VIP — Research Overview
Full Name: Vasoactive Intestinal Peptide (also called Vasoactive Intestinal Polypeptide) Pharmaceutical Designation: Aviptadil (INN for synthetic VIP) Structure: 28-amino acid neuropeptide/hormone with an alpha-helical secondary structure in physiological environments Amino Acid Sequence: His-Ser-Asp-Ala-Val-Phe-Thr-Asp-Asn-Tyr-Thr-Arg-Leu-Arg-Lys-Gln-Met-Ala-Val-Lys-Lys-Tyr-Leu-Asn-Ser-Ile-Leu-Asn-NH2 Family: Member of the secretin/glucagon superfamily of structurally related neuropeptides and hormones, which also includes secretin, glucagon, glucagon-like peptides (GLP-1, GLP-2), gastric inhibitory peptide (GIP), growth hormone-releasing hormone (GHRH), helodermin, and the closely related pituitary adenylate cyclase-activating polypeptide (PACAP). The structural conservation across this family reflects extensive divergence from a common ancestral gene. VIP and PACAP share approximately 68% amino acid sequence identity. Discovery: VIP was first isolated from porcine intestinal tissue by Sami Said and Viktor Mutt at the Karolinska Institute in 1970 (Science 169:1217-1218, PMID reference: 10.1126/science.169.3951.1217). The name “vasoactive intestinal peptide” reflects its two defining properties at discovery: its source (intestinal tissue) and its most immediately apparent biological effect (potent vasodilation). Said and Mutt subsequently identified it as a neuropeptide distributed throughout the central and peripheral nervous systems — a finding that substantially expanded its biological significance beyond its initial gut and vascular pharmacology. Endogenous Distribution: VIP is among the most widely distributed neuropeptides in the mammalian body. It is expressed by neurons in multiple brain areas and stored and released by nerve fibers innervating the heart, lungs, thyroid, kidney, urogenital tract, gastrointestinal tract, and immune organs including the spleen, thymus, bone marrow, and lymph nodes. In the gut, VIP-expressing neurons constitute a major component of the enteric nervous system. Immune cells — including CD4+ and CD8+ T lymphocytes, mast cells, and neutrophils — also produce and release VIP. The breadth of VIP expression explains the diversity of its physiological functions. Plasma Half-Life: Approximately 1-2 minutes in vivo, due to rapid enzymatic degradation primarily by neutral endopeptidases, angiotensin-converting enzyme (ACE), and mast cell tryptase. This extremely short plasma half-life is the primary pharmacological challenge for therapeutic applications and has driven development of delivery systems (liposomal encapsulation, inhalation devices) and analogs designed to extend bioavailability. Regulatory Status: VIP is not FDA-approved for any indication as a standalone therapeutic. Aviptadil (synthetic VIP) has been investigated in multiple clinical programs including Phase 2 PAH trials and COVID-19/ARDS clinical trials. No FDA marketing approval exists as of this compilation. WADA Status: Not specifically listed on the WADA prohibited list as of this compilation. Category: Endogenous neuropeptide/neurotransmitter/hormone / VPAC1/VPAC2 receptor agonist / cAMP-mediated anti-inflammatory signaling activator / vasodilator / bronchodilator / neuroimmune interface research tool / enteric nervous system regulator
Research Use Only — Disclaimer
The scientific literature on this page is provided strictly for educational and informational purposes. All Rogue Compounds products are intended for in-vitro laboratory research use only and are not approved by the FDA for human or animal consumption. The studies referenced below are independent third-party peer-reviewed publications. Rogue Compounds makes no claims that any product diagnoses, treats, cures, or prevents any disease or condition. Researchers are responsible for compliance with all applicable local, state, and federal regulations.
What Is VIP?
