IngredientsViniferin is a resveratrol-derived compound that belongs to a group of plant-produced stilbenoids, functioning as a natural defense against microbial invasion, toxins, infections, and ultraviolet radiation. Based on their structural characteristics, stilbenoids containing C6-C2-C6 backbone structures are further divided into five categories: stilbenes, oligostilbenes, bibenzyls, bisbibenzyls, and phenanthrenes. Viniferins occupy the oligostilbene subcategory and are formally classified as oxidative oligomers of resveratrol (3,4′,5-trihydroxystilbene).
The term "viniferin" does not refer to a single molecule but to a structurally diverse family of resveratrol dimers, trimers, and tetramers. Alpha-(α-) viniferin (trimer), beta-(β-) viniferin (dimer), delta-(δ-) viniferin (oxidative dehydrodimer), epsilon-(ε-) viniferin (distinct dehydrodimer), gamma-(γ-) viniferin (isomeric oligomer), vitisin A (R-viniferin), and vitisin B (R2-viniferin) are structurally diverse forms with distinct pharmacological activities.
The most common compounds found in nature are a variety of resveratrol dimers, such as ε-viniferin and δ-viniferin, and trimers, i.e., α-viniferin. For example, although the compound itself takes the form of simple resveratrol dimers and trimers, there are two stereochemical centers at positions 7a and 8a on the dihydrofuran ring, allowing the formation of four potential stereoisomers. The trans- configuration of the two hydrogens in the saturated ring system provides alpha and beta hydrogen, unlike in the cis configuration, in which both hydrogens are either on the alpha side or in the beta position.
ε-Viniferin is a dehydrodimer: trans-(−)-ε-viniferin is a dehydrodimer with a five-membered oxygen heterocyclic ring. δ-Viniferin is its structural isomer: δ-viniferin is a resveratrol dehydrodimer and is an isomer of epsilon-viniferin. α-Viniferin, by contrast, is a resveratrol trimer, while R2-viniferin (Vitisin A) and R-viniferin (Vitisin B), which are resveratrol tetramers, can also be extracted and are found in the roots of Vitis vinifera.
Similar to other stilbene derivatives, viniferin may occur in both cis and trans configurations, although the trans form is generally considered the more stable and biologically active isomer.
The best-known sources of stilbenoids are from Vitis vinifera. The rare ω-viniferin has only been reported in Vitis vinifera, which remains the most diverse natural source, producing nearly all major viniferin types including α-, ε-, δ-, ω-, trans-, R-, and R2-viniferin.
Beyond the common grapevine, individual viniferin forms are found in other plant species. ε-Viniferin is found in Vitis vinifera grapevines, in wines, in the Oriental medicinal plant Vitis coignetiae, and in the stem bark of Dryobalanops aromatica. Cis-epsilon-viniferin can be found in Paeonia lactiflora. δ-Viniferin can be isolated from stressed grapevine (Vitis vinifera) leaves; it is also found in plant cell cultures and wine, and can also be found in Rheum maximowiczii.
Within the grapevine plant itself, viniferins are distributed across multiple tissues. Vine shoots, one of the most abundant winery wastes, could be used as a source of bioactive compounds such as stilbenes. The predominant stilbenoids in vine shoots are trans-resveratrol and ε-viniferin, whose content varies depending on numerous intrinsic and extrinsic factors. The biological activity of V. vinifera is determined by the presence of high contents of polyphenols, mainly flavonoids (e.g., quercetin, kaempferol), catechin derivatives, anthocyanins, and stilbenoids (e.g., trans-resveratrol, trans-ε-viniferin).
Viniferins have also been identified in species outside the Vitaceae family. α-Viniferin, for instance, was first isolated as the anti-inflammatory constituent of Caragana chamlagu, a leguminous shrub. Five resveratrol oligomers isolated from Carex folliculata and Carex gynandra, which included one dimer, two trimers, and two tetramers — pallidol (1); α-viniferin (2) and trans-miyabenol C (3); and kobophenols A (4) and B (5) — were evaluated for antiproliferative effects.
Stilbenoids, also known as phytoalexins, are plant phenolics that are synthesized as a defense mechanism in response to abiotic and biotic stresses, such as microbial attack, toxins, infections, or UV radiation. Stilbenes are mainly synthesized by plants as phytoalexins in response to biotic and abiotic stress (e.g., pathogens, ultraviolet irradiation, heavy metal ions, mechanical damage, frost, thermal treatment, or ozone).
