Staurosporine is an alkaloid isolated from the culture broth of Streptomyces staurosporesa. It exerts antimicrobial, hypotensive, and cytotoxic activity. The main biological activity of staurosporine is the inhibition of protein kinases through the prevention of ATP binding to the kinase. This is achieved through the stronger affinity of staurosporine to the ATP-binding site on the kinase. Staurosporine is a prototypical ATP-competitive kinase inhibitor in that it binds to many kinases with high affinity, though with little selectivity. It is a potent, cell permeable protein kinase C inhibitor with an IC50 of 0.7 nM. At higher concentration (1-20 nM), staurosporine also inhibits other kinases such as PKA, PKG, CAMKII and Myosin light chain kinase (MLCK). At 50-100 nM, it is a functional neurotrophin agonist, promoting neurite outgrowth in neuroblastoma, pheochromocytoma and brain primary neuronal cultures. At 0.2- 1 uM, staurosporine induces cell apoptosis. Staurosporine is also a potent GSK-3β inhibitor with a reported IC50 value of 15 nM. In research, staurosporine is used to induce apoptosis. It has been found that one way in which staurosporine induces apoptosis is by activating caspase-3. Staurosporine was discovered to have biological activities ranging from anti-fungal to anti-hypertensive. The interest in these activities resulted in a large investigative effort in chemistry and biology and the discovery of the potential for anti-cancer treatment. Staurosporine induces apoptosis by multiple pathways and that the inhibition of more than one kinase is responsible for its potent activity. Because the mechanism of action of staurosporine is distinct from traditional anticancer drugs, this may warrant further preclinical evaluations of the antitumor potential of new staurosporine derivatives either alone or in combination with death ligands or conventional chemotherapeutic drugs.

Coniine is a neurotoxic piperidine alkaloid found in poison hemlock (Conium maculatum L.). Coniine which is considered to be racemic mixture first described by Gieseke in 1827; von Hoffman confirmed the structure in 1881; Ladenburg perfermed synthesis in 1886. Coniine enantiomers are nicotinic acetylcholine receptor (nAChR) agonists. The relative potencies of these enantiomers on TE-671 cells expressing human fetal nicotinic neuromuscular receptors had the rank order of (-)-coniine > (+/-)-coniine > (+)-coniine. The rank order potency in SH-SY5Y cells which predominately express autonomic nAChRs was: (-)-coniine>(+)-coniine> (+/-)-coniine.

Brucine is an alkaloid resembling strychnine but it is much less potent than strychnine. Brucine was first discovered in 1819 by Pelletier and Caventou in the bark of the Strychnos nux vomica tree. Brucine causes paralysis of the peripheral nerve endings and produces violent convulsions. Since brucine is a large chiral molecule, it has been used as an enantioselective recognition agent using in chiral resolution. While brucine has been shown to have good anti-tumor effects, on both hepatocellular carcinoma and breast cancer, its narrow therapeutic window has limited its use as a treatment for cancer. Brucine is also used in traditional Chinese medicine as an anti-inflammatory and analgesic agent, as well as in some Ayurveda and homeopathy drugs. Like strychnine, brucine also functions as antagonist at the glycine receptor and paralyzes the inhibitory neurons

Dezocine was discovered and patented by American Home Products Corp. in 1978. Dezocine is a partial opiate drug and was used for pain management under brand name Dalgan. But then usage of this drug was discontinued in US. Dezocine acts as a partial μ-receptor agonist, a κ-receptor antagonist, and a norepinephrine and serotonin reuptake inhibitor (via norepinephrine transporter and serotonin transporter). Dezocine shares the CNS depressant and respiratory depressant effects of opioid analgesics. Dezocine has not been shown to produce clinically significant cardiovascular adverse effects.

Aniledrine is a narcotic pain reliver. The drug was prescribed as an analgesic in anaesthesia (Leritine brand name), however, it is no longer available on the market. Although the exact mechanism is not fully understood, aniledrine appears to elicit its action by binding to endorphine receptors in CNS.

Dihydrocodeine is an opioid analgesic used as an alternative or adjunct to codeine to treat moderate to severe pain, severe dyspnea, and cough. It is semi-synthetic, and was developed in Germany in 1908 during an international search to find a more effective antitussive agent to help reduce the spread of airborne infectious diseases such as tuburculosis. It was marketed in 1911. Dihydrocodeine is metabolized to dihydromorphine -- a highly active metabolite with a high affinity for mu opioid receptors. Dihydrocodeine is used for the treatment of moderate to severe pain, including post-operative and dental pain. It can also be used to treat chronic pain, breathlessness and coughing. In heroin addicts, dihydrocodeine has been used as a substitute drug, in doses up to 2500mg/day to treat addiction.

Protoveratrine A, the principal alkaloid of Veratrum album, has been used in the treatment of hypertension but has largely been replaced by drugs with fewer adverse effects.

Aconitine is an alkaloid found in the Aconitum species. Aconitine is a highly toxic cardiotoxin and neurotoxin. In China and other countries, the herbal extract containing aconitine was used for the treatment of pain in musculoskeletal disorders, however the safety margin between therapeutic analgesic effect of aconitine and its known cardiotoxic effect is so narrow that the treatment may cause poisoning and death. The mechanism of aconitine action is explained by its ability to activate voltage-dependent sodium-ion channels.