Repositioning Candidate Details
| Candidate ID: | R0459 |
| Source ID: | DB06774 |
| Source Type: | approved |
| Compound Type: | small molecule |
| Compound Name: | Capsaicin |
| Synonyms: | |
| Molecular Formula: | C18H27NO3 |
| SMILES: | COC1=C(O)C=CC(CNC(=O)CCCC\C=C\C(C)C)=C1 |
| Structure: |
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| DrugBank Description: | Capsaicin is most often used as a topical analgesic and exists in many formulations of cream, liquid, and patch preparations of various strengths; however, it may also be found in some dietary supplements. Capsaicin is a naturally-occurring botanical irritant in chili peppers, synthetically derived for pharmaceutical formulations. The most recent capsaicin FDA approval was Qutenza, an 8% capsaicin patch dermal-delivery system, indicated for neuropathic pain associated with post-herpetic neuralgia. |
| CAS Number: | 404-86-4 |
| Molecular Weight: | 305.4119 |
| DrugBank Indication: | The capsaicin 8% patch is indicated in the treatment of neuropathic pain associated with post-herpetic neuralgia. There are multiple topical capsaicin formulations available, including creams and solutions, indicated for temporary analgesia in muscle and join pain as well as neuropathic pain. |
| DrugBank Pharmacology: | Capsaicin is a TRPV1 receptor agonist. TRPV1 is a trans-membrane receptor-ion channel complex activated by temperatures higher than 43 degrees Celsius, pH lower than 6, and endogenous lipids. When activated by a combination of these factors, the channel can transiently open and initiate depolarization due to the influx of calcium and sodium ions. Because TRPV1 is commonly expressed in A-delta and mostly C fibers, depolarization results in action potentials which send impulses to the brain and spinal cord. These impulses result in capsaicin effects of warming, tingling, itching, stinging, or burning. Capsaicin also causes more persistent activation of these receptors compared to the environmental agonists, resulting in a loss of response to many sensory stimuli, described as "defunctionalization". Capsaicin is associated with many enzymatic, cytoskeletal, and osmotic changes, as well as disruption of mitochondrial respiration, impairing nociceptor function for extended periods of time. |
| DrugBank MoA: | Capsaicin has been shown to reduce the amount of substance P associated with inflammation - however this is not believed to be its main mechanism in the relief of pain [A32319]. Capsaicin's mechanism of action is attributed to "defunctionalization" of nociceptor fibers by inducing a topical hypersensitivity reaction on the skin. This alteration in pain mechanisms is due to many of the following: temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fiber terminals. |
| Targets: | Transient receptor potential cation channel subfamily V member 1; Prohibitin-2 |
| Inclusion Criteria: |
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