Structure of Mitochonic acid 5
CAS No.: 1354707-41-7
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The BI-3802 was designed by Boehringer Ingelheim and could be obtained free of charge through the Boehringer Ingelheim open innovation portal opnMe.com, associated with its negative control.
Mitochonic acid 5 binds mitochondria and ameliorates renal tubular and cardiac myocyte damage. Mitochonic acid 5 modulates mitochondrial ATP synthesis.
Synonyms: MA-5
4.5
*For Research Use Only !
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Batch number can be found on the product's label following the word 'Batch'.
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Batch number can be found on the product's label following the word 'Batch'.
Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.
Search for reports by entering the product batch number.
Batch number can be found on the product's label following the word 'Batch'.
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CAS No. : | 1354707-41-7 |
Formula : | C18H13F2NO3 |
M.W : | 329.30 |
SMILES Code : | O=C(O)C(CC(C1=CC=C(F)C=C1F)=O)C2=CNC3=C2C=CC=C3 |
Synonyms : |
MA-5
|
MDL No. : | MFCD31657404 |
InChI Key : | BOKQALWNGNLTOC-UHFFFAOYSA-N |
Pubchem ID : | 76070959 |
GHS Pictogram: |
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Signal Word: | Warning |
Hazard Statements: | H302-H315-H319-H335 |
Precautionary Statements: | P261-P305+P351+P338 |
In Vitro:
Cell Line
|
Concentration | Treated Time | Description | References |
Human skin fibroblasts | 0.1 to 30 μM | 72 hours | MA-5 exhibited a cell-protective effect in 24/25 cases of mitochondrial disease fibroblasts, significantly reducing BSO-induced cell death and LDH level elevation. | PMC5478234 |
Mouse microglial BV-2 cells | 5 μM | 12 hours | MA-5 improved the survival of lipopolysaccharide-exposed cells, decreased the activity of caspase-3 associated with apoptosis, reduced the number of TUNEL-positive cells, and increased ATP levels in cells. MA-5 also decreased the open state of the mitochondrial permeability transition pore, reduced calcium overload and diffusion of Smac. Furthermore, MA-5 decreased the expression of apoptosis-related proteins and increased the levels of anti-apoptotic proteins, mitochondria-related proteins, and autophagy-related proteins. | PMC8328753 |
Human fibroblasts | 10 μM | MA-5 increases cellular ATP levels, reduces mitochondrial reactive oxygen species (ROS) production, and protects cells with mitochondrial dysfunction from death | PMC9455831 | |
Mouse microglial BV-2 cells | 0–10μM | 12 hours | MA-5 reduced TNFα-induced apoptosis via upregulation of Bnip3-related mitophagy, improving mitochondrial function. | PMC5887257 |
Fibroblasts from MELAS patient | 10 μM | 3 hours | MA-5 significantly increased ATP levels in fibroblasts from MELAS patients. | PMC5478234 |
Fibroblasts from Leigh syndrome patient | 10 μM | 3 hours | MA-5 significantly increased ATP levels in fibroblasts from Leigh syndrome patients. | PMC5478234 |
Human OA chondrocytes | 10 μM | 24 hours | MA-5 inhibits IL-1β-induced oxidative stress and protects chondrocytes by upregulating the SIRT3/Parkin-related autophagy signaling pathway | PMC9207248 |
Hep3B cells | 3 and 10 µM | MA-5 significantly increased intracellular ATP levels | PMC10394014 | |
Ram sperm | 0, 0.1, 1, 10, and 100 nM | 48 hours | To evaluate the effect of MA-5 on ram sperm quality, results showed that 10 nM MA-5 significantly improved sperm motility, membrane integrity, and acrosomal integrity. | PMC10854625 |
Cardiomyocytes | 5 μM | 12 hours | MA-5 administration increased cell viability and repressed apoptosis in H2O2-treated cardiomyocytes. | PMC10757297 |
In Vivo:
Species
|
Animal Model
|
Administration | Dosage | Frequency | Description | References |
Mitomouse (mouse model with mitochondrial DNA deletion mutation) | Mitochondrial disease model | Oral | 50 mg/kg body weight/day | Once daily for 30 days | MA-5 significantly reduced serum GDF-15 levels in Mitomouse, indicating its therapeutic effect in the mitochondrial disease model. | PMC5478234 |
Tags: Mitochonic acid 5 | MA-5 | Mitochonic acid5 | Mitochonic acid-5 | MA5 | MA 5 | Mitochondrial Metabolism | 1354707-41-7
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H420 | Harms public health and the environment by destroying ozone in the upper atmosphere |
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