Quick Navigation


Pterostilbene is a dimethylated derivative of resveratrol that, for some mechanisms, is more potent. It is also much better absorbed, and is commonly referred to as a 'better resveratrol'. It looks promising, but has significantly less research than its predecessor.

Our evidence-based analysis on pterostilbene features 55 unique references to scientific papers.

Research analysis led by and reviewed by the Examine team.
Last Updated:

Easily stay on top of the latest nutrition research

Become an Examine Member to get access to all of the latest nutrition research:

  • Unlock information on 400+ supplements and 600+ health topics.
  • Get a monthly report summarizing studies in the health categories that matter specifically to you.
  • Access detailed breakdowns of the most important scientific studies.

Try FREE for 14 days

Research Breakdown on Pterostilbene

1Sources and Structure


Pterostilbene (trans-3,5-dimethoxy-4-hydroxystilbene[2]) is a stilbene compound that is structurally similar to other popular stilbenes such as resveratrol or piceatannol;[3] it is named after its first discovered source (the pterocarpus genus)[4] but is also a component of blueberries and grape products. It is a phytoalexin (compound produced by plants as a defense against parasites and insects) similar to resveratrol[5] albeit more potent.[6][7]

Pterostilbene is a phytoalexin (plant chemical defense) similar to resveratrol, belonging to the stilbene class of molecules; it is named after the pterocarpus genus of plants

Its sources include:

  • Pterocarpus marsupium (Indian Kino Tree)[8] and pterocarpus santalinus (Sandalwood)[9]

  • Blueberries (92-550ng/g dry weight)[10][3]

  • Grape (Vitis vinifera) leaves[7] and berries[11]

  • Anogeissus acuminata[12]

  • The Dracaena genus[13]

  • Rheum rhaponticum (root)[14]

  • Peanuts (Arachis hypogaea)[15]

Pterostilbene is contained in low quantities in a few plants, most notably blueberries and grapes. Despite being in low concentrations, it is likely bioactive following oral ingestion of these fruits and their products (such as wine)

1.2Structure and Properties

The structure of pterostilbene is very similar to resveratrol, although the 3,5-dihydroxy part of resveratrol (the two hydroxyl groups on the benzene ring to the left) are replaced with methoxy groups.

The antioxidant capacities of resveratrol requires that there is a hydroxylation at the 4' position (right side of the molecule) and that the overall molecule is in a trans configuration rather than cis.[16][17][18][19] The above stilbenes all abide by these requirements while others such as pinosylvin do not. The methoxy groups on perostilbene appear to allow a greater antioxidative capacity relative to resveratrol.[16][17]

Pterostilbene is a methoxylated resveratrol, essentially. It has a larger difference in structure from resveratrol than piceatannol (another common stilbene compound, which is more similar to resveratrol). These three structures form the common dietary stilbenes



Pterostilbene, due to the two methoxy groups, exhibits increased hydrophobicity and oral absorption relative to resveratrol.[20] Relative to the approximate 20% bioavailability of resveratrol following oral ingestion,[21] pterostilbene's is near 80% at oral doses of 56-168mg/kg[20] and a bit lower (59.2+/-19.6% when paired with 2-hydroxypropyl-β-cyclodextrin, a delivery system[22] that complexes pterostilbene[23]) at 15mg/kg.[24] The general idea of methylated flavonoids or polyphenols having greater absorption is well known.[25]

Taking pterostilbene by itself has been noted to have a lower bioavailability (15.9+/-7.8%) than when taken as part of a delivery system, and bioavailability is further significantly reduced when taken in a fasted state (less than 5.5%).[24] Increasing the dosage to 60mg/kg under these same conditions increases the bioavailability two-fold.[24]

Sublingual absorption of pterostilbene has a bioavailability of 25.8+/-13.1%.[24]

Pterostilbene appears to be well absorbed, and better absorbed than resveratrol. While its absorption is somewhat respectable (for a polyphenolic) at lower oral doses, higher oral doses appear to actually be better absorbed than lower doses. Pterostilbene can be absorbed sublingually


