Lambertine (Dihydroberberine)

Lambertine (Dihydroberberine) at a Glance

Lambertine is a synonym, not a separate molecule. The name comes from Berberis lambertii, an Asian barberry from which a minor alkaloid was isolated and christened “lambertine”; the compound was subsequently shown to be dihydroberberine — berberine with its charged iminium bond reduced ^{1,2Reference 1PubChemDihydroberberine, CID 10217 (CAS 483-15-8; synonyms include lambertine, lambertin, dihydroumbellatine)View study →Reference 2Jeffs PW · 1967The Protoberberine AlkaloidsView study →}. Everything written about lambertine since is filed under the modern name.

That resolution changes the subject here. Under “lambertine” there is almost nothing: a handful of mid-century isolation notes and a single qualitative line in a Berberis phytochemistry review placing it among the root alkaloids of barberry, with no concentration figure attached ^{3Reference 3Mokhber-Dezfuli N et al. · 2014Phytochemistry and pharmacology of Berberis speciesView study →}. Under dihydroberberine there is a real, if small, modern literature — because the same molecule is what gut bacteria make out of swallowed berberine, and the form sold as a bioavailability-enhanced berberine supplement ^{4,6Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →}.

The honest framing: dihydroberberine behaves less like a drug in its own right than like a delivery form of berberine. It absorbs several times better, then oxidises back to berberine in the body ^{4,6Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →}. Its independent evidence is animal and cell work; the two existing human studies measured blood levels, not outcomes ^{6,7Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →Reference 7Chang C et al. · 2024Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot studyView study →}. For berberine’s own pharmacology and its substantial human trial record, see berberine — that material is deliberately not repeated here.

Lambertine Is Dihydroberberine

The synonymy is well documented, and worth stating plainly because “lambertine” still appears in constituent lists as though it were an uncharacterised mystery alkaloid.

The chemical records agree. PubChem files lambertine (and the variants lambertin and dihydroumbellatine) as synonyms of dihydroberberine, CAS 483-15-8, C₂₀H₁₉NO₄, molecular weight 337.4 ^{1Reference 1PubChemDihydroberberine, CID 10217 (CAS 483-15-8; synonyms include lambertine, lambertin, dihydroumbellatine)View study →}. The classic review of the protoberberine alkaloids records the two Berberis lambertii alkaloids berlambine and lambertine as identical to oxyberberine and dihydroberberine respectively — and notes that, at the time of writing, dihydroberberine had been reported only from that one species ^{2Reference 2Jeffs PW · 1967The Protoberberine AlkaloidsView study →}.

Structurally it is berberine, reduced. Berberine is a quaternary protoberberine: a positively charged, bright-yellow cation with a C=N⁺ iminium bond. In dihydroberberine that bond is reduced — the nitrogen becomes a neutral tertiary amine and the adjacent carbon a CH₂ — so the molecule loses its permanent positive charge and its characteristic yellow colour. It is one hydrogen pair away from berberine in each direction, which is exactly why gut bacteria can make it and why the body can turn it back ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}.

Where the botanical claim comes from. Barberry’s constituent list carries lambertine on the strength of a single line in a Berberis review, which names it among “other important alkaloids” of Berberis vulgaris alongside oxyberberine, columbamine, isocorydine, magnoflorine and oxyacanthine — qualitatively, with no quantity given ^{3Reference 3Mokhber-Dezfuli N et al. · 2014Phytochemistry and pharmacology of Berberis speciesView study →}. Independently, a 2019 pharmacology paper reported dihydroberberine from Phellodendron chinense bark, describing it as newly identified in that herb ^{9Reference 9Tan L et al. · 2019Dihydroberberine, a hydrogenated derivative of berberine firstly identified in Phellodendri Chinese Cortex, exerts anti-inflammatory effect via dual modulation of NF-κB and MAPK signaling pathwaysView study →}. Both are real reports; neither pins down how much is present.

Berberine’s Absorbable Form

The reason dihydroberberine matters is a pharmacokinetic accident.

