Decursinol: A Comprehensive Encyclopedic Reference
1. Identity: Botanical Source, Chemical Names, and Forms
1.1 Botanical Source
Decursinol is a major coumarin derived from the roots of Angelica gigas Nakai. This pyranocoumarin compound — a rare class of secondary metabolite plant products — is isolated from the roots of Angelica gigas (A. gigas), the native Korean species Angelica gigas Nakai (AGN). AGN is a Korean plant belonging to the Angelica L. genus within the Umbelliferae family, which contains more than 60 species. It is found in Korean moist soil, but is recognized as a traditional medicine mainly in Korea, China, and Japan.
As an herb plant of the genus Angelica L. in the family Umbelliferae, A. gigas is used to treat gynecological diseases and anemia, and is also used as an anti-inflammatory and analgesic agent in traditional medicine. A. gigas is mainly distributed in the north temperate zone, especially in China, Korea, and Japan.
1.2 Chemical Identity and Nomenclature
Decursinol (abbreviated as DOH in the pharmacological literature) is a pyranocoumarin. The alcoholic extracts of AGN dried root contain the signature pyranocoumarins decursin (D) and its isomer decursinol angelate (DA), which is about 50–60% as abundant as D. Decursinol (DOH) is the precursor for the synthesis of D and DA, and is detected at lower abundance than D and DA in the native plant, if at all.
In the plant's biosynthetic pathway, the attachment of a 2-methylbut-2-ene side chain results in the formation of 7-demethylsuberosin, which then undergoes cyclization to generate decursinol. Subsequent modifications of decursinol give rise to its isomeric derivatives, decursin and decursinol angelate.
AGN is unique because of the presence of substantial amounts of pyranocoumarins including decursin, decursinol, and decursinol angelate. Eleven monocoumarins, ten furocoumarins, eleven pyranocoumarins, nine volatile oils, nine flavonoids, and six other constituents of A. gigas have been identified and discussed in the literature.
1.3 Metabolic Relationship to Decursin and Decursinol Angelate
Although decursinol is less abundant than decursin and decursinol angelate in the native root, it occupies a pivotal pharmacological position because of first-pass hepatic metabolism. In rodent models, orally administered (gavage) D and DA are rapidly and extensively converted to DOH through first-pass hepatic metabolism, with a similar metabolism confirmed in humans. The pharmacokinetics of ingested AGN supplements in humans for the signature pyranocoumarins have been characterized, with decursin (D, Cmax 1x), decursinol angelate (DA, Cmax ~10x), and their common botanical precursor and hepatic metabolite decursinol (DOH, Cmax ~1000x) as the relevant circulating species. This means that following oral ingestion of AGN extract, decursinol is by far the predominant compound circulating in human plasma, making it functionally the principal active entity in the body even when decursin or decursinol angelate are the major phytochemicals in the raw plant material.
1.4 Commercial and Supplement Forms
AGN root ethanolic extracts have been marketed as dietary supplements in the United States for memory health and pain management. Commercial products containing AGN-derived pyranocoumarins include CognIQâ„¢, D-Cursinol, Decursinol-50â„¢, Ache Actionâ„¢, Fast-Acting Joint Formula, and EstroG-100â„¢. The 3-herbal mixture EstroG-100 (AGN, Cynanchum wilfordii, Phlomis umbrosa) has been found beneficial to relieve many post-menopausal symptoms in US women.
2. Traditional and Historical Use
2.1 East Asian Traditional Medicine
The root of Angelica gigas Nakai (Umbelliferae), popularly known as Korean "Dang Gui," has been used to treat female afflictions and anemia in traditional oriental herbal medicine since ancient times in Korea. The dried radix of Angelica gigas (Ag), termed "Korean Dang Gui," has been used in Korean traditional herbal medicine for the treatment of gynecological diseases such as anemia because of its hemogenic, health-promoting, analgesic, and sedative activities.
The plant has been originally employed as a tonic and for the treatment of several diseases, such as anemia, but also as a sedative or as an anodyne. The native Korean species Angelica gigas Nakai is widely used as a remedy for a variety of medical conditions including hematopoiesis, improving women's circulation, as sedatives, analgesics, and tonic.
The root of A. gigas is most commonly prepared by decocting with water, and is used as a blood tonic, for the treatment of gynecological diseases, anti-inflammatory, analgesic, and laxative.
