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Naltrexone a potential therapeutic candidate for COVID-19.
Choubey, Abhinav; Dehury, Budheswar; Kumar, Sunil; Medhi, Bikash; Mondal, Prosenjit.
  • Choubey A; School of Basic Sciences, Indian Institute of Technology Mandi, Mandi, H.P., India.
  • Dehury B; School of Biotechnology, Kalinga Institute of Industrial Technology (KIIT), Deemed to be University, Bhubaneswar, India.
  • Kumar S; ICAR-Indian Agricultural Statistical Research Institute, PUSA, New Delhi, India.
  • Medhi B; Department of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
  • Mondal P; School of Basic Sciences, Indian Institute of Technology Mandi, Mandi, H.P., India.
J Biomol Struct Dyn ; 40(3): 963-970, 2022 02.
Article in English | MEDLINE | ID: covidwho-759735
ABSTRACT
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the cause of Coronavirus Disease (COVID-19) that has resulted in a global pandemic. At the time of writing, approximately 16.06 million cases have been reported worldwide. Like other coronaviruses, SARS-CoV-2 relies on the surface Spike glycoprotein to access the host cells, mainly through the interaction of its Receptor Binding Domain (RBD) with the host receptor Angiotensin-Converting Enzyme2 (ACE2). SARS-CoV-2 infection induces a profound downstream pro-inflammatory cytokine storm. This release of the pro-inflammatory cytokines is underpinning lung tissue damage, respiratory failure, and eventually multiple organ failure in COVID-19 patients. The phosphorylation status of ERK1/2 is positively correlated with virus load and ERK1/2 inhibition suppressed viral replication and viral infectivity. Therefore, molecular entities able to interfere with binding of the SARS-CoV-2 Spike protein to ACE2, or damping hyperinflammatory cytokines storm, blocking ERK1/2 phosphorylation have a great potential to inhibit viral entry along with viral infectivity. Herein, we report that the FDA-approved non-peptide opioid antagonist drug, naltrexone suppresses high fat/LPS induced pro-inflammatory cytokine release both from macrophage cells and Adipose Tissue Macrophage. Moreover, Low Dose Naltrexone (LDN) also showed its activity as an ERK1/2 inhibitor. Notably, virtual docking and simulation data also suggest LDN may disrupt the interaction of ACE2 with RBD. LDN may be considered as a target as the treatment and (or) adjuvant therapy for coronavirus infection. Clinical toxicity measurements may not be required for LDN since naltrexone was previously tested and is an approved drug by the FDA.Communicated by Ramaswamy H. Sarma.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: COVID-19 / Naltrexone Type of study: Prognostic study Limits: Humans Language: English Journal: J Biomol Struct Dyn Year: 2022 Document Type: Article Affiliation country: 07391102.2020.1820379

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Full text: Available Collection: International databases Database: MEDLINE Main subject: COVID-19 / Naltrexone Type of study: Prognostic study Limits: Humans Language: English Journal: J Biomol Struct Dyn Year: 2022 Document Type: Article Affiliation country: 07391102.2020.1820379