Conventional therapies versus Aviptadil
Pharmacological and non-pharmacological evaluations in ARDS continue to be crucial and relevant as none of them have been found to be completely effective. Owing to the complexity of inflammation in ARDS, drugs that block only one of the inflammatory mediators have not yielded satisfactory outcomes in humans. In view of that a new drug with different mechanisms of action is expected to yield satisfactory clinical outcomes in ARDS.
Aviptadil stands the test of a drug with varying established mechanisms of action evidently supported by the significant amount of data, related to reliable clinical trials performed. Aviptadil is a synthetic form of Vasoactive Intestinal Peptide (VIP). VIP is highly expressed in the lung tissue (approximately 70%) and nasal mucosa.
If we want to summarize key mechanisms of action of Aviptadil they would include below four aspect
- Aviptadil acts as a potent anti-cytokine in the lung that provides a key defense against numerous forms of acute lung injury.
- Inhibits inflammatory cytokines like IL6 and TNF-alpha production and reverses CD4/CD8 ratio.
- Aviptadil blocks apoptosis, caspase-3 activation in the lung and preserves pulmonary tissue.
- Aviptadil increases surfactant production by up-regulation of choline phosphate cytidylyltransferase, which increases the incorporation of methyl choline into phosphatidylcholine which is the major component of pulmonary surfactant.
International data of Aviptadil has shown 75% reduction in Il-6 and led to 5.5 fold more recovery from respiratory failure. It is worthwhile to note that Aviptadil is also backed up by Indian evidence which confirms that Aviptadil when administered to COVID-19 patients with respiratory failure and ARDS led to increase in PaO2:FiO2, by 50 mmHg from baseline in 50% patients along with 20% reduction in risk of death in COVID induced ARDS. Importantly four-fold more ventilated patients were free of respiratory failure at day 3. Along with these efficacy results, Aviptadil has exhibited long term records of safety in patients of ARDS. Use of Aviptadil was safe and effective in improving the resolution of respiratory failure, shortening the time to recovery, decreasing respiratory distress and preventing death in respiratory failure patients. The rapidity and magnitude of clinical effect suggests a highly specific role of Aviptadil in combating the lethal effects of Acute Respiratory Distress Syndrome associated with COVID-19.
Aviptadil, when added to the standard of care reduces the need for oxygen supplementation, reduces the risk of death, shortens the duration of stay in the hospital. It is well proven that Aviptadil treatment results in a faster and higher rate of ARDS resolution, better improvement in PaO2/FiO2 ratio and patient survival.
References
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- Mukherjee T et al. Anticipated pharmacological role of Aviptadil on COVID-19. Environ Sci Pollut Res Int. 2022 ; 29(6):8109-8125.
- Chakraborty DS et al. Aviptadil‑ Class Effect of a Synthetic Vasoactive Intestinal Peptide as a Treatment Option in COVID-19 Patients with Severe Respiratory Failure Indian J Respir Care 2022; 11:5-10.
- Youssef, J.G.; Said, S.; Youssef, G.; Javitt, M.J.; Javitt, J.C. Treatment of Acute Respiratory Distress Syndrome with Vasoactive Intestinal Peptide. Preprints 2020, 2020070453 (doi: 10.20944 / preprints 202007.0453.v1).
- Dewan B, Shinde S. Aviptadil In Acute Respiratory Distress Syndrome Associated With Covid-19 Infection. European Journal of Pharmaceutical and Medical Research. 2022; 9(6): 243-53.
- Youssef JG, Javiti JC, Lavin P, Al-Saadi M, Zahiruddin F, et al. VIP in the Treatment of Critical Covid-19 with Respiratory Failure in Patients with Severe Comorbidity: A Prospective Externally Controlled. J Infect Dis treat. 2021; 7(8): 52.
- Youssef JG, Lee R, Javitt J, Lavin P, Jayaweera D. Effectiveness of ZYESAMI™ (Aviptadil) in accelerating recovery and shortening hospitalization in critically-ill patients with COVID-19 Respiratory Failure interim report from a phase 2b/3 multicenter trial. SSRN; 2021. DOI: 10.2139/ssrn.379426.