2.2 Traditional Indications and Preparations
AGN, an ancient medicinal plant, is widely used in several Asian countries, including Korea, Japan, and China. Both decursin and decursinol angelate have been widely utilized in conventional treatments for managing anaemia and as a sedative, anodyne, or as a tonic.
Widely growing in many Asian countries, such as Korea, Japan, and China, the roots of this plant have been traditionally used to treat hormonal imbalance and anemia, and for liver detoxification.
Some additional traditional effects attributed to the plant include antibacterial activity, acetylcholinesterase inhibitory activity, myocardial relaxant activity, protein kinase C activity, and anticancer activity against sarcoma cancer cells.
INM-176, a standardized ethanol extract of A. gigas, is traditionally used in China, Japan, and Korea to treat anemia and as a sedative, and has also been studied for its ability to improve memory impairment induced by scopolamine or Aβ1-42 protein through acetylcholinesterase inhibition and neuron-mediated protective activity.
3. Key Constituents, Chemical Relationships, and Mechanisms of Action
3.1 The Pyranocoumarin Triad
The pharmacological activity of AGN extracts is largely attributed to three closely related pyranocoumarins: decursin (D), decursinol angelate (DA), and decursinol (DOH). Cell culture structure-activity studies have uncovered distinct cellular and molecular effects of D and DA vs. their pyranocoumarin core decursinol (DOH) with respect to cancer cells and those associated with their microenvironment. These pyranocoumarin compounds, including decursinol and its derivatives decursin and decursinol angelate, have been reported to contain various biological activities such as aldolase inhibition, neuroprotection, anti-platelet, anti-bacterial, and anti-cancer activities.
3.2 Anti-inflammatory Mechanisms
In cell-culture studies, the anti-inflammatory effects of decursinol angelate on the MAP kinase and NFκB signaling pathways and the expression of pro-inflammatory cytokines were investigated in phorbol 12-myristate 13-acetate (PMA)-activated human promyelocytic leukemia (HL-60) and lipopolysaccharide (LPS)-stimulated macrophage (Raw 264.7) cell lines. PMA induced the activation of the MAP kinase–NFκB pathway and the production of pro-inflammatory cytokines in differentiated monocytes. Treatment with DA inhibited the activation of MAP kinases and the translocation of NFκB, and decreased the expression and exogenous secretion of IL-1β and IL-6.
Studies have also reported that decursin inhibits matrix metallopeptidase 9 (MMP-9)-induced cytoskeletal rearrangement by suppressing phosphoinositide 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), and NFκB activation in fibrosarcoma and breast cancer cell lines. DA inhibited the differentiation and polarization of macrophages by suppressing the expression of inflammatory cytokines and the MAPK and NFκB pathways, as well as by reducing NADPH oxidase (NOX) and iNOS levels in LPS and TPA-induced inflammatory models.
3.3 Anti-angiogenic Mechanisms
Decursin and decursinol at non-cytotoxic doses inhibited the VEGF-induced proliferation, migration, and capillary-tube formation of HUVECs. Moreover, decursin and decursinol suppressed microvessel formation on chorioallantoic membranes in fertilized eggs and in mouse Matrigel plugs. The oral administration of decursin and decursinol also reduced VEGF-induced angiogenesis in Matrigel. Furthermore, decursin and decursinol reduced the phosphorylation of ERK and JNK, but not p38 MAPK, in VEGF-stimulated HUVECs.
Decursin and decursinol angelate inhibited VEGF-induced angiogenic processes in vitro, including proliferation, migration, and tube formation of human umbilical vein endothelial cells.
3.4 Acetylcholinesterase Inhibition
Acetylcholinesterase (AChE) inhibitory activity–guided fractionation of Angelica gigas led to isolation and identification of a new coumarin, peucedanone, and 11 known coumarins. Among them, decursinol represented the highest inhibitory activity toward AChE in vitro. The correlation of the inhibitory activities of the coumarins toward AChE with their chemical structures was also studied. Several studies have shown that crude methanolic extract of Ag (AgMx) has anti-amnesic activity against scopolamine-induced cognitive impairment through inhibition of acetylcholinesterase (AChE).
3.5 Analgesic Mechanisms
Earlier experiments using receptor antagonists suggest that the antinociceptive effects of decursinol might be mediated in part via noradrenergic, serotonergic, adenosine (A2), histamine H1, and histamine H2 receptors. Interestingly, the effect of decursinol on thermal pain was not altered by the opioid receptor antagonist naloxone, suggesting that these effects might not be mediated by opioid receptor signaling pathways.
