{{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}}
Restrict the search for
amphotericin b
to a specific field?
Status:
US Approved Rx
(2004)
Source:
NDA021361
(2004)
Source URL:
First approved in 2004
Source:
NDA021361
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Rifaximin is a structural analog of rifampin and a non-systemic, gastrointestinal site-specific antibiotic. Rifaximin acts by inhibiting bacterial ribonucleic acid (RNA) synthesis and contributes to restore intestinal microflora imbalance. It is FDA approved for the treatment of travelers’ diarrhea, reduction in risk of overt hepatic encephalopathy (HE) recurrence and treatment of irritable bowel syndrome with diarrhea. More common side effects are: black, tarry stools; dizziness or lightheadedness; muscle spasm; rapid breathing; shortness of breath; trouble sleeping. Co-administration of cyclosporine, with XIFAXAN resulted in 83-fold and 124-fold increases in rifaximin mean Cmax in healthy subjects.
Status:
US Approved Rx
(2006)
Source:
NDA021501
(2006)
Source URL:
First approved in 2004
Source:
21 CFR 352
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Conditions:
Octocrylene is a compound often used as an additive in sun screen, and is thought to have skin moisturizing effects because of its emollient properties. What makes this chemical such a popular additive to sun block, is its ability to neutralize UV radiation dissipated by sunlight, and to minimize skin damage from prolonged sun exposure. Octocrylene is also often combined with avobenzone, another common sunscreen ingredient often appearing on ingredient labels. Because of its effectiveness, the chemical has been approved across the globe for use in cosmetics and skin care products, but the concentrations of this ingredient are usually limited to no more than 10 or 12 percent. However, the use of this chemical doesn’t just stop with sunscreen for face and arms, but can extend to a variety of other products, like hair spray, tannin oil, BB cream, conditioner, and CC cream, among others. Octocrylene may cause contact and photocontact allergy.
Status:
US Approved Rx
(2003)
Source:
NDA021385
(2003)
Source URL:
First approved in 2003
Source:
NDA021385
Source URL:
Class (Stereo):
CHEMICAL (RACEMIC)
Targets:
Conditions:
Sertaconazole is a azole antifungal that is FDA approved for the treatment of interdigital tinea pedis in immunocompetent patients 12 years of age and older, caused by: Trichophyton rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum. Sertaconazole interacts with 14-α demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Common adverse reactions include contact dermatitis, dry skin, burning skin and application site skin tenderness.
Status:
US Approved Rx
(2017)
Source:
NDA208385
(2017)
Source URL:
First approved in 2003
Source:
CUBICIN by CUBIST PHARMS LLC
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Daptomycin is a lipopeptide antibiotic used in the treatment of systemic and life-threatening infections caused by Gram-positive organisms. Daptomycin has a distinct mechanism of action, disrupting multiple aspects of bacterial cell membrane function. It inserts into the cell membrane in a phosphatidylglycerol-dependent fashion, where it then aggregates. The aggregation of daptomycin alters the curvature of the membrane, which creates holes that leak ions. This causes rapid depolarization, resulting in a loss of membrane potential leading to inhibition of protein, DNA, and RNA synthesis, which results in bacterial cell death. Daptomycin is bactericidal against Gram-positive bacteria only. It has proven in vitro activity against enterococci (including glycopeptide-resistant enterococci (GRE)), staphylococci (including methicillin-resistant Staphylococcus aureus), streptococci, corynebacteria and stationary-phase Borrelia burgdorferi persisters.
Status:
US Approved Rx
(2023)
Source:
ANDA079188
(2023)
Source URL:
First approved in 2003
Source:
NDA021500
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Emtricitabine was discovered by Emory researchers Dr. Dennis C. Liotta, Dr. Raymond F. Schinazi and Dr. Woo-Baeg Choi and licensed to Triangle Pharmaceuticals by Emory University in 1996. Triangle was acquired by Gilead in 2003. Emtricitabine, marketed by Gilead as Emtriva, was first approved by the U.S. Food and Drug Administration in July 2003 for the treatment of HIV infection in combination with other antiretroviral agents. Emtricitabine, a synthetic nucleoside analog of cytidine, is phosphorylated by cellular enzymes to form emtricitabine 5'-triphosphate. Emtricitabine 5'-triphosphate inhibits the activity of the HIV-1 reverse transcriptase by competing with the natural substrate deoxycytidine 5'-triphosphate and by being incorporated into nascent viral DNA which results in chain termination.
Status:
US Approved Rx
(2022)
Source:
ANDA209659
(2022)
Source URL:
First approved in 2003
Source:
NDA021602
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Bortezomib is the therapeutic proteasome inhibitor. First, which is tested in humans. The boron atom in bortezomib binds the catalytic site of the 26S proteasome with high affinity and specificity. Bortezomib is approved in the U.S. for treating relapsed multiple myeloma and mantle cell lymphoma. The 26S proteasome degrades various proteins critical to cancer cell survival, such as cyclins, tumor suppressors, BCL-2, and cyclin-dependent kinase inhibitors. Inhibition of these degradations sensitizes cells to apoptosis. Bortezomib is a potent inhibitor of 26S proteasome, which sensitizes activity in dividing multiple myeloma and leukemic cells, thus inducing apoptosis. Most commonly reported adverse reactions (incidence ≥30%) in clinical studies include asthenic conditions, diarrhea, nausea, constipation, peripheral neuropathy, vomiting, pyrexia, thrombocytopenia, psychiatric disorders, anorexia and decreased appetite, neutropenia, neuralgia, leukopenia and anemia. Co-administration of ketoconazole, a potent CYP3A inhibitor, increased the exposure of bortezomib. Co-administration of melphalan-prednisone increased the exposure of bortezomib. However, this increase is unlikely to be clinically relevant.