A single dose of 56-168mg/kg pterostilbene has noted a Cmax of 2,820ng/mL (56mg/kg) and 7,780ng/mL (168mg/kg) at a Tmax of 2 or 4 hours and half-lives of 90 and 114 minutes, respectively.[20]

56-168mg/kg pterostilbene daily for two weeks has noted a Cmax of 2,550ng/mL (56mg/kg) or 5,560ng/mL (168mg/kg) at a Tmax of 2 and 8 hours with half-lives of 96 and 114 minutes, respectively.[20] Repeated dosing appears to be associated with a higher overall AUC for 56mg/kg (15,000ng/h/mL versus 13,700ng/h/mL) but not 168mg/kg (49,600ng/h/mL versus 57,700ng/h/mL).[20]

Chronic dosing of pterostilbene appears to reduce the peak serum values while prolonging the time to reach peak levels. When looking at overall bodily exposure to pterostilbene, there isn't a predictable difference


The clearance rate of pterostilbene suggests that it readily bioaccumulates in the body[20] and the twin methoxy groups on the molecule mean it can diffuse into a cell more readily than resveratrol.[26]


While resveratrol appears to mostly be metabolized into a glucuronide conjugate, pterostilbene is mostly metabolized into pterostilbene sulfate.[20]

2.5Enzymatic Interactions

Pterostilbene has been noted to activate AMPK (albeit in prostatic cancer cells).[27]



10-30μM pterostilbene appears to reduce microglial nitric oxide production when stimulated by LPS[28] without directly scavenging the nitric oxide radicals.[29] It appears to work via inhibiting IκBα phosphorylation, and is slightly more potent than resveratrol.[29]


Pterostilbene appears to exert anxiolytic effects in the 1-2mg/kg oral dosing range in mice subjected to an elevated maze test, although it appears ineffective at 5-10mg/kg; this is thought to be related to ERK phosphorylation in the hippocampus[30] which is known to be related to anxiety and mood.[31]

3.3Memory and Learning

Isolated pterostilbene has been noted to improve cognition in aged rats when fed in the diet at 0.004-0.016% over 12-13 weeks, with the improvements correlating with hippocampal concentrations of pterostilbene.[32]

4Cardiovascular Health

4.1Blood Pressure

Supplementation of pterostilbene at 125mg twice daily appeared to reduce blood pressure (diastolic and systolic) in hypercholesteromic adults, an effect not observed with 50mg taken twice daily but partially replicated (systolic only) when 50mg was paired with 100mg grape seed extract (GSE) also taken twice daily.[33]


Pterostilbene has been noted to increase the signalling of PPARα receptors at 100µM (8-fold) and 300µM (14-fold) concentrations, with 100µM of pterostilbene being 74.2% more effective than 100µM ciprofibrate as assessed by relative luciferase units.[34] At concentrations of 1-10µM pterostilbene, the receptors were mostly inactive.[34] Since pterostilbene is known to bind to PPARα[35] it appeared to be an agonist of this receptor.

Pterostilbene may be a PPARα ligand

Oral ingestion of pterostilbene at 25mcg/kg of the diet of hamsters with high cholesterol is able to subsequently reduce LDL-C (29%) and increase HDL-C (7%),[34] and reductions in LDL-C (57%) and improvements in HDL-C (73.1%) have been noted in diabetic rats given 40mg/kg pterostilbene.[36]

Animal studies show an improvement in cholesterol metabolism with low dose supplementation of pterostilbene

When supplemented to subjects with high cholesterol (200mg/dL) and high LDL-C, pterostilbene at both doses (50mg or 125mg, both taken twice daily) appeared to increase total cholesterol and LDL cholesterol relative to placebo, with the group given the low dose pterostilbene with grape seed extract (GSE; 100mg twice daily) not seeing this increase;[33] the benefits to blood pressure seen with high dose pterostilbene were replicated with GSE.[33]