Pretreatment with naloxone partially prevented decursinol-reversal of allodynia (but not hypothermia), indicating that opioid signaling may at least partially be responsible for decursinol-induced anti-allodynia. Previous work also demonstrated that methysergide, a non-selective serotonin (5-HT) receptor antagonist, could block the antinociceptive effects of decursinol. Two selective 5-HT2A and 5-HT2C receptor antagonists have been used to probe the specific 5-HT receptor subtype(s) responsible for these effects on pain.
Administration of the decursinol precursor decursinol angelate has been shown to potentiate pentobarbital-induced sleeping behaviors through the activation of the GABAA-ergic systems.
Research has indicated that the analgesic effect of decursinol might be involved in supraspinal cyclooxygenase regulation that might overlap with APAP-induced analgesic mechanisms rather than systemic or peripheral prostaglandin modulation.
3.6 ROCK1/2 Kinase Inhibition
Given their polypharmacology nature, the pertinent mechanisms of action of the AGN pyranocoumarins are likely misrepresented by many cell culture studies that did not consider drug metabolism knowledge. Rho-associated protein kinases (ROCK1/2) have been reported as novel targets for DA and DOH. Combining this with published inhibitory activity of DOH on acetylcholinesterase, the evidence supports a multi-target pharmacological profile.
3.7 Apoptosis Induction in Cancer Cells
Existing studies indicate that decursin affects cell proliferation, apoptosis, autophagy, angiogenesis, and metastasis. It also indirectly affects the immune microenvironment and can act as a potential anticancer agent. Decursin can exert synergistic antitumor effects when used in combination with a number of common clinical anticancer drugs, enhancing chemotherapy sensitivity and reversing drug resistance in cancer cells.
4. Scientific Evidence by Area of Use
4.1 Pain and Analgesia
Preclinical evidence (animal studies): Decursinol has been demonstrated to have antinociceptive effects on various mouse pain models such as tail-flick, hot-plate, formalin, writhing, and several cytokine-induced pain tests. The antinociceptive effects of decursinol were observed at an orally-administered dose of 50 mg/kg but not at 25 or 10 mg/kg in the mouse writhing test.
Co-administration of decursinol (25 mg/kg) and acetaminophen (100 mg/kg) showed synergistic effects in mouse pain models. These results indicated that the analgesic effect of decursinol might be involved in supraspinal cyclooxygenase regulation that might overlap with APAP-induced analgesic mechanisms rather than systemic or peripheral prostaglandin modulation.
To determine if tolerance develops to the analgesic effects of decursinol in either acute and/or chemotherapy-induced neuropathic pain (CENP) models following prolonged administration, a study was performed using approximately 219 experimentally naïve eight- to ten-week-old male C57BL6/J mice.
In terms of rigor and reproducibility, neither the effects of AGN extract components on pain, nor investigations on the mechanism of action have been reported outside of Korea until relatively recently. A US-based study sought to replicate the analgesic effects of decursinol in assays for both acute thermal (tail-flick and hot plate) and neuropathic (CENP) pain.
Evidence strength: All analgesic evidence for decursinol itself is currently preclinical (animal models). No controlled human trials specifically assessing decursinol's analgesic effects have been reported in the peer-reviewed literature as of 2024–2025.
4.2 Neurodegenerative Disease and Cognitive Function
Preclinical evidence: Decursinol and decursin have neuroprotective activity against glutamate-induced neurotoxicity in rat cortical primary cells and improve scopolamine-induced amnesia in vivo with nodakenin, another component of A. gigas.
Decursin has been shown to have widely neuroprotective effects, though the underlying mechanisms between decursin and ferroptosis in Alzheimer's disease are poorly understood. The protective effect of decursin and the underlying mechanism under glutamate treatment in SH-SY5Y neuroblastoma cells has been investigated.
Several studies have shown that crude methanolic extract of AGN has anti-amnesic activity against scopolamine-induced cognitive impairment through inhibition of acetylcholinesterase (AChE).
Clinical/translational evidence: Some AGN extract-based dietary supplements have been studied for their activities against Alzheimer's type dementia in clinical trials in Korea. However, the clinical trial evidence pertaining specifically to isolated decursinol (as opposed to whole AGN extract) remains limited, and the results from Korean dementia trials have not been replicated in large independent multicenter studies.
