Neostigmine is a cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction. Neostigmine is used for the symptomatic treatment of myasthenia gravis by improving muscle tone.

Neostigmine is a cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction. Neostigmine is used for the symptomatic treatment of myasthenia gravis by improving muscle tone.

Neostigmine is a cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction. Neostigmine is used for the symptomatic treatment of myasthenia gravis by improving muscle tone.

Neostigmine is a cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction. Neostigmine is used for the symptomatic treatment of myasthenia gravis by improving muscle tone.

Solasodine is an aglycone of solamargine and solasonine, which are the major solasodine glycosides present in numerous species of the solanaceae family including potato, tomato or garden egg plant etc. In Phase II clinical trial was shown that solasodine glycosides exhibit anticancer activity against skin cancer. The effects of aglycone solasodine on cancer cells have also been investigated. Solasodine inhibits the growth of human colon and liver cancer cell. In addition, solasodine effectively inhibits proliferation of HER2-overexpressing breast cancer cells and inhibits invasion of human lung cancer cells. Solasodine possesses CNS activities such as antipyretic, anticonvulsant and memory enhancing effects. Also, solasodine has been found to possess diuretic, antifungal, hepatoprotective, immunomodulatory, anti-spermatogenetic and antiandrogenic effects.

Trimedoxime is the only one of the major bispyridinium oxime with a propylene linked between the two pyridinium rings. Trimedoxime is an oxime cholinesterase (AChE) reactivator. It was shown that trimedoxime is a more potent reactivator of the DFP-inhibited AChE than pralidoxime and a better reactivator than obidoxime in the case of the tabun-inhibited enzyme. It can be used parenterally as an antidote adjunct to atropine in treating human or animal (organophosphate group) anticholinesterase pesticide toxicity. Trimedoxime was the first oxime that was efficient in the treatment of animals intoxicated with tabun. It could also protect animals poisoned with sarin or VX, but not the ones intoxicated with soman.

Conessine is a plant steroid alkaloid that acts as a potent and specific antagonist of histamine H3 receptors. Conessine displayed high affinity at both rat and human H3 receptors (pKi = 7.61 and 8.27) and generally high selectivity against other sites, including histamine receptors H1, H2, and H4. Conessine was found to efficiently penetrate the CNS and reach very high brain concentrations. Although the very slow CNS clearance and strong binding to adrenergic receptors discouraged focus on conessine itself for further development, its potency and novel steroid-based skeleton motivated further chemical investigation. Modification based on introducing diversity at the 3-nitrogen position generated a new series of H3 antagonists with higher in vitro potency, improved target selectivity, and more favorable drug-like properties. Conessine also has high affinity for the adrenergic receptors. Conessine has being shown to possess anti-malarial activity. In India conessine finds therapeutic use for treatment of dysentery and helminthic disorders.

Trimedoxime is the only one of the major bispyridinium oxime with a propylene linked between the two pyridinium rings. Trimedoxime is an oxime cholinesterase (AChE) reactivator. It was shown that trimedoxime is a more potent reactivator of the DFP-inhibited AChE than pralidoxime and a better reactivator than obidoxime in the case of the tabun-inhibited enzyme. It can be used parenterally as an antidote adjunct to atropine in treating human or animal (organophosphate group) anticholinesterase pesticide toxicity. Trimedoxime was the first oxime that was efficient in the treatment of animals intoxicated with tabun. It could also protect animals poisoned with sarin or VX, but not the ones intoxicated with soman.

Boldine, an aporphine alkaloid, found abundantly in the leaves/bark of boldo (Peumus boldus Molina) widely consumed in the folk medicine of some regions. Boldine possesses various pharmacological properties including, anticancer activity. It exhibits a significant improvement of learning and memory through inhibition of brain acetylcholinesterase activity and alleviation of brain oxidative stress, which was shown on animal models. Boldine is a potentially useful agent for the treatment of leishmaniosis. In addition, it suppresses osteoclastogenesis, improves bone destruction and may be a potential therapeutic agent for rheumatoid arthritis. Besides, was shown, that boldine inhibits telomerase in cells treated with sub-cytotoxic concentrations. Telomerase inhibition occurs via down-regulation of human telomerase reverse transcriptase (hTERT), the catalytic subunit of the enzyme.