Myocarditis is a common inflammatory heart disease in children and young adults that may result in chronically dilated cardiomyopathy. Coxsackievirus B3 is the major etiologic agent of this disease. Current treatments for patients with viral myocarditis are almost entirely supportive. In recent years, some promising therapeutic candidates have emerged, including novel treatments and improvements of existing drugs. Among these are molecules that specially target virus entry, such as pleconaril, WIN 54954 and CAR-Fc; nucleic acid-based antiviral agents that inhibit viral translation and/or transcription, such as antisense oligodeoxynucleotide and short interfering RNA; and immunomodulatory agents that augment the host-protective immune responses to effectively clear viruses from target tissues, including interferons and immunoglobulins. In addition, certain new antiviral strategies, still in the early stages, include modulation of signal transduction pathways responsible for viral replication using enzyme inhibitors, which have revealed potential therapeutic targets for viral myocarditis. Finally, the progress in cellular cardiomyoplasty for end-stage therapy, in particular the preliminary clinical trials, is also discussed with respect to its potential future application.

01 Jun 2004·Applied Radiation and IsotopesQ3 · ENGINEERING & TECHNOLOGY

Potent antiviral agent WIN 54954: high specific activity labelling with tritium

Q3 · ENGINEERING & TECHNOLOGY

Article

Author: Richard P. Nugent ; Judith A. Egan ; Crist N. Filer

Valuable antiviral compound WIN 54954 was tritiated at high specific activity and the product was characterized.

01 Jan 2002·Scandinavian Cardiovascular JournalQ4 · MEDICINE

Cardiomyocyte Apoptosis after Antiviral WIN 54954 Treatment in Murine Coxsackievirus B3 Myocarditis

Q4 · MEDICINE

Article

Author: Timo Hyypiä ; Ville Kytö ; Tytti Vuorinen ; Jan Fohlman ; Heli Harvala ; Antti Saraste ; Nils-G. Ilbäck

OBJECTIVECardiomyocyte apoptosis (CA) is known to occur in experimental coxsackievirus B3 (CVB3) myocarditis. However, the mechanisms of CA induction are not well known. In this study we investigate the role of direct viral induction of CA in CVB3 myocarditis.DESIGNA/J mice were infected with the Woodruff strain of CVB3 and treated with WIN 54954 for 5 days thereafter. WIN 54954, a compound that inhibits early events of picornavirus infection, is known to dramatically reduce mortality in murine CVB3 myocarditis without abrogating systemic or myocardial inflammation. Presence of viral RNA (in situ hybridization), CA (TUNEL method) and histopathology were studied in transverse ventricular sections at day 7 post infection (n = 8 treated and n = 8 non-treated).RESULTSThe proportion of cardiomyocytes containing viral RNA was 89% lower in WIN 54954 treated mice when compared with non-treated mice (0.29 +/- 0.56% vs 2.76 +/- 1.65%, p = 0.003). Treatment also reduced the amount of CA by 52% compared with non-treated mice (0.20 +/- 0.06% vs 0.42 +/- 0.06%, p < 0.001). The reduction of CA by WIN treatment did not result in any increase of necrosis, in fact treatment reduced the area of necrotic lesions by 77% (2.51 +/- 1.64% vs 11.10 +/- 8.76%, p = 0.028).CONCLUSIONTaking the results of the reduced CA, necrosis and viral RNA with no effect on inflammation into account, our findings suggest the importance of direct viral effect in cardiomyocyte damage by both apoptosis and necrosis in CVB3 myocarditis.

100 Deals associated with WIN-54954

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Indication	Highest Phase	Country/Location	Organization	Date
Picornaviridae Infections	Phase 2	-	Sanofi	-
Picornaviridae Infections	Phase 2	US	Sanofi Winthrop LP	-

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