Compound Monograph
Morroniside
Morroniside is a principal secoiridoid glucoside of cornelian cherry (Cornus officinalis / shan zhu yu) and, with loganin, one of the two iridoid markers used to standardize the herb. Its pharmacology is a broad but entirely preclinical anti-diabetic-nephropathy, neuroprotective and bone-protective profile — there are no isolate human trials, the human evidence belongs to the whole fruit and its formulas, and oral bioavailability is very low (~4.3% in rats).
Sources · 3
Where Does It Come From?
Morroniside is a naturally occurring secoiridoid glucoside (iridoid glycoside), found in Cornelian cherry fruit — shan zhu yu; the principal source and QC marker, Cornus mas and Various Caprifoliaceae/Viburnaceae and Gentianaceae. It is well tolerated orally (low toxicity).
Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Morroniside at a Glance
Morroniside is a secoiridoid glucoside and, with its sibling loganin, one of the two iridoid glucosides that define cornelian cherry (Cornus officinalis, the fruit Corni Fructus / shan zhu yu) — a kidney- and liver-tonic staple of traditional Chinese medicine. The two co-occur so reliably that they are the paired quality-control markers used to authenticate and standardize the herb 1,
As a molecule in its own right, morroniside carries a broad but entirely preclinical pharmacology. The best-developed strands are protection against diabetic kidney damage and neuroprotection after cerebral ischaemia, with further signals in bone, neuropathic pain and Alzheimer’s-model tau pathology — almost all of it in cell and rodent studies 1,
Two honesty caveats run through the page. There are no clinical trials of isolated morroniside: the human evidence for its source is for the whole herb and its formulas, not the purified molecule. And morroniside has very low oral bioavailability — around 4.3% in rats — which undercuts how far in-vitro potency can translate to an oral dose 13Reference 13In vitroThe absorption of oral morroniside in rats: in vivo, in situ and in vitro studiesView study →.
Morroniside & Loganin — The Cornus Markers
Morroniside is rarely discussed alone. It is one half of a pair: morroniside and loganin are the two iridoid glucosides quantified to standardize cornelian cherry (Cornus officinalis, shan zhu yu). Because both are relatively abundant and structurally characteristic of Corni Fructus, they serve as the pharmacopoeial quality markers — the compounds an analyst measures to confirm identity, grade quality and check batch-to-batch consistency of the herb and the formulas built on it 1,
That pairing is more than a coincidence of chemistry. The two are co-extracted and co-studied: the earliest renal work isolated both from Cornus officinalis and tested them side by side against advanced-glycation-driven mesangial-cell proliferation 3Reference 3AnimalMorroniside and loganin extracted from Cornus officinalis have protective effects on rat mesangial cell proliferation exposed to advanced glycation end products by preventing oxidative stressView study →, and the modern diabetes literature treats them as a linked active duo, reviewing “loganin and morroniside” together as the iridoids behind the fruit’s anti-diabetic reputation 2Reference 2ReviewLoganin and morroniside: therapeutic effects and molecular mechanisms in diabetes mellitus and its complications — a reviewView study →. They share a common iridoid backbone and an overlapping mechanistic repertoire — anti-glycation, antioxidant, anti-inflammatory — which is why a Cornus effect can seldom be attributed to one marker over the other.
Processing matters to the pair. Cornelian cherry is used both raw and wine-steamed (a traditional preparation), and raw versus processed Corni Fructus differ measurably in iridoid content — so the morroniside : loganin ratio is itself part of what quality grading tracks 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →. The practical upshot: morroniside’s “own” pharmacology is real and isolate-tested, but its role in the herb is as a co-marker, not a lone active.
Diabetic Complications & Neuroprotection
Morroniside’s distinctive isolate signal clusters in two areas, both dominated by cornelian-cherry-derived research and both preclinical.
