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Restrict the search for
angiotensin ii
to a specific field?
Status:
US Approved Rx
(2018)
Source:
ANDA203966
(2018)
Source URL:
First approved in 2007
Source:
NDA021742
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Nebivolol is a competitive and highly selective beta-1 receptor antagonist with mild vasodilating properties, possibly due to an interaction with the L-arginine/nitric oxide pathway. In preclinical studies, nebivolol has been shown to induce endothelium-dependent arterial relaxation in a dose dependent manner, by stimulation of the release of endothelial nitric oxide. Nitric oxide acts to relax vascular smooth muscle cells and inhibits platelet aggregation and adhesion. Activation of β1-receptors by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Nebivolol blocks these receptors which reverses the effects of epinephrine, lowering the heart rate and blood pressure. In addition, beta blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels. At high enough concentrations, this drug may also bind beta 2 receptors. Marketed under the brand name BYSTOLIC, Nebivolol is indicated for
the treatment of hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions.
Status:
US Approved Rx
(2020)
Source:
ANDA213815
(2020)
Source URL:
First approved in 2005
Source:
NDA021782
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Ramelteon was approved by the United States (U.S.) in July 2005, and the Japanese Ministry of Health, Labour and Welfare in April 2010. It is currently available in the USA and Japan as ROZEREM and is indicated for the treatment of insomnia characterized by difficulty with sleep onset. In October 7, 2011, Takeda has decided to discontinue the development of ramelteon in Europe for the treatment of insomnia in order to best optimize Takeda’s resources for its research and development activities. Ramelteon is a melatonin receptor agonist with both high affinity for melatonin MT1 and MT2 receptors and selectivity over the MT3 receptor. Ramelteon demonstrates full agonist activity in vitro in cells expressing human MT1 or MT2 receptors, and high selectivity for human MT1 and MT2 receptors compared to the MT3 receptor. The activity of ramelteon at the MT1 and MT2 receptors is believed to contribute to its sleep-promoting properties since these receptors are acted upon by endogenous melatonin and are thought to be involved in the maintenance of the circadian rhythm underlying normal sleep-wake cycles. Ramelteon has no appreciable affinity for the GABA receptor complex or for receptors that bind neuropeptides, cytokines, serotonin, dopamine, noradrenaline, acetylcholine, and opiates.
Status:
US Approved Rx
(2019)
Source:
ANDA210552
(2019)
Source URL:
First approved in 2002
Source:
NDA021286
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Olmesartan medoxomil, a prodrug, is hydrolyzed to olmesartan during absorption from the gastrointestinal tract. Olmesartan is a selective AT1 subtype angiotensin II receptor antagonist. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in vascular smooth muscle. Oral olmesartan medoxomil 10-40 mg once daily is recommended for the treatment of adult patients with hypertension, this dosage has consistently helped achieve a double-digit reduction both in systolic and diastolic blood pressure, a reduction which is maintained for one year. Extensive clinical evidence from several large well designed trials and the clinical practice setting has confirmed the antihypertensive efficacy and good tolerability profile of oral olmesartan medoxomil, as monotherapy in patients with hypertension. Olmesartan medoxomil has shown no clinically important pharmacokinetic interactions with digoxin, warfarin or antacid (aluminium magnesium hydroxide). Adverse events were infrequent in clinical studies of olmesartan medoxomil and were similar to those attributed to placebo.
Status:
US Approved Rx
(2015)
Source:
ANDA204094
(2015)
Source URL:
First approved in 2002
Source:
NDA021436
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Aripiprazole is the first next-generation atypical antipsychotic. The unique actions of aripiprazole in humans are likely a combination of "functionally selective" activation of D(2) (and possibly D(3))-dopamine receptors and serotonin 5-HT(1A) receptors, coupled with inhibition of 5-HT(2A) receptors. Aripiprazole was approved by FDA (Abilify trade name) for the treatment of schizophrenia; manic and mixed episodes associated with bipolar I disorder; major depressive disorder; irritability associated with autistic disorder; Tourette’s disorder and agitation associated with schizophrenia or bipolar mania.
Status:
US Approved Rx
(2018)
Source:
ANDA208283
(2018)
Source URL:
First approved in 2002
Source:
NDA021437
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Eplerenone, an aldosterone receptor antagonist similar to spironolactone, has been shown to produce sustained increases in plasma renin and serum aldosterone, consistent with inhibition of the negative regulatory feedback of aldosterone on renin secretion. The resulting increased plasma renin activity and aldosterone circulating levels do not overcome the effects of eplerenone. Eplerenone selectively binds to recombinant human mineralocorticoid receptors relative to its binding to recombinant human glucocorticoid, progesterone and androgen receptors. Eplerenone binds to the mineralocorticoid receptor and thereby blocks the binding of aldosterone (component of the renin-angiotensin-aldosterone-system, or RAAS). Aldosterone synthesis, which occurs primarily in the adrenal gland, is modulated by multiple factors, including angiotensin II and non-RAAS mediators such as adrenocorticotropic hormone (ACTH) and potassium. Aldosterone binds to mineralocorticoid receptors in both epithelial (e.g., kidney) and nonepithelial (e.g., heart, blood vessels, and brain) tissues and increases blood pressure through induction of sodium reabsorption and possibly other mechanisms. Used for improvement of survival of stable patients with left ventricular systolic dysfunction (ejection fraction <40%) and clinical evidence of congestive heart failure after an acute myocardial infarction.
