G protein-coupled receptor allosterism and complexing¶
Christopoulos, A., & Kenakin, T. (2002). G protein-coupled receptor allosterism and complexing. Pharmacological Reviews, 54(2), 323-374.
Cited by¶
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Primes¶
- Potentiation
- Pharmacology and toxicology: Benzodiazepine potentiation of GABA receptor response (the basis for therapeutic anxiolysis, sedation, and seizure control), exemplifying the allosteric-modulator framework Christopoulos and Kenakin (2002) develop for receptor pharmacology; opioid potentiation of CNS depression by co-exposure to benzodiazepines, alcohol, sedating antihistamines, or other respiratory depressants—a major clinical cause of overdose and mortality; kindling in chronic seizure disorders, where repeated sub-threshold stimuli eventually trigger full seizures as the nervous system becomes potentiated; pharmacokinetic potentiation through competitive inhibition of the cytochrome P450 system or renal excretion pathways, causing unexpected accumulation of co-administered drugs.
This sourceFoundational review of allosteric modulation: develops the receptor-pharmacology framework underlying benzodiazepine-GABA potentiation and other allosterically potentiated drug interactions.
- Pharmacology and toxicology: Benzodiazepine potentiation of GABA receptor response (the basis for therapeutic anxiolysis, sedation, and seizure control), exemplifying the allosteric-modulator framework Christopoulos and Kenakin (2002) develop for receptor pharmacology; opioid potentiation of CNS depression by co-exposure to benzodiazepines, alcohol, sedating antihistamines, or other respiratory depressants—a major clinical cause of overdose and mortality; kindling in chronic seizure disorders, where repeated sub-threshold stimuli eventually trigger full seizures as the nervous system becomes potentiated; pharmacokinetic potentiation through competitive inhibition of the cytochrome P450 system or renal excretion pathways, causing unexpected accumulation of co-administered drugs.
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