Diabetic kidney disease is the largest strand, and it is squarely complication-focused rather than a glucose-lowering story. Morroniside and loganin, extracted from Cornus officinalis, blunted advanced-glycation-end-product (AGE)-induced mesangial-cell proliferation by curbing reactive-oxygen-species generation and restoring antioxidant enzymes 3Reference 3AnimalMorroniside and loganin extracted from Cornus officinalis have protective effects on rat mesangial cell proliferation exposed to advanced glycation end products by preventing oxidative stressView study →. In streptozotocin-diabetic rats, oral morroniside (20 and 100 mg/kg/day for 20 days) lowered serum glucose and urinary protein and reduced renal AGEs and oxidative-damage markers — protecting the kidney rather than only the blood sugar 4Reference 4AnimalProtective effects of morroniside isolated from Corni Fructus against renal damage in streptozotocin-induced diabetic ratsView study →. More recent work ties the renal benefit to lipid handling: morroniside cut renal lipid deposition in diabetic nephropathy by suppressing the NF-κB/TNF-α/SREBP1c pathway that drives lipogenic genes 5Reference 5Regulation of renal lipid deposition in diabetic nephropathy on morroniside via inhibition of NF-κB/TNF-α/SREBP1c signaling pathwayView study →. The recurring theme — anti-glycation, antioxidant, anti-inflammatory, anti-lipotoxic — is what makes morroniside a fixture of the diabetic-nephropathy literature 2Reference 2ReviewLoganin and morroniside: therapeutic effects and molecular mechanisms in diabetes mellitus and its complications — a reviewView study →.
Neuroprotection after stroke is the second strand, and it is unusually developed for an iridoid. In rat middle-cerebral-artery-occlusion models, morroniside reduced infarct volume and improved neurological scores, effects linked to its antioxidant and anti-apoptotic action 6Reference 6AnimalNeuroprotective effect of morroniside on focal cerebral ischemia in ratsView study →. Beyond simple protection, it showed a neurorestorative profile — promoting neurogenesis via Wnt/β-catenin signalling seven days post-ischaemia 7Reference 7Promoting neurogenesis via Wnt/β-catenin signaling pathway accounts for the neurorestorative effects of morroniside against cerebral ischemia injuryView study → — and it inhibited neuronal apoptosis and MMP2/9 expression in ischaemia/reperfusion injury, improving the Bcl-2/Bax ratio and lowering active caspase-3 8Reference 8Morroniside protects against cerebral ischemia/reperfusion injury by inhibiting neuron apoptosis and MMP2/9 expressionView study →.
The honest frame: this is a coherent preclinical dossier, much of it on the isolated molecule in rodents — a genuine attributional strength — but with no human isolate data and a poor-oral-bioavailability caveat that limits how far cell and high-dose findings translate 1,
What It's Used For
Morroniside’s evidence base is broad, internally consistent and entirely preclinical. The load-bearing caveat is the compound-page discipline: no human trials of the isolate, and its very low oral bioavailability means in-vitro and high-dose rodent potency overreads what an oral dose delivers 1,
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. There are no human isolate data, so scores stay modest by design.
Morroniside’s largest strand, and largely isolate work. In cells, morroniside (co-tested with loganin) blunted AGE-induced mesangial-cell proliferation by lowering ROS and restoring superoxide dismutase and glutathione peroxidase 3Reference 3AnimalMorroniside and loganin extracted from Cornus officinalis have protective effects on rat mesangial cell proliferation exposed to advanced glycation end products by preventing oxidative stressView study →.
In vivo (all rodent), oral morroniside protected the kidney in streptozotocin-diabetic rats — lowering serum glucose and urinary protein and reducing renal AGEs and oxidative damage over 20 days at 20–100 mg/kg 4Reference 4AnimalProtective effects of morroniside isolated from Corni Fructus against renal damage in streptozotocin-induced diabetic ratsView study → — and a later model attributed the renal benefit to suppressed lipid deposition via the NF-κB/TNF-α/SREBP1c axis, cutting lipogenic genes (ACC, FAS, SCD1) 5Reference 5Regulation of renal lipid deposition in diabetic nephropathy on morroniside via inhibition of NF-κB/TNF-α/SREBP1c signaling pathwayView study →.