Status:
US Approved Rx
(2001)
Source:
NDA021319
(2001)
Source URL:
First approved in 2001
Source:
NDA021319
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Dutasteride is a synthetic 4-azasteroid compound that is a selective inhibitor of both the type 1 and type 2 isoforms of steroid 5 alpha-reductase (5AR), intracellular enzymes that convert testosterone to 5 alpha-dihydrotestosterone (DHT). Type I 5a-reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and liver. Type I 5a-reductase is responsible for approximately one-third of circulating DHT. The Type II 5a-reductase isozyme is primarily found in prostate, seminal vesicles, epididymides, and hair follicles as well as liver, and is responsible for two-thirds of circulating DHT. Dutasteride inhibits the conversion of testosterone to 5 alpha-dihydrotestosterone (DHT), which is the androgen primarily responsible for the initial development and subsequent enlargement of the prostate gland. Testosterone is converted to DHT by the enzyme 5 alpha-reductase, which exists as 2 isoforms, type 1 and type 2. Dutasteride is a competitive and specific inhibitor of both type 1 and type 2 5 alpha-reductase isoenzymes, with which it forms a stable enzyme complex. Dissociation from this complex has been evaluated under in vitro and in vivo conditions and is extremely slow. Used for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate gland to improve symptoms, and reduce the risk of acute urinary retention and the need for surgery. Marketed under the brand name Avodart.
Status:
US Approved Rx
(2021)
Source:
ANDA213541
(2021)
Source URL:
First approved in 2001
Source:
NDA021356
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
(R)-9-(2-Phosphonylmethoxypropyl)adenine (PMPA known as tenofovir) is an antiviral drug. Diphosphate of PMPA acts as a selective inhibitor of the HIV-1 reverse
transcriptase. Tenofovir disoproxil was approved for clinical use for the treatment of HIV infection (AIDS) and chronic HBV infection.
Status:
US Approved Rx
(2002)
Source:
NDA021386
(2002)
Source URL:
First approved in 2001
Source:
ZOMETA by NOVARTIS
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Zoledronic acid (Reclast, Aclasta, Zometa) is an intravenous, highly potent amino-bisphosphonate approved worldwide, including in the USA, EU and Japan for use in patients with primary or secondary osteoporosis or low bone mass (approved indications vary between countries). Its high affinity to and long half-life in bone, and long duration of action allow for once-yearly administration, which has the potential to improve adherence to therapy. Zoledronic acid once yearly for up to 3 years improved bone mineral density (BMD) at several skeletal sites, reduced fracture risk and bone turnover, and/or preserved
bone structure and mass relative to placebo in clinical studies in patients with primary or secondary osteoporosis. While additional benefits were seen when treatment was continued for up to 6 years, as evidenced by a reduced risk of vertebral fractures and higher BMD relative to 3 years’ therapy, there was the minimal advantage of treatment beyond 6 years. Therefore, in patients with low fracture risk, treatment discontinuation should be considered after approximately 5 years’ therapy. Zoledronic acid administered annually or once in 2 years was also effective in preventing bone loss in patients with low bone mass. Zoledronic acid was generally well tolerated, with the most common adverse events (AEs) being transient, mild-to-moderate post-infusion symptoms, which decreased with subsequent infusions.
Status:
US Approved Rx
(2018)
Source:
ANDA206812
(2018)
Source URL:
First approved in 2001
Source:
NDA021345
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Fondaparinux is a synthetic and specific inhibitor of activated Factor X (Xa). By selectively binding to antithrombin III (ATIII), fondaparinux sodium potentiates (about 300 times) the innate neutralization of Factor Xa by ATIII. Neutralization of Factor Xa interrupts the blood coagulation cascade and thus inhibits thrombin formation and thrombus development. Fondaparinux is indicated for the prophylaxis of deep vein thrombosis (DVT), which may lead to pulmonary embolism (PE): in patients undergoing hip fracture surgery, including extended prophylaxis; in patients undergoing hip replacement surgery; in patients undergoing knee replacement surgery; in patients undergoing abdominal surgery who are at risk for thromboembolic complications. The most serious adverse reactions reported with Fondaparinux are bleeding complications and thrombocytopenia. Agents that may enhance the risk of hemorrhage should be discontinued prior to initiation of therapy with Fondaparinux unless these agents are essential.
Status:
US Approved Rx
(2005)
Source:
ANDA077636
(2005)
Source URL:
First approved in 2000
Source:
NDA020789
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Zonisamide is an antiseizure drug chemically classified as a sulfonamide and unrelated to other antiseizure agents. The precise mechanism by which zonisamide exerts its antiseizure effect is unknown, although it is believed that the drug blocks sodium and calcium channels, which leads to the suppression of neuronal hypersynchronization (i.e. convulsions). Sonisamide has also been found to potentiate dopaminergic and serotonergic neurotransmission but does not appear to potentiate syanptic activity by GABA (gamma amino butyric acid). Zonisamide binds to sodium channels and voltage sensitive calcium channels, which suppresses neuronal depolarization and hypersynchronization. Zonisamide also inhibits carbonic anhydrase to a weaker extent, but such an effect is not thought to contribute substantially to the drug's anticonvulsant activity. Zonisamide is approved in the United States, United Kingdom, and Australia for adjunctive treatment of partial seizures in adults and in Japan for both adjunctive and monotherapy for partial seizures (simple, complex, secondarily generalized), generalized (tonic, tonic-clonic (grand mal), and atypical absence) and combined seizures.
