[7] This drug was developed by Olactec Therapeutics with the purpose of decreasing IL-1β peripheral inflammation by binding to the NLRP3 protein and inhibiting the formation of the NLRP3 inflammasome.
Dapansutrile has tested in clinical trials and has been proposed as a beneficial compound for the remedy of osteoarthritis, and gouty arthritis.
[1] Dapansutrile is a β-sulfonyl nitrile compound with four carbon, seven hydrogen, one nitrogen, two oxygen, and one sulfur atom (Figure 2).
This reaction produces crude methylsulfonylpropionitrile which is then purified through dissolution into acetone, filtration of the sodium bromide bi-product, solvent exchange via distillation, and recrystallization from ethanol.
Murine macrophages were used and stimulated with lipopolysaccharides and either flagellin or the dsDNA analog Poly(dA:dT) to activate inflammasomes such as NLRC4 and AIM 2 respectively.
[9] Subjects presented no changes in blood pressure (systolic and diastolic), urinalysis, heart rate, liver function enzymes or acute phase proteins in the cohort after an 8-day trial with up to daily 1,000 mg dosing of dapansutrile.
[13] Dapansutrile was used in the Experimental Autoimmune Encephalomyelitis (EAE) mouse model to understand its possible underlying effects for MS.
[14] Currently, it is unclear whether the drug could inhibit microglial reactivity, but currently it has no known benefits to aid in the prevention of dementia and cognitive function.
In essence, the drug reduced joint inflammation, as well as interleukin levels[6] demonstrating its therapeutic benefit for this disease.
[17] They have carried out a Phase 1 double blinded study with a total of 30 subjects to assess the drug's safety and pharmacodynamics.
[17] Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) / COVID-19: Dapansutrile has been proposed by a number of scientists as a measure to reduce cardiovascular outcomes that seem to be brought on by COVID-19.
[18] The rationale behind using Dapansutrile is to inhibit the NLRP3 inflammasome and reduce the chances of a cytokine storm which seems to cause multi-organ failure in COVID-19 patients.
[19] NLRP3 not only activates cytokines but other key players that can inflict myocardial damages, and Acute Respiratory Distress Syndrome (ARDS), and its inhibition has been found to deter these outcomes.