Fenbutrazate is a prodrug of phenmetrazine, a psychostimulant for the treatment of obesity. Fenbutrazate acts as an agonist of monoamine transportes upon conversion to the active metabolite. The drug is no longer marketed due to its addictive profile.

Masitinib is a new orally administered tyrosine kinase inhibitor that targets mast cells and macrophages, important cells for immunity, through inhibiting a limited number of kinases. Based on its unique mechanism of action, masitinib can be developed in a large number of conditions in oncology, in inflammatory diseases, and in certain diseases of the central nervous system. In oncology due to its immunotherapy effect, masitinib can have an effect on survival, alone or in combination with chemotherapy. Through its activity on mast cells and consequently the inhibition of the activation of the inflammatory process, masitinib can have an effect on the symptoms associated with some inflammatory and central nervous system diseases and the degeneration of these diseases. AB Science is developing masitinib in multiple sclerosis and alzheimer's disease. Masitinib targets kinases, including c-Kit, PDGFR, and Lyn. It is used in the treatment of mast cell tumors in animals, specifically dogs. Since its introduction in November 2008 it has been distributed under the commercial name Masivet. It has been available in Europe since the second part of 2009. In the USA it is distributed under the name Kinavet.

Mefenorex or (+/-)N-(3-chloropropyl)-1-methyl-2-phenylethylamine is an N-alkylated analogue of amphetamine. The therapeutic efficacy of mefenorex as an adjunctive support in the treatment of obesity for limited periods of time, as well as its ability to be well tolerated, has been amply demonstrated. Mefenorex is considered to be racemic mixture, no available data regarding enantiospecific pharmacological activity of the compound.

Amineptine is a selective inhibitor of dopamine reuptake. The drug was developed in France and was marketed for the treatment of depressive disorders under the name Survector among the others. Amineptine was withdrawn from the French market in 1999 because of abuse and drug dependence and because of its hepatic (cholestatic injuries) and cutaneous (acne) adverse effects.

Fonzine (also known as dimetotiazine) is an analgesics and anti-inflammatory agent marketed in Japan and Europe under the name Migristene and indicated for the treatment of migraine and headaches secondary to other disease. Fonzine exerts its activity by inhibiting serotonin and histamine H1 receptors.

Methenolone (also known as primobolan) was described in 1960. Squibb Company began producing injectable drug in 1962. Methenolone originally was prescribed in case of muscle loss after operations, infections, long-term illnesses, aggressive therapy with corticoids or malnutrition, and in some cases it was used to treat osteoporosis and breast cancer. Methenolone was commonly used to promote weight gain in infants, weighing less than normal, without any side effects. Methenolone is an anabolic steroid, modification of dihydrotestosterone (DHT) with weak androgenic activity and a moderate anabolic effect. A notable trait of methenolone is that it can firmly bind to androgen receptors, stronger than testosterone. Adult doses for the treatment of aplastic anemia are usually in a range of 1–3 mg/kg per day. Adverse side effects include fluid and electrolyte retention, hypercalcaemia, increased bone growth and skeletal weight. In men, additional side priapism, azoospermia, hirsutism, male pattern baldness, acne andoedema. In women, side effects include virilization, amenorrhoea, menstrual irregularities, suppressed lactation, and increased libido. In children, side effects may include virilization symptoms. Metenolone may enhance effects of antidiabetics, ciclosporin, levothyroxine, warfarin. Resistance to the effects of neuromuscular blockers may occur, and metenolone also has the potential to interfere with glucose tolerance and thyroidfunction tests. Metenolone enanthate (methenolone enanthate) is an ester derivative of methenolone sold commonly under the brand names Primobolan (tablet form) orPrimobolan Depot (injectable). When it interacts with the aromatase enzyme it does not form any estrogens. It is used by people who are very susceptible to estrogenic side effects, having lowerestrogenic properties than nandrolone. This trait makes primobolan to be a good fat burner. Primobolan does not convert into estradiol. As an anabolic steroid, the use of metenolone is banned from use in sports governed by the World Anti-Doping Agency. Belarusian shot putter Nadzeya Ostapchuk was stripped of her gold medal after testing positive for metenolone at the London 2012 Olympic Games. She has been excluded from future IOC events. The NBA and NBPA also banned the use of methenolone under the Anti-Drug Program. In February 2013, Hedo Türkoğlu of the Orlando Magic was suspended for 20 games without pay by the league after testing positive for methenolone. In December 2013, Natalia Volgina was stripped of her 2013 Old Mutual Two Oceans Marathon title and received a two-year competition ban, subsequent to a final guilty verdict for using the steroid Metenolone.

