SELENATE ION is a compound containing an oxoanion with selenium in its highest oxidation state of VI. Selenates are analogous to sulfates and have similar chemistry, but unlike sulfate, selenate is a good oxidizer. Selenate is the form required by organisms that need selenium as a micronutrient. These organisms have the ability to acquire, metabolize and excrete selenium. The level at which selenium becomes toxic varies from species to species and is related to other environmental factors like pH and alkalinity that influence the concentration of selenite over selenate. Selenate and other forms of selenium are highest in areas where ancient seas have evaporated. These areas are enriched in selenium and over millennia, biologic adaptation has occurred.

Doconexent (Docosahexaenoic acid, DHA) is an omega-3 fatty acid that is a primary structural component of the human brain, cerebral cortex, skin, and retina. DHA is widely used as a food supplement, and is beleived to support healthy brain development in young childred, prevent cardiovascular disease and cognitive decline during Alzheimer's disease. Most of these claims, however, were not supported by clinical trials. DHA spray is used as a tanner.

Erythorbic acid, an epimer of L-ascorbic acid, is used in the United States as a food additive. It was studied, that erythorbic acid enhanced of iron absorption and could play a major role in enhancing iron bioavailability from mixed diets that include foods preserved with erythorbic acid. In addition, was investigated if the erythorbic acid could influence on the metabolism of vitamin C in young women, and obtained results showed, that prolonged ingestion of erythorbic acid had no effect on vitamin C uptake or clearance from the body.

Hemin (trade name Panhematin) is a protoporphyrin IX containing a ferric iron ion (heme B) with a chloride ligand, which is is indicated for the amelioration of recurrent attacks of acute intermittent porphyria temporally related to the menstrual cycle in susceptible women. Manifestations such as pain, hypertension, tachycardia, abnormal mental status and mild to progressive neurologic signs may be controlled in selected patients with this disorder. the therapy for the acute porphyrias is not curative. Heme acts to limit the hepatic and/or marrow synthesis of porphyrin. This action is likely due to the inhibition of δ-aminolevulinic acid synthetase, the enzyme which limits the rate of the porphyrin/heme biosynthetic pathway. The exact mechanism by which hematin produces symptomatic improvement in patients with acute episodes of the hepatic porphyrias has not been elucidated.

The iodate ion is an oxoanion of iodine bearing a negative charge and containing three oxygen atoms. Because it is more stable than iodide, most health authorities preferentially recommend iodate as an additive to salt for correcting iodine deficiency. In humans and rats, oral bioavailability of iodine from iodate is virtually equivalent to that from iodide. When given intravenously to rats, or when added to whole blood or tissue homogenates in vitro or to foodstuff, iodate is quantitatively reduced to iodide by nonenzymatic reactions, and thus becomes available to the body as iodide. Therefore, except perhaps for the gastrointestinal mucosa, exposure of tissues to iodate might be minimal. At much higher doses given intravenously (i.e., above 10 mg/kg), iodate is highly toxic to the retina. Ocular toxicity in humans has occurred only after exposure to doses of 600 to 1,200 mg per individual. Oral exposures of several animal species to high doses, exceeding the human intake from fortified salt by orders of magnitude, pointed to corrosive effects in the gastrointestinal tract, hemolysis, nephrotoxicity, and hepatic injury.

Magnesium isoglycyrrhizinate is a magnesium salt form of isoglycyrrhizinate, a derivative of glycyrrhizic acid extracted from the roots of the plant Glycyrrhiza glabra. Magnesium isoglycyrrhizinate has anti-inflammatory, antioxidant and hepatoprotective activities. The drug is believed to be a free radical scavenger and to modulate the activity of hepatic enzymes. Magnesium isoglycyrrhizinate was investigated in clinical trials to restore hepatic impairments caused by chemotherapy drugs and as a treatment of chronic liver diseases.

Xaliproden is an orally active 5HT1-A receptor antagonist that was being developed by Sanofi. It has been evaluated for the treatment of Alzheimer's disease and amyotrophic lateral sclerosis (ALS), and protection against peripheral neurotoxicity associated with certain cancer chemotherapies. Two large, 18-month, clinical trials of xaliproden (monotherapy or adjunctive therapy, respectively) in patients with mild to moderate AD (MMSE, 16–26, inclusive) were completed in 2007. Failure to demonstrate sufficient efficacy in both trials resulted in cancelation of the xaliproden development program for AD in September 2007.

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.

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.

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.