δ-Viniferin is a grapevine phytoalexin following stresses like fungal infection (by Plasmopara viticola, the agent of downy mildew), UV light irradiation or ozone treatment. In cell cultures, the use of methyl jasmonate and jasmonic acid as elicitors stimulates δ-viniferin biosynthesis. Stilbene synthase (STS) is the key enzyme involved in stilbene biosynthetic pathways. Resveratrol serves as the monomeric building block; its oxidative cyclization by peroxidases produces the dimeric viniferins, and further oxidative coupling generates higher oligomers.
Solid by-products generated in the winemaking process can comprise valuable bioactive substances such as resveratrol and viniferin, which can be used in a whole range of sectors including medicine, pharmacy, and the cosmetic industry. Stilbene complex mixtures from Vitis vinifera L. wastes (cane, wood, and root) have recently been used as a cheap source of bioactive compounds for the development of natural fungicides.
Commercially, viniferin is most commonly encountered as a standardized extract of grapevine shoot (sarment or cane) material. One proprietary preparation, Vineatrol®30, is a grapevine-shoot extract standardized to contain both trans-resveratrol and trans-ε-viniferin. There are monographs published by respected organizations such as the EMA-HMPC (European Medicines Agency Committee on Herbal Medicinal Products), FDA (Food and Drug Administration), and EFSA (European Food Safety Authority) on the applicability of V. vinifera raw materials. In addition, there are nine V. vinifera raw materials which can be used in cosmetics that are listed in the CosIng (Cosmetics Ingredient) database, namely: fruit, skin (peel), seed, leaf, flower, root, shoot, stem, and bud.
Stilbenoids, also known as phytoalexins, are plant phenolics synthesized as a defense mechanism in response to abiotic and biotic stresses. The best-known sources of stilbenoids are from Vitis vinifera. The scientific identification of discrete viniferin molecules is a relatively modern achievement — the term and its chemical characterization emerged in the late 20th century — but the plant sources from which viniferins are extracted have long histories of traditional use.
Grapes, grape leaves, grape seeds, and grapevine bark have been used medicinally across European, Middle Eastern, and Asian traditions for millennia. In classical Mediterranean medicine, grapevine sap, leaves, and preparations from the cane were employed for purposes including wound healing, inflammation, and digestive complaints. Vitis coignetiae, one of the identified plant sources of ε-viniferin, is also recognized in Oriental herbal medicine, used historically in East Asian traditions. However, no historical source attributed specific effects to viniferin as a discrete chemical entity, since the isolation and naming of individual viniferins only occurred with modern analytical chemistry. The traditional use context is best understood as applying to whole-plant or crude extracts rather than to viniferin specifically.
Resveratrol and viniferin as the most common stilbene derivatives in grape cane, also known as phytoalexins, are important in food production and also can be very useful in various branches of science thanks to their potential antioxidant activity. Vitis vinifera (vine grape, Vitaceae) is one of the best-known fruit crops with wide applications in the food, pharmaceutical and cosmetic industries. The main cultivation regions of V. vinifera are located in Europe (France, Italy and Spain), Asia (China) and the Americas (United States, Argentina and Chile).
Different forms of viniferin exist, including alpha-viniferin (α-viniferin), beta-viniferin (β-viniferin), delta-viniferin (δ-viniferin), epsilon-viniferin (ε-viniferin), gamma-viniferin (γ-viniferin), R-viniferin (vitisin A), and R2-viniferin (vitisin B). All of these forms exhibit a range of important biological activities and, therefore, have several possible applications in clinical research and future drug development.
A wide variety of natural stilbene derivatives have been identified and their structure ranges from monomers to octamers possessing different substituents at various positions, like glycosyl, hydroxyl, methyl, or isopropyl groups. Among the viniferin forms, ε-viniferin and α-viniferin have received the most scientific attention; ε-viniferin and α-viniferin have been the most studied for their biological activities.
Stilbenes are polyphenols known for their antioxidant and anti-inflammatory activities. The main compound of this family is resveratrol, the oligomerization of which can produce numerous stilbenes containing up to eight resveratrol units. Despite the structural similarities between resveratrol and ε-viniferin, these compounds modulate some neurobiological effects in different ways. Furthermore, ε-viniferin has been reported to have more effective antioxidant and anti-inflammatory activities than resveratrol.