HDL cholesterol was noted to be unchanged overall, but in people not on cholesterol medication taking the higher dose of pterostilbene there was a decrease relative to control.[33]

High doses of pterostilbene supplementation (50-125mg twice daily) appear to increase, rather than decrease, cholesterol and LDL levels in subjects who already have high LDL concentrations; those not on cholesterol lowering medications also noted a decrease in HDL cholesterol


Serum triglycerides were reduced by 30% following six weeks of supplementation with 40mg/kg pterostilbene in diabetic rats, the potency exceeding that of 500mg/kg metformin but not fully normalizing relative to nondiabetic control.[36]

In humans (hypercholesterolemic but with normal triglycerides) given 50mg or 125mg pterostilbene twice daily over the course of 52 days, there were no observable changes in serum triglyceride concentrations relative to control; the addition of 100mg grape seed extract to the low dose group also did not confer any beenfits.[33]

5Interactions with Glucose Metabolism

5.1Blood Glucose

25mcg/kg of pterostilbene to the diets of hypercholesterolemic hamsters is able to reduce blood glucose by 14%[34] and in diabetic rats 40mg/kg pterostilbene for six weeks a reduction in glucose with a concomitant increase in insulin was noted;[36] this extended to otherwise healthy rats to a lesser degree (6.3% reduction)[36] and in hyperglycemic rats the potency of pterostilbene (40mg/kg) is comparable to metformin (500mg/kg).[36][37]

6Inflammation and Immunology


Pterostilbene has been noted to inhibit LPS-induced PGE2 production from white blood cells with an IC50 value of 1.0+/-0.6µM (compared to the IC50 of resveratrol at 3.2+/-1.4µM)[4] and can inhibit iNOS activity in macrophages with an IC50 of 9.9µg/mL (comparable to resveratrol and weaker than parthenolide from feverfew at 0.42µg/mL).[15]

Pterostilbene may exert antiinflammatory effects at low concentrations with a potency greater than resveratrol; these effects may be relevant to oral supplementation of higher doses of pterostilbene

Neutrophils are known to produce oxidation when activated via the NADPH oxidase enzyme[38] which may lead to injury in excessive levels (despite being protective against bacterial invaders at lower activity);[39] resveratrol has previously been implicated as an NADPH oxidase inhibitor, and this activity appears to extend to pterostilbene as it can reduce chemiluminescence of neutrophils (an indication of antioxidant activity[40]).[41] And while pterostilbene doesn't inherently affect superoxide levels in neutrophils,[42] 100µM is able to reduce superoxide production and subsequent myeloperoxidase (MPO) production to around 60% of control with lower concentrations ineffective.[42]

When comparing potencies, pterostilbene appears to be less effective than resveratrol[43] (assessed by IC50 values of reducing extracellular chemiluminescence) with pterostilbene also being less potent than piceatannol, and the potency of curcumin lying between resveratrol and piceatannol.[44][41][45] When looking at intracellular chemiluminescence, curcumin seems most potent (IC50 3.57µM to pterostilbene's 21.58µM) and resveratrol is intermediate to the two.[43]

Reduced chemiluminescence has been noted in rats following ingestion of 30mg/kg pterostilbene (partial reduction), suggesting that the above is biologically relevant in higher doses to a small degree.[46]

Pterostilbene appears to reduce oxidation in neutrophils (the main mechanism of action of spirulina), although the effect seems to occur only at very high concentrations. It appears to be active following oral ingestion, but not to a large degree

6.2Joint Inflammation

30mg/kg pterostilbene in a rat model of arthritis has shown weak anti-inflammatory effects, having no significant effect on hind paw volume (a marker of edema) or MPO while minorly reducing chemiluminescence (a marker of neutrophil oxidation).[46]

Current preliminary evidence suggests no significant benefit of pterostilbene on inflammation, just a minor antioxidative effect