Vasoactive Intestinal Peptide is a 28-amino acid neuropeptide that occupies a unique position in biomedical research as one of the most biologically multifunctional endogenous peptides known — simultaneously a neurotransmitter, a hormone, a vasodilator, a bronchodilator, an immunomodulator, a secretagogue, and a circadian rhythm regulator. The diversity of VIP’s physiological roles reflects its receptor distribution: VPAC1 and VPAC2 receptors are expressed on virtually every tissue type in the body, and VIP is released at the neuroimmune interface — the molecular junction where the nervous system communicates with the immune system — in both directions.
VIP’s pharmacological significance as a research tool lies in its role as the endogenous “brake” on inflammatory responses. When immune cells activate and produce pro-inflammatory cytokines, the nervous system responds by releasing VIP into the local tissue environment, where it binds VPAC receptors on immune cells and activates anti-inflammatory signaling cascades that downregulate the inflammatory response. This feedback mechanism — neurons releasing VIP to modulate local immune activity — constitutes a fundamental component of the neuroimmune regulatory network that prevents inflammatory responses from becoming uncontrolled and self-damaging.
The consequence of this biology is that VIP deficiency is associated with exaggerated inflammatory responses, and VIP excess or supplementation attenuates them. This has been directly demonstrated: VIP-knockout mice are dramatically more susceptible to LPS-induced septic shock, develop bronchial asthma and pulmonary hypertension spontaneously, and show elevated pro-inflammatory cytokines in inflammatory challenge models compared to wild-type animals. Conversely, exogenous VIP administration reduces symptoms and mortality in experimental models of an extraordinary range of inflammatory and autoimmune conditions — sepsis, rheumatoid arthritis, Crohn’s disease, experimental autoimmune encephalomyelitis (the mouse model of multiple sclerosis), type 1 diabetes, pancreatitis, pulmonary hypertension, and Sjogren’s syndrome among many others. This breadth of preclinical efficacy reflects VIP’s action at a regulatory node that is relevant across all inflammatory conditions, not just one pathway.
The VIP/PACAP Family and Receptor System
VIP is one of two closely related neuropeptides in the VIP/PACAP subfamily. PACAP (pituitary adenylate cyclase-activating polypeptide) exists as PACAP-38 (38 amino acids) and PACAP-27 (27 amino acids) and shares 68% amino acid sequence identity with VIP in its N-terminal region. Their shared sequence explains why both peptides bind VPAC receptors with high and essentially equal affinity.
The receptor system for VIP and PACAP consists of three G-protein coupled receptors (GPCRs) belonging to Class B (secretin receptor family):
VPAC1 (VIP/PACAP receptor type 1): Widely expressed throughout the body — lungs, liver, jejunum, T lymphocytes (particularly CD4+ T cells), and many other tissues. Mediates the majority of VIP’s anti-inflammatory effects in immune cells. Constitutively expressed on resting immune cells. Binds both VIP and PACAP with equal high affinity. Primary mediator of VIP’s effects in most peripheral inflammatory contexts.
VPAC2 (VIP/PACAP receptor type 2): More concentrated in the central nervous system, smooth muscle, T lymphocytes (particularly CD8+ and memory T cells), and certain immune cell populations. Expression is inducible — upregulated on lymphocytes following antigen activation. Also binds VIP and PACAP with equal high affinity. VPAC2 plays an important role in circadian rhythm regulation through its expression in the suprachiasmatic nucleus (SCN).
PAC1 (PACAP-selective receptor): Selective for PACAP, with much lower affinity for VIP. Primary target for PACAP’s distinct CNS effects. Not a primary target of VIP at physiological concentrations.
All three receptors are Gs-protein coupled, activating adenylyl cyclase and elevating intracellular cyclic AMP (cAMP) as the primary second messenger. This cAMP elevation drives the anti-inflammatory transcriptional program through protein kinase A (PKA) → CREB phosphorylation, combined with PKA-mediated inhibition of pro-inflammatory transcription factors NF-kB, AP-1, and IRF. VPAC receptors also signal through additional pathways — phospholipase C (PLC), phosphoinositide-3-kinase (PI3K), and EPAC (exchange protein directly activated by cAMP) — adding complexity to the downstream effects.
