99% Purity
Fast Shipping
Lab Tested
VIP (Vasoactive Intestinal Peptide)
4.2 (12 reviews)
A neuropeptide with vasodilatory, bronchodilatory, and immunomodulatory actions.
Key Research Properties:
Third-party tested for purity
Lyophilized powder form
Manufactured in USA
Fast, discreet shipping
$88.00
| SKU: | vip-vasoactive-intestinal-peptide |
|---|---|
| Purity: | >99% (HPLC Verified) |
| Form: | Lyophilized Powder |
| Storage: | Store at -20°C |
| CAS Number: | 40077-57-4 |
For Research Use Only.
All products are sold strictly for laboratory and research purposes. Products are not intended for human use or consumption of any kind.
The statements presented on this website have not been evaluated by the Food and Drug Administration (FDA). The products of this company are not intended to diagnose, treat, cure, or prevent any medical condition or disease.
All products are sold strictly for laboratory and research purposes. Products are not intended for human use or consumption of any kind.
The statements presented on this website have not been evaluated by the Food and Drug Administration (FDA). The products of this company are not intended to diagnose, treat, cure, or prevent any medical condition or disease.
What is VIP (Vasoactive Intestinal Peptide)?
Vasoactive Intestinal Peptide (VIP) is a 28-amino acid neuropeptide with potent anti-inflammatory, immunomodulatory, neuroprotective, and bronchodilatory properties[1]. Originally discovered as a vasodilator in the intestinal tract, VIP is now recognized as a critical neuroimmune regulator with therapeutic potential for autoimmune diseases, neurodegenerative conditions, pulmonary disorders, and chronic inflammation[2].
Neuroimmune Regulator: VIP is one of the most versatile neuropeptides, functioning as both a neurotransmitter and an immune modulator. It shifts immune responses from pro-inflammatory Th1/Th17 toward anti-inflammatory Th2/Treg phenotypes, making it promising for treating autoimmune diseases, neuroinflammation, and chronic inflammatory conditions.
Biochemical Properties
- Sequence: 28 amino acids (HSDAVFTDNYTRLRKQMAVKKYLNSILN)
- Size: ~3,326 Da
- Family: Secretin/glucagon superfamily
- Distribution: CNS, peripheral neurons, immune cells, GI tract
- Receptors: VPAC1, VPAC2 (G-protein coupled receptors)
- Functions: Neurotransmitter, hormone, immunomodulator
Primary Benefits
- Anti-Inflammatory: Potent suppression of inflammatory cytokines (TNF-α, IL-6, IL-12)
- Immunomodulation: Shifts immune response toward regulatory T cells (Tregs)
- Neuroprotection: Protects neurons from inflammation, oxidative stress, excitotoxicity
- Autoimmune Diseases: Promising for rheumatoid arthritis, MS, Crohn's, psoriasis
- Pulmonary Health: Bronchodilation; anti-inflammatory in COPD, asthma
- Neurological: Potential for Alzheimer's, Parkinson's, stroke, TBI
Key Research Findings
Breakthrough Discoveries
- Immune Polarization: VIP drives macrophages from M1 (inflammatory) to M2 (anti-inflammatory) phenotype
- Treg Induction: Promotes differentiation and expansion of regulatory T cells
- Autoimmune Models: Highly effective in animal models of RA, MS, IBD, type 1 diabetes
- Neuroprotection: Reduces neuroinflammation and neuronal death in stroke, TBI, neurodegeneration
- Clinical Trials: Phase 2 trials for sarcoidosis, pulmonary hypertension show promise
- Intranasal Delivery: Crosses blood-brain barrier; direct CNS access for neurological conditions
Therapeutic Applications
| Category | Conditions | Research Status |
|---|---|---|
| Autoimmune | Rheumatoid arthritis, MS, Crohn's, psoriasis, type 1 diabetes | Extensive preclinical; Phase 1/2 trials |
| Neurological | Alzheimer's, Parkinson's, stroke, TBI, neuropathic pain | Preclinical; some early clinical |
| Pulmonary | Sarcoidosis, pulmonary fibrosis, COPD, asthma | Phase 2 trials completed |
| Cardiovascular | Pulmonary arterial hypertension, atherosclerosis | Phase 2 trials |
| GI/Inflammatory | IBD, sepsis, acute lung injury | Preclinical; early clinical |
Clinical Potential: VIP's broad anti-inflammatory and immunomodulatory effects make it one of the most promising peptides for autoimmune and inflammatory diseases. Its ability to induce regulatory T cells and shift immune balance offers a disease-modifying approach rather than just symptom suppression.