Antioxidant studies showed that ε-viniferin exhibited a 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging half-maximal inhibitory concentration (IC₅₀) of about 80 µM.
Suppression of nuclear factor kappa B (NF-κB), cyclooxygenase-2 (COX-2), and prostaglandin E₂ are among the anti-inflammatory mechanisms attributed to viniferin forms. α-Viniferin was found to inhibit cyclooxygenase activity and cytotoxic activity, and its anti-inflammatory activity has been attributed to its inhibition of cyclooxygenase-2 and inducible nitric oxide synthase, as well as suppression of signal transduction and activation of transcription-1 (STAT-1).
trans-(−)-ε-Viniferin preserves mitochondrial membrane potential and reduces reactive oxygen species (ROS) levels induced by mutant huntingtin. Moreover, viniferin increases mitochondrial SIRT3 levels, activates AMP-activated protein kinase (AMPK), and replenishes cellular NAD+ levels. The increased NAD+ leads to activation of SIRT3 deacetylase activity and enhances the antioxidant activity of target substrate Mn-SOD.
SIRT3 is required for the neuroprotection of viniferin, as inhibition of SIRT3 abolished the protection.
These effects involve multiple molecular targets and signaling pathways associated with glucose homeostasis, insulin signaling, oxidative stress, and inflammation. Viniferin has been reported to modulate glucose metabolism by enhancing insulin sensitivity and glucose uptake in peripheral tissues. ε-Viniferin has been shown to activate the AMPK pathway, which plays a pivotal role in regulating cellular energy metabolism and homeostasis. ε-Viniferin has been shown to activate AMPK in skeletal muscle and liver tissues, leading to promoting glucose uptake, fatty acid oxidation, and inhibiting hepatic gluconeogenesis.
Viniferin shows potential against multiple cancers by inducing apoptosis, cell cycle arrest, ROS production, and synergizing with chemotherapy, with 2R-viniferin acting via a p53-dependent mechanism. R2-viniferin causes an increase in intracellular reactive oxygen species (ROS), thereby inhibiting the p38/ERK MAPK signaling pathway, arresting the cell cycle in G2/M, and elevating the ratio of Bax/Bcl-2 proteins, predictive of apoptosis.
Alpha-viniferin inhibits melanin production in melasma and freckles by inhibiting protein kinase A (PKA) activation and reassociation between catalytic and regulatory subunits in cAMP-elevated melanocytes.
Huntington's Disease (Preclinical): To develop more potent neuroprotective agents from natural products, researchers screened a unique collection of 22 stilbenic compounds consisting of naturally occurring resveratrol monomers and oligomers, as well as semisynthetic resveratrol derivatives. They demonstrated that trans-(−)-ε-viniferin preserves mitochondrial membrane potential and reduces reactive oxygen species levels induced by mutant huntingtin. The study showed, for the first time, that mutant huntingtin down-regulates SIRT3 protein levels and provided evidence that the neuroprotective role of viniferin is mediated by SIRT3, and that viniferin further enhances the activity of the antioxidant enzyme Mn-SOD and activates AMPK. Together, the results indicate that viniferin enhances mitochondrial function and antioxidant activity via an increase of SIRT3 and activation of AMPK and downstream signaling pathways. This evidence is entirely preclinical (cell-based), with no human trials conducted.
Parkinson's Disease (Preclinical): ε-Viniferin has neuroprotective effects in Huntington's disease by activating the SIRT3/LKB1/AMPK signaling pathway; however, it remained unknown whether ε-viniferin also has a neuroprotective role in Parkinson's disease. A Parkinson's disease cell model was induced by exposing SH-SY5Y cells to 3.0 μM rotenone for 24 hours, and cells were then treated with 1.0 μM ε-viniferin for 24 hours. Treatment with ε-viniferin upregulated SIRT3 expression, which promoted FOXO3 deacetylation and nuclear localization. ε-Viniferin also increased ATP production and decreased reactive oxygen species production. Furthermore, ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis, and restored the expression of mitochondrial homeostasis-related proteins.
The polyphenol trans-ε-viniferin is a dimer of resveratrol reported to hold antioxidant and anti-inflammatory properties. A separate study aimed to evaluate the neuroprotective potential of viniferin in nerve growth factor (NGF)-differentiated PC12 cells, a dopaminergic cellular model of Parkinson's disease, and to assess its anti-inflammatory properties in a N9 microglia–neuronal PC12 cell co-culture system. All evidence in this area is preclinical; no clinical trials in human Parkinson's or Huntington's patients have been reported.
