ArticleFrontiers in immunology2023
Brensocatib, an oral, reversible inhibitor of dipeptidyl peptidase 1, mitigates interferon-α-accelerated lupus nephritis in mice.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Impact of dipeptidyl peptidase I and neutrophil serine proteases on neutrophil functional responses.Frontiers in pharmacology · 2026Article
- Cathepsin C-driven enhancement of neutrophil extracellular trap formation contributes to acute lung injury.iScience · 2025Article
- Identification of Marrubiin as a Cathepsin C Inhibitor for Treating Rheumatoid Arthritis.Molecules (Basel, Switzerland) · 2025Article
- Induction of LY6E regulates interleukin-1β production, potentially contributing to the immunopathogenesis of systemic lupus erythematosus.Cell communication and signaling : CCS · 2025Article
- Therapeutically targeting proinflammatory type I interferons in systemic lupus erythematosus: efficacy and insufficiency with a specific focus on lupus nephritis.Frontiers in immunology · 2024Review
- Targeting cathepsin C ameliorates murine acetaminophen-induced liver injury.Theranostics · 2024Article
- Pharmacologic inhibition of dipeptidyl peptidase 1 (cathepsin C) does not blockFrontiers in pharmacology · 2024Article
- Brensocatib (an oral, reversible inhibitor of dipeptidyl peptidase-1) attenuates disease progression in two animal models of rheumatoid arthritis.Frontiers in immunology · 2023Article
- Dipeptidyl peptidase 1 inhibition as a potential therapeutic approach in neutrophil-mediated inflammatory disease.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils have been implicated in initiating and perpetuating systemic lupus erythematosus and the resultant kidney damage in lupus nephritis (LN) patients, in part through an excessive release of neutrophil serine proteases (NSPs). NSP zymogens are activated by dipeptidyl peptidase 1 (DPP1) during neutrophil maturation and released by mature neutrophils in response to inflammatory stimuli. Thus, a potential strategy to attenuate disease progression in LN would be to inhibit DPP1. We tested whether brensocatib, a highly selective and reversible DPP1 inhibitor, could mitigate LN progression in an interferon-alpha (IFNα)-accelerated NZB/W F1 mouse model. To confirm brensocatib's pharmacodynamic effect on NSPs in this mouse strain, repeated dose studies were conducted for 7 and 14 days in naïve NZB/W F1 mice
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Registered trials
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