for uptake into cells. The higher concentration of the thiol metabolite in normal tissues is available to bind to, and thereby detoxify, reactive metabolites of cisplatin. This thiol metabolite can also scavenge reactive oxygen species generated by exposure to either cisplatin or radiation. Healthy cells are preferentially protected because amifostine and metabolites are present in healthy cells at 100-fold greater concentrations than in tumor cells.
Status:
US Approved Rx
(2012)
Source:
ANDA091541
(2012)
Source URL:
First approved in 1995
Source:
NDA020387
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Losartan is a selective, competitive angiotensin II receptor type 1 (AT1) antagonist. Losartant is recommended as one of several preferred agents for the initial management of hypertension. Administration of losartan reduces the risk of stroke in patients with hypertension and left ventricular hypertrophy. Losartan is indicated for the treatment of diabetic nephropathy with an elevated serum creatinine and proteinuria in patients with type 2 diabetes and a history of hypertension.
Status:
US Approved Rx
(2017)
Source:
NDA208630
(2017)
Source URL:
First approved in 1995
Source:
ANDA077614
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Aminolevulinic Acid is the first compound in the porphyrin synthesis pathway. The metabolism of aminolevulinic acid (ALA) is the first step in the biochemical
pathway resulting in heme synthesis. Aminolevulinic acid is not a photosensitizer, but rather a
metabolic precursor of protoporphyrin IX (PpIX), which is a photosensitizer. The synthesis of ALA is
normally tightly controlled by feedback inhibition of the enzyme, ALA synthetase, presumably by
intracellular heme levels. ALA, when provided to the cell, bypasses this control point and results in the
accumulation of PpIX, which is converted into heme by ferrochelatase through the addition of iron to the PpIX nucleus. Marketed under the brand name LEVULAN KERASTICK for Topical Solution plus blue light illumination using the BLU-U Blue Light Photodynamic Therapy Illuminator, it is indicated for the treatment of minimally to moderately
thick actinic keratoses (Grade 1 or 2, see table 2 for definition) of the face or scalp. Aminolevulinic acid is also being studied in the treatment of other conditions and types of cancer. An orally-administered in vivo diagnostic agent, Aminolevulinic acid, is used in photodynamic diagnosis
(PDD) whose aim is to help doctors visualize the tumor tissue during surgical resection of malignant glioma, it is
already sold in over 20 European countries including Germany and the U.K. According to the presumed mechanism of action, photosensitization following application of aminolevulinic acid (ALA) topical solution occurs through the metabolic conversion of ALA to protoporphyrin IX (PpIX), which accumulates in the skin to which aminolevulinic acid has been applied. When exposed to light of appropriate wavelength and energy, the accumulated PpIX produces a photodynamic reaction, a cytotoxic process dependent upon the simultaneous presence of light and oxygen. The absorption of light results in an excited state of the porphyrin molecule, and subsequent spin transfer from PpIX to molecular oxygen generates singlet oxygen, which can further react to form superoxide and hydroxyl radicals. Photosensitization of actinic (solar) keratosis lesions using aminolevulinic acid, plus illumination with the BLU-UTM Blue Light Photodynamic Therapy Illuminator (BLU-U), is the basis for aminolevulinic acid photodynamic therapy (PDT).
Status:
US Approved Rx
(2009)
Source:
ANDA090258
(2009)
Source URL:
First approved in 1995
Source:
NDA020560
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Alendronic acid is a bisphosphonate drug used for osteoporosis, osteogenesis imperfecta, and several other bone diseases. It is marketed alone as well as in combination with vitamin D. Alendronate inhibits osteoclast-mediated bone-resorption. Like all bisphosphonates, it is chemically related to inorganic pyrophosphate, the endogenous regulator of bone turnover. But while pyrophosphate inhibits both osteoclastic bone resorption and the mineralization of the bone newly formed by osteoblasts, alendronate specifically inhibits bone resorption without any effect on mineralization at pharmacologically achievable doses. Its inhibition of bone-resorption is dose-dependent and approximately 1,000 times stronger than the equimolar effect of the first bisphosphonate drug, etidronate. Under therapy, normal bone tissue develops, and alendronate is deposited in the bone-matrix in a pharmacologically inactive form. For optimal action, enough calcium and vitamin D are needed in the body in order to promote normal bone development. Hypocalcemia should, therefore, be corrected before starting therapy. Treatment of post-menopausal women and people with osteogenesis imperfecta over the age of 22 with alendronic acid has demonstrated normalization of the rate of bone turnover, significant increase in BMD (bone mineral density) of the spine, hip, wrist and total body, and significant reductions in the risk of vertebral (spine) fractures, wrist fractures, hip fractures, and all non-vertebral fractures. In the Fracture Intervention Trial, the women with the highest risk of fracture (by virtue of pre-existing vertebral fractures) were treated with Fosamax 5 mg/day for two years followed by 10 mg/day for the third year. This resulted in approximately 50% reductions in fractures of the spine, hip, and wrist compared with the control group taking placebos. Both groups also took calcium and vitamin D.
Status:
US Approved Rx
(2012)
Source:
ANDA202176
(2012)
Source URL:
First approved in 1995
Source:
NDA020406
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Levolansoprazole is the levorotary (L-enantiomer) form of proton-pump inhibitor (PPI) Lansoprazole. Lansoprazole is a racemic 1:1 mixture of the enantiomers dexlansoprazole (Dexilant, formerly named Kapidex) and Levolansoprazole. Lansoprazole has used to the treatment of acid-reflux disorders (GERD), peptic ulcer disease, H. pylori eradication, and prevention of gastrointestinal bleeds with NSAID use. Levolansoprazole is extensively metabolized in the liver. Two metabolites have been identified in measurable quantities in plasma (the hydroxylated sulfinyl and sulfone derivatives of Levolansoprazole).