Gut bacteria make it. Berberine is notoriously badly absorbed. Work published in 2015 showed that intestinal bacteria carrying nitroreductases reduce berberine to dihydroberberine in the gut lumen, and that dihydroberberine is absorbed at roughly five times berberine’s rate. Once through the intestinal wall it is non-enzymatically oxidised back to berberine in the tissue, so what circulates is berberine again. Antibiotic-treated mice converted less berberine and got less of its glucose- and lipid-lowering effect ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}.

So it functions as a prodrug. Giving dihydroberberine directly skips the microbial step. In high-fat-fed rodents it produced better in-vivo results than berberine at equivalent doses — less adiposity and tissue triglyceride accumulation — while acting through the same mechanism, inhibition of mitochondrial respiratory complex I and consequent AMPK activation ^{5Reference 5Turner N et al. · 2008Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex IView study →}.

Two small human studies confirm the exposure advantage. In a randomised crossover pilot in five men, 100 mg dihydroberberine produced a peak plasma berberine concentration of 3.76 ± 1.4 ng/mL against 0.4 ± 0.17 ng/mL from 500 mg of berberine — roughly an order of magnitude more from a fifth of the dose. Glucose and insulin did not change, which the authors attributed to the short protocol and healthy participants ^{6Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →}. A second pilot in nine volunteers found dihydroberberine gave higher blood concentrations of berberine metabolites than a micellar berberine formulation, though a lower proportion of unmetabolised berberine ^{7Reference 7Chang C et al. · 2024Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot studyView study →}.

The practical consequence: dihydroberberine’s systemic pharmacology is largely berberine’s pharmacology at a higher plasma concentration. Where the compound has been studied on its own terms, that work is below.

What It's Used For

The dihydroberberine literature is small, recent and almost entirely preclinical — mouse and cell models plus two human pharmacokinetic pilots. It is also scattered: single studies reach into premature ovarian insufficiency ^{17Reference 17Deng D et al. · 2024AnimalDihydroberberine alleviates Th17/Treg imbalance in premature ovarian insufficiency mice via inhibiting Rheb/mTOR signalingView study →} and colorectal cancer ^{18Reference 18Xu L et al. · 2026Dihydroberberine regulates the ferroptosis-autophagy positive feedback loop in colorectal cancer by targeting PANX2View study →} without follow-up. No efficacy outcome has been tested in humans.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Note that the top row scores a pharmacokinetic endpoint measured in humans, not a clinical benefit; every therapeutic row below it is animal-only.

01Delivering berberine (oral bioavailability)Promising46%Two small human PK pilots + rodent PK + a defined microbial mechanism ^{4,6,7,8Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →Reference 7Chang C et al. · 2024Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot studyView study →Reference 8Buchanan B et al. · 2018Comparative pharmacokinetics and safety assessment of transdermal berberine and dihydroberberineView study →}

02Glycaemic and metabolic effectsShaky30%Rodent adiposity/triglyceride work and β-cell/glucokinase studies; human glucose unchanged ^{5,6,15Reference 5Turner N et al. · 2008Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex IView study →Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →Reference 15Zhang C et al. · 2026Dihydroberberine normalizes insulin secretion by regulating glucokinaseView study →}

03Anti-inflammatory and colitisShaky26%Three mouse inflammation models + a DSS colitis model ^{9,10Reference 9Tan L et al. · 2019Dihydroberberine, a hydrogenated derivative of berberine firstly identified in Phellodendri Chinese Cortex, exerts anti-inflammatory effect via dual modulation of NF-κB and MAPK signaling pathwaysView study →Reference 10Li C et al. · 2021AnimalDihydroberberine, an isoquinoline alkaloid, exhibits protective effect against dextran sulfate sodium-induced ulcerative colitis in miceView study →}

04Anti-hyperuricaemic and nephroprotectiveShaky16%One mouse study with an in-vitro xanthine-oxidase IC₅₀ ^{11Reference 11Xu L et al. · 2021AnimalAnti-hyperuricemic and nephroprotective effects of dihydroberberine in potassium oxonate- and hypoxanthine-induced hyperuricemic miceView study →}

05AnticancerShaky14%Isolated cell-line and analogue studies, no replication ^{16,18Reference 16Dai B et al. · 2017Dihydroberberine exhibits synergistic effects with sunitinib on NSCLC NCI-H460 cells by repressing MAP kinase pathways and inflammatory mediatorsView study →Reference 18Xu L et al. · 2026Dihydroberberine regulates the ferroptosis-autophagy positive feedback loop in colorectal cancer by targeting PANX2View study →}

Mechanisms

The first two rows are the ones that define this molecule. Dihydroberberine is a chemical intermediate on berberine’s own absorption route, and its therapeutic targets are berberine’s targets reached more efficiently — which is why the interesting questions here are pharmacokinetic rather than pharmacodynamic.

