Mechanisms of action of hydroxychloroquine and chloroquine:implications for rheumatology
Abstract
Despite widespread clinical use of antimalarial drugs such as hydroxychloroquine and chloroquine in the treatment of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and other inflammatory rheumatic diseases, insights into the mechanism of action of these drugs are still emerging. Hydroxychloroquine and chloroquine are weak bases and have a characteristic 'deep' volume of distribution and a half-life of around 50 days. These drugs interfere with lysosomal activity and autophagy, interact with membrane stability and alter signalling pathways and transcriptional activity, which can result in inhibition of cytokine production and modulation of certain co-stimulatory molecules. These modes of action, together with the drug's chemical properties, might explain the clinical efficacy and well-known adverse effects (such as retinopathy) of these drugs. The unknown dose-response relationships of these drugs and the lack of definitions of the minimum dose needed for clinical efficacy and what doses are toxic pose challenges to clinical practice. Further challenges include patient non-adherence and possible context-dependent variations in blood drug levels. Available mechanistic data give insights into the immunomodulatory potency of hydroxychloroquine and provide the rationale to search for more potent and/or selective inhibitors.
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Hydroxychloroquine interferes with TLRs and cyclic GMP-AMP synthase (cGAS), dampening downstream pro-inflammatory cytokine and type I IFN production.
“Hydroxychloroquine is an anti-malarial that interferes with TLRs and cyclic GMP-AMP synthase (cGAS), dampening downstream pro-inflammatory cytokine and type I IFN production (60).”
From Immunomodulation in Administration of RAAV: Preclinical and Clinical Adjuvant Pharmacotherapies (2021) · cites this paper as [60]
Endosomal acidification is essential for rAAV escape, and hydroxychloroquine increases endosomal and lysosomal pH, so the effect may not be replicated or consistent with systemic application.
“However, endosomal acidification is essential for rAAV escape (84), and hydroxychloroquine increases endosomal and lysosomal pH (60), this effect may not be replicated or consistent with systemic application.”
From Immunomodulation in Administration of RAAV: Preclinical and Clinical Adjuvant Pharmacotherapies (2021) · cites this paper as [60]
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- Authors
- Schrezenmeier, E., & Dörner, T.
- Affiliations
- Charité – Universitätsmedizin Berlin (DE)
- German Rheumatism Research Centre (DE)
- Corresponding author
- Dörner, Thomas
- Venue
- Nature Reviews Rheumatology
- Published
- 2020-02-07
- Volume
- 16
- Issue
- 3
- Pages
- 155-166
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- OpenAlex
- W3004709581
- Cited by
- 1,468
- References
- 189
- Citations by year
- 2026: 93 · 2025: 127 · 2024: 154 · 2023: 162 · 2022: 197 · 2021: 270 · 2020: 464 · 2019: 1
- FWCI
- 42.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (Do491/10–1)
- Leibniz-Gemeinschaft
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
- Keywords
- hydroxychloroquine, chloroquine, mechanism of action, rheumatoid arthritis, systemic lupus erythematosus, immunomodulation, lysosomal activity, autophagy, cytokine production, retinopathy, dose-response relationship, patient adherence, antimalarial drugs
- MeSH terms
- Antimalarials, Arthritis, Rheumatoid, Chloroquine, Humans, Hydroxychloroquine, Rheumatology, Treatment Outcome
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