ABT-116
ABT-116 is an orally active antagonist of transient receptor potential vanilloid type 1 (TRPV1). ABT-116 has analgesic efficacy. ABT-116 can be used for the research of neurological disease.
For research use only. We do not sell to patients.
- CAS No.: 1008529-42-7
- Formula: C23H27F3N4O
- Molecular Weight:432.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
TRPV1 |
Cellular Effect
|
Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HEK293 | IC50 |
15 nM
Compound: 21
|
Antagonist activity at human TRPV1 expressed in HEK293 cells assessed as inhibition of N-arachidonoyl-dopamine-induced effect
Antagonist activity at human TRPV1 expressed in HEK293 cells assessed as inhibition of N-arachidonoyl-dopamine-induced effect
|
[PMID: 20457518] |
| HEK293 | IC50 |
7 nM
Compound: 21
|
Antagonist activity at human TRPV1 expressed in HEK293 cells assessed as inhibition of capsaicin-induced effect at pH 5.5
Antagonist activity at human TRPV1 expressed in HEK293 cells assessed as inhibition of capsaicin-induced effect at pH 5.5
|
[PMID: 20457518] |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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CAS No. 1008529-42-7
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Molecular Weight 432.48
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Formula C23H27F3N4O
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SMILES
O=C(NCC1=CC=C(C(F)(F)F)C=C1CCC(C)(C)C)NC2=CC=CC3=C2C=NN3C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)