Mito-4509
Explore a selection of our essential drug information below, or:
Identification
- Generic Name
- Mito-4509
- DrugBank Accession Number
- DB05846
- Background
Mito-4509 is a non-feminizing estrogen analog that could affect mitochondrial metabolic pathways. It is used to treat Parkinson's Disease, Alzheimer's Disease, Retinal Disorders and other neurologic Disorders.
- Type
- Small Molecule
- Groups
- Investigational
- Synonyms
- Not Available
Pharmacology
- Indication
Investigated for use/treatment in alzheimer's disease, neurologic disorders, parkinson's disease, and retinal disorders (unspecified).
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- Pharmacodynamics
Not Available
- Mechanism of action
MITO-4509 is an orally-administered drug candidate that shows neuro-protective activity and reductions in beta-amyloid in animal models of Alzheimer's disease, and is well tolerated in a completed human Phase I trial. In addition to Alzheimer's disease, MITO-4509 shows potential for use in Parkinson's disease, Friedreich's ataxia, retinitis pigmentosa, and mild cognitive impairment ("MCI" is often considered a precursor to Alzheimer's disease).
Target Actions Organism UAmyloid-beta precursor protein Not Available Humans - Absorption
Not Available
- Volume of distribution
Not Available
- Protein binding
Not Available
- Metabolism
- Not Available
- Route of elimination
Not Available
- Half-life
Not Available
- Clearance
Not Available
- Adverse Effects
- Improve decision support & research outcomesWith structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates. View sample adverse effects data in our new Data Library!Improve decision support & research outcomes with our structured adverse effects data.
- Toxicity
Not Available
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.Not Available
- Food Interactions
- Not Available
Categories
- Drug Categories
- Not Available
- Classification
- Not classified
- Affected organisms
- Not Available
Chemical Identifiers
- UNII
- Not Available
- CAS number
- Not Available
- InChI Key
- Not Available
- InChI
- Not Available
- IUPAC Name
- Not Available
- SMILES
- Not Available
References
- General References
- Johnston TH, Brotchie JM: Drugs in development for Parkinson's disease. Curr Opin Investig Drugs. 2004 Jul;5(7):720-6. [Article]
- External Links
- PubChem Substance
- 347910266
Clinical Trials
- Clinical Trials
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Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
- Not Available
- Prices
- Not Available
- Patents
- Not Available
Properties
- State
- Solid
- Experimental Properties
- Not Available
- Predicted Properties
- Not Available
- Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Not Available
- Chromatographic Properties
Collision Cross Sections (CCS)
Not Available
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- General Function
- Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis (PubMed:25122912). Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(o) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1 (By similarity). By acting as a kinesin I membrane receptor, plays a role in axonal anterograde transport of cargo towards synapses in axons (PubMed:17062754, PubMed:23011729). Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1
- Specific Function
- DNA binding
- Gene Name
- APP
- Uniprot ID
- P05067
- Uniprot Name
- Amyloid-beta precursor protein
- Molecular Weight
- 86942.715 Da
Drug created at November 18, 2007 18:28 / Updated at June 12, 2020 16:52