Pharmacokinetics

This is the compound’s entire reason for existing in the literature. Berberine’s oral bioavailability is famously poor — well under 1% — and dihydroberberine is nature’s workaround: gut nitroreductases reduce it, the reduced form crosses the intestinal wall about five times faster, and non-enzymatic oxidation converts it back to berberine on the other side ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}. Because of that reversion, plasma assays after a dihydroberberine dose measure berberine, and there is no published half-life or clearance figure for dihydroberberine as a circulating species in humans.

The human numbers are limited to two pilots. A randomised crossover in five men gave a peak plasma berberine of 3.76 ± 1.4 ng/mL after 100 mg dihydroberberine versus 0.4 ± 0.17 ng/mL after 500 mg berberine ^{6Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →}. A nine-volunteer study comparing dihydroberberine with micellar berberine found higher metabolite exposure from dihydroberberine but a lower fraction of unmetabolised berberine, with distinct handling of the berberrubine and thalifendine metabolites ^{7Reference 7Chang C et al. · 2024Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot studyView study →}. In rats, transdermal dihydroberberine gave an AUC of 187.3 ng·h/mL against 26.5 ng·h/mL for oral berberine, sustained over 14 days of dosing ^{8Reference 8Buchanan B et al. · 2018Comparative pharmacokinetics and safety assessment of transdermal berberine and dihydroberberineView study →}.

The caveat that matters: even the “high” human figure is a few nanograms per millilitre, which is orders of magnitude below the micromolar concentrations used in the cell studies above. Better than berberine is not the same as enough.

Clinical Trials

Two small pharmacokinetic pilots, no efficacy trials. Neither human study was powered for, or found, a clinical effect: glucose and insulin were unchanged in the crossover trial ^{6Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →}, and the second study measured metabolite profiles only ^{7Reference 7Chang C et al. · 2024Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot studyView study →}. Everything therapeutic is preclinical.

Last checked: July 2026.

Isolate vs. Plant Studies

Unusually for a plant constituent, there is no whole-plant literature to weigh against the isolate. Every study cited here used pure dihydroberberine — synthesised or purified — and none used a Berberis extract standardised to it. That is partly a strength (nothing here is confounded by co-occurring alkaloids) and partly a symptom: the compound’s occurrence in barberry root is documented only qualitatively ^{3Reference 3Mokhber-Dezfuli N et al. · 2014Phytochemistry and pharmacology of Berberis speciesView study →}, so no one has ever produced an extract with a known dihydroberberine content to test.

It also means the herbal inference runs the wrong way. Someone taking a barberry or goldenseal preparation is not getting a meaningful dose of dihydroberberine from the plant; they are getting berberine, some of which their gut bacteria convert into dihydroberberine before absorption ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}. The molecule is more accurately described as a step in the metabolism of a herbal alkaloid than as a herbal active in its own right — which is also why the microbiome-dependence finding matters: mice with depleted gut flora absorbed less and responded less ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}.

Prevalence in Nature

Dihydroberberine is a trace constituent with no published concentration data anywhere. The 1967 protoberberine review recorded it from Berberis lambertii only, under the name lambertine, noting that its co-alkaloid oxyberberine (berlambine) occurred more widely ^{2Reference 2Jeffs PW · 1967The Protoberberine AlkaloidsView study →}. A 2014 review of Berberis phytochemistry lists lambertine among the alkaloids reported from barberry (Berberis vulgaris) root, in a single qualitative sentence with no quantity ^{3Reference 3Mokhber-Dezfuli N et al. · 2014Phytochemistry and pharmacology of Berberis speciesView study →}. In 2019 it was reported from Phellodendron chinense bark, described there as newly identified in that herb ^{9Reference 9Tan L et al. · 2019Dihydroberberine, a hydrogenated derivative of berberine firstly identified in Phellodendri Chinese Cortex, exerts anti-inflammatory effect via dual modulation of NF-κB and MAPK signaling pathwaysView study →}. No source has been assigned a percentage of dry weight.

