Does anyone have hard information as to why Abbot dropped the nicotinic agonist ABT 594 in phase 2 trials?
it is an interesting molecule based on the extremely dangerous poison and potent non opioid analgesic Epibatidine, the toxin originally from an Ecuadorian poison frog (200x as strong as morphine hype). Epibatidine has a minimal theraputic index effecting the heart and causing convulsions followed by death at doses only slightly higher than the analgesic doses.
ABT 594 was Abbots modification of the epibatidine lead compound
They have a newer nicotinic agonist ABT 894 in human trials, perhaps that was why the earlier ABT 594 was dropped. but I don't think they have released the structure, has anyone any guesses as to the structure of ABT 894??
Next question, which subtypes of the nACh receptor are interesting in terms of releasing DA from where it is co-located with dopaminergic neurons?
I know that ibogaine is relatively selective on one subtype in contrast to the rest of its diverse and messy pharmacology.
it is an interesting molecule based on the extremely dangerous poison and potent non opioid analgesic Epibatidine, the toxin originally from an Ecuadorian poison frog (200x as strong as morphine hype). Epibatidine has a minimal theraputic index effecting the heart and causing convulsions followed by death at doses only slightly higher than the analgesic doses.
ABT 594 was Abbots modification of the epibatidine lead compound
They have a newer nicotinic agonist ABT 894 in human trials, perhaps that was why the earlier ABT 594 was dropped. but I don't think they have released the structure, has anyone any guesses as to the structure of ABT 894??
Next question, which subtypes of the nACh receptor are interesting in terms of releasing DA from where it is co-located with dopaminergic neurons?
I know that ibogaine is relatively selective on one subtype in contrast to the rest of its diverse and messy pharmacology.