Non-Small Cell Lung Cancer (Preclinical): A study evaluated the effectiveness of α-viniferin and ε-viniferin using MTT assay. Results showed that α-viniferin was more effective than ε-viniferin in reducing the viability of NCI-H460 cells, a type of non-small cell lung cancer. Annexin V/7AAD assay results provided further evidence that the decrease in cell viability observed in response to α-viniferin treatment was due to the induction of apoptosis in NCI-H460 cells.
Resveratrol oligomers, including vitisin A, (−)-vitisin B, and (+)-hopeaphenol, have been found to have promising anti-cancer properties due to their ability to inhibit the activity of the human SIRT1 enzyme.
Colon Cancer (Preclinical): In a study, five resveratrol oligomers isolated from Carex folliculata and Carex gynandra — including α-viniferin — along with resveratrol were evaluated for antiproliferative effects against human colon cancer (HCT-116, HT-29, Caco-2) and normal human colon (CCD-18Co) cells. Although not cytotoxic, the resveratrol oligomers, as well as resveratrol, inhibited growth of the human colon cancer cells. Among the six stilbenoids, α-viniferin was most active against the colon cancer cells with IC₅₀ values of 6–32 μM (>2-fold compared to normal colon cells). Moreover, α-viniferin at 20 μM did not induce apoptosis but arrested cell cycle (in the S-phase) for the colon cancer but not the normal colon cells.
Prostate Cancer (Preclinical): Researchers investigated the cytotoxic/growth-inhibiting properties of the resveratrol tetramer r-viniferin on the prostate cancer cell line LNCaP and compared them with those of resveratrol. Using the sulforhodamine B assay followed by cell cycle analysis via flow cytometry and commercially available apoptosis/necrosis assay kits, they showed that both compounds were able to inhibit the growth of LNCaP cells and to induce a cell cycle arrest in the G1 phase. r-Viniferin was significantly more potent in inhibiting cellular growth than resveratrol and was the only compound that increased the apoptotic cellular fraction as well as the activity of apoptosis-associated enzymes.
In a separate prostate cancer study, researchers investigated the therapeutic efficacy and mechanism of α-viniferin, an oligostilbene of trimeric resveratrol, against human prostate cancer cells, and found that it markedly inhibited the proliferation of LNCaP, DU145, and PC-3 cancer cells in a time- and dose-dependent manner, and had strong cytotoxicity in non-androgen-dependent prostate cancer cells. In addition, it inhibited AR downstream expression in LNCaP cells and inhibited activation of GR signaling pathway in DU145 and PC-3.
Hepatocellular Carcinoma (Preclinical): R2-viniferin demonstrated an IC₅₀ of 9.7 µM against hepatocellular carcinoma HepG2 cells at 72 h, mediated through apoptosis and cell-cycle arrest. The stilbene tended to arrest cell cycle at G2/M, and it also increased intracellular reactive oxygen species, caspase 3 activity, and the ratio of Bax/Bcl-2 proteins, indicative of apoptosis. The distinctive toxicity of R2-viniferin on HepG2 encourages research into the underlying mechanism to develop the oligostilbene as a therapeutic agent against hepatocellular carcinoma.
Evidence strength for anticancer activity: All anticancer findings reported above are based on in vitro (cell culture) studies. No controlled clinical trials in human cancer patients have been conducted for any viniferin form. The evidence is considered preliminary.
In vivo studies reinforce viniferin's antidiabetic effects. Oral administration of viniferin in diabetic rodent models resulted in significantly decreased fasting blood glucose levels and improved lipid profiles. ε-Viniferin was confirmed to have a higher anti-adipogenesis activity in 3T3-L1 cells. It significantly suppressed lipid accumulation and the expression of the adipogenesis marker gene PPAR gamma. When compared with a high-fat-diet control mice group, there was reduced body weight, as well as liver triglyceride levels following ε-viniferin treatment. The levels of plasma insulin and leptin were significantly improved.
Evidence strength: Evidence is restricted to in vitro cell models and animal studies. No human clinical trials on viniferin for diabetes or metabolic syndrome have been reported.