Gap: all rodent/cell, no human isolate trials; the human anti-diabetic evidence for its source is the whole herb / formula, and poor oral bioavailability limits achievable renal exposure 1,
A developed, coherent isolate signal in rat stroke models. Morroniside reduced infarct volume and improved neurological scores after middle-cerebral-artery occlusion, consistent with antioxidant and anti-apoptotic action 6Reference 6AnimalNeuroprotective effect of morroniside on focal cerebral ischemia in ratsView study →; beyond protection it was neurorestorative, promoting neurogenesis through Wnt/β-catenin signalling (↑ Wnt3a, β-catenin, Tcf-4) for brain recovery a week post-ischaemia 7Reference 7Promoting neurogenesis via Wnt/β-catenin signaling pathway accounts for the neurorestorative effects of morroniside against cerebral ischemia injuryView study →; and in ischaemia/reperfusion it inhibited neuronal apoptosis and MMP2/9, improving the Bcl-2/Bax ratio and lowering active caspase-3 8Reference 8Morroniside protects against cerebral ischemia/reperfusion injury by inhibiting neuron apoptosis and MMP2/9 expressionView study →.
Gap: all rodent, all the isolated molecule, acute stroke paradigms; no human data, and central exposure of an orally poorly-absorbed glucoside is unquantified 6,
A bone thread that fits cornelian cherry’s traditional “kidney-tonic” use. Isolated morroniside enhanced osteoblast differentiation (alkaline-phosphatase activity, osteogenic genes) while suppressing osteoclast differentiation, and in ovariectomized mice (2 and 10 mg/kg/day for 12 weeks) it prevented the loss of bone mineral density and microarchitecture 9Reference 9In vitroAnti-osteoporotic effect of morroniside on osteoblast and osteoclast differentiation in vitro and ovariectomized mice in vivoView study →.
Gap: rodent/cell only, single-programme evidence, no human data 9Reference 9In vitroAnti-osteoporotic effect of morroniside on osteoblast and osteoclast differentiation in vitro and ovariectomized mice in vivoView study →.
The most mechanistically distinctive finding. Morroniside is an orthosteric agonist of the glucagon-like-peptide-1 (GLP-1) receptor: it protected microglial and GLP-1-receptor-expressing cells from hydrogen-peroxide oxidative damage, and its antinociceptive effect in nerve-injured rats was completely blocked by a GLP-1-receptor antagonist, pinning the action to spinal GLP-1 receptors 10Reference 10Morroniside, a secoiridoid glycoside from Cornus officinalis, attenuates neuropathic pain by activation of spinal glucagon-like peptide-1 receptorsView study →.
This is an unusual, specific target for a plant iridoid and overlaps the receptor biology behind its Alzheimer’s-model effects.
Gap: a single (if elegant) rodent study of the isolate; no human confirmation, and the systemic exposure needed is unaddressed given poor oral absorption 10,
A mechanistically tight cellular signal. In an okadaic-acid model of neurodegeneration (SK-N-SH cells), morroniside inhibited tau hyperphosphorylation by activating protein phosphatase 2A (PP2A) — reducing demethylated/phosphorylated inactive PP2A — with the effect lost when PP2A was silenced, indicating a direct PP2A-activating action 11Reference 11Morroniside-induced PP2A activation antagonizes tau hyperphosphorylation in a cellular model of neurodegenerationView study →. This dovetails with its GLP-1-receptor agonism, a second neuroprotective route 10Reference 10Morroniside, a secoiridoid glycoside from Cornus officinalis, attenuates neuropathic pain by activation of spinal glucagon-like peptide-1 receptorsView study →.