Mechanism of Action — The Anti-Inflammatory Program
Macrophage and microglia programming — the core innate immune mechanism: VIP acts on macrophages and microglia (the CNS resident macrophage equivalent) to simultaneously suppress pro-inflammatory mediator production and stimulate anti-inflammatory mediator production. On the suppression side: VIP inhibits production of TNF-alpha, IL-6, IL-12, IL-1beta, the chemokines responsible for immune cell recruitment, PGE2 (by inhibiting COX-2), and nitric oxide (by inhibiting inducible NO synthase, iNOS). On the induction side: VIP stimulates production of IL-10 (the master anti-inflammatory cytokine) and IL-1Ra (the endogenous IL-1 receptor antagonist). This simultaneous pro/anti-inflammatory mediator balance shift — not simply suppressing immune activation but redirecting it toward a resolution phenotype — is the cellular basis for VIP’s therapeutic effects across inflammatory disease models.
Dendritic cell modulation — Th1/Th17 to Treg shift: VIP acts on dendritic cells (DCs) — the professional antigen-presenting cells that determine whether T-cell responses differentiate toward inflammatory (Th1, Th17) or regulatory (Treg) phenotypes. VIP reduces costimulatory molecule expression (CD80/CD86) on mature DCs, impairing their ability to activate Th1 cells. VIP also promotes the generation of tolerogenic dendritic cells (tDCs) — a DC subtype that drives the differentiation of naive T cells into induced regulatory T cells (iTreg) rather than inflammatory Th1 or Th17 cells. This DC-mediated induction of peripheral iTreg is one of VIP’s most powerful anti-autoimmune mechanisms, creating a population of self-antigen-specific suppressor T cells that prevent and reverse autoimmune responses.
Regulatory T-cell induction: Through the tDC pathway and through direct effects on T cells, VIP promotes the generation and maintenance of regulatory T cells (Treg) — CD4+CD25+FOXP3+ lymphocytes that suppress antigen-specific immune responses. This iTreg induction provides lasting immunological tolerance that outlasts the direct pharmacological effect of VIP itself, which is pharmacologically significant given VIP’s short plasma half-life.
Th1/Th17 suppression, Th2 promotion: VIP shifts the T-cell cytokine balance away from the Th1 profile (IFN-gamma, TNF-alpha, IL-2 — associated with autoimmunity and cellular inflammation) and Th17 profile (IL-17 — associated with rheumatoid arthritis, inflammatory bowel disease, psoriasis) toward the Th2 profile (IL-4, IL-5, IL-10 — associated with antibody-mediated immunity and anti-inflammatory responses). This shift provides the molecular basis for VIP’s efficacy across Th1- and Th17-driven autoimmune conditions.
Vasodilation and smooth muscle relaxation: Through VPAC receptors on vascular smooth muscle, VIP activates adenylyl cyclase → cAMP → PKA → phosphorylation of myosin light chain kinase (MLCK) → smooth muscle relaxation → vasodilation. In systemic vasculature this produces blood pressure reduction. In pulmonary vasculature — where VIP-expressing nerve fibers are particularly dense and VPAC receptors are highly expressed on pulmonary artery smooth muscle — this produces selective pulmonary vasorelaxation that is directly therapeutically relevant to pulmonary arterial hypertension.
Bronchodilation: VIP is one of the most potent endogenous bronchodilators in the human airway. VIP-containing nerve fibers innervate airway smooth muscle throughout the bronchial tree, and VPAC receptors on bronchial smooth muscle cells mediate cAMP-driven smooth muscle relaxation. VIP deficiency in the lungs correlates with bronchospasm, and exogenous VIP produces rapid bronchodilation. This mechanism, combined with VIP’s anti-inflammatory effects on airway macrophages and mast cells, provides the pharmacological rationale for VIP in pulmonary conditions including asthma and COPD.
