The roots are taken as a vermifuge and leaf juice, softened in oil, are applied to treat ulcers, parasitic skin infections or fever.

The plant is used for pain relief, and in the Indian Ocean islands, a decoction of the leaves is used to bath children with eczema.

The active compound (quisqualic acid) resembles the action of the anthelmintic α-santonin, so in some countries the seeds of the plants are used to substitute for the drug.

[12] The quisqualic acid can be now commercially synthesized, and it functions as an antagonist for its receptor, found in the mammalian central nervous system.

Amine group of serine has to be protected, so di-tert-butyldicarbonate in isopropanol and aqueous sodium hydroxide was added, at room temperature.

T-Boc protected serine was treated with one equivalent of isobutyl chloroformate and N-methylmorpholine in dry THF, resulting in mixed anhydride.

The hydroxamate proceeds to be converted into β – lactam, which was hydrolyzed to the hydroxylamino acid (77) by treatment with one equivalent of sodium hydroxide.

[citation needed] As mentioned, binding of quisqualic acid to these receptors leads to an influx of calcium and sodium ions into the neurons, which triggers downstream signaling cascades.

Calcium signaling involves protein effectors such as kinases (CaMK, MAPK/ERKs), CREB-transcription factor and various phosphatases.

[19] A greater dose of quisqualic acid over activates these receptors that can induce seizures, due to prolonged action potentials firing the neurons.

Like Glutamate, quisqualic acid binds to this receptor and shows even a higher potency, mainly for mGlu1 and mGlu5 and exert its effects through a complex second messenger system.

[23] Activation of group 1 mGluRs are implicated in synaptic plasticity and contribute to both neurotoxicity and neuroprotection such as protection of the retina against NMDA toxicity, mentioned above.

Quisqualic acid is an excitatory amino acid (EAA) and a potent agonist of metabotropic glutamate receptors, where evidence shows that activation of these receptors may cause a long lasting sensitization of neurons to depolarization, a phenomenon called the “Quis effect ”.

[17] Since then, its main use in research has been as template for excitotoxic models of spinal cord injury (SCI) studies.

When injected into the spinal cord, quisqualic acid can cause excessive activation of glutamate receptors, leading to neuronal damage and loss.

[29] This excitotoxic model has been used to study the mechanisms of SCI and to develop potential treatments for related conditions.

Several studies have demonstrated experimentally the similarity between the pathology and symptoms of SCI induced by quisqualic acid injections and those observed in clinical spinal cord injuries.

However, even though the bioavailability is not well established, studies in rats suggest that age may play a role in the presence of administered quisqualic acid effects.

The ADME (absorption, distribution, metabolism and excretion) process has been studied by means of various animal models in the laboratory.

Distribution: knowing the receptors it binds to, it can be readily predicted where the acid is present such as: hippocampus, basal ganglia, olfactory regions.

It is worth mentioning that the pharmacokinetics of quisqualic acid has not been extensively studied and there is sparse information available on its ADME process.