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Hydroxychloroquine (HCQ) is an antimalarial drug developed in the 1940s by chemists at Winthrop Chemical Company, a subsidiary of Sterling Drug. Derived from chloroquine (itself synthesized in 1934 by Bayer), HCQ was introduced in 1955 as a safer alternative with fewer side effects. Originally used to treat malaria, it later became a cornerstone therapy for autoimmune diseases like lupus and rheumatoid arthritis due to its anti-inflammatory properties. Its development was part of a broader effort to improve quinine-based treatments during World War II.
Hydroxychloroquine has garnered interest for its potential anticancer effects, primarily observed in preclinical studies. It inhibits autophagy—a process cancer cells use to survive stress—leading to cell death, reduced tumor growth, and enhanced sensitivity to other therapies in lab and animal models. While human clinical trials are limited as of April 2025, its repurposing potential continues to drive research.
Preclinical research suggests HCQ may affect the following cancers. These findings are preliminary and await robust human clinical validation:
HCQ accumulates in the parasite’s food vacuole, raising pH and inhibiting heme polymerization. This disrupts parasite metabolism, killing Plasmodium species responsible for malaria.
HCQ modulates the immune system by inhibiting toll-like receptor signaling and reducing pro-inflammatory cytokine production, alleviating symptoms in lupus and rheumatoid arthritis.
HCQ blocks autophagy by preventing lysosome acidification, stopping cancer cells from recycling nutrients under stress. This halts proliferation, particularly in autophagy-dependent cancers like pancreatic cancer, as seen in cell lines and mouse models.
By inhibiting autophagy, HCQ increases reactive oxygen species (ROS) and mitochondrial stress, triggering caspase-mediated apoptosis. Studies show this effect in breast and lung cancer cells, often via p53 or MAPK pathways.
HCQ sensitizes cancer cells to chemotherapy (e.g., gemcitabine) and radiation by blocking protective autophagy. Preclinical data suggest it enhances cell death in pancreatic and colorectal cancers when combined with these treatments.