Benexate is an active ingredient of benexate.CD or benexate hydrochloride betadex, a beta-cyclodextrin complex. Benexate was approved for the treatment of Gastric Ulcer in Japan. The terapeuthic effect of benexate is associated with promotion of prostaglandin synthesis, inhibition of acid secretion and increase in mucosal blood flow.

Linsidomine (SIN-1, chemically 3-morpholinosydnonimin), is a vasodilator and antianginal drug. It is the direct hepatic metabolite of molsidomine. The dosage recommended by its manufacturer for its initial purpose, coronary angiography, is 0.4-1 mg. Contrary to molsidomine, which is widely used as an antianginal drug, linsidomine is used only for coronary angiography. The plasma half-life of Linsidomine is about 1 hour. Linsidomine is nonenzymatically metabolized to SIN-1A which spontaneously releases NO. NO, probably released directly from nonadrenergic, noncholinergic (NANC) nerves in the penis, is believed to cause smooth muscle relaxation by stimulating the soluble form of guanylate cyclase leading to an increase of intracellular cyclic guanosine 3',5' monophosphate (cGMP) with subsequent smooth muscle relaxation. Linsidomine also hyperpolarizes the cell membrane, making the smooth muscle less susceptible to adrenergic stimulation. NO further interacts with platelets when released intraluminally causing an increase in cGMP that decreases platelet aggregation and adhesion

Mifamurtide (liposomal muramyl tripeptide phosphatidylethanolamine; trade name Mepact) is an immunomodulator with antitumor effects that appear to be mediated via activation of monocytes and macrophages. After intravenous administration, mifamurtide is selectively phagocytosed by monocytes and macrophages. Cytosolic Mifamurtide specifically interacts with nucleotide-binding oligomerization domain 2 (NOD2) receptor that induces nuclear factor (NF)-kB activation and is implicated in innate immune defense. Activation of monocyte-mediated tumoricidal function was observed following in vivo treatment with mifamurtide in phase I/II clinical trials. Intravenous administration of mifamurtide inhibited tumor growth and increased survival in rodent models of lung and liver metastasis. In a large, randomized, open-label, multicenter, phase III trial, the addition of adjuvant (postoperative) mifamurtide to three- or four-drug combination chemotherapy (doxorubicin, cisplatin, and high-dose methotrexate with, or without, ifosfamide) was associated with a statistically significant improvement in overall survival in patients with newly diagnosed, high-grade, non-metastatic, resectable osteosarcoma. The pattern of outcome was generally similar in a small cohort of patients with metastatic disease who were enrolled in this trial. Mifamurtide is generally well tolerated; adverse events attributed to administration of the drug include chills, fever, headache, nausea, and myalgias. In the EU, mifamurtide is indicated in children, adolescents, and young adults for the treatment of high-grade, resectable, non-metastatic osteosarcoma after macroscopically complete surgical resection; it is administered by intravenous infusion in conjunction with postoperative multiagent chemotherapy. In the US, mifamurtide is currently an investigational agent that holds orphan drug status for the treatment of osteosarcoma.

Calcium dobesilate (brand name Doxium) is a veno-tonic drug, which is widely prescribed in more than 60 countries from Europe, Latin America, Asia and the Middle East for three main indications: chronic venous disease, diabetic retinopathy and the symptoms of haemorrhoidal attack. This drugs also in the phase III of clinical trial is an effective adjuvant therapy, with an absence of significant side-effects, in patients with venous ulcers and stasis dermatitis. It was suggested, that the inhibitory effect of calcium dobesilate on platelet function is mediated through the cyclic AMP pathway, and probably through activation of adenyl cyclase.

Pyritinol is a semi natural analogue of water soluble vitamin B6. Pyritinol was synthetized way back in 1961 by Merck Laboratories. After years of research, it entered the market in the 1970s, where it was used for clinical applications – including treating stroke patients and those with Alzheimer’s. Since the 1990s, it has been sold as a nootropic dietary supplement in the United States and many other parts of the world. Pyritinol, unlike many other nootropics, has been approved for use as a medical treatment in countries around the world. Doctors in many European countries use Pyritinol to treat patients with chronic degenerative brain disorders – like dementia. Countries where Pyritinol is an approved treatment include Austria, Germany, France, Greece, Italy, and Portugal. France has approved the use of Pyritinol – but only as a treatment for rheumatoid arthritis. Pyritinol is not currently licensed for use in the United Kingdom, but in most other countries, it’s available online or through drug stores as an over the counter substance. Pyritinol is marketed under the brand names Encephabol, Encefabol and Cerbon 6. One of the known mechanisms of action of Pyritinol involves increasing choline uptake into your neurons and thereby increasing acetylcholine levels. Pyritinol is also a great effective precursor to dopamine, which is one of the neurotransmitter mood-boosters in the brain. Pyritinol has better conversion into the neurochemical. This drug increases dopamine, which can keep the brain from anxiety because a lower dopamine level is connected to mood disorders and depression.

