Benidipine is an orally triple L-, T-, and N-type calcium channel blocker for the treatment of hypertension and angina pectoris synthesized and developed by Kyowa Hakko Kogyo Co., Ltd. Benidipine, approved in Japan in November 1991, has become one of the three best selling CCBs and is highly useful as a potent, long-lasting antihypertensive and antianginal agent.

Aminothiazole is a heterocyclic amine, commonly used as a starting point for synthesis of many compounds. In 1940s aminothiazole was used for the treatment of thyrotoxicosis. It has a direct action on the thyroid and acts by inhibiting T4 synthesis and accelerating its deiodination. Aminothiazole is an inhibitor of inducible NO synthetase (IC50 18 uM).

Kainic acid (kainate) is a natural marine acid present in some seaweed. Kainic acid is a potent neuroexcitatory amino acid that acts by activating receptors for glutamate, the principal excitatory neurotransmitter in the central nervous system. Kainic acid is commonly injected into laboratory animal models to study the effects of experimental ablation. Kainic acid is a direct agonist of the glutamic kainate receptors and large doses of concentrated solutions produce immediate neuronal death by overstimulating neurons to death. Such damage and death of neurons is referred to as an excitotoxic lesion. Thus, in large, concentrated doses kainic acid can be considered a neurotoxin, and in small doses of dilute solution kainic acid will chemically stimulate neurons. Kainic acid is utilised in primary neuronal cell cultures and acute brain slice preparations [5] to study of the physiological effect of excitotoxicity and assess the neuroprotective capabilities of potential therapeutics. Kainic acid is a potent central nervous system excitant that is used in epilepsy research to induce seizures in experimental animals, at a typical dose of 10–30 mg/kg in mice. In addition to inducing seizures, kainic acid is excitotoxic and epileptogenic. Kainic acid induces seizures via activation of kainate receptors containing the GluK2 subunit and also through activation of AMPA receptors, for which it serves as a partial agonist.

Tropisetron (Tropisetron-AFT) is a potent and selective serotonin 3 (5-hydroxytryptamine3; 5-HT3) receptor antagonist with antiemetic properties, probably mediated via antagonism of receptors both at peripheral sites and in the central nervous system. Surgery and treatment with certain substances, including some chemotherapeutic agents, may trigger the release of serotonin from enterochromaffin-like cells in the visceral mucosa and initiate the emesis reflex and its accompanying feeling of nausea. Tropisetron (Tropisetron-AFT) selectively blocks the excitation of the presynaptic 5-HT3 receptors of the peripheral neurons in this reflex, and may exert additional direct actions within the CNS on 5-HT3 receptors mediating the actions of vagal input to the area postrema.

Hypericin (4,5,7,4',5',7'-hexahydroxy-2,2'-dimethylnaphtodianthrone) is a naturally occurring chromophore found in some species of the genus Hypericum, especially Hypericum perforatum L. (St. John's wort), and in some basidiomycetes (Dermocybe spp.) or endophytic fungi (Thielavia subthermophila). Among its antidepressant and light-dependent antiviral actions, hypericin is a powerful natural photosensitizer that is applicable in the photodynamic therapy (PDT) of various oncological diseases. Hypericin may act as an inhibitor of enzymes such as MAO (monoaminoxidase), PKC (protein kinase C), dopamine-beta-hydroxylase, reverse transcriptase, telomerase and CYP (cytochrome P450), has yielded results supporting therapeutic potential. Research of hypericin and its effect on GABA-activated (gamma amino butyric acid) currents and NMDA (N-methyl-D-aspartat) receptors also indicate the therapeutic potential of this substance whereby new insights in stroke research (apoplexy) are expected. Topical SGX301 (synthetic hypericin as a potent photosensitizer in photodynamic therapy) is in phase 3 for the treatment of cutaneous T-cell lymphoma.

Huperzine A is a plant alkaloid derived from Club moss plant, Huperzine serrata, which is a member or the Lycopodium species. Huperzine-A is in phase III clinical trial in the USA (Alzheimer disease) and is available as a dietary supplement. It selectively and reversibly inhibits acetylcholinesterase. Huperzine A is also a NMDA receptor antagonist, which protects the brain against glutamate induced damage, and it increases nerve growth factor levels. Huperzine A is used for Alzheimer's disease, memory and learning enhancement, and age-related memory impairment. It is also used for treating a muscle disease called myasthenia gravis, for increasing alertness and energy, and for protecting against agents that damage the nerves such as nerve gases. It can cause some side effects including nausea, diarrhea, vomiting, sweating, blurred vision, slurred speech, restlessness, loss of appetite, contraction and twitching of muscle fibers, cramping, increased saliva and urine, inability to control urination, high blood pressure, and slowed heart rate. Various medications used for glaucoma, Alzheimer's disease, and other conditions (Cholinergic drugs) interacts with Huperzine A.

