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Treatment of lung inflammation and fibrosis caused by COVID-19
Preparing for a phase 2 clinical trial in the U.S. for moderate and severe COVID-19 patients
- Acute Respiratory Distress Syndrome (ARDS) Is the leading cause of death for COVID-19 patients
- ARDS induces acute pulmonary inflammation and fibrosis due to the disruption of immune homeostatis by continuously inducing an overactive state of the immune system
- Anti-inflammatory and anti-fibrotic drugs are being developed worldwide for the treatment of COVID-19.
Efficacy has been verified in various animal models, including ARDS models
Limited safety concerns based on results from a Phase 1 clinical study in healthy adults
Completed development of oral formulation of ivaltinostat for ease of use
- Inhibition of key mechanisms of inflammatory cytokine production (reduction of angiotensinogen expression)
- Anti-inflammatory function in acute lung injury mouse model (reduction of inflammatory cytokines IL-6, IL-1β, TNF-α expression)
- Anti-inflammatory function in flu virus infection mouse model (reduction of inflammatory cytokines TNF-α and IFN-γ expression)
- Suppression of immune hypersensitivity reaction through regulation of neutrophil count
- Inhibition of the expression of fibrotic proteins (Collagen-1, Vimentin, Fibronectin)
Yoon, G.E. et al. Histone deacetylase inhibitor CG200745 ameliorates high-fat diet-induced hypertension via inhibition of angiotensin II production. Schmiedebergs Arch. Pharmacol. 393, 491-500 (2020).
Kim, Y.S. et al. The anti-fibrotic effects of CG-745, an HDAC inhibitor, in bleomycin and PHMG-induced mouse models. Molecules 24, 2792 (2019).