Substance P: Neuropeptide Research Guide

In 1931, two scientists in a London laboratory discovered a mysterious powder that caused intestinal tissue to contract. They called it "substance P"—the "P" standing for the powdered preparation they'd isolated. Nearly a century later, this pioneering neuropeptide remains one of the most studied molecules in neuroscience, with roles spanning pain transmission, inflammation, mood regulation, and cancer biology.

Substance P belongs to the tachykinin family of neuropeptides and acts primarily through the neurokinin-1 (NK1) receptor. Its discovery predates nearly all other neuropeptides, making it a foundational molecule in understanding how the nervous and immune systems communicate. Today, drugs that block substance P's receptor treat millions of chemotherapy patients, and research continues to explore its therapeutic potential for conditions ranging from chronic pain to depression.

This guide translates the science of substance P into clear, actionable information for researchers, clinicians, and anyone seeking to understand this versatile signaling molecule.

Quick Facts
What Is Substance P?
Mechanisms of Action
Clinical Relevance
- NK1 Receptor Antagonists
- FDA-Approved Applications
Research Applications
Safety and Considerations
Frequently Asked Questions
Bottom Line
References

Quick Facts

Property	Details
Full Name	Substance P
Type	Tachykinin neuropeptide
Amino Acids	11 (undecapeptide)
Sequence	Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH₂ (RPKPQQFFGLM-NH₂)
Molecular Weight	1,348 Da
Primary Receptor	Neurokinin-1 receptor (NK1R)
Gene	TAC1 (tachykinin precursor 1)
Discovered	1931 (Ulf von Euler and John H. Gaddum)
Structure Determined	1971 (Chang, Leeman & Niall)

What Is Substance P?

Substance P is an 11-amino-acid neuropeptide that functions as both a neurotransmitter and neuromodulator throughout the nervous system. As the founding member of the tachykinin family, it was the first neuropeptide discovered that could trigger rapid contraction of intestinal smooth muscle—a property reflected in the "tachy-" (rapid) prefix.

The peptide consists of the sequence Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met with an amide group at the C-terminus. This structural arrangement creates an amphiphilic molecule: positively charged residues cluster at the N-terminus, while hydrophobic residues occupy the C-terminus. All tachykinins share a conserved carboxy-terminal sequence (Phe-X-Gly-Leu-Met-NH₂, where X is a hydrophobic amino acid) that enables receptor binding and activation.

The TAC1 gene encodes substance P along with related peptides including neurokinin A (NKA), neuropeptide K (NPK), and neuropeptide gamma through alternate processing. This single gene thus generates multiple bioactive peptides with overlapping but distinct functions.

Substance P is synthesized primarily in neurons but also produced by immune cells including macrophages, eosinophils, lymphocytes, and dendritic cells. This dual origin allows substance P to mediate interactions between the nervous and immune systems—a property that makes it important in conditions ranging from arthritis to inflammatory bowel disease.

The discovery story began in 1930 when Ulf von Euler, working as a postgraduate student in H.H. Dale's laboratory in London, tested an intestinal extract for biological activity. The extract produced powerful contractions in isolated rabbit intestine that weren't blocked by atropine and couldn't be explained by known compounds. Dale suggested collaboration with J.H. Gaddum, and after systematic investigation, they confirmed the presence of a novel active agent. They purified it to a powder form, giving rise to the name "substance P." The complete amino acid sequence wouldn't be determined for another 40 years.

Mechanisms of Action

NK1 Receptor Binding and Signaling

Substance P exerts most of its biological effects through the neurokinin-1 receptor (NK1R), a G protein-coupled receptor (GPCR) consisting of seven transmembrane helical segments. While substance P can also bind NK2 and NK3 receptors, NK1R represents its primary and highest-affinity target.

The binding process involves amino acid residues in the receptor's extracellular loops and transmembrane regions. When substance P binds NK1R, the receptor undergoes rapid internalization via clathrin-dependent endocytosis. The substance P-NK1R complex travels to acidified endosomes where it dissociates, after which the NK1R recycles quickly back to the plasma membrane—a process that allows sustained or repeated signaling.

