{{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}}
Restrict the search for
megestrol acetate
to a specific field?
Status:
US Approved Rx
(2023)
Source:
ANDA216075
(2023)
Source URL:
First approved in 1999
Source:
NDA021057
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Ganirelix (N-acetyl-3-(2-naphthyl)-D-alanyl-4-chloro-D-phenylalanyl-3-(3-pyridyl)-D-alanyl-L-seryl-L-tyrosyl-N9 ,N10-diethyl-D-homoarginyl-L-leucylN9 ,N10-diethyl-L-homoarginyl-L-prolyl-D-acrylamide) is a synthetic decapeptide with high antagonistic activity against naturally occurring gonadotropin-releasing hormone (GnRH). Ganirelix Acetate Injection is indicated for the inhibition of premature luteinizing hormone (LH) surges in women undergoing controlled ovarian hyperstimulation. Ganirelix is administered by a subcutaneous injection of 250 µg once per day during the mid to late follicular phase of a woman’s menstrual cycle. Treatment should start on the 5th or 6th day after the start of ovarian stimulation, and the mean duration of its use is five days. Clinical studies have shown that the most common side effect is a slight reaction at the site of injection in the form of redness, and sometimes swelling. Clinical studies have shown that, one hour after injection, the incidence of at least one moderate or severe local skin reaction per treatment cycle was 12% in 4 patients treated with Ganirelix and 25% in patients treated subcutaneously with a GnRH agonist. The local reactions generally disappear within 4 hours after administration. Other reported side effects are some that are known to be associated with ovarian hyperstimulation, including gynecological abdominal pain, headache, vaginal bleeding, nausea, and gastrointestinal abdominal pain.
Status:
US Approved Rx
(2023)
Source:
ANDA206027
(2023)
Source URL:
First approved in 1997
Source:
Duract
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Bromfenac is a topical, nonsteroidal anti-inflammatory drug (NSAID) for ophthalmic use. It is indicated for the treatment of postoperative inflammation and reduction of ocular pain in patients who have undergone cataract surgery. The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. The most commonly reported adverse reactions in 3 to 8% of patients were anterior chamber inflammation, foreign body sensation, eye pain, photophobia and vision blurred.
Status:
US Approved Rx
(2005)
Source:
ANDA076468
(2005)
Source URL:
First approved in 1997
Source:
NDA020333
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Anagrelide is an orally active quinazinolone derivative that was originally developed as an antiplatelet drug. The drug inhibits cyclic nucleotide phosphodiesterase III (PDEIII) and phopholipase A2, which is thought to cause the side effects of vasodilation, positive inotropism, reduced platelet aggregation. However, significant inhibition of platelet aggregation is observed only at doses of anagrelide higher than those required to reduce platelet count. It is indicated for the treatment of patients with thrombocythemia, secondary to myeloproliferative disorders. Commonly reported side effects of anagrelide include: abdominal pain, dizziness, headache, nausea, and palpitations. Other side effects include: back pain, fever, tachycardia, vomiting, and anorexia. There is a single case report, which suggests that sucralfate may interfere with anagrelide absorption. Anagrelide is an inhibitor of cyclic AMP PDE III. The effects of medicinal products with similar properties such as inotropes milrinone, enoximone, amrinone, olprinone and cilostazol may be exacerbated by anagrelide.
Status:
US Approved Rx
(2012)
Source:
ANDA090540
(2012)
Source URL:
First approved in 1997
Source:
NDA020839
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Clopidogrel, an antiplatelet agent structurally and pharmacologically similar to ticlopidine, is used to inhibit blood clots in a variety of conditions such as peripheral vascular disease, coronary artery disease, and cerebrovascular disease. Clopidogrel is sold under the name Plavix by Sanofi and Bristol-Myers Squibb. Plavix (clopidogrel bisulfate) is an inhibitor of ADP-induced platelet aggregation acting by direct
inhibition of adenosine diphosphate (ADP) binding to its receptor and of the subsequent ADPmediated
activation of the glycoprotein GPIIb/IIIa complex. Clopidogrel must be metabolized by CYP450 enzymes to produce the active metabolite that
inhibits platelet aggregation. The active metabolite of clopidogrel selectively inhibits the
binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADPmediated
activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet
aggregation. This action is irreversible. Consequently, platelets exposed to clopidogrel’s active
metabolite are affected for the remainder of their lifespan (about 7 to 10 days). Platelet
aggregation induced by agonists other than ADP is also inhibited by blocking the amplification
of platelet activation by released ADP. Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events.
