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Itália – Drogas anabolizantes podem combater a perda de força da distrofia muscular mas com efeitos colaterais indesejados. GLPG0492 é um novo não-esteróides modulador seletivo do receptor de andrógeno que está atualmente em desenvolvimento para doenças músculo-esqueléticas, como sarcopenia e caquexia. Os resultados com esta droga foram favoráveis, resultando em aumento do desempenho físico e melhora das alterações patológicas. Os resultados foram semelhantes aos observados com corticóides e com esteróides anabolizantes.
O resumo em inglês pode ser lido abaixo:
(Pharmacological Research, 2013)GLPG0492, A NOVEL SELECTIVE ANDROGEN RECEPTOR MODULATOR, IMPROVES MUSCLE PERFORMANCE IN THE EXERCISED-MDX MOUSE MODEL OF MUSCULAR DYSTROPHY
Anna Cozzoli, Roberta Francesca Capogrosso, Valeriana Teresa Sblendorio, Maria Maddalena Dinardo, Catherine Jagerschmidt, Florence Namour, Giulia Maria Camerino, Annamaria De Luca
Anabolic drugs may counteract muscle wasting and dysfunction in Duchenne Muscular Dystrophy (DMD); however, steroids have unwanted side effects. We focused on GLPG0492, a new non-steroidal selective androgen receptor modulator that is currently under development for musculo-skeletal diseases such as sarcopenia and cachexia. GLPG0492 was tested in the exercised mdx mouse model of DMD in a 4-week trial at a single high dose (30 mg/kg, 6 day/week s.c.), and the results were compared with those from the administration of (-methylprednisolone (PDN; 1 mg/kg, i.p.) and nandrolone (NAND, 5 mg/kg, s.c.). This assessment was followed by a 12-week dose-dependence study (0.3-30 mg/kg s.c.). The outcomes were evaluated in vivo and ex vivo on functional, histological and biochemical parameters. Similar to PDN and NAND, GLPG0492 significantly increased mouse strength. In acute exhaustion tests, a surrogate of the 6-min walking test used in DMD patients, GLPG0492 preserved running performance, whereas vehicle- or comparator-treated animals showed a significant increase in fatigue (30-50%). Ex vivo, all drugs resulted in a modest but significant increase of diaphragm force. In parallel, a decrease in the non-muscle area and markers of fibrosis was observed in GLPG0492- and NAND-treated mice. The drugs exerted minor effects on limb muscles; however, electrophysiological biomarkers were ameliorated in extensor digitorum longus muscle. The longer dose-dependence study confirmed the effect on mdx mouse strength and resistance to fatigue and demonstrated the efficacy of lower drug doses on in vivo and ex vivo functional parameters. These results support the interest of further studies of GLPG0492 as a potential treatment for DMD.
Fonte: http://distrofiamuscular.net/noticias.htm
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