{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Search results for m root_references_citation in Reference Text / Citation (approximate match)
Status:
US Approved Rx
(1987)
Source:
ANDA070738
(1987)
Source URL:
First approved in 1978
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Verapamil is a FDA approved drug used to treat high blood pressure and to control chest pain. Verapamil is an L-type calcium channel blocker that also has antiarrythmic activity. The R-enantiomer is more effective at reducing blood pressure compared to the S-enantiomer. However, the S-enantiomer is 20 times more potent than the R-enantiomer at prolonging the PR interval in treating arrhythmias. Verapamil inhibits voltage-dependent calcium channels. Specifically, its effect on L-type calcium channels in the heart causes a reduction in ionotropy and chronotropy, thuis reducing heart rate and blood pressure. Verapamil's mechanism of effect in cluster headache is thought to be linked to its calcium-channel blocker effect, but which channel subtypes are involved is presently not known.
Status:
US Approved Rx
(2020)
Source:
ANDA213324
(2020)
Source URL:
First approved in 1977
Source:
FLEXERIL by JANSSEN RES AND DEV
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Cyclobenzaprine is a centrally-acting muscle relaxant which boosts levels of norepinephrine and binds to serotonin receptors in the brain to reduce spasm. Cytochromes P-450 3A4, 1A2, and, to a lesser extent, 2D6, mediate N-demethylation, one of the oxidative pathways for cyclobenzaprine. Cyclobenzaprine relieves skeletal muscle spasm of local origin without interfering with muscle function. Drowsiness, fatigue and sedation (up to 40%) is the most common side effect of Cyclobenzaprine. It may have life-threatening interactions with monoamine oxidase (MAO) inhibitors. Postmarketing cases of serotonin syndrome have been reported during combined use of cyclobenzaprine and other drugs such as selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), tramadol, bupropion, meperidine, verapamil, or MAO inhibitors.
Status:
US Approved Rx
(2005)
Source:
NDA021807
(2005)
Source URL:
First approved in 1977
Source:
NOLVADEX by ASTRAZENECA
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Tamoxifen (brand name Nolvadex), is selective estrogen receptor modulators (SERM) with tissue-specific activities for the treatment and prevention of estrogen receptor positive breast cancer. Tamoxifen itself is a prodrug, having relatively little affinity for its target protein, the estrogen receptor (ER). It is metabolized in the liver by the cytochrome P450 isoform CYP2D6 and CYP3A4 into active metabolites such as 4-hydroxytamoxifen (4-OHT) (afimoxifene) and N-desmethyl-4-hydroxytamoxifen (endoxifen) which have 30–100 times more affinity with the ER than tamoxifen itself. These active metabolites compete with estrogen in the body for binding to the ER. In breast tissue, 4-OHT acts as an ER antagonist so that transcription of estrogen-responsive genes is inhibited. Tamoxifen has 7% and 6% of the affinity of estradiol for the ERα and ERβ, respectively, whereas 4-OHT has 178% and 338% of the affinity of estradiol for the ERα and ERβ. The prolonged binding of tamoxifen to the nuclear chromatin of these results in reduced DNA polymerase activity, impaired thymidine utilization, blockade of estradiol uptake, and decreased estrogen response. It is likely that tamoxifen interacts with other coactivators or corepressors in the tissue and binds with different estrogen receptors, ER-alpha or ER-beta, producing both estrogenic and antiestrogenic effects. Tamoxifen is currently used for the treatment of both early and advanced estrogen receptor (ER)-positive (ER+) breast cancer in pre- and post-menopausal women. Additionally, it is the most common hormone treatment for male breast cancer. Patients with variant forms of the gene CYP2D6 (also called simply 2D6) may not receive full benefit from tamoxifen because of too slow metabolism of the tamoxifen prodrug into its active metabolites. Tamoxifen is used as a research tool to trigger tissue-specific gene expression in many conditional expression constructs in genetically modified animals including a version of the Cre-Lox recombination technique. Tamoxifen has been shown to be effective in the treatment of mania in patients with bipolar disorder by blocking protein kinase C (PKC), an enzyme that regulates neuron activity in the brain. Researchers believe PKC is over-active during the mania in bipolar patients.
Status:
US Approved Rx
(1988)
Source:
ANDA072206
(1988)
Source URL:
First approved in 1975
Source:
LOXITANE by TEVA BRANDED PHARM
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Loxapine is a dibenzoxazepine tricyclic antipsychotic agent, available for oral and inhalatory administration, classified as a typical antipsychotic. Loxapine acts as an antagonist at central serotonin and dopamine receptors. Adasuve (loxapine inhalation powder) is a prescription medicine that is used to treat acute agitation in adults with schizophrenia or bipolar I disorder.
