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Restrict the search for
amphotericin b
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There is one exact (name or code) match for amphotericin b
Status:
US Approved Rx
(1995)
Source:
NDA050724
(1995)
Source URL:
First approved in 1958
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Amphotericin B used to treat progressive, potentially life-threatening fungal infections, such as oral thrush, vaginal candidiasis and esophageal candidiasis in patients with normal neutrophil counts. Also, Amphotericin B is often used in otherwise-untreatable protozoan infections such as visceral leishmaniasis and primary amoebic meningoencephalitis. As with other polyene antifungals, amphotericin B binds with ergosterol, a component of fungal cell membranes, forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl−) leakage, which is the primary effect leading to fungal cell death.
When administered concurrently, the following drugs may interact with amphotericin B: Antineoplastic agents, Corticosteroids and Corticotropin (ACTH); Digitalis glycosides; Flucytosine; Imidazoles (e.g., ketoconazole, miconazole, clotrimazole, fluconazole, etc.); Zidovudine; Skeletal muscle relaxants (tubocurarine); Rifabutin; Leukocyte transfusions. The adverse reactions most commonly observed are: fever; malaise; weight loss; hypotension; tachypnea; anorexia; nausea; vomiting; diarrhea; dyspepsia; cramping epigastric pain; normochromic, normocytic anemia; pain at the injection site with or without phlebitis or thrombophlebitis; generalized pain, including muscle and joint pains; headache; decreased renal function and renal function abnormalities.
Status:
US Approved Rx
(1995)
Source:
NDA050724
(1995)
Source URL:
First approved in 1958
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
Amphotericin B used to treat progressive, potentially life-threatening fungal infections, such as oral thrush, vaginal candidiasis and esophageal candidiasis in patients with normal neutrophil counts. Also, Amphotericin B is often used in otherwise-untreatable protozoan infections such as visceral leishmaniasis and primary amoebic meningoencephalitis. As with other polyene antifungals, amphotericin B binds with ergosterol, a component of fungal cell membranes, forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl−) leakage, which is the primary effect leading to fungal cell death.
When administered concurrently, the following drugs may interact with amphotericin B: Antineoplastic agents, Corticosteroids and Corticotropin (ACTH); Digitalis glycosides; Flucytosine; Imidazoles (e.g., ketoconazole, miconazole, clotrimazole, fluconazole, etc.); Zidovudine; Skeletal muscle relaxants (tubocurarine); Rifabutin; Leukocyte transfusions. The adverse reactions most commonly observed are: fever; malaise; weight loss; hypotension; tachypnea; anorexia; nausea; vomiting; diarrhea; dyspepsia; cramping epigastric pain; normochromic, normocytic anemia; pain at the injection site with or without phlebitis or thrombophlebitis; generalized pain, including muscle and joint pains; headache; decreased renal function and renal function abnormalities.
Status:
US Approved Rx
(2024)
Source:
NDA219008
(2024)
Source URL:
First approved in 2024
Source:
NDA219008
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Status:
US Approved Rx
(2024)
Source:
NDA218033
(2024)
Source URL:
First approved in 2024
Source:
NDA218033
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
BIIB-024, also known as MLN2480, and AMG 2112819, is an oral, selective pan-Raf kinase inhibitor. The Raf kinases (A-Raf, B-Raf and C-Raf) are key regulators of cell proliferation and survival within the mitogen-activated protein kinase (MAPK) pathway. The MAPK pathway is frequently disregulated in human cancers, often via activating mutations of Ras or Raf. BIIB-024 inhibits MAPK pathway signaling in BRAF mutant and some RAS mutant preclinical cancer models at concentrations that are tolerated in vivo. BIIB-024 is most potent in BRAF mutant melanoma models but also has single agent activity in some RAS mutant models. The combination of BIIB-024 with TAK-733 inhibits the growth of a broader range of RAS mutant tumor models than single agent BIIB-024, including primary human tumor xenograft models of melanoma and CRC. BIIB-024 is in phase I clinical trials for the treatment of malignant melanoma and solid tumours.