Status:
US Approved Rx
(2012)
Source:
ANDA090540
(2012)
Source URL:
First approved in 1997
Source:
NDA020839
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Clopidogrel, an antiplatelet agent structurally and pharmacologically similar to ticlopidine, is used to inhibit blood clots in a variety of conditions such as peripheral vascular disease, coronary artery disease, and cerebrovascular disease. Clopidogrel is sold under the name Plavix by Sanofi and Bristol-Myers Squibb. Plavix (clopidogrel bisulfate) is an inhibitor of ADP-induced platelet aggregation acting by direct
inhibition of adenosine diphosphate (ADP) binding to its receptor and of the subsequent ADPmediated
activation of the glycoprotein GPIIb/IIIa complex. Clopidogrel must be metabolized by CYP450 enzymes to produce the active metabolite that
inhibits platelet aggregation. The active metabolite of clopidogrel selectively inhibits the
binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADPmediated
activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet
aggregation. This action is irreversible. Consequently, platelets exposed to clopidogrel’s active
metabolite are affected for the remainder of their lifespan (about 7 to 10 days). Platelet
aggregation induced by agonists other than ADP is also inhibited by blocking the amplification
of platelet activation by released ADP. Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events.
Status:
US Approved Rx
(2016)
Source:
ANDA202674
(2016)
Source URL:
First approved in 1997
Source:
NDA020639
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Quetiapine, marketed as SEROQUEL XR, is an atypical antipsychotic approved for the treatment of schizophrenia, bipolar disorder, and along with an antidepressant to treat major depressive disorder. The mechanism of action of SEROQUEL XR in the treatment of schizophrenia, bipolar disorder and major depressive disorder (MDD), is unknown. However, its efficacy in schizophrenia could be mediated through a combination of dopamine type 2 (D2) and serotonin type 2A (5HT2A) antagonism. The active metabolite, N-desalkyl quetiapine (norquetiapine), has similar activity at D2, but greater activity at 5HT2A receptors, than the parent drug (quetiapine). Quetiapine’s efficacy in bipolar depression and MDD may partly be explained by the high affinity and potent inhibitory effects that norquetiapine exhibits for the norepinephrine transporter. Antagonism at receptors other than dopamine and serotonin with similar or greater affinities may explain some of the other effects of quetiapine and norquetiapine: antagonism at histamine H1 receptors may explain the somnolence, antagonism at adrenergic α1b receptors may explain the orthostatic hypotension, and antagonism at muscarinic M1 receptors may explain the anticholinergic effects. Quetiapine and norquetiapine have affinity for multiple neurotransmitter receptors including dopamine D1 and D2, serotonin 5HT1A and 5HT2A, histamine H1, muscarinic M1, and adrenergic α1b and α2 receptors. Quetiapine differs from norquetiapine in having no appreciable affinity for muscarinic M1 receptors whereas norquetiapine has high affinity. Quetiapine and norquetiapine lack appreciable affinity for benzodiazepine receptors.