Its natural context is the standard protoberberine suite — it travels with berberine, palmatine, jatrorrhizine, columbamine and magnoflorine, and with the bisbenzylisoquinolines berbamine and oxyacanthine in the same roots and barks, all of them dwarfed by berberine itself ^{3Reference 3Mokhber-Dezfuli N et al. · 2014Phytochemistry and pharmacology of Berberis speciesView study →}.

The larger share of dihydroberberine that exists in the world is not in plants at all. It is generated in the intestine of anyone taking berberine, by bacterial nitroreductases ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}, and it is manufactured as a supplement ingredient by chemical reduction of berberine.

Discovery & Synthesis

The name lambertine was given to an alkaloid isolated from Berberis lambertii, alongside a second alkaloid named berlambine for the same species. Both names were later retired as identities: berlambine proved to be oxyberberine, and lambertine to be dihydroberberine — a conclusion already recorded in the standard review of the protoberberine alkaloids by 1967 ^{2Reference 2Jeffs PW · 1967The Protoberberine AlkaloidsView study →}. As a chemical entity, dihydroberberine long predated its botanical isolation; it is the straightforward two-electron reduction product of berberine, and was already familiar to alkaloid chemists as a berberine derivative and a reference point in protoberberine reaction chemistry ^{2Reference 2Jeffs PW · 1967The Protoberberine AlkaloidsView study →}.

Manufacture today is entirely semi-synthetic. No one extracts dihydroberberine from plants — the natural abundance is too low to be worth it. Commercial material is made by reducing berberine, which is itself extracted cheaply from Berberis, Coptis or Phellodendron roots and bark, or produced synthetically. Because dihydroberberine oxidises back to berberine readily, formulation and storage stability are practical concerns for the finished ingredient. Synthetic dihydroberberine and tetrahydroberberine analogues have also been prepared for anticancer screening, a separate medicinal-chemistry thread from the natural product ^{16Reference 16Dai B et al. · 2017Dihydroberberine exhibits synergistic effects with sunitinib on NSCLC NCI-H460 cells by repressing MAP kinase pathways and inflammatory mediatorsView study →}.

Patents: not yet researched.

Toxicity & Safety

Dihydroberberine carries a low flag on the strength of a dedicated toxicology package — but that package is short, and the compound converts to berberine in the body, so berberine’s cautions should be assumed to apply until shown otherwise.

Safety at a Glance

✅ Low / no toxicityCardiac cautionDrug interactions

• A real toxicology dataset exists. Non-genotoxic in bacterial and mammalian assays; acute oral LD₅₀ above 2,000 mg/kg in rats; 90-day rat NOAEL of 100 mg/kg body weight per day — the highest dose tested ^{12Reference 12Lewis KD · 2022Toxicological assessment of dihydroberberineView study →}.
• No liver or kidney signal in the rodent PK work. ALT, ALP, creatinine and BUN unchanged over 14 days of dosing, with no change in CYP3A4 expression ^{8Reference 8Buchanan B et al. · 2018Comparative pharmacokinetics and safety assessment of transdermal berberine and dihydroberberineView study →}.
• An unresolved cardiac-channel signal. Dihydroberberine blocks the hERG potassium channel concentration-dependently in HEK293 cells and disrupts its trafficking to the membrane — a QT-prolongation flag that has not been followed up in animals or people ^{13Reference 13Yu D et al. · 2017Inhibitory effects and mechanism of dihydroberberine on hERG channels expressed in HEK293 cellsView study →}.
• Inherit berberine’s interaction profile. Since absorbed dihydroberberine becomes berberine, the known berberine cautions — CYP3A4/P-glycoprotein interactions, and displacement of bilirubin from albumin — should be treated as applying, though none has been tested for dihydroberberine itself ^{14Reference 14Wang D · 2026Dihydroberberine in metabolic disorders: bioavailability, molecular mechanisms, toxicology, and future perspectivesView study →}.
• Effectively no human safety data. Total human exposure in the published literature is fourteen people across two single-dose pilot studies ^{6,7Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →Reference 7Chang C et al. · 2024Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot studyView study →}.