Status:
US Approved Rx
(2024)
Source:
NDA217686
(2024)
Source URL:
First approved in 2024
Source:
NDA217686
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
ACT-132577 is the major and pharmacologically active metabolite of macitentan (ACT-064992), which is dual ETA/ETB endothelin (ET) receptor antagonist designed for tissue targeting.
Status:
US Approved Rx
(2024)
Source:
NDA215192
(2024)
Source URL:
First approved in 2024
Source:
NDA215192
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Vadadustat is an Hypoxia-inducible factor (HIF) prolyl hydroxylase (PH) enzyme inhibitor. Patients with chronic kidney disease (CKD) have reduced levels of erythropoietin (EPO) and iron in the body, which can result in decreased number of oxygen-carrying red blood cells (RBCs) (anemia). The deficiency in RBCs causes inadequate oxygen delivery to cells and tissues. Vadadustat simulates the hypoxia response pathway by stabilizing key regulatory proteins called HIFs. Under normal conditions, when sufficient oxygen is present, HIF proteins are targeted for degradation by HIF-PH to maintain homeostasis in RBC production. Under conditions of hypoxia, HIF-PH activity is reduced, resulting in HIF stabilization. Stable HIF moves to the nucleus, where it activates target genes that increase EPO synthesis, resulting in the production of new RBCs, and suppression of hepcidin to promote iron absorption and mobilization. Vadadustat is currently in the phase 3 stage of development for the treatment of anemia secondary to CKD.
Status:
US Approved Rx
(2023)
Source:
NDA218276
(2023)
Source URL:
First approved in 2023
Source:
NDA218276
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(2023)
Source:
NDA216059
(2023)
Source URL:
First approved in 2023
Source:
NDA216059
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Pirtobrutinib is a small molecule, noncovalent inhibitor of BTK. BTK is a signaling protein of the B-cell antigen receptor (BCR) and cytokine receptor pathways. In B-cells, BTK signaling results in activation of pathways necessary for B-cell proliferation, trafficking, chemotaxis, and adhesion. Pirtobrutinib binds to wild type BTK and BTK harboring C481 mutations, leading to inhibition of BTK kinase activity. In nonclinical studies, pirtobrutinib inhibited BTK-mediated B-cell CD69 expression and inhibited malignant B-cell proliferation. Pirtobrutinib showed dose-dependent anti-tumor activities in BTK wild type and BTK C481S mutant mouse xenograft models. On January 27, 2023, the Food and Drug Administration (FDA) granted accelerated approval to pirtobrutinib (Jaypirca, Eli Lilly and Company) for relapsed or refractory mantle cell lymphoma (MCL) after at least two lines of systemic therapy, including a BTK inhibitor.
Status:
US Approved Rx
(2023)
Source:
NDA216834
(2023)
Source URL:
First approved in 2023
Source:
NDA216834
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Status:
US Approved Rx
(2023)
Source:
NDA216993
(2023)
Source URL:
First approved in 2023
Source:
NDA216993
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Targets:
Quizartinib (AC220) is an orally bioavailable, small molecule receptor tyrosine kinase inhibitor that is being developed by Daiichi Sankyo Company (previously Ambit Biosciences) and Astellas Pharma as a treatment for acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL) and advanced solid tumours. The highest affinity target identified for Quizartinib was FLT3. The only other kinases with binding constants within 10-fold that for FLT3 were the closely related receptor tyrosine kinases KIT, PDGFRA, PDGFRB, RET, and CSF1R. Kinase inhibition of (mutant) KIT, PDGFR and FLT3 isoforms by quizartinib leads to potent inhibition of cellular proliferation and induction of apoptosis in in vitro leukemia models as well as in native leukemia blasts treated ex vivo.
Status:
US Approved Rx
(2023)
Source:
NDA216718
(2023)
Source URL:
First approved in 2023
Source:
NDA216718
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Omaveloxolone (RTA-408) is a synthetic triterpenoid exerting antioxidant inflammation modulator properties. It activates the transcription factor Nrf2 and inhibits NF-κB signaling. Omaveloxolone demonstrated antioxidant, anti-inflammatory, and anticancer activities. Reata Pharmaceuticals is developing omaveloxolone for the treatment of cancers, Friedreich's ataxia and mitochondrial disorders.