Activation of NK1R triggers multiple intracellular signaling cascades. The major pathways include:

Phosphoinositide hydrolysis leading to formation of inositol trisphosphate (IP3) and diacylglycerol (DAG)
Calcium mobilization through IP3-mediated release from intracellular stores
Cyclic AMP (cAMP) production through adenylyl cyclase activation
MAPK pathway activation involving mitogen-activated protein kinases

These signaling events occur in a context-dependent manner, with different cell types and tissues exhibiting distinct response patterns. The magnitude and duration of substance P release correlates with stimulus intensity and frequency—more potent or frequent stimuli allow substance P to diffuse farther from release sites, activating approximately 3- to 5-times more NK1R-expressing neurons.

Pain Transmission

Substance P plays a well-established role in nociception, the sensory process that detects and transmits pain signals. The peptide is expressed in dorsal root ganglion (DRG) neurons—the primary sensory neurons that detect painful stimuli in the periphery and transmit signals to the central nervous system.

When tissue damage or noxious stimuli activate sensory nerve endings, substance P is released from the central terminals of these neurons in the dorsal horn of the spinal cord. There, substance P acts on NK1 receptors located on second-order neurons that relay pain signals to higher brain centers. Substance P often coexists with glutamate, the primary excitatory neurotransmitter, creating a coordinated pain signaling system.

The observation that substance P concentrates in the dorsal (sensory) horn but not the ventral (motor) horn of the spinal cord provided early evidence for its sensory function. Experimental studies showed that noxious stimuli trigger substance P release proportional to stimulus intensity, and that NK1R activation facilitates pain signal transmission.

However, the clinical picture proved more complex than animal models suggested. Despite strong preclinical evidence, NK1 receptor antagonists have shown disappointing results in pain clinical trials, with no clear analgesic efficacy demonstrated across various pain conditions. This disconnect between animal studies and human trials remains an active area of investigation and suggests that pain processing in humans involves redundant pathways that can compensate when substance P signaling is blocked.

Elevated cerebrospinal fluid (CSF) levels of substance P have been documented in fibromyalgia, with concentrations two to three times higher than in healthy controls. This finding supports a role for central sensitization—a state of heightened pain sensitivity that characterizes fibromyalgia and many chronic pain syndromes.

Neurogenic Inflammation

Substance P mediates neurogenic inflammation—a local inflammatory response triggered by sensory nerve activation. When peripheral terminals of sensory neurons are stimulated by injury, infection, or certain irritants, they release substance P directly into surrounding tissues.

Released substance P triggers several pro-inflammatory events:

Vasodilation: Substance P causes blood vessels to widen, increasing blood flow to affected areas. This effect depends on nitric oxide release from endothelial cells.
Increased vascular permeability: Blood vessel walls become more permeable, allowing plasma proteins and immune cells to enter tissues more easily.
Leukocyte recruitment: Substance P induces expression of adhesion molecules on endothelial cells, facilitating attachment and migration of white blood cells to sites of injury or infection.
Immune cell activation: Substance P acts directly on resident and infiltrating immune cells to boost their inflammatory functions.

These mechanisms explain why blocking substance P has shown therapeutic benefit in conditions driven by neurogenic inflammation, including certain types of inflammatory bowel disease, where substance P levels correlate with disease activity in the affected intestinal tissue.

Conditions associated with neurogenic inflammation include eczema, psoriasis, rosacea, asthma, migraine, and rheumatoid arthritis, where substance P levels are elevated in synovial fluid and serum and correlate with disease severity.

Emesis (Nausea and Vomiting)

Substance P plays a dominant role in triggering nausea and vomiting, particularly the delayed phase that occurs 2-5 days after chemotherapy administration. This mechanism has proven clinically important, as blocking substance P prevents chemotherapy-induced nausea and vomiting (CINV) in millions of patients annually.

The emetic pathway involves both peripheral and central components:

Peripheral pathway: Chemotherapy drugs damage enterochromaffin cells in the gastrointestinal tract, triggering release of serotonin (5-HT). Serotonin activates 5-HT3 receptors on vagal afferent nerve terminals, which then release substance P. NK1 receptors are located on these vagal afferents, suggesting that locally released substance P may contribute to acute CINV during the first 24 hours after chemotherapy.

Central pathway: Chemotherapy triggers substance P release from neurons in the brainstem, particularly in the nucleus tractus solitarius (NTS) and area postrema—brain regions that coordinate the vomiting reflex. Released substance P binds to NK1 receptors in these vomiting centers, initiating the emetic response. This central mechanism predominantly drives delayed CINV.

