Repositioning Candidate Details

Candidate ID: R1550
Source ID: DB14999
Source Type: approved; investigational
Compound Type: biotech
Compound Name: Human interferon beta
Synonyms: Fibroblast interferon; FIF; Interferon beta; Interferon beta (human); Interferon-beta
Molecular Formula: --
SMILES: --
DrugBank Description: Human interferon beta is a polypeptide used in the management of relapsing forms of Multiple Sclerosis (MS), and was initially approved by the FDA in 1992. Multiple Sclerosis is a devastating neurodegenerative disease that is usually progressive and significantly debilitating with a profound impact on the quality of life. Interferon beta is currently being studied as a possible treatment for COVID-19, which results from infection with the novel 2019 SARS-CoV-2 virus. Interferon-beta has been used in the past in clinical studies with other coronaviruses due to its demonstrated activity against the virus causing Middle Eastern Respiratory Syndrome (MERS). It is therefore a potential drug candidate for SARS-CoV-2 based on viral genetic similarity.
CAS Number: 74899-71-1
Molecular Weight:
DrugBank Indication: This drug is indicated to treat relapsing forms of Multiple Sclerosis (MS) in adults, which includes clinically isolated syndrome, relapsing-remitting disease, as well as active secondary progressive disease.
DrugBank Pharmacology: Interferon-beta has antiviral and immunomodulatory effects. It reduces demyelination, the main component of Multiple Sclerosis pathophysiology, reducing the clinical frequency of MS attacks and slowing disease progression. In vitro studies have shown that beta interferon reduces the replication of certain coronaviruses in lung tissue. Retrospective studies using combinations of and beta interferon showed improved survival against MERS-CoV, the virus that causes Middle Eastern Respiratory Syndrome (MERS).
DrugBank MoA: Part of the pathophysiology of MS is immune cell activation in addition to degradation of the blood–brain barrier (BBB), resulting in both neural demyelination and axon injury. Immunomodulating drugs such as interferon-beta decrease the inflammation that results in demyelination of nerves. Binding of interferon-beta to type 1 interferon receptors induces a series of beneficial transcriptional JAK/STAT pathway changes. This decreases antigen presentation as well as the proliferation of inflammatory T-cells, reducing the inflammation associated with MS. It also changes the expression of cytokine and matrix metalloproteinase (MMP).
Targets: Interferon alpha/beta receptor 1 binder
Inclusion Criteria: Therapeutic strategy associated