Disease relevance of CLOFENAPATE

• Administration of 25 mg/kg/day methyl clofenapate to Alpk/APfSD rats for up to 4 days gave rise to hepatomegaly resulting from a combination of hepatocyte hyperplasia, mainly in the periportal region of the lobule, and centrilobular cell hypertrophy [1].

High impact information on CLOFENAPATE

• We now present evidence to demonstrate that such cells respond to methyl clofenapate, a peroxisome proliferator [2].
• Comparative effects of clofibrate and methyl clofenapate on morphological transformation and intercellular communication of Syrian hamster embryo cells [3].
• Both were able to suppress spontaneous and TGF beta 1-induced apoptosis in rat and guinea pig hepatocytes although the effects of MCP were weak (P < or = 0.05) compared with nafenopin or Wy-14 643 (P < or = 0.01) [4].
• With increasing length of exposure to methyl clofenapate the number of peroxisomes located in this region during mitosis increased [1].
• Feeding the hypolipidemic compounds, beta-diethylaminoethyl-alpha-p-chlorophenoxyisobutyrate hydrochloride, Nafenopin and Clofenapate did not significantly alter catalase levels [5].

Biological context of CLOFENAPATE

• Juxtaposition of peroxisomes and chromosomes in mitotic hepatocytes following methyl clofenapate administration to rats [1].
• Chronic exposure to clofenapate leads to an increase in palmitate utilization through both oxidation and, as previously shown (Verrando et al., 1981), esterification [6].

Anatomical context of CLOFENAPATE

• There was no increase in lysosomes in the renal tubules of methy l clofenapate treated animals [7].
• The effects of hypolipidemic drugs such as clofenapate observed on a long-term basis in vitro are consistent with the results of studies on adipose tissue in vivo [8].

References