NFAT signaling suppression in pulmonary vasculature: In pulmonary arterial hypertension, a key molecular driver of the pathological smooth muscle cell proliferation and vascular remodeling characteristic of the disease is dysregulated calcineurin-NFAT (nuclear factor of activated T cells) signaling. VIP suppresses NFAT activation in pulmonary vascular smooth muscle cells — providing a mechanistic explanation for why VIP gene knockout mice develop spontaneous pulmonary hypertension and why VIP deficiency is found in idiopathic PAH patients. This NFAT suppression mechanism positions VIP not merely as a vasodilator but as a modulator of the underlying vascular remodeling process in PAH.
Gut function regulation: In the enteric nervous system, VIP is a primary inhibitory neurotransmitter that coordinates intestinal smooth muscle relaxation, sphincter control, water and ion secretion by intestinal epithelium, and blood flow regulation in the gut wall. This physiological role explains why VIPomas (VIP-secreting tumors) cause Verner-Morrison syndrome — characterized by watery diarrhea, hypokalemia, and achlorhydria — and why VIP is relevant to inflammatory bowel disease research.
Published Research
Study 1 — Discovery and Characterization
Authors: Said SI, Mutt V Year: 1970 Journal: Science Reference: Science 1970;169(3951):1217-1218
VIP was first reported in this landmark Science paper by Sami Said and Viktor Mutt, describing isolation of a polypeptide with broad biological activity from porcine small intestine. Said and Mutt identified the vasodilatory activity that gave VIP its name, and established the foundational structural characterization of the 28-amino acid sequence.
The conservation of VIP’s amino acid sequence across mammalian species — human VIP is identical to porcine VIP in its core functional regions — was documented in early structural characterization studies and argues for a fundamental physiological role that strong evolutionary pressure has maintained. This high conservation distinguishes VIP from peptides whose sequences diverge substantially across species.
Over five decades of subsequent research has established VIP as a master regulator of the neuroimmune interface — a significance not anticipated at discovery from its vasodilatory properties alone.
Study 2 — VIP in Experimental Rheumatoid Arthritis: Proof-of-Concept for Autoimmune Application
Authors: Gonzalez-Rey E, Chorny A, Delgado M et al. (Instituto de Parasitología y Biomedicina Lopez Neyra, Granada) Year: 2007 (and companion publications from Delgado laboratory, 2002-2010) Journal: Arthritis and Rheumatism and related journals
This series of studies from Mario Delgado’s laboratory at the Spanish National Research Council established VIP as a viable candidate for autoimmune arthritis treatment — the most clearly validated single inflammatory disease application in the preclinical VIP literature.
VIP administration in the collagen-induced arthritis (CIA) mouse model — the standard preclinical model of human rheumatoid arthritis — completely abrogated joint swelling and destruction of cartilage and bone in treated animals versus saline controls. The magnitude of protection was remarkable — not just reduction in severity but complete joint preservation at the doses studied.
The therapeutic effect was mechanistically characterized as a dual downregulation of both the inflammatory component of arthritis (reduced TNF-alpha, IL-6, IL-17 in joint fluid; reduced macrophage activation; reduced neutrophil infiltration) and the autoimmune component (suppressed Th1/Th17 autoimmune T-cell responses; increased Treg cells specific for collagen autoantigens). This mechanistic dual action — simultaneously anti-inflammatory and pro-tolerogenic — produced more complete protection than anti-inflammatory agents alone and established VIP as potentially superior to pure anti-cytokine approaches in autoimmune contexts.
Human relevance was supported by the finding that immune cells from rheumatoid arthritis patients express lower VPAC1 receptor levels than cells from healthy controls — and respond poorly to VIP stimulation — suggesting that reduced endogenous VIP signaling may contribute to the failure of the normal neuroimmune brake in RA patients.
Study 3 — Pulmonary Arterial Hypertension: VIP Deficiency and Clinical Trials
Authors: Multiple; Leuchte HH et al. (inhaled aviptadil); Said SI (VIP gene in PAH) Years: 2008 (inhaled aviptadil study), 2009 (VIP gene PAH model), 2012 (Phase 2 RCT results) Journals: European Respiratory Journal, PMID 18978135; Proceedings of the American Thoracic Society; American Journal of Respiratory and Critical Care Medicine
This research program established the strongest translational case for VIP in any specific indication by demonstrating: (1) endogenous VIP deficiency in PAH patients, (2) a causal mechanism linking VIP absence to pulmonary vascular remodeling, and (3) clinical pharmacological evidence that exogenous inhaled VIP produces pulmonary vasodilation in PAH patients.
