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The anti-leprosy drug clofazimine reduces polyQ toxicity through activation of PPARγ.
EBioMedicine
May 2024
Science for Life Laboratory, Division of Genome Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, S-171 21, Stockholm, Sweden; Genomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, 28029, Spain. Electronic address:
Article Synopsis
- PolyQ diseases are serious brain disorders caused by a repeated section of DNA, and they currently have no good treatments.
- Researchers tested many drugs and found that clofazimine, a medication used for leprosy, can help reduce the toxicity caused by a harmful protein related to Huntington's disease.
- The study shows that clofazimine works by improving cell energy production and may help treat polyQ diseases in the future.
Case Report: Rifampicin-Induced Thrombocytopenia in a Patient with Borderline Lepromatous Leprosy.
Am J Trop Med Hyg
October 2020
2Department of Leprosy, Shanghai Dermatology Hospital, Shanghai, People's Republic of China.
Rifampicin is a highly effective antibacterial drug and an important component of multidrug therapy used to treat leprosy. Side effects of rifampicin are rare with the once-a-month dosage regimen of anti-leprosy multidrug therapy. Here, we report a case of rifampicin-induced thrombocytopenia during anti-leprosy treatment.
View Article and Find Full Text PDFFatal course of clofazimine-induced pulmonary crystal deposition in a patient with Melkersson-Rosenthal syndrome.
Int J Clin Pharmacol Ther
September 2020
A wide variety of drugs and substances have the potential to damage the respiratory system by different mechanisms. Clofazimine is an anti-leprosy drug that is normally only prescribed for a few years. It has a very long half-life, and crystalline deposition of the drug in various tissues has been documented.
View Article and Find Full Text PDFMultiple docking analysis and absorption, distribution, metabolism, excretion, and toxicity screening of anti-leprosy phytochemicals and dapsone against dihydropteroate synthase of .
Int J Mycobacteriol
January 2020
Molecular Genetics Research Laboratory, Bai Jerbai Wadia Hospital for Children, Mumbai, Maharashtra, India.
Background: Leprosy is a neglected tropical disease affecting millions of people. The current treatment against leprosy includes various antibacterial drugs of which dapsone is known to bind to dihydropteroate synthase of Mycobacterium leprae. Dapsone is an expensive antibacterial drug with many side effects.
View Article and Find Full Text PDFMycobacterium leprae infection causes bone lesions and osteoporosis, however, the effect of antileprosy drugs on the bone is unknown. We, therefore, set out to address it by investigating osteogenic differentiation from bone marrow (BM)-derived mesenchymal stem cells (MSCs). Out of 7 antileprosy drugs, only clofazimine (CFZ) reduced MSCs viability (IC50 ∼ 1 μM) and their osteogenic differentiation but increased adipogenic differentiation on a par with rosiglitazone, and this effect was blocked by a peroxisome proliferator-activated receptor gamma antagonist, GW9662.
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