The distinction between acute and delayed phases is clinically significant. While 5-HT3 receptor antagonists (like ondansetron) effectively prevent acute CINV by blocking serotonin signaling, NK1 receptor antagonists are required to prevent the substance P-mediated delayed phase.

Clinical Relevance

NK1 Receptor Antagonists

The discovery that substance P mediates nausea and vomiting led to development of NK1 receptor antagonists—drugs designed to block the neurokinin-1 receptor and prevent substance P signaling. These represent a major therapeutic advance, particularly in oncology supportive care.

NK1 antagonists are highly selective compounds that can cross the blood-brain barrier to occupy NK1 receptors in the central nervous system. This property is important because the delayed phase of CINV originates primarily from central substance P release in brainstem vomiting centers.

Key characteristics of NK1 antagonists include:

High selectivity: Modern NK1 antagonists show minimal binding to other neurokinin receptors (NK2, NK3) or other receptor systems
Blood-brain barrier penetration: PET studies demonstrate that therapeutic doses achieve substantial NK1R occupancy in the human brain
Long half-life: Most NK1 antagonists have half-lives of 9-13 hours, providing sustained receptor blockade

The class includes several FDA-approved drugs (see below) and investigational compounds being studied for additional indications beyond antiemetic use.

FDA-Approved Applications

Aprepitant (Emend) became the first FDA-approved NK1 receptor antagonist in 2003 for prevention of chemotherapy-induced nausea and vomiting. Available in oral formulation, aprepitant is given before chemotherapy and for several days afterward to prevent both acute and delayed CINV.

Key properties:

Oral bioavailability: 60-65%
Protein binding: >95%
Half-life: 9-13 hours
Metabolism: Primarily via CYP3A4

Aprepitant shows approximately 3,000-fold selectivity for NK1R over NK3R and 45,000-fold selectivity over NK2R. Importantly, it has no affinity for serotonin, dopamine, or corticosteroid receptors—the other main targets of antiemetic drugs—allowing combination therapy without receptor competition.

Fosaprepitant is an intravenous prodrug of aprepitant, offering the same therapeutic effects with the convenience of single-dose IV administration.

Rolapitant (Varubi) and netupitant (in combination with palonosetron as Akynzeo) represent second-generation NK1 antagonists with similar antiemetic efficacy but different pharmacokinetic profiles and drug interaction patterns.

These drugs are typically combined with 5-HT3 receptor antagonists and corticosteroids in guideline-recommended regimens for preventing CINV in patients receiving moderately or highly emetogenic chemotherapy. The addition of NK1 antagonists to standard antiemetic regimens has substantially reduced delayed nausea and vomiting, improving quality of life for cancer patients.

NK1 antagonists are also approved for prevention of postoperative nausea and vomiting (PONV), though this represents a less common clinical use.

Research Applications

Pain Research

Substance P has been studied extensively in pain research, with investigations spanning acute nociception, chronic pain conditions, and central sensitization. Key research areas include:

Acute pain mechanisms: Studies examining how substance P release and NK1R activation in the spinal dorsal horn contribute to normal pain signaling. Research has established that substance P acts synergistically with glutamate to facilitate pain transmission and that NK1R-expressing neurons in the dorsal horn project to higher brain centers involved in pain perception.

Chronic pain conditions: Elevated CSF substance P levels have been documented in fibromyalgia, with two- to three-fold increases compared to healthy controls. However, substance P's role in pain chronicity is complex, and NK1 antagonists have failed to demonstrate analgesic efficacy in multiple clinical trials despite compelling preclinical data.

Central sensitization: The state of heightened nervous system reactivity that characterizes many chronic pain conditions. Excess substance P in the CNS may contribute to lowered pain thresholds and amplified pain responses seen in conditions like fibromyalgia, irritable bowel syndrome, and temporomandibular disorders.

Opioid interactions: Research exploring how substance P interacts with opioid systems, including whether chronic opioid use alters substance P signaling and whether this contributes to opioid-induced hyperalgesia.

Despite substantial preclinical evidence linking substance P to pain, the clinical failure of NK1 antagonists as analgesics remains a significant disappointment. This disconnect has prompted researchers to reconsider assumptions about pain mechanisms derived from animal models and to recognize that human pain processing involves redundant pathways that may compensate when single targets are blocked.