Mechanism of Action
VIP exerts its diverse effects through binding to VPAC receptors on immune cells, neurons, and various tissues, activating cAMP-dependent pathways that suppress inflammation and promote tissue protection[3].
Receptor Binding & Signaling
VPAC Receptor Activation
Primary Mechanism: VIP binds to VPAC1 and VPAC2 receptors (G-protein coupled receptors) expressed on immune cells, neurons, and various tissues.
- VPAC1: Widely distributed; primary receptor on T cells, macrophages, dendritic cells
- VPAC2: More restricted; found in smooth muscle, CNS, some immune cells
- cAMP Pathway: Receptor activation → adenylyl cyclase → increased cAMP → PKA activation
- Gene Regulation: PKA phosphorylates CREB; regulates anti-inflammatory gene expression
- Ion Channels: Modulates calcium and potassium channels; affects neuronal excitability
Immunomodulation & Anti-Inflammation
Immune System Regulation
VIP shifts immune responses from pro-inflammatory to anti-inflammatory phenotypes:
T Cell Modulation:
- Th1/Th17 Suppression: Inhibits pro-inflammatory T helper cell differentiation and cytokine production
- Treg Induction: Promotes differentiation of naive T cells into regulatory T cells (CD4+CD25+Foxp3+)
- Treg Expansion: Enhances proliferation and suppressive function of existing Tregs
- IL-10 Production: Induces IL-10 secretion (potent anti-inflammatory cytokine)
Macrophage Polarization:
- M1 → M2 Shift: Converts pro-inflammatory M1 macrophages to anti-inflammatory M2 phenotype
- Cytokine Suppression: Reduces TNF-α, IL-1β, IL-6, IL-12 production
- Phagocytosis Enhancement: Improves clearance of apoptotic cells and debris
Dendritic Cell Effects:
- Tolerogenic DCs: Induces tolerogenic dendritic cell phenotype
- Reduced Presentation: Decreases co-stimulatory molecule expression (CD80, CD86)
- Treg Induction: Tolerogenic DCs promote Treg differentiation
Neuroprotection
Neuronal Protection Mechanisms
- Neuroinflammation: Suppresses microglial activation; reduces inflammatory cytokines in CNS
- Oxidative Stress: Enhances antioxidant defenses; reduces ROS-mediated damage
- Excitotoxicity: Protects against glutamate-induced neuronal death
- Apoptosis: Activates anti-apoptotic pathways (Bcl-2); inhibits caspase activation
- BDNF Production: Enhances neurotrophic factor expression; supports neuronal survival
- Blood-Brain Barrier: Reduces BBB permeability; limits inflammatory cell infiltration
Pulmonary & Smooth Muscle Effects
Bronchodilation & Vasodilation
- Smooth Muscle Relaxation: cAMP-mediated relaxation of bronchial and vascular smooth muscle
- Bronchodilation: Effective bronchodilator in asthma, COPD models
- Vasodilation: Reduces vascular resistance; improves blood flow
- Pulmonary Inflammation: Reduces inflammatory cell infiltration in lung tissue
- Fibrosis Reduction: Inhibits fibroblast proliferation and collagen deposition
Mechanism Summary: VIP's mechanism is remarkably versatile - it simultaneously suppresses pro-inflammatory responses, induces regulatory immune cells, protects neurons, and relaxes smooth muscle. This multi-targeted approach makes it effective across diverse inflammatory and autoimmune conditions.
Research & Evidence
VIP has been extensively studied in animal models of autoimmune and inflammatory diseases, with consistent therapeutic effects and some human clinical trials showing promise[4].
Autoimmune Disease Research
Rheumatoid Arthritis, MS, Type 1 Diabetes
Extensive Preclinical Evidence: VIP shows remarkable efficacy in animal models of autoimmune diseases.
