Abstract |
The efficacy of the proapoptotic cytokine tumor necrosis factor ( TNF) alpha-inhibiting compound CPI-1189 has been demonstrated in various cell culture and animal models of chronic neurodegenerative and inflammatory diseases. CPI-1189 intracellularly inhibits the p38 mitogen-activated protein kinase phosphoactivation, thereby protecting against TNF alpha-induced neurodegeneration. Clinical proof-of-concept phase IIa trials in patients with Parkinson's disease and AIDS dementia complex were successful. These studies demonstrated clinical relevance for treatment with CPI-1189 (50 to 100 mg/day), which attenuated the deterioration in cognitive and/or motor function without any relevant side effects. Since the importance of neuroprotection is emerging, in particular in neurodegenerative diseases with concomitant observed immunological pro-apoptotic alterations in the central nervous system, long-term application of CPI-1189 could represent a promising future therapeutic alternative, in addition to neuroprotective compounds such as selegiline.
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Authors | Thomas Müller |
Journal | Current opinion in investigational drugs (London, England : 2000)
(Curr Opin Investig Drugs)
Vol. 3
Issue 12
Pg. 1763-7
(Dec 2002)
ISSN: 1472-4472 [Print] England |
PMID | 12528314
(Publication Type: Journal Article, Review)
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Chemical References |
- Butanes
- Nitrogen Oxides
- CPI 1189
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Topics |
- Animals
- Butanes
(chemistry, pharmacology, therapeutic use)
- Clinical Trials as Topic
(statistics & numerical data)
- Drug Industry
(legislation & jurisprudence, methods)
- Humans
- Neurodegenerative Diseases
(drug therapy)
- Nitrogen Oxides
(chemistry, pharmacology, therapeutic use)
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