Similar research challenges exist with other neuropeptides like Selank and Semax, where promising preclinical findings don't always translate directly to clinical efficacy.

Mood and Anxiety Disorders

Substance P and NK1 receptors are distributed throughout brain regions involved in emotion regulation, including the hypothalamus, amygdala, periaqueductal gray, lateral septum, nucleus accumbens, and locus coeruleus. This distribution pattern, combined with evidence that emotional stressors trigger substance P release in these areas, suggests a role in mood and anxiety disorders.

Depression: CSF substance P concentrations are elevated 51% in patients with major depressive disorder compared to healthy controls. Substance P is often colocalized with monoamine neurotransmitters (serotonin, norepinephrine, dopamine) in brain regions implicated in depression, suggesting potential interactions with classical antidepressant mechanisms.

A landmark study with MK-869, a selective NK1 antagonist, showed significant antidepressant activity versus placebo in a double-blind trial, with fewer sexual side effects than the SSRI comparator paroxetine. This finding generated substantial excitement about NK1 antagonists as a novel antidepressant class. However, a subsequent phase 3 trial failed to replicate these effects, and clinical development of NK1 antagonists for depression was largely abandoned.

Post-Traumatic Stress Disorder: CSF substance P levels are elevated in PTSD patients, with marked increases (up to 169% above baseline) observed when PTSD symptoms are triggered by traumatic reminders. These findings implicate CNS substance P release in acute PTSD symptoms and suggest a role for chronic substance P dysregulation in PTSD pathophysiology.

Anxiety disorders: Research in animal models shows that emotional stressors produce pronounced and long-lasting increases (up to 150%) in substance P release in the medial amygdala—a brain region involved in fear and anxiety responses. Clinical trials with NK1 antagonists have shown some benefit in anxiety symptoms, though results have been mixed.

The pattern emerging from mood and anxiety research mirrors that seen in pain: compelling biological evidence for substance P involvement, but inconsistent translation to clinical efficacy when NK1 receptors are blocked pharmacologically. This may reflect compensatory mechanisms, inadequate receptor occupancy, or fundamental differences between animal models and human psychiatric conditions.

Inflammatory Conditions

Substance P's role in neurogenic inflammation has made it a target of interest for multiple inflammatory conditions. Research has explored both the basic mechanisms by which substance P promotes inflammation and potential therapeutic applications of blocking these effects.

Inflammatory bowel disease: Elevated substance P levels and upregulated NK1R expression have been reported in the intestinal tissue of patients with Crohn's disease and ulcerative colitis, with levels correlating with disease activity. Substance P released from enteric neurons and immune cells promotes intestinal inflammation through multiple mechanisms including increased vascular permeability, immune cell recruitment, and direct activation of inflammatory pathways in intestinal epithelial cells.

Rheumatoid arthritis: Substance P concentrations are elevated in synovial fluid and serum of RA patients, and NK1R mRNA is upregulated in synoviocytes. Early research found that blocking substance P reduced the severity of experimental arthritis in animal models, suggesting therapeutic potential.

Asthma and respiratory inflammation: Substance P is released from sensory nerve endings in airways in response to irritants and allergens, contributing to bronchospasm, mucus secretion, and airway inflammation. NK1 antagonists have been investigated for potential benefit in asthma, though clinical development has been limited.

Dermatologic conditions: Neurogenic inflammation contributes to eczema, psoriasis, and rosacea pathophysiology. Substance P released from cutaneous sensory nerves triggers mast cell degranulation, vasodilation, and recruitment of inflammatory cells to skin lesions.

Research with anti-inflammatory peptides like KPV has shown that targeting inflammatory pathways at multiple levels may offer therapeutic advantages over blocking single mediators like substance P.

Cancer Research

An emerging area of substance P research explores its role in cancer biology and the potential therapeutic application of NK1 receptor antagonists as anticancer agents. This represents a dramatic expansion from the peptide's original role as an antiemetic.

Substance P in tumor biology: Research has found that substance P and NK1R are overexpressed in a wide variety of cancers, including leukemia, glioblastoma, astrocytoma, neuroblastoma, melanoma, and cancers of the breast, ovary, prostate, lung, pancreas, and thyroid. In these contexts, substance P acts as a mitogen (growth-promoting factor) that affects tumor cell proliferation, survival, migration, and metastasis.

