2. Metabolic Enzyme/Protease
  3. Mitochondrial Metabolism
  4. Bevemipretide trihydrochloride

Bevemipretide trihydrochloride  (Synonyms: SBT-272 trihydrochloride)

Cat. No.: HY-156600A
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Bevemipretide trihydrochloride (SBT-272 trihydrochloride) is a blood-brain barrier-permeable mitochondrial function repair agent. Bevemipretide trihydrochloride stabilizes cardiolipin in the inner mitochondrial membrane, restores mitochondrial structure, respiratory function, motor capacity and upper motor neuron health. Bevemipretide trihydrochloride reduces astrogliosis and microgliosis in mice with amyotrophic lateral sclerosis. Bevemipretide trihydrochloride prevents stroke-induced mitochondrial dysfunction. Bevemipretide trihydrochloride is applicable to research related to amyotrophic lateral sclerosis, Parkinson's disease, dementia with Lewy bodies and Huntington's disease.

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Bevemipretide trihydrochloride

Bevemipretide trihydrochloride Chemical Structure

CAS No. : 2589640-11-7

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Description

Bevemipretide trihydrochloride (SBT-272 trihydrochloride) is a blood-brain barrier-permeable mitochondrial function repair agent. Bevemipretide trihydrochloride stabilizes cardiolipin in the inner mitochondrial membrane, restores mitochondrial structure, respiratory function, motor capacity and upper motor neuron health. Bevemipretide trihydrochloride reduces astrogliosis and microgliosis in mice with amyotrophic lateral sclerosis. Bevemipretide trihydrochloride prevents stroke-induced mitochondrial dysfunction. Bevemipretide trihydrochloride is applicable to research related to amyotrophic lateral sclerosis, Parkinson's disease, dementia with Lewy bodies and Huntington's disease[1][2].

In Vitro

Bevemipretide (100 nM; 30 min anoxia exposure followed by reoxygenation and 10 min monitoring) trihydrochloride significantly reduces mitochondrial H2O2 release and the H2O2/O2 ratio in permeabilized rat myocardial fibers treated with hypoxia-reoxygenation stress[1].
Bevemipretide (100 nM; 3 days) trihydrochloride improves mitochondrial ultrastructural integrity, increases mitochondrial membrane polarization in corticospinal motor neurons (CSMN) from prp-hTDP-43A315T-UeGFP mice by reducing mitochondrial aggregates, increasing the number of cristae, and restoring the percentage of intact cristae[1].
Bevemipretide (10 nM-1 μM; 3 days) trihydrochloride dose-dependently improves mitochondrial motility in mouse CSMNs expressing prp-hTDP-43A315T-UeGFP, increases the proportion of cells with mitochondria in axons, enhances axonal growth, and ameliorates neurite branching and dendritic morphology[1].
Bevemipretide (100 nM) trihydrochloride binds to cardiolipin in hTDP-43 neurons and restores mitochondrial structure[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Bevemipretide trihydrochloride Related Antibodies
In Vivo

Bevemipretide (2 mg/kg; s.c.; administered twice: 30 minutes before ischemia and 5 minutes before reperfusion) trihydrochloride provides 81% protection against ischemia-reperfusion-induced elevation of blood urea nitrogen (BUN) and 86% protection against ischemia-reperfusion-induced elevation of creatinine in rats with acute kidney injury[1].
Bevemipretide (1-5 mg/kg; s.c.; administered twice at 20 h intervals) trihydrochloride prevents stroke-induced mitochondrial dysfunction by maintaining the respiratory control ratio in the rat brain[1].
Bevemipretide (1-5 mg/kg, i.p. daily for 60 days) trihydrochloride exerts neuroprotective effects in ALS mice with TDP-43 pathology by preserving the number of corticospinal motor neurons, reducing astrogliosis and microgliosis, decreasing the level of ubiquitinated protein inclusions, and improving mitochondrial ultrastructure[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: hsd:Sprague Dawley® (male, 275-300 g, ischemia-reperfusion induced)[1]
Dosage: 2 mg/kg
Administration: s.c.; 2 doses: 30 min pre-ischemia and 5 min pre-reperfusion
Result: Reduced post-ischemia plasma blood urea nitrogen levels to 19.2 mg/dL.
Reduced post-ischemia creatinine levels to 0.4 mg/dL.
Animal Model: hsd:Sprague Dawley® (male, 275-300 g, ET-1-induced middle cerebral artery occlusion)[1]
Dosage: 1 mg/kg; 5 mg/kg
Administration: s.c.; 2 doses: 48 h and 28 h pre-decapitation
Result: Preserved mitochondrial respiratory control ratio (RCR) values comparable to sham controls in rats treated with 1 mg/kg or 5 mg/kg.
Animal Model: prp-hTDP-43A315T-UeGFP (female, C57BL/6 J background, transgenic TDP-43 A315T mutation)[1]
Dosage: 1 mg/kg/day; 5 mg/kg/day
Administration: i.p.; daily; 60 days starting at postnatal day 60
Result: Increased CSMN retention to 51.4 (1 mg/kg/day) and 49.9 (5 mg/kg/day).
Reduced activated astrocytes to 20.1 (1 mg/kg/day) and 24 (5 mg/kg/day).
Reduced activated microglia to 9.1 (1 mg/kg/day) and 13.3 (5 mg/kg/day).
Reduced CSMN with ubiquitinated protein inclusions to 26.1% (1 mg/kg/day) and 27.5% (5 mg/kg/day).
Increased mitochondria with visible cristae to 82.2% and reduced mitochondrial clumps per CSMN to 0.69 at 5 mg/kg/day.
Molecular Weight

717.13

Formula

C31H48Cl3N9O4
CAS No.
SMILES

CC(C=C(C=C1C)O)=C1C[C@H](NC([C@H](N)CCCNC(N)=N)=O)C(N[C@H](C2=NC(CC3=CC=CC=C3)=NO2)CCCCN)=O.Cl.Cl.Cl
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Bevemipretide trihydrochloride Related Classifications

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Keywords:

Bevemipretide trihydrochloride2589640-11-7SBT-272 trihydrochlorideMitochondrial MetabolismcardiolipinmicrogliosisParkinson's diseasehTDP-43 miceupper motor neuronprp-hTDP-43A315T-UeGFP mouse CSMNamyotrophic lateral sclerosisastrogliosiscorticospinal motor neuronTDP-43 pathologyInhibitorinhibitorinhibit

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