7Interactions with Cancer Metabolism


Resveratrol has previously been noted to increase apoptosis via the Notch signalling pathway[47][48] (which induces Cyclin D1 and survivin as it is prosurvival[49][50]) which appears to extend to pterostilbene in lung cancer cells (A549) with an IC50 value on cell growth of 3.476µM.[51] Pterostilbene appears to reduce the Notch1-dependent survial while induces production of reactive oxygen species, leading to apoptosis.[51]

Pterostilbene appears to reduce viability of lung cancer cells in vitro, and does so at a concentration that is probably relevant to oral supplementation

8Longevity and Life Extension


Pterostilbene (70μM) has been noted to upregulate a variety of mitochondrial genes in a yeast assay (148 up and 13 downregulated) involved in respiration, electron transport, mitochondrial protein targeting, and mitochondrial protein synthesis.[52]

The oxidative stress seen during the aging process in neurons appears to be attenuated with low dietary levels of pterostilbene (0.004-0.016% of the diet), with a potency greater than resveratrol.[32][53]

9Safety and Toxicology


In mice, doses of pterostilbene up to 3,000mg/kg daily (500-fold the estimated human intake) have failed to exert any significant clinical or biochemical toxicity.[54]

Pterostilbene up to 250mg daily (125mg twice daily) in humans over the course of 6-8 weeks has failed to cause any biochemical or clinical signs of toxicity, with side effects not significantly different than placebo aside from one dropout due to worsening cholesterol[55] which may be related to an increase in LDL-C seen with this dose when tested elsewhere in hypercholesterolemic adults.[33]