Mechanisms: Substance P-NK1R signaling in cancer cells activates pathways involved in cell division, resistance to apoptosis (programmed cell death), angiogenesis (new blood vessel formation), and metastatic spread. NK1R activation can also promote drug resistance through various mechanisms.

NK1 antagonists as anticancer agents: Preclinical studies show that NK1 antagonists exert antitumor, antiproliferative, anti-survival, antiangiogenic, and antimetastatic effects. These drugs promote tumor cell death through apoptosis in a concentration-dependent manner, with effects observed across multiple cancer types.

Aprepitant repurposing: The FDA-approved antiemetic aprepitant has shown promise in cancer research beyond its standard indication. Studies demonstrate that aprepitant can sensitize tumor cells to conventional chemotherapy drugs including arsenic trioxide, vincristine, etoposide, and doxorubicin. This is particularly significant given that drug resistance accounts for over 90% of deaths in patients receiving chemotherapy or targeted anticancer treatments.

Clinical development: While preclinical data supporting NK1 antagonists as anticancer agents is substantial, clinical trials evaluating these drugs for cancer treatment remain limited. The safety profile established through years of antiemetic use positions aprepitant and related compounds favorably for repurposing trials.

This research direction illustrates how substance P's biological roles extend far beyond neurotransmission into fundamental processes like cell proliferation and survival. Just as oxytocin's functions extend beyond social bonding to include cancer-relevant pathways, substance P appears to serve multiple distinct functions depending on cellular context.

Safety and Considerations

Substance P itself is not administered therapeutically, so safety considerations focus primarily on drugs that block the NK1 receptor.

NK1 receptor antagonist safety: Aprepitant and related NK1 antagonists have been used in millions of patients since FDA approval in 2003, establishing an extensive safety database. Common side effects are generally mild and include tiredness, decreased appetite, diarrhea, abdominal pain, hiccups, itching, and transient changes in blood pressure.

Drug interactions: Aprepitant is metabolized primarily by CYP3A4 and can affect levels of other drugs metabolized by this enzyme system. This requires attention to potential interactions with chemotherapy drugs, immunosuppressants, anticoagulants, and other medications with narrow therapeutic windows. Rolapitant and other second-generation NK1 antagonists have different CYP interaction profiles that may offer advantages in specific clinical situations.

Pregnancy and lactation: NK1 antagonists are generally avoided during pregnancy unless clearly needed, as animal studies have shown potential fetal effects at high doses. Whether substance P itself or NK1R blockade affects fetal development in humans remains incompletely characterized.

Research context: In research settings involving substance P measurement or NK1R studies, considerations include appropriate sample collection and handling for peptide stability, recognition that substance P levels can be influenced by stress and inflammation, and understanding that single-timepoint measurements may not reflect dynamic changes in substance P signaling.

Immune function: Given substance P's role in coordinating neuroimmune interactions, there is theoretical concern that chronic NK1R blockade might affect immune responses. However, clinical experience with NK1 antagonists has not revealed significant immunosuppression, though patients receiving these drugs for cancer are simultaneously receiving chemotherapy, making this difficult to assess definitively.

For researchers working with related neuropeptides like ACTH or defensins, similar considerations about neuroimmune effects and complex signaling networks apply.

Frequently Asked Questions

What does substance P do in the body?

Substance P functions as a neurotransmitter and neuromodulator with multiple roles including pain signal transmission in the spinal cord, triggering neurogenic inflammation when released from sensory nerve endings, causing nausea and vomiting when released in brainstem vomiting centers, and modulating immune cell function. Its effects depend on which tissues express NK1 receptors and the context in which substance P is released.

Why is it called substance P?

The name derives from the original 1931 discovery by Ulf von Euler and John Gaddum, who isolated the compound as a powder from equine brain and intestine. The "P" stands for the powdered preparation they used in their experiments. The complete chemical structure wasn't determined until 1971, 40 years after the initial discovery.

How does substance P relate to pain?

Substance P is released from sensory neurons in the spinal cord in response to painful stimuli and activates NK1 receptors on neurons that transmit pain signals to the brain. CSF levels are elevated in chronic pain conditions like fibromyalgia. However, despite strong evidence linking substance P to pain mechanisms, drugs that block NK1 receptors have failed to provide pain relief in clinical trials, suggesting human pain involves compensatory pathways.