Azosemide is a monosulfamyl belonging to the class of loop diuretics, used to treat hypertension, edema, and ascites. Azosemide inhibits sodium and chloride reabsorption throughout the thick ascending limb of the loop of Henle. The exact mechanism of action is not fully understood, but it mainly acts on both the medullary and cortical segments of the thick ascending limb of the loop of Henle. Delayed tolerance was demonstrated in humans by homeostatic mechanisms (principally an increase in aldosterone secretion and perhaps also an increase in the reabsorption of solute in the proximal tubule). After oral administration to healthy humans in the fasting state, the plasma concentration of azosemide reached its peak at 3–4 h with an absorption lag time of approximately 1 h and a terminal half-life of 2–3 h. The estimated extent of absolute oral bioavailability in humans was approximately 20.4%. After oral administration of the same dose of azosemide and furosemide, the diuretic effect was similar between the two drugs, but after intravenous administration, the effect of azosemide was 5.5–8 times greater than that in furosemide. This could be due to the considerable first-pass effect of azosemide. Azosemide is actively secreted in the renal proximal tubule possibly via nonspecific organic acid secretory pathway in humans. Thus, the amount of azosemide that reaches its site of action could be significantly modified by changes in the capacity of this transport system. This capacity, in turn, could be predictably changed in disease states, resulting in decreased delivery of the diuretic to the transport site, as well as in the presence of other organic acids such as nonsteroidal anti-inflammatory drugs which could compete for active transport of azosemide.

Periciazine (INN), also known as pericyazine (BAN) or Propericiazine, is a drug that belongs to the phenothiazine class of typical antipsychotics. Pericyazine is not approved for sale in the United States. It is commonly sold in Canada and Russia under the tradename Neuleptil and in the United Kingdom and Australia under the tradename Neulactil. The primary uses of pericyazine include the short-term treatment of severe anxiety or tension and in the maintenance treatment of psychotic disorders such as schizophrenia. There is insufficient evidence to determine whether periciazine is more or less effective than other antipsychotics. Pericyazine is a rather sedating and anticholinergic antipsychotic, and despite being classed with the typical antipsychotics, its risk of extrapyramidal side effects is comparatively low. It has a relatively high risk of causing hyperprolactinemia and a moderate risk of causing weight gain and orthostatic hypotension.

Gemigliptin, an orally active, CD26 antigen (dipeptidyl peptidase IV or DPP IV) antagonist, was developed by LG Life Sciences (Seoul, Korea) and was approved by the Ministry of Food and Drug safety in June 2012 for the treatment of Type 2 diabetes mellitus. Zemiglo is the brand name of gemigliptin. The company also signed licensing agreement with multinational pharmaceutical companies including Sanofi (Paris, France), and at present gemigliptin is approved in India, Columbia, Costa Rica, Panama, Ecuador and a few other countries. Registration studies are currently ongoing in several countries including Russia, Mexico and Thailand. Various studies have proven the efficacy and safety of gemigliptin for the treatment of T2DM, both as monotherapy as well as in combination with other anti-diabetic drugs. Gemigliptin binds to the S1, S2, and S2 extensive subsites of the DPP-4 enzyme. The piperidinone group of gemigliptin binds to the S1 subsite, where the upside F atom on the piperidin ring forms a hydrogen bond with the side chain of Tyr631 and the downside F atom makes a hydrophobic interaction with the side chain of Tyr666 and Tyr662. In addition, the key interaction occurs between the CF3 groups on the pyrimidino piperidine and the S2 extensive subsite of the DPP-4 substrate, which enhances the potency of the drug and increases its selectivity as well. Gemigliptin is a reversible and competitive inhibitor of DPP-4 enzyme with a Ki value of 7.25 ± 0.67 nM. It acts as a long-acting DPP-4 inhibitor which inhibits DPP-4 in a dose-dependent manner. In addition, it showed at least >23,000 fold selectivity for proteases such as DPP-8, DPP-9, and fibroblast activating protein – α. By preventing degradation of GLP-1 by DPP-4 inhibition, it increases insulin secretion, reduces glucagon secretion, decreases HbA1c, and prevents β-cell damage. Gemigliptin has also been investigated for the treatment of cancer and cisplatin adverse reaction.

Eberconazole is an antifungal drug with broad antimicrobial spectrum of activity. The drug was developed and approved in Spain (Ebernet 1% cream) for the treatment of tinea. Eberconazole exerts fungicidal or fungistatic activity depending on concentration, being fungicidal at higher concentration and fungistatic at lower concentrations. Eberconazole prevents fungal growth by inhibiting ergosterol synthesis, an essential component of the fungal cytoplasmic membrane leading to structural and functional changes. It prevents the fungal ergosterol synthesis by inhibiting lanosterol 14alpha-demethylase enzyme that is responsible for the formation of 14 alpha-methylsterols (precursor of ergosterols).