Obidoxime is an antidote for organophosphorous nerve agent poisoning including chlorosarin, cyclosarin (GF), R-33 (VR), R-VX, sarin (GB), tabun (GA), VX, chlorosoman, soman (GD), and organophosphorous pesticides. It acts as an acetylcholinesterase (AChE) reactivator. In combination with atropine obidoxime can be used to treat super toxic organophosphate poisoning by relieving the symptoms of skeletal neuromuscular blocking that occurs during a cholinergic crisis.

Budipine is an antiparkinsonian drug, which was developed by Byk Gulden (now Takeda) for the treatment of Parkinson's disease. The drug has multiple mechanisms of action: it was found to interfere with dopamine biosynthesis, mainly by inhibiting MAO-B enzyme and stimulating aromatic L-amino acid decarboxylase. Also the drug inhibits the dopamine re-uptake and has weak affinity to NMDA and muscarinic receptors. Budipine passes the blood-brain barrier, is metabolized by hydroxylation, and is excreted by both in urine and feces within 24 h.

METHYLMETHIONINE (S-Methionine methyl sulfonium, SMMS) chloride is a derivative of methionine metabolism in some plants. Methylmethionine has therapeutic effects on gastrointestinal ulceration potentially via its ability to promote dermal fibroblast migration and growth. The natural derivative Methylmethionine is biosynthesized from L-methionine which is first converted to S-adenosylmethionine. The subsequent conversion, involving replacement of the adenosyl group by a methyl group is catalyzed by the enzyme methionine S-methyltransferase. Methylmethionine is particularly abundant in plants, being more abundant than methionine. S-Methylmethionine is sometimes referred to as vitamin U, but it is not considered a true vitamin. The term was coined in 1950 by Garnett Cheney for uncharacterized anti-ulcerogenic factors in raw cabbage juice that may help speed healing of peptic ulcers.

Lobenzarit is an immunomodulator and antioxidative agent, which has been used successfully in Japan for the treatment of rheumatoid arthritis. Lobenzarit is a scavenger of oxygen-free radicals such as hydroxyl radicals, superoxide, peroxyl and singlet oxygen. Side effects of this medicine are: decreased/considerably increased urinary volume, bloody urine, frequent urination.

Scientists at Parke-Davis first synthesized Pramiracetam (brand name Pramistar) in the late 1970’s. It was first tested with Alzheimer’s patients. Seeing mixed results, the company tried it with major depressive disorder and licensed it as an orphan drug to Menarini. Pramiracetam is a central nervous system stimulant and nootropic agent belonging to the racetam family of drugs. Pramistar is used for the treatment of concentration and memory disturbances caused by the degeneration of brain cells or to diseases of the blood vessels supplying the brain, conditions that arise both in elderly patients (aged over 65 years). By stimulating choline uptake, pramiracetam indirectly modulates the release of acetylcholine and stimulates increased activity in the hippocampus. Because this part of the brain is absolutely crucial to the memory function, the general stimulation that pramiracetam creates can improve both the formation of new memories and the retention of reference or long-term memories. The increased activity in the hippocampus also increases cerebral blood flow, which enhances alertness and improves cognitive abilities in general. Pramiracetam may have other mechanisms of action as well. Researchers have hypothesized that in addition to its action in the brain, pramiracetam acts outside the brain in peripheral sites that rely on the adrenal glands. Animal studies suggest that pramiracetam may also increase or restore brain membrane fluidity, which facilitates cell signaling. Unlike many other racetam class nootropics, pramiracetam does not appear to strongly alter either wakefulness or emotional states. This can be explained by pramiracetam’s very limited influence on the production and release of serotonin, GABA and dopamine, the neurotransmitters that have the greatest effect on mood and anxiety levels.