α-Viniferin, a bioactive phytochemical compound, has been reported to have excellent anti-Staphylococcus efficacy as a topical agent. However, before 2021, no clinical trials had been conducted to elucidate its efficacy. A study aimed to investigate the antibacterial efficacy of α-viniferin against S. aureus in a ten-day clinical trial. α-Viniferin showed 50% minimum inhibitory concentrations (MIC₅₀ values) of 7.8 μg/mL in culture broth medium.
α-Viniferin was administered in the nares three times a day for ten days using a sterile cotton swab stick. Nasal swab specimens were collected before (0 days) and after finishing the trial (10th day), and then analyzed. 16S ribosomal RNA-based amplicon sequencing analysis showed that S. aureus reduced from 51.03% to 23.99% at the genus level. RNA-seq analysis was also conducted to gain insights into molecular mechanisms of α-viniferin against S. aureus, which revealed that some gene groups were reduced in 5-fold FC cutoff at two times MIC conditions. The study results demonstrate α-viniferin as a potential S. aureus-specific drug candidate.
Evidence strength: This is a small, single-arm, topical application trial published in the Polish Journal of Microbiology (2021). While it constitutes the only direct human clinical trial data for any viniferin form, it was a preliminary proof-of-concept study with limited sample size and no comparator arm. No oral antimicrobial clinical trials exist for viniferin.
When vascular endothelial cells (VECs) were exposed to ε-viniferin, endothelial NO synthase was activated and the expression of sirtuin 1 (SIRT1) and HO-1 was induced.
A grapevine shoot extract (GSE) was administered to an isoproterenol-induced myocardial injury animal model. The extract alleviated the associated symptoms, i.e., the plasma lipid profile was improved, while the disturbed plasma ion concentration, the cardiac dysfunction markers, the DNA laddering, and the necrosis of myocardial tissue were diminished. This was an animal study using a mixed extract (containing both trans-resveratrol and trans-ε-viniferin), and the specific contribution of viniferin versus resveratrol was not isolated.
Evidence strength: Cardiovascular evidence for viniferin specifically is preclinical (cell-based and animal model). No human cardiovascular trials have been completed.
Treatment with α-viniferin dose-dependently inhibited α-MSH-induced melanin production, as did arbutin, in which α-viniferin was more effective (>5-fold) than arbutin in the comparison with IC₅₀ values. α-Viniferin also inhibited histamine- or N6,2'-O-dibutyryl (db)-cAMP-induced melanin production in B16-F0 cells.
The beneficial properties of stilbenes for human health include protective effects against cancer, diabetes, neurodegenerative diseases such as Alzheimer's disease, and coronary heart disease. They are also used as multifunctional ingredients in cosmetics. The anti-melanogenic activity of α-viniferin is considered one of its strongest commercially exploited properties, but clinical evidence from controlled human trials remains absent from the published literature.
Research isolated stilbenes from Vitis vinifera grapevine shoots to perform biological assays against amyloid-β peptide aggregation. Known compounds isolated included (E)-ε-viniferin (trans-ε-viniferin) and ω-viniferin, and their structures were established on the basis of detailed spectroscopic analysis. α-Viniferin is a trimer of resveratrol and has various pharmacological activities including anti-Alzheimer's disease, anti-tuberculosis, anti-tumor, anti-inflammatory and anti-diabetic. Evidence for Alzheimer's-related benefits is currently limited to in vitro assays; no human clinical data are available.
Natural stilbenes were shown to possess a wide range of biological activities, such as antioxidant, anti-inflammatory, antihyperglycemic, cardioprotective, neuroprotective, and antineoplastic properties.
Primary pharmacokinetic (PK) studies reveal that viniferin isomers, particularly δ- and ε-viniferin, generally exhibit very low oral bioavailability (< 3%). This is attributed to a combination of poor absorption and extensive first-pass metabolism (glucuronidation and sulfation). Species differences in metabolism are notable; for instance, sulfation plays a larger role in ε-viniferin metabolism in vitro in humans compared to rats.
Oral bioavailability of α-viniferin was found to be 4.2% in rat pharmacokinetic studies. Unlike resveratrol, ε-viniferin and α-viniferin are quickly absorbed in vivo experiments as reported by many pharmacokinetic studies.