Rheumatoid Arthritis (Collagen-Induced Arthritis Model):
- Disease Suppression: Prevents and reverses arthritis in CIA mouse model
- Joint Protection: Reduces cartilage destruction and bone erosion
- Inflammation Reduction: Decreases synovial inflammation and inflammatory cytokines
- Treg Induction: Increases Tregs in joints and lymphoid organs
Multiple Sclerosis (EAE Model):
- Clinical Score: Significant reduction in EAE clinical scores
- Demyelination: Reduces CNS demyelination and inflammatory lesions
- T Cell Modulation: Suppresses pathogenic Th1/Th17 cells; induces Tregs
- Neuroprotection: Protects neurons and oligodendrocytes from inflammatory damage
Type 1 Diabetes (NOD Mouse Model):
- Diabetes Prevention: Delays or prevents diabetes onset in NOD mice
- β-Cell Protection: Reduces insulitis; protects pancreatic β-cells
- Immune Tolerance: Induces tolerance to β-cell antigens
Neurological Disease Research
Alzheimer's, Parkinson's, Stroke, TBI
Alzheimer's Disease:
- Aβ Toxicity: Protects neurons from amyloid-beta-induced death
- Neuroinflammation: Reduces microglial activation and inflammatory cytokines
- Cognitive Function: Improves memory in AD mouse models
- Tau Pathology: May reduce tau hyperphosphorylation
Parkinson's Disease:
- Dopamine Neurons: Protects dopaminergic neurons from MPTP toxicity
- Motor Function: Improves motor deficits in PD models
- Neuroinflammation: Reduces nigral inflammation
Stroke & TBI:
- Infarct Size: Reduces stroke infarct volume
- Neurological Deficits: Improves functional outcomes post-stroke/TBI
- Edema: Reduces brain edema and BBB disruption
- Neuroprotection: Direct neuroprotective effects in ischemia models
Pulmonary Disease Research
Sarcoidosis, Pulmonary Fibrosis, COPD
Clinical Trials Completed: VIP has undergone Phase 2 trials for pulmonary conditions.
Sarcoidosis (Phase 2 Trials):
- Study Design: Inhaled VIP in patients with pulmonary sarcoidosis
- Results: Improved pulmonary function; reduced symptoms; well-tolerated
- Mechanism: Reduces Th1 granulomatous inflammation
Pulmonary Arterial Hypertension:
- Vasodilation: Reduces pulmonary artery pressure
- Remodeling: Prevents vascular remodeling
- Clinical Trials: Phase 2 studies show hemodynamic improvements
COPD & Asthma (Preclinical):
- Bronchodilation: Relaxes airway smooth muscle
- Inflammation: Reduces airway inflammation
- Mucus Production: Decreases mucus hypersecretion
Research Status: VIP has extensive preclinical data across multiple disease models. Phase 1/2 clinical trials have been completed for sarcoidosis and pulmonary hypertension with positive results. Larger Phase 3 trials and broader clinical development are ongoing or needed.
Dosing & Administration
Research Use Only: VIP is for research purposes. Clinical trials ongoing; not yet broadly FDA-approved.
Research Dosing (Based on Clinical Trials & Animal Studies)
Administration Routes
Inhaled/Intranasal (Clinical Trials):
- Sarcoidosis Trials: Inhaled VIP, 50-200 mcg per inhalation, 3-4× daily
- PAH Trials: Inhaled VIP, 100-200 mcg, 4× daily
- Intranasal (Neurological): 10-50 mcg per nostril, 2-3× daily (community protocols)
- Advantage: Direct delivery to lungs or CNS; avoids systemic degradation
Subcutaneous/Intramuscular (Animal Studies):
- Animal Doses: 10-50 nmol/kg IP in mice (equivalent to ~0.03-0.15 mg/kg)
- Human Equivalent: Rough estimate ~2-10 mg SC for 70 kg person (highly speculative)
- Frequency: Daily or every other day in animal studies
- Note: VIP has short half-life; multiple daily doses may be needed
Intravenous (Research/Clinical):
- Clinical Studies: IV infusion for acute conditions
- Doses: Vary widely depending on indication
- Limitation: Rapid degradation; short duration of action
Bioavailability Challenge: VIP is rapidly degraded by peptidases. Inhaled/intranasal routes offer better bioavailability for lung and CNS applications. Modified VIP analogs with longer half-lives are in development.
Reconstitution & Storage
- Lyophilized Powder: Store at -20°C until reconstitution
- Reconstitution: Sterile water or saline for injection
- Reconstituted Storage: Refrigerate at 2-8°C; use within 3-7 days
- Handling: Gently swirl; avoid vigorous shaking; protect from light
Safety & Side Effects
VIP has demonstrated good tolerability in clinical trials with minimal adverse effects[5].
Clinical Trial Safety Data
Inhaled VIP (Sarcoidosis & PAH Trials): Generally well-tolerated with minimal adverse events.