Status:
US Approved Rx
(2019)
Source:
ANDA206285
(2019)
Source URL:
First approved in 2003
Source:
NDA021368
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Tadalafil is used to treat male erectile dysfunction (impotence) and pulmonary arterial hypertension (PAH). Part of the physiological process of erection involves the release of nitric oxide (NO) in the corpus cavernosum. This then activates the enzyme guanylate cyclase which results in increased levels of cyclic guanosine monophosphate (cGMP), leading to smooth muscle relaxation in the corpus cavernosum, resulting in increased inflow of blood and an erection. Tadalafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum. This means that, with tadalafil on board, normal sexual stimulation leads to increased levels of cGMP in the corpus cavernosum which leads to better erections. Without sexual stimulation and no activation of the NO/cGMP system, tadalafil should not cause an erection.Tadalafil inhibits the cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum located around the penis. Penile erection during sexual stimulation is caused by increased penile blood flow resulting from the relaxation of penile arteries and corpus cavernosal smooth muscle. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cGMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum. The inhibition of phosphodiesterase type 5 (PDE5) by tadalafil enhances erectile function by increasing the amount of cGMP. Tadalafil is used for the treatment of erectile dysfunction.
Status:
US Approved Rx
(2013)
Source:
ANDA202051
(2013)
Source URL:
First approved in 2002
Source:
HEPSERA by GILEAD
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Conditions:
The potential antiviral effect of adefovir, an acyclic nucleoside phosphonate analog of 2′-deoxyadenosine monophosphate, was first studied by Holý and De Clercq in 1980s.
Adefovir is an acyclic nucleotide analog of adenosine monophosphate which is phosphorylated to the active metabolite adefovir diphosphate by cellular kinases. Adefovir diphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate and by causing DNA chain termination after its incorporation into viral DNA. Oral adefovir dipivoxil is effective and generally well tolerated in HBeAg-positive and -negative patients chronically infected with wild-type or lamivudine-resistant HBV.
Status:
US Approved Rx
(2017)
Source:
ANDA205529
(2017)
Source URL:
First approved in 2002
Source:
ELOXATIN by SANOFI AVENTIS US
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Oxaliplatin (brand name Eloxatin), a new generation of platinum derivatives discovered by Prof Kidani in 1976 at Nagoya University in Japan, was licensed-in and developed by Debiopharm. Eloxatin is typically administered in combination with fluorouracil and leucovorin for the adjuvant treatment of stage III colon cancer and for the treatment of advanced carcinoma of the colon or rectum. Oxaliplatin undergoes nonenzymatic conversion in physiologic solutions to active derivatives via displacement of the labile oxalate ligand. Several transient reactive species are formed, including monoaquo and diaquo 1,2-diaminocyclohexane (DACH) platinum, which covalently bind with macromolecules. Both inter- and intrastrand Pt-DNA crosslinks are formed. Crosslinks are formed between the N7 positions of two adjacent guanines (GG), adjacent adenine-guanines (AG), and guanines separated by an intervening nucleotide (GNG). These crosslinks inhibit DNA replication and transcription. Cytotoxicity is cell-cycle nonspecific.
Status:
US Approved Rx
(2009)
Source:
NDA022387
(2009)
Source URL:
First approved in 2002
Source:
NDA021272
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Treprostinil (marketed under the trade names Remodulin for infusion) is a vasodilator that is used for the treatment of pulmonary arterial hypertension. Pulmonary arterial hypertension (PAH) is a disease in which blood pressure is abnormally high in the arteries between the heart and lungs. PAH is characterized by symptoms of shortness of breath during physical exertion. The condition can ultimately lead to heart failure. Treprostinil is a potent oral antiplatelet agent. The major pharmacologic actions of treprostinil are direct vasodilation of pulmonary and systemic arterial vascular beds and inhibition of platelet aggregation. In animals, the vasodilatory effects reduce right and left ventricular afterload and increase cardiac output and stroke volume. Other studies have shown that treprostinil causes a dose-related negative inotropic and lusitropic effect. No major effects on cardiac conduction have been observed. Treprostinil had high affinity for the Prostaglandin D2 receptor (DP1), Prostaglandin E2 receptor EP2 subtype (EP2) and Prostaglandin D2 receptor (IP) receptors (Ki 4.4, 3.6 and 32 nM, respectively), low affinity for EP1 and EP4 receptors and even lower affinity for EP3, Prostaglandin F (FP) and thromboxane (TP) receptors. Treprostinil has demonstrated a unique effect on PPAR gamma, a transcription factor important in vascular pathogenesis as a mediator of proliferation, inflammation and apoptosis. Through a complementary, yet cyclic AMP-independent pathway, treprostinil activates PPARs, another mechanism that contributes to the anti-growth benefits of the prostacyclin class.