  1. ^ Qureshi AA, et al. Suppression of Nitric Oxide Production and Cardiovascular Risk Factors in Healthy Seniors and Hypercholesterolemic Subjects by a Combination of Polyphenols and Vitamins. J Clin Exp Cardiolog. (2012)
  2. ^ McCormack D, McFadden D. A review of pterostilbene antioxidant activity and disease modification. Oxid Med Cell Longev. (2013)
  3. ^ a b Rimando AM, et al. Resveratrol, pterostilbene, and piceatannol in vaccinium berries. J Agric Food Chem. (2004)
  4. ^ a b Hougee S, et al. Selective COX-2 inhibition by a Pterocarpus marsupium extract characterized by pterostilbene, and its activity in healthy human volunteers. Planta Med. (2005)
  5. ^ Langcake P. Disease resistance of Vitis spp. and the production of the stress metabolites resveratrol, epsiton-viniferin, alpha-viniferin and pterostilbene. Physiol Plant Pathol. (1981)
  6. ^ Alessandro M, et al. Bioassays on the Activity of Resveratrol, Pterostilbene and Phosphorous Acid towards Fungi Associated with Esca of Grapevine. Pytopathol Mediterr. (2000)
  7. ^ a b Langcake P, Cornford CA, Pryce RJ. Identification of pterostilbene as a phytoalexin from Vitis vinifera leaves. Phytochem. (1979)
  8. ^ Maurya R, et al. Constituents of Pterocarpus marsupium: an ayurvedic crude drug. Phytochemistry. (2004)
  9. ^ Seshadri TR. Polyphenols of Pterocarpus and Dalbergia woods. Phytochem. (1972)
  10. ^ Rodríguez-Bonilla P, et al. Development of a reversed phase high performance liquid chromatography method based on the use of cyclodextrins as mobile phase additives to determine pterostilbene in blueberries. J Chromatogr B Analyt Technol Biomed Life Sci. (2011)
  11. ^ Adrian M, et al. Stilbene content of mature Vitis vinifera berries in response to UV-C elicitation. J Agric Food Chem. (2000)
  12. ^ Rimando AM, et al. Revision of the NMR Assignments of Pterostilbene and of Dihydrodehydrodiconieferyl alcohol: Cytotoxic Constituents from Anogeissus acuminata. Nat Prod Lett. (1994)
  13. ^ Fan LL, et al. Simultaneous quantification of five major constituents in stems of Dracaena plants and related medicinal preparations from China and Vietnam by HPLC-DAD. Biomed Chromatogr. (2009)
  14. ^ Püssa T, et al. Polyphenolic composition of roots and petioles of Rheum rhaponticum L. Phytochem Anal. (2009)
  15. ^ a b Sobolev VS, et al. Biological activity of peanut (Arachis hypogaea) phytoalexins and selected natural and synthetic Stilbenoids. J Agric Food Chem. (2011)
  16. ^ a b Ovesná Z, Horváthová-Kozics K. Structure-activity relationship of trans-resveratrol and its analogues. Neoplasma. (2005)
  17. ^ a b Hasiah AH, et al. Cytotoxic and antioxidant effects of methoxylated stilbene analogues on HepG2 hepatoma and Chang liver cells: Implications for structure activity relationship. Hum Exp Toxicol. (2011)
  18. ^ Cheng JC, et al. Structure-activity relationship studies of resveratrol and its analogues by the reaction kinetics of low density lipoprotein peroxidation. Bioorg Chem. (2006)
  19. ^ Stivala LA, et al. Specific structural determinants are responsible for the antioxidant activity and the cell cycle effects of resveratrol. J Biol Chem. (2001)
  20. ^ a b c d e f g Kapetanovic IM, et al. Pharmacokinetics, oral bioavailability, and metabolic profile of resveratrol and its dimethylether analog, pterostilbene, in rats. Cancer Chemother Pharmacol. (2011)
  21. ^ Athar M, et al. Resveratrol: a review of preclinical studies for human cancer prevention. Toxicol Appl Pharmacol. (2007)
  22. ^ Thatiparti TR, Shoffstall AJ, von Recum HA. Cyclodextrin-based device coatings for affinity-based release of antibiotics. Biomaterials. (2010)
  23. ^ López-Nicolás JM, et al. Physicochemical study of the complexation of pterostilbene by natural and modified cyclodextrins. J Agric Food Chem. (2009)
  24. ^ a b c d Yeo SC, Ho PC, Lin HS. Pharmacokinetics of pterostilbene in Sprague-Dawley rats: The impacts of aqueous solubility, fasting, dose escalation, and dosing route on bioavailability. Mol Nutr Food Res. (2013)
  25. ^ Wen X, Walle T. Methylated flavonoids have greatly improved intestinal absorption and metabolic stability. Drug Metab Dispos. (2006)
  26. ^ Lin HS, Yue BD, Ho PC. Determination of pterostilbene in rat plasma by a simple HPLC-UV method and its application in pre-clinical pharmacokinetic study. Biomed Chromatogr. (2009)
  27. ^ Lin VC, et al. Activation of AMPK by pterostilbene suppresses lipogenesis and cell-cycle progression in p53 positive and negative human prostate cancer cells. J Agric Food Chem. (2012)
