Hi doctorchou2-ga, and thanks for your question.
After several unsuccessful searches, I finally came up with a useful
reference. It turns out that normeperidine is a nonopioid metabolite
of meperidine with half the analgesic potency. It also,
unfortunately, has about 2-3 times the excitatory stimulous of
meperidine in the central nervous system, which is the primary source
of the drug's toxicity.
Here is the relevant passage and reference for the article I mentioned above:
"Meperidine is metabolized in the body by two different pathways. The
predominant pathway is hepatic carboxylesterase metabolism to
meperidinic acid, an inactive metabolite. The most clinically
significant pathway is N-demethylation by the hepatic cyto-chrome
P-450 system to normeperidine, a nonopioid active metabolite. This
metabolic process is carried out in the microsomal hydroxylation
enzyme system. Normeperidine can be metabolized to either
normeperidinic acid by carboxylesterase or by microsomal hydroxylation
to N-hydroxynormeperidine followed by renal elimination.[24?34] The
active nonopioid neurotoxic metabolite normeperidine has half the
analgesic potency of meperidine but two to three times the potency as
a central nervous system (CNS) excitatory agent.[28,35] An overlooked
clinical iatrogenic event is the propensity of normeperidine to
precipitate anxiety, hyperreflexia, myoclonus, seizures, and mood
changes within 24 hours."
Latta KS, Ginsberg B, Barkin RL. Meperidine: a critical review. Am J
Ther. 2002 Jan-Feb;9(1):53-68. Review.
Using Google Scholar:
receptor affinity meperidine normeperidine
I hope this information is useful. Please request any clarification
prior to rating.