Encapsulation of ε-viniferin into multilamellar liposomes (MLL) improved its pharmacokinetic behavior in rats compared with free ε-viniferin. While encapsulation did not markedly alter plasma levels of the native compound, it significantly prolonged the half-life of its major glucuronide metabolite (εVG), increasing it almost three-fold (approximately 119 min vs. 38 min for the free form), and doubled plasma and tissue exposure to εVG. Moreover, encapsulated ε-viniferin led to higher concentrations in metabolically active tissues, including liver, kidneys, and adipose depots.
These findings highlight that nanocarriers may enhance the stability and systemic persistence of viniferin metabolites, representing a promising avenue to overcome bioavailability barriers typical of plant-derived stilbenoids.
Reported dosages are sourced directly from specific studies and reflect the experimental conditions used, not clinically established human therapeutic doses:
The confirmation of viniferin concentrations' therapeutic efficacy in humans is still required. The pharmaceutical industry faces a significant challenge in applying this molecule clinically; it needs to be studied in greater depth to understand its bioavailability, metabolic pathways and human toxicity, and thus the need to improve the field of clinical medicine is a challenge in producing commercially viable medicine.
To date, human safety data on viniferins remain confined to topical use. Challenges such as low bioavailability and isomerization are the major bottlenecks for the development of stilbenes as therapeutic drugs. No long-term oral safety or toxicology data from human clinical trials have been published for any viniferin form.
A key safety concern identified in laboratory research is the inhibition of cytochrome P450 enzymes by α-viniferin. Herb–drug interactions are the source of the most harmful complications in patients co-administered herbal and modern medicines, and are caused by modulation of the activities of drug metabolizing enzymes. Researchers investigated the inhibitory effects of α-viniferin on the activities of 9 human cytochrome P450 (CYP) isoforms using a cocktail of probe substrates and LC–MS/MS in pooled human liver microsomes. α-Viniferin strongly inhibited 7 of the 9 CYP isoforms (except CYP2A6 and CYP2E1).
Furthermore, α-viniferin strongly inhibited CYP2C19-mediated omeprazole 5-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation with IC₅₀ values of 0.93 and 1.2 μM, respectively. CYP3A4 and CYP2C19 are major enzymes responsible for the metabolism of a wide range of clinically used drugs; inhibition in vitro at these concentrations signals a potential for pharmacokinetic herb-drug interactions, though this has not been characterized in human subjects.
ε-Viniferin has also been noted to inhibit human cytochrome P450 enzymes: it shows human cytochrome P450 enzymes inhibition activity.
α-Viniferin at concentrations with antimelanogenic activity did not disturb the viability or proliferation of melanocytes, excluding nonspecific cytotoxicity. In several in vitro studies, effects on cancer cells were observed at concentrations that did not affect normal cells, suggesting some degree of selectivity, but this has not been confirmed in humans.
The confirmation of viniferin concentrations' therapeutic efficacy in humans is still required. The pharmaceutical industry faces a significant challenge in applying this molecule clinically; it needs to be studied in greater depth to understand its bioavailability, metabolic pathways and human toxicity. The studies indicated that viniferin is a potentially active molecule and that structural modifications to viniferin may lead to new drug development, with improved bioavailability.
The body of scientific research on viniferins is substantial at the preclinical level but markedly limited with respect to human clinical evidence. The diverse studies conducted on viniferin cover anti-inflammatory, antipsoriasis, antidiabetic, antiplasmodic, anticancer, anti-angiogenic, antioxidant, anti-melanogenic, neurodegenerative effects, antiviral, antimicrobial, antifungal, antidiarrhea, anti-obesity, and anthelminthic activities. However, the overwhelming majority of these observations derive from cell-culture (in vitro) and animal (in vivo) experiments. The single published human clinical trial tested only the topical antibacterial efficacy of α-viniferin against nasal S. aureus colonization. A separate human bioavailability study examined a 500 mg single dose of a standardized grapevine-shoot extract. Neither study establishes a therapeutic dose or a safety profile for systemic, long-term viniferin supplementation.
Viniferins, oligomeric structures 'constructed by nature' on a structural platform of resveratrol, deserve extraordinary attention because they might offer a wide spectrum of pharmacological effects that can be prospectively utilized to improve human health. The consensus in the peer-reviewed literature is that viniferin research is promising but remains in an early stage, and that rigorous human trials are needed before any therapeutic claims can be validated.
Health conditions that Viniferin may help support.
Body systems that Viniferin may help support.
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