Full Safety & Interactions Detail

The dedicated toxicology package. A 2022 assessment found dihydroberberine non-genotoxic in bacterial reverse-mutation and mammalian assays, established an acute oral LD₅₀ above 2,000 mg/kg in female rats, and set a 90-day no-observed-adverse-effect level of 100 mg/kg body weight per day in Sprague-Dawley rats — noting that this was the highest dose tested, so the true NOAEL may be higher ^{12Reference 12Lewis KD · 2022Toxicological assessment of dihydroberberineView study →}. This is more toxicological groundwork than most minor plant alkaloids ever receive, and it is the main reason for the low grading.

The hERG question. Against that, dihydroberberine inhibited hERG (IKr) potassium channels expressed in HEK293 cells in a concentration-dependent manner, binding aromatic residues in the channel pore and additionally reducing the mature 155-kDa form while increasing the immature 135-kDa form — i.e. both a direct block and a trafficking defect ^{13Reference 13Yu D et al. · 2017Inhibitory effects and mechanism of dihydroberberine on hERG channels expressed in HEK293 cellsView study →}. hERG block is the standard in-vitro predictor of QT prolongation. No in-vivo cardiac study, ECG data or human cardiac observation exists for dihydroberberine, and a 2026 review names this as the outstanding safety item ^{14Reference 14Wang D · 2026Dihydroberberine in metabolic disorders: bioavailability, molecular mechanisms, toxicology, and future perspectivesView study →}. Anyone with a QT-prolonging medication list or a known arrhythmia should treat this as unresolved rather than reassuring.

Interactions are un-tested but inheritable. No drug-interaction study has been run on dihydroberberine. The rat transdermal work found no effect on simvastatin pharmacokinetics and no change in hepatic CYP3A4 expression over 14 days ^{8Reference 8Buchanan B et al. · 2018Comparative pharmacokinetics and safety assessment of transdermal berberine and dihydroberberineView study →}, which is mildly reassuring but is one drug in one species. The more important point is structural: dihydroberberine is oxidised back to berberine after absorption ^{4Reference 4Feng R et al. · 2015Transforming berberine into its intestine-absorbable form by the gut microbiotaView study →}, so berberine’s documented interactions — raised cyclosporine levels via CYP3A4 and P-glycoprotein, and potent displacement of bilirubin from albumin — are the realistic risk model here, and the higher plasma berberine that dihydroberberine delivers could in principle make them more likely, not less ^{14Reference 14Wang D · 2026Dihydroberberine in metabolic disorders: bioavailability, molecular mechanisms, toxicology, and future perspectivesView study →}. See berberine for that interaction profile in full.

Reproductive and developmental (prose only). No reproductive-toxicity study of dihydroberberine exists. One 2024 mouse study used it therapeutically in a premature-ovarian-insufficiency model, reporting an improved Th17/Treg balance via Rheb/mTOR signalling ^{17Reference 17Deng D et al. · 2024AnimalDihydroberberine alleviates Th17/Treg imbalance in premature ovarian insufficiency mice via inhibiting Rheb/mTOR signalingView study →} — a treatment finding, not a safety one, and not evidence of reproductive safety either way. Berberine’s own contraindication in pregnancy and breastfeeding rests on bilirubin displacement and kernicterus risk; nothing about the reduced form removes that concern. Pregnancy and lactation decisions belong to the herb or product page where intake is decided, not to this molecule page.

What is not known. There is no repeat-dose human data, no long-term data of any kind, no carcinogenicity study, and no assessment in children, older adults or people with liver or kidney impairment.

Dosage

There is no established human dose for dihydroberberine, and none at all for “lambertine” as a botanical constituent. The figures below are research and product doses, listed for reference only.

The commercial logic of the ingredient is that a 100–200 mg dose is intended to substitute for a much larger berberine dose, on the basis of the plasma-concentration comparison alone ^{6Reference 6Moon JM et al. · 2021RCTAbsorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trialView study →}. No trial has confirmed that the substitution produces an equivalent clinical effect, and no dose-ranging or repeat-dose human study has been published. These are doses studied in research and are not a personal recommendation.