Evidence strength: Primarily preclinical (in vitro and rodent models). The AChE-inhibitory mechanism offers a plausible biological rationale, but human evidence specific to decursinol as an isolated compound is preliminary.
4.3 Oncology (Anticancer Activity)
In vitro evidence — cancer cell lines: Decursin demonstrated cytotoxic effects on U87 and C6 glioma cells in a dose-dependent manner but not in primary glial cells. Additionally, decursin increased apoptotic bodies and phosphorylated JNK and p38 in U87 cells, and also down-regulated Bcl-2 as well as cell cycle dependent proteins. Decursin-induced apoptosis was dependent on caspase activation in U87 cells. These data provide evidence that decursin induces apoptosis in glioblastoma cells, making it a potential candidate as a chemotherapeutic drug against brain tumor.
Research revealed for the first time that decursin had excellent inhibitory effects on VEGF-induced vascular formation in human umbilical vein endothelial cells (HUVECs), fertilized eggs, and intramuscular animal models in vitro. Decursin had significant in vivo antiangiogenic effects, primarily via preventing the angiogenesis generated by vascular endothelial growth factor by reducing ERK and JNK activation in HUVECs.
Decursinol angelate (DA), derived from AGN, has demonstrated anti-cancer effectiveness through the induction of intrinsic and extrinsic apoptosis pathways, inhibition of cancer cell proliferation, anti-neovascularization, anti-inflammatory and anti-oxidative activities, and stimulation of the immune process.
Human pharmacokinetic trial: A clinical trial investigated the pharmacokinetics of a single oral dose of decursin and decursinol angelate-enriched dietary supplement Cogni-Q. In this study, a total of 20 healthy subjects, each taking 119 mg of decursin and 77 mg of decursinol angelate, were enrolled. The results provided credibility to the safety data using rodent models. Analyses of plasma samples using UHPLC-MS/MS showed mean time to peak concentration (Tmax) of 2.1, 2.4, and 3.3 hours and mean peak concentration (Cmax) of 5.3, 48.1, and 2,480 nmol/L for D, DA, and DOH, respectively.
A second clinical trial was approved (NCT05375539): a Phase I study entitled "Angelica herbal supplement AGN-CognI.Q acute dose safety and pharmacokinetics dose-response in prostate cancer patients (PK Dose Trial)" aiming to obtain acute dose safety and PK/PD data in a dose–response design.
Evidence strength: Substantial preclinical (in vitro and animal) evidence exists for anticancer properties of decursin and its metabolite decursinol, spanning multiple cancer types. No completed randomized controlled clinical trials demonstrating therapeutic efficacy against cancer in humans have been published. Further studies are still needed to assess the genotoxicity and reproductive toxicity of decursin, among others, in order to support anticancer studies.
4.4 Anti-inflammatory Activity
Several studies have characterized the anti-inflammatory, anticancer, and anti-angiogenic properties of decursin in various cancers, including myelogenous leukemia cell lines. The anti-inflammatory mechanism operates primarily through inhibition of NF-κB and MAPK pathways in cell culture models. Despite the well-documented anti-inflammatory effects of DA in preclinical models, the mechanisms underlying these effects are not yet fully understood.
Evidence strength: Preclinical only. No controlled human trials specifically evaluating decursinol's anti-inflammatory properties have been conducted to date.
4.5 Metabolic Syndrome and Related Conditions
Both decursin, the main constituent of A. gigas, and an ethanol extract of A. gigas inhibited the formation of new fat in mice fed a high-fat diet, alleviated nonalcoholic fatty liver disease and dyslipidemia, and also reduced high-fat-diet-induced glucose and insulin intolerance, hepatic steatosis and inflammation, and hypertriglyceridemia.
Evidence strength: Preclinical only (rodent high-fat diet models). No human trials on decursinol specifically for metabolic syndrome have been reported.
4.6 Additional Areas Under Investigation
Reported in vivo medicinal activities of AGN and/or its pyranocoumarins and furanocoumarin nodakenin span cancer, pain, memory loss, cerebral ischemia reperfusion stroke, metabolic syndrome and vascular endothelial dysfunctions, anxiety, sleep disorder, epilepsy, inflammatory bowel disease, osteoporosis, and osteoarthritis. All of these additional areas are currently at the preclinical stage; human clinical trials in these domains specifically using decursinol have not been published.