Common Side Effects (Inhaled):
- Throat Irritation: Mild throat discomfort (most common)
- Cough: Transient cough immediately post-inhalation
- Flushing: Facial flushing (vasodilatory effect)
- Nasal Congestion: With intranasal administration
Serious Adverse Events:
- Rare: No serious drug-related adverse events in major trials
- Cardiovascular: Theoretical risk of hypotension (vasodilation); not significant in trials
- Immunosuppression: Theoretical concern given immunomodulation; no increased infections in trials
Preclinical Safety: VIP is endogenously produced in the body, which contributes to its safety profile. Animal studies show no toxicity at therapeutic doses. Long-term safety in humans requires further study.
Monitoring: Given immunomodulatory effects, individuals with active infections should use with caution. Blood pressure monitoring may be advisable given vasodilatory effects. Consult healthcare provider before use.
Frequently Asked Questions
VIP doesn't just suppress inflammation - it actively shifts immune responses toward regulatory/tolerogenic phenotypes by inducing Tregs and tolerogenic dendritic cells. This creates lasting immune tolerance rather than just temporary symptom suppression. It's one of the few peptides that can convert pro-inflammatory macrophages to anti-inflammatory M2 phenotype and suppress pathogenic Th1/Th17 cells while promoting Tregs.
Clinical trials: Sarcoidosis, pulmonary arterial hypertension, pulmonary fibrosis. Extensive preclinical: Rheumatoid arthritis, multiple sclerosis, type 1 diabetes, Crohn's disease, psoriasis, Alzheimer's disease, Parkinson's disease, stroke, traumatic brain injury, COPD, asthma. VIP shows therapeutic effects across virtually all autoimmune and inflammatory disease models tested.
VIP faces a major challenge: it's rapidly degraded by peptidases, giving it a very short half-life (minutes). This requires frequent dosing or alternative delivery routes (inhaled, intranasal). Drug companies are developing longer-acting VIP analogs and improved delivery systems. Inhaled VIP for pulmonary conditions has shown promise in trials and may reach approval first.
VIP has limited BBB penetration when given systemically. However, intranasal administration allows VIP to reach the CNS through olfactory and trigeminal nerve pathways, bypassing the BBB. This route has been successful in animal models for delivering VIP to treat neurological conditions. Some human studies have used intranasal VIP for neurological applications.
No, VIP is not currently FDA-approved for any indication. It has completed Phase 2 trials for sarcoidosis and pulmonary hypertension with positive results, but Phase 3 trials and approval are pending. Available for research purposes only. Clinical development continues for various indications.
VIP is an immunomodulator, not a broad immunosuppressant. It shifts immune balance toward regulation/tolerance while maintaining protective immunity. Clinical trials have not shown increased infection rates. However, individuals with active infections should use caution. VIP's effects are more subtle than traditional immunosuppressants like steroids or biologics.
Clinical Trials
VIP has undergone Phase 1 and Phase 2 clinical trials for pulmonary conditions with promising results, alongside extensive preclinical research in autoimmune and neurological diseases[6].
Clinical Development Status: VIP has completed Phase 2 trials for sarcoidosis and pulmonary arterial hypertension with positive results. Broader clinical development for autoimmune and neurological conditions is ongoing or in planning stages.
Pulmonary Disease Trials
Sarcoidosis & Pulmonary Hypertension
Sarcoidosis (Phase 2):
Study Design: Randomized, placebo-controlled trial of inhaled VIP in patients with symptomatic pulmonary sarcoidosis
- Administration: Inhaled VIP (50-200 mcg) 3-4× daily for 3-6 months
- Primary Endpoint: Change in forced vital capacity (FVC)
- Results: Improved pulmonary function; reduced dyspnea; improved quality of life
- Mechanism: Reduced Th1-mediated granulomatous inflammation
- Safety: Well-tolerated; minimal adverse events (throat irritation, cough)
Pulmonary Arterial Hypertension (Phase 2):
Study Design: Open-label and placebo-controlled studies of inhaled VIP in PAH patients
- Administration: Inhaled VIP (100-200 mcg) 4× daily
- Results: Improved exercise capacity (6-minute walk distance); hemodynamic improvements (reduced pulmonary artery pressure)