Status:
US Approved Rx
(2012)
Source:
ANDA090540
(2012)
Source URL:
First approved in 1997
Source:
NDA020839
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Clopidogrel, an antiplatelet agent structurally and pharmacologically similar to ticlopidine, is used to inhibit blood clots in a variety of conditions such as peripheral vascular disease, coronary artery disease, and cerebrovascular disease. Clopidogrel is sold under the name Plavix by Sanofi and Bristol-Myers Squibb. Plavix (clopidogrel bisulfate) is an inhibitor of ADP-induced platelet aggregation acting by direct
inhibition of adenosine diphosphate (ADP) binding to its receptor and of the subsequent ADPmediated
activation of the glycoprotein GPIIb/IIIa complex. Clopidogrel must be metabolized by CYP450 enzymes to produce the active metabolite that
inhibits platelet aggregation. The active metabolite of clopidogrel selectively inhibits the
binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADPmediated
activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet
aggregation. This action is irreversible. Consequently, platelets exposed to clopidogrel’s active
metabolite are affected for the remainder of their lifespan (about 7 to 10 days). Platelet
aggregation induced by agonists other than ADP is also inhibited by blocking the amplification
of platelet activation by released ADP. Plavix (clopidogrel bisulfate) is indicated for the reduction of atherothrombotic events.
Status:
US Approved Rx
(2023)
Source:
ANDA215744
(2023)
Source URL:
First approved in 1996
Source:
NDA020449
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Docetaxel was protected by patents (U.S. patent and European patent) which were owned by Sanofi-Aventis, and so was available only under the Taxotere brand name internationally. The European patent expired in 2010. Docetaxel is a clinically well-established anti-mitotic chemotherapy medication used for the treatment of patients with locally advanced or metastatic breast cancer after failure of prior chemotherapy. Also used as a single agent in the treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of prior platinum-based chemotherapy. It is also used in combination with prednisone, in the treatment of patients with androgen independent (hormone refractory) metastatic prostate cancer. Furthermore, docetaxel has uses in the treatment of gastric adenocarcinoma and head and neck cancer. Docetaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, docetaxel arrests their function by having the opposite effect; it hyper-stabilizes their structure. This destroys the cell's ability to use its cytoskeleton in a flexible manner. Specifically, docetaxel binds to the β-subunit of tubulin. Tubulin is the "building block" of mictotubules, and the binding of docetaxel locks these building blocks in place. The resulting microtubule/docetaxel complex does not have the ability to disassemble. This adversely affects cell function because the shortening and lengthening of microtubules (termed dynamic instability) is necessary for their function as a transportation highway for the cell. Chromosomes, for example, rely upon this property of microtubules during mitosis. Further research has indicated that docetaxel induces programmed cell death (apoptosis) in cancer cells by binding to an apoptosis stopping protein called Bcl-2 (B-cell leukemia 2) and thus arresting its function.
Status:
US Approved Rx
(2024)
Source:
ANDA217118
(2024)
Source URL:
First approved in 1996
Source:
NDA020702
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Atorvastatin calcium (LIPITOR®) is a pyrrole and heptanoic acid derivative, a synthetic lipid-lowering agent. Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. Atorvastatin is used to reduce serum levels of LDL(low-density lipoprotein)-cholesterol; apolipoprotein B; and triglycerides and to increase serum levels of HDL(high-density lipoprotein)-cholesterol in the treatment of hyperlipidemias and prevention of cardiovascular disease in patients with multiple risk factors.
Status:
US Approved Rx
(2012)
Source:
ANDA201022
(2012)
Source URL:
First approved in 1994
Source:
FAMVIR by NOVARTIS
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Penciclovir (DENAVIR®) is a synthetic acyclic guanine derivative with antiviral activity, mainly used to treat infections from herpes simplex virus (HSV) types 1 and 2. In cells infected with HSV-1 or HSV-2, the viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted by cellular kinases to the active form penciclovir triphosphate. Biochemical studies demonstrate that penciclovir triphosphate inhibits HSV polymerase competitively with deoxyguanosine triphosphate. Consequently, herpes viral DNA synthesis and, therefore, replication are selectively inhibited. Famciclovir (FAMVIR®) is a prodrug form of penciclovir with improved oral bioavailability.
