Acetamiprid is a carboxamidine that is acetamidine in which the amino hydrogens are substituted by a (6-chloropyridin-3-yl)methyl and a methyl group while the hydrogen attached to the imino nitrogen is replaced by a cyano group. It has a role as a neonicotinoid insectide, an environmental contaminant and a xenobiotic. It is a monochloropyridine, a nitrile and a carboxamidine. It derives from a 2-chloropyridine. Acetamiprid is an insecticide that is currently approved for EU use. It is highly soluble in water and is volatile. Based on its chemical properties it would not be expected to leach to groundwater. It is not persistence in soil systems but may be very persistent in aquatic systems under certain conditions. It has a moderate mammalian toxicity and it has a high potential for bioaccumulation. Acetamiprid is a recognised irritant. It is highly toxic to birds and earthworms and moderately toxic to most aquatic organisms. Acetamiprid is a nicotinic agonist that reacts with nicotinic acetylcholine receptors (nACh-R). The activation of the nACh-R receptors causes hyperactivity and muscle spasms, and eventually death.

CGP-47645 (also known as Leflutrozole) is an orally active non-steroidal aromatase aromatase inhibitor which is under development by Mereo BioPharma and Novartis for the treatment of hypogonadism in men.

Oxidopamine (6-Hydroxydopamine) is an antagonist of the neurotransmitter dopamine with potential antineoplastic activity. 6-Hydroxydopamine (6-HOD) can be taken up by selective adrenergic terminals, thereby causing acute degeneration of adrenergic terminals that leads to depletion of norepinephrine, and of dopamine in the dopamine-sensitive sites. This agent is auto-oxidated at physiological pH that leads to the formation of reactive free radicals, thereby leading to cytotoxicity in neural cells. 6-Hydroxydopamine is often used to induce CNS and sympathetic neural lesions that model aging and various nervous disorders in animal systems. The growth of C-1300 neuroblastoma was markedly slowed in 6-hydroxydopamine-treated mice. The growth of the A-10 breast adenocarcinoma was also significantly retarded in 6-hydroxydopamine-treated mice but the growth of B-16 melanoma was not affected.

Trigonellamide (1-Methylnicotinamide) is a metabolite of nicotinamide and is produced primarily in the liver by nicotinamide N-methyltransferase. Trigonellamide may be an endogenous activator of prostacyclin (PGI2) production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system. The mechanisms of action of Trigonellamide involve the activation of PGI2 release driven by cyclooxygenase 2 (COX-2). PGI2 releasing capacity of 1- Trigonellamide was shown to afford not only anti-thrombotic but also fibrinolytic, anti-inflammatory and gastroprotective effects. Interestingly, Trigonellamide did not directly either affect the activity of leucocytes or release PGI2 in the perfused rat hindquarters model. Still, Trigonellamide, due to its PGI2 releasing capacity, might serve as a hepatoprotective agent that protects against Concanavalin-A induced liver injury through the downregulation of interleukin-4 (IL-4) and tumor necrosis factor-α signalization (TNF-α). In addition to its anti-platelet, anti-thrombotic and anti-inflammatory activities, 1-MNA has also been shown to restore endothelial function in diabetic hyperglycemic rats, as well as to improve endothelial function in humans. PGI2 displays anti-metastatic activity, and the PGI2 releasing activity of Trigonellamide, the potential application of exogenous Trigonellamide to prevent metastatic cancer.

Pentapiperide is an anticholinergic drug with antisecretory and antimotility activity on the upper gastrointestinal tract, which was used as adjunctive therapy for relieving the symptoms of peptic ulcer. pentapiperide methylsulfate) has approximately the same in vitro antispasmodic activity as atropine. In vivo, however, the quaternary ammonium compounds such as pentapiperide methylsulfate are less readily absorbed from the gastrointestinal tract than are the tertiary amines such as atropine. Pentapiperide methylsulfate is contraindicated in patients with glaucoma or a predisposition to glaucoma, in patients with pyloric obstruction or stenosis, gastric retention, known or suspected obstructive disease of the gastrointestinal tract, and urinary bladder neck obstruction. It is also contraindicated in prostatic hypertrophy, stenosing peptic ulcer, megaesophagus, organic cardiospasm, and in patients with a hypersensitivity to the drug. Xerostomia was the most frequently encountered complaint. In decreasing order of frequency, visual blurring, difficult micturition, constipation, and nausea were reported.

Perfosfamide is the active metabolite of the nitrogen mustard cyclophosphamide with potent antineoplastic and immunosuppressive properties. Perfosfamide alkylates DNA, thereby inhibiting DNA replication and RNA and protein synthesis. The incubation of normal human marrow cells with perfosfamide has a toxic effect on granulocyte-macrophage progenitor cells that is dose as well as white blood cell concentration dependent. It is likely that this dependency of the perfosfamide stem cell effect is caused not only by the target white blood cell concentration but by the suspension’s total protein concentration. Autologous bone marrow transplantation with perfosfamide purging in patients with acute myeloid leukemia in second complete remission produced results similar to that reported with allogeneic bone marrow transplantation. Perfosfamide had been in phase III clinical trial for the treatment of acute myeloid leukemia. However, this development was discontinued.

1-aminocyclopropanecarboxylic acid (ACPC) is a non-proteinogenic alpha-amino acid consisting of cyclopropane having amino and carboxy substituents both at the 1-position. It has a role as a plant metabolite and a member of ethylene releasers. ACPC is produced endogenously in the tomato and other higher plants as a product of the action of 1-aminocyclopropane-1-carboxylic acid synthase in the biosynthesis of ethylene. It is a monocarboxylic acid and a non-proteinogenic alpha-amino acid. It derives from a cyclopropanecarboxylic acid. ACPC is a partial agonist at the strychnine-insensitive glycine recognition site on the N-methyl-D-aspartate (NMDA) receptor complex in the mammalian central nervous system with preclinical activity in animal models of neuroprotection and psychiatric illnesses. Half-maximal activation by ACPC as a glycine-site agonist was 0.7 to 0.9 microM. Half-maximal inhibition by ACPC was dependent on NMDA concentration. Peak responses to a >100 microM ACPC pulse in the presence of 1 microM glutamate were similar to those of glycine but decayed to a steady-state amplitude below that of glycine. The removal of ACPC initially caused an increase in inward current followed by a subsequent decrease to baseline levels. This suggests that relief of low-affinity antagonism occurs before high-affinity agonist dissociation. ACPC is shown to block convulsions and death produced by NMDA exposure, significantly reducing seizure induction and cell death of NMDA-treated hippocampal neurons.