NCT04803227

Safety and Tolerability of Emricasan in Symptomatic Outpatients Diagnosed With Mild-COVID-19

Terminated Phase 1 Last updated 4 January 2022

What this trial tests

Phase 1 trial testing Emricasan in Covid19 in 13 participants. Terminated before completion.

Timeline

11 March 2021

Primary endpoint
28 May 2021

28 May 2021

Quick facts

Lead sponsor	Histogen
Phase	Phase 1
Status	Terminated
Study type	INTERVENTIONAL
Allocation	randomized
Design	parallel
Masking	triple
Primary purpose	treatment
Enrollment	13
Start date	11 March 2021
Primary completion	28 May 2021
Estimated completion	28 May 2021
Sites	1 location across United States

Drugs / interventions tested

• Emricasan — full drug profile →
• Placebo

Conditions studied

• Covid19 — all drugs for Covid19 →

Sponsor

Histogen — full company profile →

Who can join

18 and older, any sex, with Covid19. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

Treatments for COVID-19 are urgently needed. Emricasan (EMR) is a pan caspase inhibitor. Caspase-1 plays a role in a form of cell death called pyroptosis. EMR inhibits pyroptosis. The Investigators have shown that peripheral blood lymphocytes of COVID-19 patients overexpress caspase-1, providing evidence for pyroptosis. A recent European study corroborate the Investigators finding as they have shown evidence for the activation of the inflammasome in COVID-19.

Publications & conference data

8 peer-reviewed publications reference this trial (live from Europe PMC):

1. IL-1 and autoinflammatory disease: biology, pathogenesis and therapeutic targeting.
   Broderick L, Hoffman HM. · · 2022 · cited 112× · PMID 35729334 · DOI 10.1038/s41584-022-00797-1
2. Cell deaths: Involvement in the pathogenesis and intervention therapy of COVID-19.
   Li X, Zhang Z, Wang Z, Gutiérrez-Castrellón P, et al · · 2022 · cited 58× · PMID 35697684 · DOI 10.1038/s41392-022-01043-6
3. Caspases and therapeutic potential of caspase inhibitors in moderate-severe SARS-CoV-2 infection and long COVID.
   Plassmeyer M, Alpan O, Corley MJ, Premeaux TA, et al · · 2022 · cited 50× · PMID 33993490 · DOI 10.1111/all.14907
4. NLRP3 inflammasome activation in COVID-19: an interlink between risk factors and disease severity.
   Amin S, Aktar S, Rahman MM, Chowdhury MMH. · · 2022 · cited 37× · PMID 34838941 · DOI 10.1016/j.micinf.2021.104913
5. The role of reactive oxygen species in severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) infection-induced cell death.
   Xie J, Yuan C, Yang S, Ma Z, et al · · 2024 · cited 14× · PMID 39516736 · DOI 10.1186/s11658-024-00659-6
6. Drug-target identification in COVID-19 disease mechanisms using computational systems biology approaches.
   Niarakis A, Ostaszewski M, Mazein A, Kuperstein I, et al · · 2023 · cited 10× · PMID 38414974 · DOI 10.3389/fimmu.2023.1282859
7. Understanding the immunological aspects of SARS-CoV-2 causing COVID-19 pandemic: A therapeutic approach.
   Das A, Roy S, Swarnakar S, Chatterjee N. · · 2021 · cited 6× · PMID 34303849 · DOI 10.1016/j.clim.2021.108804
8. Small Molecules for the Treatment of Long-COVID-Related Vascular Damage and Abnormal Blood Clotting: A Patent-Based Appraisal.
   Samarelli F, Graziano G, Gambacorta N, Graps EA, et al · · 2024 · cited 5× · PMID 38543815 · DOI 10.3390/v16030450