  28. ^ Carey AN, et al. Stilbenes and Anthocyanins Reduce Stress Signaling in BV-2 Mouse Microglia. J Agric Food Chem. (2013)
  29. ^ a b Meng XL, et al. Effects of resveratrol and its derivatives on lipopolysaccharide-induced microglial activation and their structure-activity relationships. Chem Biol Interact. (2008)
  30. ^ Al Rahim M, et al. Anxiolytic Action of Pterostilbene: Involvement of Hippocampal ERK Phosphorylation. Planta Med. (2013)
  31. ^ Einat H, et al. The role of the extracellular signal-regulated kinase signaling pathway in mood modulation. J Neurosci. (2003)
  32. ^ a b Joseph JA, et al. Cellular and behavioral effects of stilbene resveratrol analogues: implications for reducing the deleterious effects of aging. J Agric Food Chem. (2008)
  33. ^ a b c d e f Riche DM1, et al. Pterostilbene on metabolic parameters: a randomized, double-blind, and placebo-controlled trial. Evid Based Complement Alternat Med. (2014)
  34. ^ a b c d Rimando AM, et al. Pterostilbene, a new agonist for the peroxisome proliferator-activated receptor alpha-isoform, lowers plasma lipoproteins and cholesterol in hypercholesterolemic hamsters. J Agric Food Chem. (2005)
  35. ^ Mizuno CS, et al. Design, synthesis, biological evaluation and docking studies of pterostilbene analogs inside PPARalpha. Bioorg Med Chem. (2008)
  36. ^ a b c d e Pari L, Satheesh MA. Effect of pterostilbene on hepatic key enzymes of glucose metabolism in streptozotocin- and nicotinamide-induced diabetic rats. Life Sci. (2006)
  37. ^ Manickam M, et al. Antihyperglycemic activity of phenolics from Pterocarpus marsupium. J Nat Prod. (1997)
  38. ^ El-Benna J, Dang PM, Gougerot-Pocidalo MA. Priming of the neutrophil NADPH oxidase activation: role of p47phox phosphorylation and NOX2 mobilization to the plasma membrane. Semin Immunopathol. (2008)
  39. ^ Babior BM. Phagocytes and oxidative stress. Am J Med. (2000)
  40. ^ Jancinová V, et al. The combined luminol/isoluminol chemiluminescence method for differentiating between extracellular and intracellular oxidant production by neutrophils. Redox Rep. (2006)
  41. ^ a b Perecko T, et al. Structure-efficiency relationship in derivatives of stilbene. Comparison of resveratrol, pinosylvin and pterostilbene. Neuro Endocrinol Lett. (2008)
  42. ^ a b Mačičková T, et al. Effect of stilbene derivative on superoxide generation and enzyme release from human neutrophils in vitro. Interdiscip Toxicol. (2012)
  43. ^ a b Drábiková K, et al. Polyphenol derivatives - potential regulators of neutrophil activity. Interdiscip Toxicol. (2012)
  44. ^ Jancinová V, et al. Decreased activity of neutrophils in the presence of diferuloylmethane (curcumin) involves protein kinase C inhibition. Eur J Pharmacol. (2009)
  45. ^ Nosal R, et al. Suppression of oxidative burst in human neutrophils with the naturally occurring serotonin derivative isomer from Leuzea carthamoides. Neuro Endocrinol Lett. (2010)
  46. ^ a b Macickova T, et al. In vivo effect of pinosylvin and pterostilbene in the animal model of adjuvant arthritis. Neuro Endocrinol Lett. (2010)
  47. ^ Lin H, et al. Notch-1 activation-dependent p53 restoration contributes to resveratrol-induced apoptosis in glioblastoma cells. Oncol Rep. (2011)
  48. ^ Truong M, et al. Resveratrol induces Notch2-mediated apoptosis and suppression of neuroendocrine markers in medullary thyroid cancer. Ann Surg Oncol. (2011)
  49. ^ Meng RD, et al. gamma-Secretase inhibitors abrogate oxaliplatin-induced activation of the Notch-1 signaling pathway in colon cancer cells resulting in enhanced chemosensitivity. Cancer Res. (2009)
  50. ^ Chen Y, et al. Notch-1 signaling facilitates survivin expression in human non-small cell lung cancer cells. Cancer Biol Ther. (2011)
  51. ^ a b Yang Y, et al. Pterostilbene exerts antitumor activity via the Notch1 signaling pathway in human lung adenocarcinoma cells. PLoS One. (2013)
  52. ^ Pan Z, et al. Identification of molecular pathways affected by pterostilbene, a natural dimethylether analog of resveratrol. BMC Med Genomics. (2008)
  53. ^ Chang J, et al. Low-dose pterostilbene, but not resveratrol, is a potent neuromodulator in aging and Alzheimer's disease. Neurobiol Aging. (2012)
  54. ^ Ruiz MJ, et al. Dietary administration of high doses of pterostilbene and quercetin to mice is not toxic. J Agric Food Chem. (2009)
  55. ^ Riche DM, et al. Analysis of safety from a human clinical trial with pterostilbene. J Toxicol. (2013)