5. Body Systems and Health Areas of Association
- Nervous system: Decursinol has various pharmacological effects against inflammation, angiogenesis, nociceptive pain, and Alzheimer's disease. Neuroprotection against glutamate-induced neurotoxicity and AChE inhibition are the primary mechanistic associations.
- Musculoskeletal / pain: Antinociceptive activity demonstrated across multiple animal pain models including thermal, chemical, and neuropathic modalities, involving serotonergic and noradrenergic pathways.
- Oncological: Both in vitro and in vivo studies have demonstrated that decursin has potential neuroprotective, anti-inflammatory, anti-melanogenic, anti-angiogenic, antioxidant, and anti-visceral properties.
- Vascular / cardiovascular: Anti-angiogenic effects mediated via the VEGFR-2 / ERK / JNK pathway have been documented in vitro and in animal models.
- Immune / inflammatory: Suppression of NF-κB translocation, MAP kinase activation, and pro-inflammatory cytokine (IL-1β, IL-6) expression in macrophage cell lines.
- Gynecological / endocrine: Traditionally, A. gigas has been used as an immune-booster in the treatment of gynecological disorders and anemia.
- Hepatic / metabolic: Preclinical evidence for effects on hepatic steatosis, dyslipidemia, and glucose metabolism in rodent models.
6. Pharmacokinetics and Dosage
6.1 Absorption and Bioavailability
Following oral administration, decursinol exhibited high oral bioavailability (>45%) and rapid absorption (Tmax, 0.4–0.9 hours) over the dose range studied in rats. Decursinol exhibited high stability to oxidative and glucuronic metabolism in human and rat liver microsomes. In Caco-2 cell monolayers, decursinol showed high permeability (>14 × 10−6 cm/s) at all tested concentrations in the absorptive direction, which saturated at 100 μM.
Secretion increased in a concentration-dependent manner, with an efflux ratio of more than 2 at 50 μM, indicating the participation of an active efflux transporter such as P-glycoprotein, multidrug resistance protein 2, or breast cancer resistance protein.
6.2 Protein Binding and Distribution
The fraction of decursinol not bound to plasma proteins was 25–26% in the rat and 9–18% in humans. In human plasma, but not rat plasma, the percentage of unbound decursinol was concentration-dependent.
6.3 Human Pharmacokinetics
Analyses of plasma samples from the first-in-human study using UHPLC-MS/MS showed mean time to peak concentration (Tmax) of 2.1, 2.4, and 3.3 hours, and mean peak concentration (Cmax) of 5.3, 48.1, and 2,480 nmol/L for D, DA, and DOH, respectively. The terminal elimination half-life (t1/2) for D and DA was similar (17.4 and 19.3 hours) and each was much longer than that of DOH (7.4 hours).
The mean area under the curve (AUC0–48h) for D, DA, and DOH was estimated as 37, 335, and 27,579 h·nmol/L, respectively. Gender-wise, men absorbed the parent compounds faster and took shorter time to reach DOH peak concentration. The human data supported an extensive conversion of D and DA to DOH, even though humans metabolized DA slightly slower than rodents.
This first-in-human single dose PK study of D and DA was delivered through Cogni.Q dietary supplement. The data support the similarity of metabolic fate(s) of D and DA in humans and rodents, with suggestion of a potential slower metabolism of DA in humans than in rodents. The results provide credence to using rodent models to evaluate efficacy and safety data to benefit the clinical translation of AGN phytochemicals.
6.4 Dosages Reported in Studies
- Mouse analgesic studies (oral): The antinociceptive effects of decursinol were observed at an orally-administered dose of 50 mg/kg, but not at 25 or 10 mg/kg, in mice.
- Mouse sedation/GABA studies (oral): Oral administration of decursinol angelate at 10, 25, and 50 mg/kg markedly suppressed spontaneous locomotor activity and prolonged sleeping time.
- Human PK study (single oral dose): Twenty healthy subjects each took 119 mg of decursin and 77 mg of decursinol angelate in the pharmacokinetic study.
- Rodent anticancer efficacy models: The dosages of AGN used in rodent anti-cancer models ranged from 100–200 mg/kg, equivalent to 20–100 mg/kg of D/DA depending on extraction procedures.
No established therapeutic dosage for decursinol as an isolated compound has been determined in human clinical trials. The single PK study cited above was a pharmacokinetic, not a dose-efficacy, trial.