Idiopathic pulmonary arterial hypertension (IPAH) patients were found to have significantly lower lung VIP content than normal controls — establishing VIP deficiency as a pathological feature of the disease rather than merely an incidental finding. VIP gene-knockout mice develop spontaneous pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular remodeling — confirming that VIP deficiency is causally related to the PAH phenotype rather than correlative.
The mechanistic link was identified as dysregulated calcineurin-NFAT signaling: absent VIP allows NFAT to drive smooth muscle proliferation and vascular remodeling that would be suppressed by normal VIP-VPAC signaling.
Leuchte et al. (2008) conducted an acute hemodynamic study where 20 PAH patients inhaled a single 100 microgram dose of aviptadil (inhaled VIP) during right-heart catheterization. Aviptadil produced a small but statistically significant selective pulmonary vasodilation, improved stroke volume, and improved mixed venous oxygen saturation. Six of 20 patients experienced pulmonary vascular resistance reduction greater than 20% — a clinically meaningful acute response.
The subsequent Phase 2 randomized controlled trial (MG-101) published its results after delay via the American Journal of Respiratory and Critical Care Medicine. The trial did not meet its pre-specified primary endpoints for acute hemodynamic improvement or for 3-month outcomes. However, investigators noted that some patients on long-term aviptadil showed clinical stabilization or improvement, and the rights to aviptadil were subsequently acquired by LungRx for further US development. Further US PAH development did not advance to Phase 3.
Study 4 — Sarcoidosis: Phase 2 Open-Label Clinical Evidence
Authors: Multiple (Hamzeh N, Voelkel NF, and collaborators) Year: Multiple publications 2003-2010
This open Phase 2 study treated 20 patients with histologically proven sarcoidosis and active disease with nebulized VIP for 4 weeks. VIP inhalation was safe, well-tolerated, and significantly reduced TNF-alpha production by cells isolated from bronchoalveolar lavage (BAL) fluids — directly demonstrating pharmacological anti-inflammatory effect on sarcoid alveolitis in human lungs.
Sarcoidosis is characterized by noncaseating granulomas where excessive TNF-alpha production by pulmonary macrophages drives granuloma formation. VIP’s suppression of macrophage TNF-alpha production is mechanistically precisely relevant to this pathology.
This study represents the clearest published demonstration of VIP’s anti-inflammatory mechanism operating in human lung tissue in a clinical setting — a particularly important data point given the route of administration (inhaled) that is most likely to achieve therapeutic concentrations in lung while minimizing systemic hypotension.
Study 5 — COVID-19 ARDS: Aviptadil IV Clinical Trial
Authors: Youssef JG, Lavin P, Schoenfeld DA et al. Year: 2022 Journal: Critical Care Medicine PMID: 36044317
This 60-day randomized controlled trial evaluated intravenous aviptadil (VIP) in patients with critical COVID-19 respiratory failure. The study was motivated by VIP’s dual mechanisms relevant to COVID-19: pulmonary vasoprotection and anti-inflammatory/cytokine storm suppression — specifically the suppression of the TNF-alpha, IL-6, and IL-12 that drive COVID-19 cytokine storm and lung injury.
The study enrolled patients with confirmed COVID-19 and respiratory failure requiring mechanical ventilation or high-flow oxygen. The aviptadil arm received IV VIP over the first 12 hours. Primary outcomes included survival at 60 days and respiratory recovery.
The trial demonstrated that aviptadil was safely administered in the critical COVID-19 setting. Clinical outcomes, while showing numerical improvement trends in the aviptadil group, produced mixed results across the primary and secondary endpoints in this relatively small trial. The study established proof-of-safety and proof-of-pharmacological-concept for IV aviptadil in the COVID-19 context and contributed to the body of evidence guiding subsequent development decisions.