Flupirtine is a triaminopyridine derivative having a chemical structure - 2-amino-3-ethoxy-carbonylamino-6-4-fluoro-benzylamino-pyridine. The basic molecule used for synthesis of flupirtine was 2, 6-dichoro 3-nitropyridine. It was first synthesized in 1980s in Germany and was marketed by Degussa Pharma. Flupirtine is a centrally acting, non-opioid analgesic that is available in a number of European countries for the treatment of a variety of pain states. The therapeutic benefits seen with flupirtine relate to its unique pharmacological properties. Flupirtine displays indirect NDMA receptor antagonism via activation of potassium channels and is the first representative of a pharmacological class denoted the 'selective neuronal potassium channel openers'. The generation of the M-current is facilitated by flupirtine via the opening of neuronal Kv7 potassium channels. The opening of these channels inhibits exaggerated neuronal action potential generation and controls neuronal excitability. Neuronal hyperexcitability is a physiological component of many pain states such as chronic pain, migraine and neurogenic pain.

Zimeldine was one of the first selective serotonin reuptake inhibitors to be marketed as an antidepressant under the brand names Zimeldine, Normud, and Zelmid. Zimelidine was developed in the late 1970s and early 1980s by Arvid Carlsson, who was then working for the Swedish company Astra AB. While zimelidine had a very favorable safety profile, within a year and a half of its introduction, rare case reports of Guillain–Barré syndrome emerged that appeared to be caused by the drug, prompting its withdrawl from the market.

Alizapride is a dopamine antagonist with prokinetic and antiemetic effects used in the treatment of nausea and vomiting, including postoperative nausea and vomiting. The anti-emetic action of Alizapride is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone (CTZ) in the central nervous system (CNS)—this action prevents nausea and vomiting triggered by most stimuli. Structurally similar to metoclopramide and, therefore, shares similar other attributes related to emesis and prokinetics.

Lomerizine (INN) (also known as KB-2796) is a diphenylpiperazine class L-type and T-type calcium channel blocker with relatively selective CNS effects. Voltage dependent L-type Ca2+ channels play an important role Ca2+ influx. L-type calcium currents typically require a strong depolarization for activation and are long-lasting. The common pharmacological profile of L-type channels is determined by the α1 subunit, which forms the Ca2+ selective. Lomerizine was developed as a potential agent for the selective improvement of the ocular or cerebrovascular circulation with minimal adverse cardiovascular effects, and it is used as an anti- migraine drug. Lomerizine selectively relaxes smooth muscle cells by inhibiting L-type Ca2+ influx, thereby reducing tone and increasing blood flow in cerebral vessels. Lomerizine also shows neuroprotective effects against secondary degeneration resulting from injury in retinal ganglion cells. While some calcium-channel blockers, such as flunarizine, act on the dopaminergic system, lomerizine is ineffective in vivo at inhibiting the release of dopamine. However, it has been observed to weakly inhibit the binding of [3H]spiperone to D2 dopamine receptors in vitro. While researchers are unsure of the reason for this difference, one hypothesis is that the doses administered cannot reach a high enough concentration in the brain to affect D2 receptors.