Gap: in-vitro cellular model only, no in-vivo or human tau/cognition data for the isolate 11Reference 11Morroniside-induced PP2A activation antagonizes tau hyperphosphorylation in a cellular model of neurodegenerationView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Advanced glycation end products (AGEs) / ROS | anti-glycation; ↓ ROS, ↑ SOD/GPx | diabetic nephropathy (mesangial protection) |
| NF-κB / TNF-α / SREBP1c | suppressed → ↓ renal lipid deposition | diabetic nephropathy (lipotoxicity) |
| Wnt/β-catenin (Wnt3a, β-catenin, Tcf-4) | activated → neurogenesis / neurorestoration | post-ischaemic brain recovery |
| Neuronal apoptosis; MMP2/9; caspase-3; Bcl-2/Bax | apoptosis and MMP2/9 suppressed | cerebral ischaemia/reperfusion |
| Osteoblast vs osteoclast differentiation | osteogenesis favoured; resorption suppressed | anti-osteoporotic |
| GLP-1 receptor | orthosteric agonism | neuropathic pain; neuroprotection |
| Protein phosphatase 2A (PP2A) | activated → ↓ tau hyperphosphorylation | Alzheimer’s-model tau pathology |
| CYP3A (rat liver) | induced (↑ activity/mRNA/protein) | drug-interaction potential (see Toxicity) |
The reproduced core is an antioxidant / anti-glycation / anti-inflammatory programme shared with loganin, layered with two more specific actions — GLP-1-receptor agonism and PP2A activation — that give the neuropathic-pain and tau strands their identity. The CYP3A row is a pharmacokinetic/interaction finding, not a therapeutic effect.
Pharmacokinetics
Morroniside is a hydrophilic iridoid glucoside with very low oral bioavailability. A dedicated rat study reports an absolute oral bioavailability of only ~4.3%, with linear dose-proportional kinetics across the range tested 13Reference 13In vitroThe absorption of oral morroniside in rats: in vivo, in situ and in vitro studiesView study →; Caco-2 monolayer work characterises it as a poorly absorbed compound whose transport combines passive diffusion with efflux-transporter-mediated handling (BCRP and MRP2), a mechanistic reason for the low absorption 1,
Clinical Trials
There are no controlled trials of isolated morroniside. Its human footprint is entirely indirect, through the whole cornelian-cherry fruit (shan zhu yu) and multi-herb formulas — most famously Liu Wei Di Huang Wan — where morroniside is one of several actives and serves, with loganin, as a standardization marker rather than the tested agent 1,
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate; human data belong to whole Cornus officinalis / formulas) | — | — | Broad(renal-led; neuroprotective, bone, neuropathic pain, tau) |
Last checked: July 2026.
Isolate vs. Plant Studies
The split is clean and, on the mechanism side, favourable. Morroniside’s pharmacology is overwhelmingly the isolated molecule — the AGE/mesangial and STZ-diabetic-kidney studies 3,
The human evidence inverts this: it belongs to the whole herb. Cornelian cherry (shan zhu yu) is used clinically as a fruit and inside formulas such as Liu Wei Di Huang Wan, where morroniside is a quality marker (with loganin) quantified for batch consistency rather than the demonstrated active 1,
Its Role in Plants
In the plant, morroniside belongs to the iridoid / secoiridoid glucosides — a class of bitter, often deterrent compounds stored as inert glucosides and mobilised on tissue damage, whose broad ecological role is chemical defence against herbivores and pathogens. It is biosynthesised through the iridoid pathway (from geraniol via the loganin route that also yields its co-marker loganin), and transcriptomic work in Cornus officinalis has begun to map the genes governing its accumulation, implicating early terpenoid-pathway enzymes such as HMG-CoA synthase and a geranyl-diphosphate synthase in fruit iridoid content 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →. As always, a molecule’s role in plant metabolism is plant biology, not human pharmacology, and does not predict what it does as a medicine.
Prevalence in Nature
Morroniside is a characteristic iridoid glucoside of the genus Cornus, and its headline source is cornelian cherry (Cornus officinalis, Cornaceae) — the fruit Corni Fructus / shan zhu yu, in which morroniside is, with loganin, a principal iridoid and pharmacopoeial quality marker used to authenticate and standardize the herb 1,
Absolute content is rarely reported as a clean % dry weight and varies widely with species, plant part, ripeness and (for cornelian cherry) processing — raw versus wine-steamed Corni Fructus differ measurably in iridoid content 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →. A reliable cross-source concentration ranking therefore does not exist here and is tracked as a gap rather than asserted.