References

1. PubChem. Dihydroberberine, CID 10217 (CAS 483-15-8; synonyms include lambertine, lambertin, dihydroumbellatine). National Library of Medicine. https://pubchem.ncbi.nlm.nih.gov/compound/10217
2. Jeffs PW (1967). The Protoberberine Alkaloids. In: The Alkaloids: Chemistry and Physiology, pp. 41–115. https://doi.org/10.1016/S1876-0813(08)60198-0
3. Mokhber-Dezfuli N, Saeidnia S, Gohari AR, Kurepaz-Mahmoodabadi M (2014). Phytochemistry and pharmacology of Berberis species. Pharmacognosy Reviews. https://pubmed.ncbi.nlm.nih.gov/24600191/
4. Feng R, Shou JW, Zhao ZX, et al. (2015). Transforming berberine into its intestine-absorbable form by the gut microbiota. Scientific Reports. https://pubmed.ncbi.nlm.nih.gov/26174047/
5. Turner N, Li JY, Gosby A, et al. (2008). Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I. Diabetes. https://pubmed.ncbi.nlm.nih.gov/18285556/
6. Moon JM, Ratliff KM, Hagele AM, et al. (2021). Absorption kinetics of berberine and dihydroberberine and their impact on glycemia: a randomized, controlled, crossover pilot trial. Nutrients. https://pubmed.ncbi.nlm.nih.gov/35010998/
7. Chang C, Roh YS, Du M, et al. (2024). Differences in metabolite profiles of dihydroberberine and micellar berberine in Caco-2 cells and humans — a pilot study. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/38891813/
8. Buchanan B, Meng Q, Poulin MM, et al. (2018). Comparative pharmacokinetics and safety assessment of transdermal berberine and dihydroberberine. PLoS One. https://pubmed.ncbi.nlm.nih.gov/29579096/
9. Tan L, Wang Y, Ai G, et al. (2019). Dihydroberberine, a hydrogenated derivative of berberine firstly identified in Phellodendri Chinese Cortex, exerts anti-inflammatory effect via dual modulation of NF-κB and MAPK signaling pathways. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/31401380/
10. Li C, Dong N, Wu B, et al. (2021). Dihydroberberine, an isoquinoline alkaloid, exhibits protective effect against dextran sulfate sodium-induced ulcerative colitis in mice. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/34253428/
11. Xu L, Lin G, Yu Q, et al. (2021). Anti-hyperuricemic and nephroprotective effects of dihydroberberine in potassium oxonate- and hypoxanthine-induced hyperuricemic mice. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/33959014/
12. Lewis KD, Falk M (2022). Toxicological assessment of dihydroberberine. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/35868606/
13. Yu D, Lv L, Fang L, et al. (2017). Inhibitory effects and mechanism of dihydroberberine on hERG channels expressed in HEK293 cells. PLoS One. https://pubmed.ncbi.nlm.nih.gov/28763460/
14. Wang D, Tang Y (2026). Dihydroberberine in metabolic disorders: bioavailability, molecular mechanisms, toxicology, and future perspectives. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/42398618/
15. Zhang C, Zhang X, Zhang Q, et al. (2026). Dihydroberberine normalizes insulin secretion by regulating glucokinase. Diabetes, Obesity and Metabolism. https://pubmed.ncbi.nlm.nih.gov/41077968/
16. Dai B, et al. (2017). Dihydroberberine exhibits synergistic effects with sunitinib on NSCLC NCI-H460 cells by repressing MAP kinase pathways and inflammatory mediators. Journal of Cellular and Molecular Medicine. https://pubmed.ncbi.nlm.nih.gov/28444871/
17. Deng D, et al. (2024). Dihydroberberine alleviates Th17/Treg imbalance in premature ovarian insufficiency mice via inhibiting Rheb/mTOR signaling. Molecular Medicine. https://pubmed.ncbi.nlm.nih.gov/39472803/
18. Xu L, et al. (2026). Dihydroberberine regulates the ferroptosis-autophagy positive feedback loop in colorectal cancer by targeting PANX2. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/42401068/

View all 18 references▾