[3] Neurokinin A is ubiquitous in both the central and peripheral mammalian nervous systems, and seems to be involved in reactions to pain and the inflammatory responses.

[2] It has various roles in the body of humans and other animals, specifically stimulation of extravascular smooth muscle, vasodilation, hypertensive action, immune system activation, and pain management.

Modified from: Sun J, Ramnath RD, Tamizhselvi R, Bhatia M."Neurokinin A engages neurokinin-1 receptor to induce NF-kappaB-dependent gene expression in murine macrophages: implications of ERK1/2 and PI 3-kinase/Akt pathways."

[5] Additionally both SP neurokinin A is found in the neurosensory system and modulates a wide range of inflammatory and tissue repairing processes [1].

In various tissues, such as the skin, the release of bioactive tachykinins by sensory nerve fibers C, that extend from the dorsal root ganglia into the epidermis, directly influence the activity of keratinocytes.

The overstimulation of the hypothalamic–pituitary–adrenal axis system and elevated secretion of corticotropin-releasing hormone from the hypothalamus, have been studied in many clinical manifestations of pathological depression.

[5] Studies have shown that stress-induced activation of the noradrenergic prefrontal lobe system may be under the control of both endogenously released corticotropin-releasing hormone and SP and neurokinin A.

[7] Inflammatory responses within the central nervous system (CNS) are often the result of traumatic injury or exposure to infectious agents.

There is significant evidence to indicate that tachykinins are a major component of the neural inflammatory response at peripheral tissues as well as the CNS.

[8] The ability to regulate tachykinin secretion represents an important mechanism for designing potentially useful drugs to treat inflammation.

The diverse responses that are triggered by locally released tachykinins produce beneficial effects such as modulation of ganglion transmission.

[5] Neurokinin A binds to the G-protein coupled receptor ultimately increasing the release of inositol-phosphate and calcium second messengers.

[17] MEN 11420 has been demonstrated to be a potent, selective and competitive antagonist of tachykinin NK2 receptors, both in animal and human models.

In vivo animal models, MEN 11420 produces an effective and long-lasting blockade of the NK2 receptors expressed in the smooth muscle of the intestinal, genito-urinary and respiratory tract.

[8] A number of approaches have been utilized to study the role that neurokinin A plays in the manifestation and continuation of human affective disorders.

Tachykinin ligands have been extensively studied and determined to be functionally linked to the control of affective phenotypes in a complex physiological manner.

[8] Experimentally when substance P is injected into the rat hippocampus, it significantly lowers the initiation threshold for seizures induced in a dose-dependent manner.