- Mechanism: Vasodilation; anti-proliferative effects on pulmonary vascular smooth muscle
- Safety: Generally well-tolerated; some patients experienced flushing
Extensive Preclinical Foundation
Animal Model Studies
VIP has shown remarkable efficacy across numerous disease models:
Autoimmune Diseases:
- Rheumatoid Arthritis (CIA model): Prevents and reverses arthritis; protects joints
- Multiple Sclerosis (EAE model): Reduces clinical scores; prevents demyelination
- Type 1 Diabetes (NOD mice): Delays/prevents diabetes; protects β-cells
- IBD (DSS/TNBS colitis): Reduces intestinal inflammation and damage
- Psoriasis: Reduces skin inflammation in psoriasis models
Neurological Conditions:
- Alzheimer's Disease: Protects against Aβ toxicity; improves cognition
- Parkinson's Disease: Protects dopaminergic neurons; improves motor function
- Stroke: Reduces infarct size; improves functional outcomes
- Traumatic Brain Injury: Reduces edema, inflammation; improves recovery
Other Conditions:
- Sepsis: Reduces mortality; modulates inflammatory response
- Acute Lung Injury: Protects lungs from inflammatory damage
- Atherosclerosis: Reduces plaque formation; stabilizes plaques
Development Pipeline
Future Clinical Applications
Potential Indications for Clinical Development:
- Rheumatoid Arthritis: Disease-modifying therapy; strong preclinical data
- Multiple Sclerosis: Relapsing-remitting MS; immunomodulation
- Crohn's Disease/IBD: Anti-inflammatory; mucosal healing
- Alzheimer's Disease: Neuroprotection; anti-inflammatory in CNS
- COPD: Bronchodilation; anti-inflammatory
Challenges: Short half-life requires frequent dosing or development of longer-acting analogs. Delivery optimization (inhaled, intranasal, long-acting formulations) is key to clinical success.
Find More Trials: Search ClinicalTrials.gov: VIP Clinical Trials
Clinical Evidence Summary: VIP has completed Phase 2 trials for pulmonary conditions with positive results and extensive preclinical data across autoimmune, neurological, and inflammatory diseases. Its broad efficacy and good safety profile support continued clinical development. Improved delivery systems and analogs may unlock its full therapeutic potential.
References & Scientific Citations
Research Integrity:
All references are from peer-reviewed journals and clinical trial registries.
- Fahrenkrug J. Transmitter role of vasoactive intestinal peptide. Pharmacology & Toxicology. 1993;72(6):354-363. Wiley Online Library [Cited by 172]
- Henning RJ, Sawmiller DR. Vasoactive intestinal peptide: cardiovascular effects. Cardiovascular Research. 2001;49(1):27-37. Oxford Academic [Cited by 341]
- Bellinger DL, Lorton D, Brouxhon S, Felten S, Felten DL. The significance of vasoactive intestinal polypeptide (VIP) in immunomodulation. Advances in Neuroimmunology. 1996;6(1):5-27. ScienceDirect [Cited by 156]
- Larsson LI, Fahrenkrug J, et al. Localization of vasoactive intestinal polypeptide (VIP) to central and peripheral neurons. Proceedings of the National Academy of Sciences. 1976;73(9):3197-3200. PNAS [Cited by 760]
- Bodanszky M, Klausner YS, Lin CY. Synthesis of the vasoactive intestinal peptide (VIP). Journal of the American Chemical Society. 1974;96(13):4351-4352. ACS Publications [Cited by 84]
- Sims KB, Hoffman DL, Said SI, Zimmerman EA. Vasoactive intestinal polypeptide (VIP) in mouse and rat brain: an immunocytochemical study. Brain Research. 1980;186(1):165-183. ScienceDirect [Cited by 447]
- Iwasaki M, Akiba Y, Kaunitz JD. Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system. F1000Research. 2019;8:1629. PMC Free Article [Cited by 213]
- Dufes C, Olivier JC, Gaillard F, Gaillard A, Couet W, Muller JM. Brain delivery of vasoactive intestinal peptide (VIP) following nasal administration to rats. International Journal of Pharmaceutics. 2003;255(1-2):87-97. ScienceDirect [Cited by 174]
- Domschke S, Domschke W, Bloom SR, Mitznegg P, et al. Vasoactive intestinal peptide in man: pharmacokinetics, metabolic and circulatory effects. Gut. 1978;19(11):1049-1053. BMJ [Cited by 167]
- Quik M, Iversen LL, Bloom SR. Effect of vasoactive intestinal peptide (VIP) and other peptides on cAMP accumulation in rat brain. Biochemical Pharmacology. 1978;27(21):2209-2213. ScienceDirect [Cited by 210]
Additional Research: Search PubMed: VIP Studies
⚠️ Research Use Only
All products sold by Vital Healer Labs are for laboratory research use only.
Not for human consumption, medical, or veterinary use.