7. Safety Considerations and Interactions
7.1 General Safety Profile
Preclinical and clinical studies indicated that AGN and decursin/DA were quite safe to animals and humans. The results of the human PK study provided credibility to the safety data obtained using rodent models. The efficacy, safety, and pharmacokinetic mechanisms of both compounds in rodents have been well reproduced in humans.
However, further studies are still needed to assess the genotoxicity and reproductive toxicity of decursin, among others, in order to support anticancer studies of decursin. The absence of completed long-term human trials means that a comprehensive safety profile cannot be fully established at present.
7.2 Efflux Transporter Interactions
Secretion of decursinol in Caco-2 monolayers increased in a concentration-dependent manner, with an efflux ratio of more than 2 at 50 μM, indicating the participation of an active efflux transporter such as P-glycoprotein, multidrug resistance protein 2, or breast cancer resistance protein. This finding is pharmacokinetically significant: compounds that are substrates of P-glycoprotein may interact with other P-gp substrates or inhibitors, potentially altering circulating concentrations of co-administered drugs.
7.3 Interactions with Analgesic Drugs
Co-administration of decursinol (25 mg/kg) and acetaminophen (100 mg/kg) showed synergistic effects in mouse analgesic models. However, the co-administration of decursinol and aspirin did not show any differences at doses of 10 or 25 mg/kg and 50 or 100 mg/kg, respectively. Although this was demonstrated in animal models, it suggests a mechanism-based interaction potential with APAP-type (supraspinal COX-mediated) analgesics that has not been evaluated in humans.
7.4 Opioid Receptor Interactions
Pretreatment with naloxone partially prevented decursinol-reversal of allodynia (but not hypothermia), indicating that opioid signaling may at least partially be responsible for decursinol-induced anti-allodynia. This suggests that in contexts of neuropathic pain, decursinol may interact with opioid receptor pathways, though the clinical implications remain uninvestigated.
7.5 Hormone-Related Exclusions in Clinical Trials
The human PK clinical trial excluded subjects taking oral contraception, hormone-containing IUDs, contraception implants, or Depo medroxyprogesterone injections, as well as those taking any food or herbal supplements containing AGN within 30 days of the study, and female subjects that were pregnant, less than 6 months postpartum, or breastfeeding. These exclusions reflect investigator concern about potential hormonal interactions, reflecting the plant's traditional use for gynecological conditions. However, specific interaction data in humans are lacking.
7.6 Metabolic Enzyme Stability
Decursinol exhibited high stability to oxidative and glucuronic metabolism in human and rat liver microsomes. This metabolic stability may reduce the likelihood of CYP450-mediated drug interactions arising from competitive substrate inhibition, though formal human DDI studies have not been conducted.
7.7 Protein Binding Considerations
The fraction of decursinol not bound to plasma proteins was 25–26% in the rat and 9–18% in humans. In human plasma, but not rat plasma, the percentage of unbound decursinol was concentration-dependent. The concentration-dependent protein-binding behavior in humans is pharmacologically noteworthy, as it may affect the free (pharmacologically active) fraction at varying doses in a non-linear manner.
7.8 Gaps in Safety Evidence
As of the most recent literature (2024–2025), no phase II or phase III clinical trials testing therapeutic efficacy or extended-duration safety of decursinol as an isolated compound have been published. More clinical research is suggested to establish proper efficacy, safety, and human dosage. Although research using cell culture is indispensable for preliminary screening of anti-cancer agents, these models could not fully replicate the complex interactions and microenvironments present in an in vivo setting. Consequently, the observed effects on cell viability and apoptosis may not fully translate to clinical efficacy.
Summary of Evidence Strength
Decursinol's pharmacological profile is supported by a substantial body of preclinical research — encompassing in vitro cell culture work and rodent in vivo models — across anti-inflammatory, antinociceptive, neuroprotective, anticancer, and antiangiogenic domains. The single first-in-human PK study (NCT02114957, n=20) established that oral bioavailability and metabolic conversion from decursin and decursinol angelate are broadly similar in humans and rodents, lending translational credibility to preclinical findings. A Phase I prostate cancer PK/PD dose-response trial (NCT05375539) was approved but its results have not yet been published in peer-reviewed literature. For all areas of claimed activity, the evidence remains at the preliminary-to-emerging stage, with no completed randomized controlled trials demonstrating therapeutic efficacy in humans as of the period covered by the sources consulted.
References
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