Discovery & Synthesis
Morroniside is a twentieth-century iridoid whose name derives from its Cornus source (the cornelian-cherry lineage), from whose fruit it was isolated and characterized during the modern phytochemical study of Corni Fructus; the exact first-isolation author and year are not cleanly documented in the sources gathered here. Its structure is that of a secoiridoid / iridoid glucoside, and research-grade material is obtained by extraction — chiefly from Cornus officinalis fruit — using macroporous-resin enrichment (AB-8 or D101 resins) followed by HPLC purification to high purity (~98–99%), because the molecule is relatively abundant there and its glucoside chemistry makes isolation far more practical than total synthesis 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →. Total chemical synthesis is not the supply route and is not well documented here.
Patents: not yet researched.
Toxicity & Safety
Morroniside reads as a low-toxicity iridoid glucoside — it is a marker constituent of a fruit (shan zhu yu) eaten and decocted for centuries and taken inside widely-used formulas, and preclinical studies report no acute toxicity signal at the doses used 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →. The rating stays off “none” for evidentiary reasons: there is no comprehensive isolate toxicology package (no definitive LD50, genotoxicity or repeat-dose organ-toxicity dataset) for pure morroniside — a gap the review literature explicitly flags as needing to be filled before clinical use — and its very low oral bioavailability means real-world isolate exposure is limited 1,
- A long-used dietary/medicinal-plant iridoid. A quality marker of cornelian cherry (shan zhu yu) and a constituent of long-used TCM formulas, with no acute toxicity signal in rodent studies 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →.
- Real-world exposure is whole-herb and low. People meet morroniside as a fruit/formula constituent, not as a concentrated isolate, and its oral absorption is poor (~4.3% in rats) 13Reference 13In vitroThe absorption of oral morroniside in rats: in vivo, in situ and in vitro studiesView study →.
- No comprehensive isolate toxicology. No definitive LD50, genotoxicity or repeat-dose package for the pure compound; safety is inferred from the whole herb, not established for the molecule 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →.
- A CYP3A-induction interaction flag. Repeated morroniside induced hepatic CYP3A in rats and lowered exposure to the CYP3A substrate midazolam — a plausible herb–drug interaction route to watch, not yet characterised in humans 12Reference 12AnimalInduction of CYP3A by morroniside in ratsView study →.
- In-vitro potency overreads oral exposure. Very low bioavailability and efflux-transporter handling limit how far cell/high-dose findings translate 1,
13Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →Reference 13In vitroThe absorption of oral morroniside in rats: in vivo, in situ and in vitro studiesView study → .
Full Safety & Interactions Detail
Morroniside carries a low flag. It is a principal iridoid and pharmacopoeial marker (with loganin) of cornelian cherry (Cornus officinalis, shan zhu yu), a fruit with a long dietary and medicinal history, and it is a constituent of extensively-used multi-herb formulas such as Liu Wei Di Huang Wan; rodent efficacy studies report no acute toxicity signal at the doses used 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →.
The caveats are largely evidentiary. First, there is no comprehensive isolate toxicology — no definitive LD50, genotoxicity or repeat-dose organ-toxicity dataset for pure morroniside — so its safety is inferred from the whole herb, not demonstrated for the molecule, and the review literature explicitly calls for chronic and acute toxicity studies before clinical use 1Reference 1ReviewA review of the sources and pharmacological research of morronisideView study →.
Second, unlike most plant iridoids there is a concrete interaction signal: repeated morroniside induced hepatic CYP3A in rats — increasing CYP3A activity, mRNA and protein and reducing the exposure of the CYP3A probe midazolam — so a herb–drug interaction with CYP3A-metabolised medicines is biologically plausible, though its human relevance is unquantified 12Reference 12AnimalInduction of CYP3A by morroniside in ratsView study →.
Third, very low oral bioavailability (~4.3% in rats, with efflux-transporter-limited absorption) both limits real-world isolate exposure and means high-dose or parenteral preclinical findings do not transfer cleanly to oral use 1,
Reproductive note (prose only). No dedicated reproductive- or developmental-toxicity dataset exists for isolated morroniside. Any pregnancy/lactation caution around morroniside-containing herbs (chiefly cornelian cherry) belongs to the source herb and is a decision made on the herb or product page where intake is decided — not on this molecule page.