VIP and CIRS — What the Evidence Actually Shows
Chronic Inflammatory Response Syndrome (CIRS) is a diagnostic and treatment framework developed primarily by Ritchie Shoemaker, MD, for a constellation of symptoms attributed to biotoxin exposure from water-damaged buildings, Lyme disease, and related environmental toxin sources. VIP nasal spray (typically 50 micrograms per nostril, 2-4 times daily) is used as a final intervention in the Shoemaker protocol after other measures have addressed upstream inflammatory markers.
The biological rationale for VIP in CIRS is internally coherent: VIP is an endogenous anti-inflammatory neuropeptide; CIRS is proposed to involve a state of chronic immune dysregulation; therefore restoring VIP signaling could modulate the chronic inflammatory state. Shoemaker has published case series and observational data showing improvements in the complex inflammatory marker panel (TGF-beta1, MMP-9, VEGF, C4a) and patient-reported symptoms associated with VIP treatment in CIRS patients.
What the evidence does not include: placebo-controlled randomized trials of VIP nasal spray for CIRS. CIRS is not a recognized diagnosis in mainstream medicine and does not appear in ICD classification systems. The diagnostic criteria, laboratory markers, and treatment protocols associated with CIRS are not validated through independent multicenter research.
Researchers evaluating VIP in this context should understand that the endogenous biology of VIP is well-established and pharmacologically real, while the specific CIRS clinical framework and the VIP nasal spray application within it have not been validated by controlled clinical research meeting standard evidence thresholds. The biology is sound; the clinical evidence for this specific application is limited to observational data.
VIP in Inflammatory Bowel Disease — Preclinical Evidence
VIP’s endogenous role in the enteric nervous system and its immunomodulatory properties make inflammatory bowel disease a rationally motivated research application. In preclinical studies using the trinitrobenzene sulfonic acid (TNBS) mouse model of Crohn’s disease, VIP administration significantly reduced colitis severity — decreasing colon inflammation scores, reducing pro-inflammatory cytokine levels, and preventing mucosal damage. Similar protective effects have been demonstrated in DSS-colitis models. The mechanistic logic is direct: the inflamed IBD gut has elevated Th1/Th17 activity and reduced regulatory T-cell function; VIP’s Th1/Th17 suppression and Treg induction directly address both components. Human clinical trials in IBD have not yet been conducted.
The Half-Life Problem and Drug Delivery Research
VIP’s 1-2 minute plasma half-life is its primary pharmacological limitation. Rapid degradation by endopeptidases, ACE, and mast cell tryptase prevents sustained pharmacological effects from systemic injection. Multiple strategies for overcoming this limitation have been investigated:
Liposomal and phospholipid encapsulation: Incorporating VIP into phospholipid formulations protects it from enzymatic degradation and — importantly — changes its conformation from random coil to alpha-helix, which increases VPAC receptor binding affinity. VIP in phospholipid formulations has been successfully used in animal pulmonary hypertension models. The Aviptadil inhaled formulations for PAH clinical trials used this delivery approach.
Neutral endopeptidase inhibitors: Co-administration of NEP inhibitors that block VIP degradation has been shown to dramatically augment and prolong VIP’s hemodynamic effects in PAH models — suggesting that pharmacological NEP inhibition combined with VIP administration could enable clinical efficacy from doses that would otherwise be cleared too rapidly.
Slow-release microspheres and nanoparticle systems: Extended-release VIP formulations are under investigation for chronic inflammatory disease applications.
VIP analogs: Structural modifications to VIP that increase metabolic stability while preserving or enhancing VPAC receptor affinity are an active area of pharmaceutical research. VPAC1-selective agonists and long-acting VIP analogs represent the most likely clinical development path for VIP-based therapeutics in chronic inflammatory conditions.