What drugs block substance P?

NK1 receptor antagonists including aprepitant (Emend), fosaprepitant, rolapitant (Varubi), and netupitant (in Akynzeo) block substance P signaling by preventing the peptide from binding to its primary receptor. These drugs are FDA-approved for preventing chemotherapy-induced and postoperative nausea and vomiting. They are highly selective for NK1R and can cross the blood-brain barrier to block central substance P effects.

Does substance P cause depression?

Research shows that CSF substance P levels are 51% higher in patients with major depression compared to healthy controls, suggesting a role in depressive pathology. However, the relationship is complex. An early clinical trial showed that blocking NK1 receptors had antidepressant effects, but later trials failed to replicate this benefit, and NK1 antagonists are not used clinically for depression. Substance P may be elevated as a consequence rather than a cause of depression, or compensatory mechanisms may limit the benefit of blocking a single pathway.

Is substance P involved in inflammation?

Yes, substance P is a key mediator of neurogenic inflammation—a process where sensory nerve activation triggers local inflammatory responses. Released substance P causes vasodilation, increases vascular permeability, recruits immune cells, and directly activates inflammatory pathways. Elevated substance P levels have been found in inflammatory bowel disease, rheumatoid arthritis, and inflammatory skin conditions, with levels often correlating with disease activity.

Can substance P levels be measured?

Yes, substance P can be measured in cerebrospinal fluid (CSF), blood plasma, or tissues using immunoassay techniques like ELISA. However, measurement is primarily a research tool rather than a clinical diagnostic test. Substance P is released in response to stress and inflammation, so levels can fluctuate based on multiple factors, making single-timepoint measurements difficult to interpret clinically.

What is the relationship between substance P and cancer?

Emerging research shows that substance P and its NK1 receptor are overexpressed in many cancer types, where the peptide acts as a growth factor promoting tumor cell proliferation, survival, and metastasis. NK1 receptor antagonists like aprepitant show anticancer effects in laboratory studies and can sensitize tumor cells to chemotherapy drugs. Clinical trials exploring NK1 antagonists as cancer treatments are in early stages, representing a potential repurposing opportunity for these FDA-approved antiemetics.

Bottom Line

Substance P represents one of the most extensively studied neuropeptides in biomedical research. Discovered in 1931 and structurally characterized in 1971, this 11-amino-acid peptide has proven to be a versatile signaling molecule with roles spanning pain transmission, inflammation, emesis, mood regulation, and even cancer biology.

The clinical success of NK1 receptor antagonists as antiemetics demonstrates that blocking substance P can provide meaningful therapeutic benefit. Aprepitant and related drugs have improved quality of life for millions of chemotherapy patients by preventing nausea and vomiting—one of the most dreaded side effects of cancer treatment.

However, substance P research also illustrates how biological complexity can confound efforts to translate mechanism into therapy. Despite compelling evidence for substance P's involvement in pain and depression, NK1 antagonists have failed to provide consistent benefit in these conditions during clinical trials. This disconnect between preclinical promise and clinical reality has prompted researchers to reconsider how findings from animal models translate to human disease.

Emerging research on substance P's role in cancer biology offers a potential new direction for NK1 antagonists, with preclinical data suggesting antitumor effects and drug sensitization. Whether this translates to clinical benefit remains to be determined through ongoing trials.

For researchers and clinicians, substance P exemplifies both the power and limitations of targeting single molecules in complex biological systems. The peptide participates in multiple physiological processes, interacts with numerous other signaling pathways, and can be compensated for by redundant mechanisms. Understanding substance P requires appreciating this complexity rather than expecting simple cause-and-effect relationships.

As research continues, substance P will likely reveal additional layers of biological function and may yet yield therapeutic applications beyond antiemetic use. Its history as a pioneering neuropeptide whose name reflects a time before peptide chemistry existed serves as a reminder of how far neuroscience has advanced—and how much remains to be discovered.

Disclaimer: This article is for informational purposes only and is not medical advice. Substance P is not available as a therapeutic agent for direct administration. NK1 receptor antagonists like aprepitant are prescription medications that should only be used under medical supervision. The research discussed includes investigational applications that are not FDA-approved. Consult qualified healthcare providers for medical decisions.

Table of Contents