Biguanide has been investigated for the treatment of Diabetes Mellitus. The term "biguanidine" often refers specifically to a class of drugs that have a broad range of medical indications. Besides recent experiments have shown that biguanide could be a modifiable pharmacophore for the synthesis of therapeutic cysteinyl cathepsins inhibitors with a wide range of potencies and specificities. It is known that excessive activities of cysteinyl cathepsins contribute to the progress of many diseases.

Arpromidine is a potent histamine H2-receptor agonist and weak NPY Y1 antagonist. In the isolated aperfused heart, arpromidine was more potent in increasing cardiac contractile force and coronary flow but less effective on heart rate and less arrhythmogenic. Arpromidine may be considered a new lead for the development of "cardiohistaminergics". In the arpromidine series the order of potency found in guinea-pig atria was in good agreement with the results from isolated perfused guinea-pig hearts. In particular, the two-fold halogenated arpromidine analogues proved to be more potent positive inotropic agents than impromidine with lower stimulating effects on heart rate and reduced arrhythmogenic properties.

Debrisoquin is an antihypertensive drug having guanethidine-like properties, which inhibits monoamine oxidase (MAO) and does not enter the brain. Debrisoquine was used for the treatment of hypertension. Debrisoquine hydroxylation phenotype has been the most used test in humans to evaluate CYP2D6 activity. Two debrisoquine hydroxylation phenotypes have been described: poor and extensive metabolizers. A group with a very low debrisoquine metabolic ratio within the extensive metabolizers, named ultrarapid metabolizers, has also been distinguished. This CYP2D6 variability can be for a large part alternatively determined by genotyping, which appears to be of clinical importance given CYP2D6 involvement in the metabolism of a large number of commonly prescribed drugs.

Adrenochrome monoaminoguanidine (S-Adchnon) is a hemostatic capillary-stabilizing agent demonstrating pharmacological effects against radiation injury by reducing side effects of radiation therapy on hematopoietic organ. Synthesized by a dehydrating reaction of adrenochrome and aminoguanidine it has superior properties than adrenochrome, an oxidation product of adrenalin remarkable for its efficiency as a haemostatic agent at very small doses and for its more rapid and equally intense action than that of adrenalin. Adrenochrome does not alter the cardiac rhythm and does not cause any hypertension or internal haemorrhages and would be suitable for therapeutic applications, however, its instability, in aqueous or alcoholic solution, makes its use substantially impossible. S-Adchnon was devised, approved by the Japanese Ministry of Health, Labor and Welfare in 1962 and used widely in Japan. Adrenochrome monoaminoguanidine has negligible toxicity, stable and could be made into salts for aqueous dosage, especially for injection. Adrenochrome monoaminoguanidine methanesulfonate (AMM) enhances the recovery from radiation-induced leukopenia in rabbits and in humans, and inhibits the increases in chromosome aberrations in peripheral lymphocytes of patients with cervical carcinoma under radiotherapy. It has been shown that the radiation-induced initial decrease in number of peripheral blood leukocytes (PBL) is not affected by AMM, but recovery from the decrease is enhanced, shortening the period of leukopenia. This suggests that AMM may not exert its effects by protecting PBL directly but by protecting stem and/or progenitor cells in hematogenesis which proliferate and differentiate to PBL after irradiation. In in vitro colony formation method AMM demonstrated a protective effect on the survival of GM-CFC, a hematopoietic progenitor cells. Differential action on cancer and normal tissue by AMM and cytochrome C combined with radiotherapy was demonstrated. AMM in combination with cytochrome C augumented natural killer (NK) cells activity in KSN nude mice, protected potent NK cells in patients with lung cancer against radiotherapy and sensitized the human lung cancer xenografts to radiotherapy. Thus, AMM and cytochrome C may have the potential as a differential modulator of radiosensitivity of normal tissues and of tumors.

Dinotefuran is a new furanicotinyl insecticide which represents the third generation of neonicotinoid group. Dinotefuran, which was developed by Mitsui Chemicals, Inc., was registered in Japan April 24, 2002 and the registration has been submitted to the Environment Protection Agency (EPA) in the USA. Dinotefuran was granted Organophosphorus Alternative and Reduced Risk Status by the EPA. Dinotefuran exhibits a insecticidal activity against Hemiptera, Lepidoptera, Coleoptera, Diptera, Dictyoptera and Thysanoptera. Furthermore, it has very low phytotoxicity so that it can be utilized for many kinds of crops. Dinotefuran is water-soluble and has excellent systemic and translaminar action in many plants. This property enables dinotefuran to be applied using various methods and various formulations. The binding assay using insect nAChRs and the electrophysiological study showed that dinotefuran acted on nAChRs as an agonist. However, in the binding study, the affinity of dinotefuran against the binding site of other neonicotinoids was very low, suggesting that this compound acts on a different site than other neonicotinoids.

Guanoxan is 2-guanidinomethylbenzo-1,4-dioxan. It acts as a blocker of alpha-2 adrenoceptors. The clinical use of this drug has been in the treatment of hypertension. Both systolic and diastolic pressures are lowered in the lying and standing positions.

Guanazodine is a new antihypertensive drug. Guanazodine caused a sustained decrease in the systemic blood pressure of spontaneously hypertensive rats, renal hypertensive dogs and normal cats. No tachyphylaxis developed when the drug was administered orally. The heart rate decreased. Guanazodine relaxed the cat nictitating membrane, attenuated the positive chronotropic response to sympathetic nerve stimulation in anesthetized dogs and in isolated rabbit aorta to transmural electrical stimulation. Guanazodine potentiated the pressor response to noradrenaline but attenuated the response to tyramine in anesthetized cats. It may be concluded that the hypotensive effect of guanazodine is related to adrenergic neuron blocking action, the noradrenaline-depleting action in peripheral tissues is similar to the effect of guanethidine and bethanidine. However, this drug is less potent than guanethidine. Toxicity and side effects appear to be less with guanazodine than with guanethidine and bethanidine.

Aganodine, an imidazoline/ alpha-2 receptor agonist, can lower intraocular pressure in the sympathetic neurons of the eye and possibly in the central nervous system.

Aptiganel (CNS 1102, Cerestat), a selective ligand with antagonized properties for the ion-channel site of the N-methyl-D-aspartate receptor-channel complex, was developed as a neuroprotective agent for focal brain ischemia. However, in the clinical trials in patients with acute ischemic stroke aptiganel was not efficacious at either of the tested doses and may be harmful. That is why its further study was discontinued.