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Restrict the search for
tyrosine
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Here are the exact (name or code) matches for tyrosine
Status:
US Previously Marketed
Source:
TPN by INTL MINERALS
(1961)
Source URL:
First approved in 1961
Source:
TPN by INTL MINERALS
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Tyrosine (L-form) is a non-essential amino acid, which is primarily required for the protein synthesis. This amino acid is the precursor of dopamine, norepinephrine, and epinephrine; therefore the lower concentration of tyrosine could be a peripheral marker of the hyperdopaminergic condition hypothesized to explain psychosis. Tyrosine supplements can improve cognition, increase energy, reduce anxiety, reduce depression, reduce levels of pain.
Status:
US Previously Marketed
Source:
TPN by INTL MINERALS
(1961)
Source URL:
First approved in 1961
Source:
TPN by INTL MINERALS
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Tyrosine (L-form) is a non-essential amino acid, which is primarily required for the protein synthesis. This amino acid is the precursor of dopamine, norepinephrine, and epinephrine; therefore the lower concentration of tyrosine could be a peripheral marker of the hyperdopaminergic condition hypothesized to explain psychosis. Tyrosine supplements can improve cognition, increase energy, reduce anxiety, reduce depression, reduce levels of pain.
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:
NDA217900
(2024)
Source URL:
First approved in 2024
Source:
NDA217900
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
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:
NDA218171
(2024)
Source URL:
First approved in 2024
Source:
NDA218171
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
X-396 (Ensartinib) is a novel, potent anaplastic lymphoma kinase (ALK) small molecule tyrosine kinase inhibitor (TKI) with additional activity against MET, ABL, Axl, EPHA2, LTK, ROS1 and SLK. Ensartinib has demonstrated activity in ALK treatment naïve and previously treated patients and has a generally well tolerated safety profile. Ensartinib is currently in a global phase 3 trial in ALK positive non-small cell lung cancer (NSCLC) patients. The phase 1/2 clinical findings support the preclinical results that the use of ensartinib may result in favorable therapeutic outcomes in patients with ALK NSCLC, including patients with CNS metastases. In this study, ensartinib was generally well tolerated with the most common adverse event being a rash.
Status:
US Approved Rx
(2023)
Source:
NDA215830
(2023)
Source URL:
First approved in 2023
Source:
NDA215830
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Ritlecitinib is an orally administered, covalent small-molecule selective dual inhibitor of JAK3 and the TEC kinase family. In vitro studies showed ritlecitinib covalently binds to JAK3 and is more than 10 000 times more potent against JAK3 than against JAK1, JAK2, and tyrosine kinase. Ritlecitinib also inhibits the five members of the TEC kinase family. Ritlecitinib irreversibly inhibits Janus kinase 3 (JAK3) and TEC kinase family by blocking the adenosine triphosphate (ATP) binding site. In cellular settings, ritlecitinib inhibits cytokine induced STAT phosphorylation mediated by JAK3-dependent receptors.
Additionally, ritlecitinib inhibits signaling of immune receptors dependent on TEC kinase family members.The FDA has approved ritlecitinib (LITFULO; Pfizer Inc), a once daily oral treatment, for individuals aged 12 years and older with severe alopecia areata. This makes ritlecitinib, in the 50 mg dosage, the first and only treatment approved by the FDA for adolescents with severe alopecia areata. The approval was based on the results of the ALLEGRO phase 2b/3 trial (NCT03732807), which included 718 individuals who had 50% or more scalp hair loss measured by the Severity of Alopecia Tool. Investigators of the study evaluated the safety and efficacy of ritlecitinib at 118 different sites in 18 different countries. Regulatory applications for LITFULO in alopecia areata have been submitted to countries around the world for review, including China, the European Union, Japan, and the United Kingdom. The European Medicines Agency (EMA) has accepted the Marketing Authorization Application (MAA) for ritlecitinib with a decision anticipated in the third quarter of 2023. LITFULO is also being evaluated for vitiligo, Crohn’s disease, and ulcerative colitis.
Status:
US Approved Rx
(2023)
Source:
NDA216873
(2023)
Source URL:
First approved in 2023
Source:
NDA216873
Source URL:
Class (Stereo):
CHEMICAL (ACHIRAL)
Conditions:
Momelotinib (CYT387) is an ATP-competitive small molecule that potently inhibits JAK1/JAK2 kinases. Momelotinib is developing by Gilead Sciences for the oral treatment of pancreatic and non-small cell lung cancers, and myeloproliferative disorders (including myelofibrosis, essential thrombocythaemia and polycythaemia vera).
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:
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.