Safety Profile and Predictable Adverse Effects
VIP’s adverse effect profile is mechanistically predictable from its pharmacology and is primarily driven by vasodilation. The dominant predictable adverse effect of systemic VIP administration is hypotension — blood pressure reduction — resulting from smooth muscle relaxation in peripheral vasculature. This is not an idiosyncratic toxicity but an on-target pharmacological effect that is dose-dependent and managed by limiting systemic exposure.
In clinical studies, facial flushing, transient blood pressure reduction, and tachycardia have been the most consistently reported adverse events with systemic VIP administration — all mechanistically consistent with vasodilation and consequent baroreceptor-mediated heart rate compensation. These effects are transient and dose-related.
Inhaled VIP produces substantially less systemic hypotension than intravenous or subcutaneous VIP because it achieves high local concentrations in pulmonary tissue (where vasodilation is therapeutically desired) while minimizing systemic exposure. This is the primary pharmacological rationale for the inhaled route in PAH and pulmonary inflammatory conditions.
VIP is not associated with immune suppression, infection risk, organ toxicity, or the safety concerns associated with broader immunosuppressants. Its modulating rather than suppressing immune action maintains the capacity for protective immune responses against pathogens.
Current Research Status
VIP research remains highly active across multiple domains. The strongest current clinical development focus is inhaled and intravenous aviptadil for pulmonary conditions (PAH, COVID-19 ARDS, and related respiratory inflammatory conditions). Academic research continues extensively on VIP’s role in autoimmune conditions — particularly rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, and type 1 diabetes models — and on the neuroimmune regulatory network of which VIP is a central component. Development of stable, long-acting VPAC receptor agonists that overcome VIP’s half-life limitation remains an active pharmaceutical research priority. Clinical translation to autoimmune indications beyond the pulmonary system awaits Phase 2 trials that match the strength of the preclinical evidence base.
Reconstitution Note
VIP is supplied as lyophilized powder. Bacteriostatic water is the standard reconstitution solvent for research use. VIP dissolves readily in aqueous solution. Protect from light and from repeated freeze-thaw cycles. VIP is susceptible to enzymatic degradation at physiological temperature; reconstituted solutions should be used promptly or stored refrigerated. Always confirm the recommended solvent against the specific lot datasheet before reconstitution.
In-Use Period and Storage
Before Reconstitution — Lyophilized Powder
Rogue Compounds stores all products refrigerated prior to shipping to maintain compound integrity from production through to delivery. Upon receipt researchers should store vials at 2 to 8 degrees Celsius immediately. Keep vials sealed, dry, and away from direct light until ready for use. Do not freeze. Repeated freeze-thaw cycling has been documented in peer-reviewed pharmaceutical formulation literature to accelerate structural degradation even in dry powder form, potentially compromising molecular integrity and experimental reproducibility.
Why We Refrigerate Instead of Freeze
Freezing and thawing introduces mechanical and osmotic stress at the molecular level. Published pharmaceutical research identifies freeze-thaw cycling as a significant risk factor for loss of structural integrity in peptides and protein-based compounds. To protect compound quality at every stage of handling and fulfillment, Rogue Compounds maintains refrigerated rather than frozen cold chain storage throughout the entire process.
After Reconstitution — Liquid Solution
Store reconstituted solutions refrigerated at 2 to 8 degrees Celsius immediately after preparation. VIP in aqueous solution is susceptible to enzymatic degradation if left at room temperature — refrigerated storage is essential. Protect from light. Avoid repeated freeze-thaw cycles. Use within the timeframe recommended for the individual compound. Label each aliquot with the compound name, concentration, date of reconstitution, and diluent used. Discard any solution that shows visible particulate matter, discoloration, or signs of degradation.
Note: Storage and in-use recommendations on this page are provided as general laboratory guidance based on standard peptide handling practices documented in peer-reviewed pharmaceutical literature. Researchers should always refer to the individual compound’s published research literature and datasheet for any specific requirements. All products sold by Rogue Compounds are intended strictly for in-vitro laboratory research use only.
Available from Rogue Compounds
View the VIP product page: https://roguecompounds.com/product/vip/