Dosage
There is no established or recommended human dose for isolated morroniside — it has never been given to people as an isolate for therapy. Cited figures are preclinical research doses: micromolar concentrations in vitro, and roughly 2–270 mg/kg in rodents depending on the model — from 2–10 mg/kg in the bone study 9Reference 9In vitroAnti-osteoporotic effect of morroniside on osteoblast and osteoclast differentiation in vitro and ovariectomized mice in vivoView study → and 20–100 mg/kg in the diabetic-kidney work 4Reference 4AnimalProtective effects of morroniside isolated from Corni Fructus against renal damage in streptozotocin-induced diabetic ratsView study → up to 30–270 mg/kg in the cerebral-ischaemia studies 6,
References
- Shi P, Zheng B, Zhang S, Guo Q (2024). A review of the sources and pharmacological research of morroniside. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/39301568/
- Jiang W, et al. (2025). Loganin and morroniside: therapeutic effects and molecular mechanisms in diabetes mellitus and its complications — a review. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/40714074/
- Xu H, Shen J, Liu H, Shi Y, Li L, Wei M (2006). Morroniside and loganin extracted from Cornus officinalis have protective effects on rat mesangial cell proliferation exposed to advanced glycation end products by preventing oxidative stress. Canadian Journal of Physiology and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/17487235/
- Yokozawa T, Yamabe N, Kim HY, Kang KS, Hur JM, Park CH, Tanaka T (2008). Protective effects of morroniside isolated from Corni Fructus against renal damage in streptozotocin-induced diabetic rats. Biological & Pharmaceutical Bulletin. https://pubmed.ncbi.nlm.nih.gov/18591786/
- Zhu W, Chen M, Wang Y, Chen Y, Zhang Y, Wang Y, Liu P, Li P (2023). Regulation of renal lipid deposition in diabetic nephropathy on morroniside via inhibition of NF-κB/TNF-α/SREBP1c signaling pathway. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/37769864/
- Wang W, Xu J, Li L, Wang P, Ji X, Ai H, Zhang L, Li L (2010). Neuroprotective effect of morroniside on focal cerebral ischemia in rats. Brain Research Bulletin. https://pubmed.ncbi.nlm.nih.gov/20637265/
- Sun FL, Wang W, Zuo W, Xue JL, Xu JD, Ai HX, Zhang L, Wang XM, Ji XM (2014). Promoting neurogenesis via Wnt/β-catenin signaling pathway accounts for the neurorestorative effects of morroniside against cerebral ischemia injury. European Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/24876057/
- Zeng G, Ding W, Li Y, Sun M, Deng L (2018). Morroniside protects against cerebral ischemia/reperfusion injury by inhibiting neuron apoptosis and MMP2/9 expression. Experimental and Therapeutic Medicine. https://pubmed.ncbi.nlm.nih.gov/30186462/
- Lee CG, Kim J, Yun SH, Hwang S, Jeon H, Park E, Jeong SY (2021). Anti-osteoporotic effect of morroniside on osteoblast and osteoclast differentiation in vitro and ovariectomized mice in vivo. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/34638983/
- Xu M, Wu HY, Liu H, Gong N, Wang YR, Wang YX (2017). Morroniside, a secoiridoid glycoside from Cornus officinalis, attenuates neuropathic pain by activation of spinal glucagon-like peptide-1 receptors. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/28098360/
- Yang CC, Kuai XX, Gao WB, Yu JC, Wang Q, Li L, Zhang L (2016). Morroniside-induced PP2A activation antagonizes tau hyperphosphorylation in a cellular model of neurodegeneration. Journal of Alzheimer’s Disease. https://pubmed.ncbi.nlm.nih.gov/26836014/
- Xiong S, Li J, Zhang W, Wang X, Zhang Z (2015). Induction of CYP3A by morroniside in rats. Journal of Pharmacological Sciences. https://pubmed.ncbi.nlm.nih.gov/25953268/
- Xiong S, Li Y, Mu Y, Zhang Z (2019). The absorption of oral morroniside in rats: in vivo, in situ and in vitro studies. Acta Pharmaceutica. https://doi.org/10.2478/acph-2019-0012