Status:
US Approved Rx
(1986)
Source:
ANDA070974
(1986)
Source URL:
First approved in 1974
Source:
COMBIPRES by BOEHRINGER INGELHEIM
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Clonidine is a centrally acting α2 adrenergic agonist and imidazoline receptor agonist used to treat high blood pressure, attention deficit hyperactivity disorder, anxiety disorders, tic disorders, withdrawal (from either alcohol, opioids, or smoking), migraine, menopausal flushing, diarrhea, and certain pain conditions. Clonidine treats high blood pressure by stimulating α2 receptors in the brain, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem. This binding decreases presynaptic calcium levels, thus inhibiting the release of norepinephrine (NE). It has also been proposed that the antihypertensive effect of clonidine is due to agonism on the I1 receptor (imidazoline receptor), which mediates the sympatho-inhibitory actions of imidazolines to lower blood pressure. Clonidines mechanism of action in the treatment of ADHD is to increase noradrenergic tone in the prefrontal cortex (PFC) directly by binding to postsynaptic α2A adrenergic receptors and indirectly by increasing norepinephrine input from the locus coeruleus. Clonidine indicated in the treatment of hypertension. Clonidine hydrochloride tablets may be employed alone or concomitantly with other antihypertensive agents. The US Food and Drug Administration (FDA) has approved clonidine for the treatment of attention deficit hyperactivity disorder (ADHD), under the trade name of Kapvay alone or with stimulants in 2010, for pediatric patients aged 6–17 years.
Status:
US Approved Rx
(2018)
Source:
ANDA207707
(2018)
Source URL:
First approved in 1974
Source:
INTROPIN by HOSPIRA
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Dopamine, a sympathomimetic amine vasopressor, is the naturally occurring immediate precursor of norepinephrine. G protein-coupled dopamine receptors (D1, D2, D3, D4, and D5) mediate all of the physiological functions of the catecholaminergic neurotransmitter dopamine, ranging from voluntary movement and reward to hormonal regulation and hypertension. Dopamine HCl is indicated for the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure.
Status:
US Approved Rx
(1996)
Source:
NDA020372
(1996)
Source URL:
First approved in 1973
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Molybdenum-99 (99Mo, half-life = 66 h) is a parent radionuclide of a diagnostic nuclear isotope. It decays in technetium-99 m (half-life = 6 h), which is used in over 30 million procedures per year around the world. Between 95 and 98 percent of Mo-99 is currently being produced using highly enriched uranium (HEU) targets. Other medical isotopes such as iodine-131 (I-131) and xenon-133 (Xe-133) are by-products of the Mo-99 production process and will be sufficiently available if Mo-99 is available.
Status:
US Approved Rx
(1996)
Source:
ANDA074549
(1996)
Source URL:
First approved in 1970
Source:
NDA016812
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Ketamine (brand name Ketalar) is a cyclohexanone derivative used for induction of anesthesia. Ketalar is indicated as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation; also, it is indicated for the induction of anesthesia prior to the administration of other general anesthetic agents. Ketamine blocks NMDA receptors through an interaction with sites thought to be located within the ion channel pore region. However, the complete pharmacology of ketamine is more complex, and it is known to directly interact with a variety of other sites to varying degrees. Recently, it was shown that inclusion of the NR3B subunit does not alter the ketamine sensitivity of recombinant NR1/NR2 receptors expressed in oocytes. Likewise, 100 μM ketamine produced only weak inhibition of the glycine-induced current of NR1/NR3A/NR3B receptors. The side effects of ketamine noted in clinical studies include psychedelic symptoms (hallucinations, memory defects, panic attacks), nausea/vomiting, somnolence, cardiovascular stimulation and, in a minority of patients, hepatoxicity. The recreational use of ketamine is increasing and comes with a variety of additional risks ranging from bladder and renal complications to persistent psychotypical behaviour and memory defects. Ketamine was first synthesized in 1962 by Calvin Stevens at Parke-Davis Co (now Pfizer) as an alternative anesthetic to phencyclidine. It was first used in humans in 1965 by Corssen and Domino and was introduced into clinical practice by 1970.
Status:
US Approved Rx
(2012)
Source:
ANDA090979
(2012)
Source URL:
First approved in 1970
Source:
NDA050162
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Clindamycin phosphate is the prodrug of clindamycin with no antimicrobial activity in vitro but can be rapidly converted in vivo to the parent drug, clindamycin, by phosphatase ester hydrolysis. It is indicated in the treatment of serious infections caused by susceptible anaerobic bacteria: Lower respiratory tract infections including pneumonia, empyema, and lung abscess caused by anaerobes; Skin and skin structure infections; Gynecological infections including endometritis, nongonococcal tubo-ovarian abscess, pelvic cellulitis, and postsurgical vaginal cuff infection caused by susceptible anaerobes; Intra-abdominal infections; Septicemia; Bone and joint infections. Orally and parenterally administered clindamycin has been associated with severe colitis, which may end fatally. Abdominal pain, gastrointestinal disturbances, gram-negative folliculitis, eye pain and contact dermatitis have also been reported in association with the use of topical formulations of clindamycin. Clindamycin has been shown to have neuromuscular blocking properties that may enhance the action of other neuromuscular blocking agents
Status:
US Approved Rx
(2014)
Source:
ANDA203428
(2014)
Source URL:
First approved in 1966
Source:
NDA016273
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
Furosemide, a sulfonamide-type loop diuretic structurally related to bumetanide, is used to manage hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome. Furosemide inhibits water reabsorption in the nephron by blocking the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. This is achieved through competitive inhibition at the chloride binding site on the cotransporter, thus preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron. Because the thick ascending limb is responsible for 25% of sodium reabsorption in the nephron, furosemide is a very potent diuretic. Furosemide is sold under the brand name Lasix among others.