Risotilide is a Class III antiarrhythmic agent that inhibits the voltage-dependent potassium channel. Risotilide prolongs cardiac action potentials and refractory periods. It was shown to reduce ventricular vulnerability in a study on arrhythmogenic effects of left ventricular hypertrophy (LVH) in the intact heart in cats. Phase I and II trials have been conducted, but development of this drug has been discontinued.

Dexniguldipine (B8509-035, (-)-(R)-niguldipine) is a new dihydropyridine derivative, that exerts selective antiproliferative activity in a variety of tumor models and, in addition, has a high potency in overcoming multidrug resistance. Dexniguldipine is ( - )-(R)-enantiomer of niguldipine, of which the ( )-(S)-enantiomer shows pronounced cardiovascular hypotensive activity due to its high affinity for the voltage-dependent Ca2 channel. As compared with the (S)-enantiomer, the (R)-enantiomer has a 40-fold lower affinity for the Ca 2 channel and, accordingly, only minimal hypotensive activity in animal pharmacology models. Dexniguldipine have shown antiproliferative activity in several tumor cell lines, but the concentrations necessary to inhibit growth have varied by several orders of magnitude between cell lines. Initial results of preclinical investigations for the evaluation of the mechanism of its antiproliferative activity demonstrate that dexniguldipine interferes with intracellular signal transduction by affecting phosphoinositol pathways, protein kinase C expression, and intracellular Ca 2 metabolism. In a series of human tumor xenografts in vitro, dexniguldipine demonstrated selective antiproliferative activity against several tumor types, e.g., melanoma and renal-cell carcinoma. Striking results were obtained in a hamster model, in which neuroendocrine lung tumors could be completely eradicated by 20 weeks of oral treatment with 32.5mg/kg dexniguldipine, whereas Clara-cell-type lung tumors were not affected. In in vitro studies, dexniguldipine has been found to bind to P-glycoprotein (P-gp) and to enhance the cytotoxicity of chemotherapeutic agents such as doxorubicin and etoposide in several cell lines The synergistic effect may well be associated with the reversal of multidrug resistance (MDR) related to the activity of P-gp. In the clinical therapy of cancer, resistance to many cytostatic drugs is a major cause of treatment failure. However, the high potency of dexniguldipine (about 10-fold as compared with that of verapamil in vitro) and its low cardiovascular activity provide the opportunity to achieve blood or tumor concentrations that might be high enough to overcome Mdr 1 resistance in patients without producing dose-limiting cardiovascular effects.

Clofilium is a quaternary ammonium compound that acts as potassium channel blocker. Clofilium is a class III agent. Clofilium increases atrial and ventricular effective refractory period without changing conduction time and, despite no apparent change in premature ventricular complex frequency, it can abolish the ability to induce ventricular tachycardia by programmed stimulation and is also well tolerated.

Butaclamol is an antipsychotic drug, which was studied for the treatment of schizophrenia. This drug has never marketed and now is used in research, because of its action as a dopamine receptor-blocking agent. Butaclamol consists of the two forms: (-)-butaclamol, an inactive drug and (+)-butaclamol, a potent neuroleptic drug.

Actinoquinol is sunscreen agent that absorbs Ultraviolet B light. Actinoquinol in combination with hyaluronic acid drops might be helpful for the human eye in the defense against photooxidative and other oxidative processes.

Sophocarpine is a dehydrogenation derivative of the bis-quinolizidine alkaloid matrine. Sophocarpine is also an active component in sophora alkaloids, which possess a variety of pharmacological effects such as anti-inflammation, immunity regulation, antivirus, and anti-tumor actions. Sophocarpine is able to block HERG K+ channel. It is Na+ channel inward current inhibitor. It activates the AMPK signaling pathway and inhibits the TLR4-downstream pathway.

Sophocarpine is a dehydrogenation derivative of the bis-quinolizidine alkaloid matrine. Sophocarpine is also an active component in sophora alkaloids, which possess a variety of pharmacological effects such as anti-inflammation, immunity regulation, antivirus, and anti-tumor actions. Sophocarpine is able to block HERG K+ channel. It is Na+ channel inward current inhibitor. It activates the AMPK signaling pathway and inhibits the TLR4-downstream pathway.

Verticine is a steroidal alkaloid compound extracted from the Fritillaria species of medicinal plants. Verticine was not only able to block the Nav1.7 ion channel but also preferably inhibited the Kv1.3 ion channel. It inhibits the production of inflammatory cytokines induced by LPS through blocking MAPKs and NF-κB signaling pathways. Verticine inhibited the hERG peak tail currents in a concentration dependent manner. Verticine exhibits anti-inflammatory, antitussive, antihypertensive and pain suppression properties.