Damnacanthal

Damnacanthal at a Glance

Damnacanthal is an anthraquinone — 3-hydroxy-1-methoxy-2-formylanthraquinone — best known as the characteristic root pigment of noni (Morinda citrifolia, Rubiaceae) and as a research-grade kinase inhibitor sold by reagent suppliers. It is the single most-studied bioactive isolated from noni, and its literature is dominated by cancer-cell pharmacology ^{10Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}.

Its scientific fame rests on one property: it is a potent, selective inhibitor of p56lck, a Src-family tyrosine kinase central to T-cell signalling ^{1Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →}. Beyond p56lck it inhibits several other kinases — c-Met, VEGFR-2, focal adhesion kinase — reverses the Ras-transformed cell phenotype, and induces apoptosis across a range of tumour cell lines ^{2,3,4Reference 2Hiramatsu T et al. · 1993Induction of normal phenotypes in ras-transformed cells by damnacanthal from Morinda citrifoliaView study →Reference 3García-Vilas JA et al. · 2015Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cellsView study →Reference 4García-Vilas JA et al. · 2017The noni anthraquinone damnacanthal is a multi-kinase inhibitor with potent anti-angiogenic effectsView study →}.

Two honest caveats frame everything below. First, every anticancer and mechanistic result is preclinical — cell-culture and rodent work on the isolated molecule, with no human trials of damnacanthal itself. Second, although noni is marketed heavily on damnacanthal’s reputation, the molecule is concentrated in noni root, is scarce in the fruit and juice most people consume, and the one human noni cancer trial used fruit capsules and saw no tumour response ^{9Reference 9Issell BF et al. · 2009Clinical trialUsing quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II doseView study →}.

Damnacanthal & the p56lck / Tyrosine-Kinase Story

The reason damnacanthal appears in reagent catalogues at all is a single, well-characterised biochemical result. In 1995 Faltynek and colleagues showed damnacanthal is a highly potent, selective inhibitor of p56lck (Lck) — a lymphocyte-specific Src-family tyrosine kinase that sits at the top of T-cell-receptor signalling. It inhibited p56lck autophosphorylation with an IC₅₀ of ~17 nM, was >100-fold selective over the serine/threonine kinases PKA and PKC and >40-fold selective over four receptor tyrosine kinases, and worked by competing at the peptide-substrate site while behaving as a mixed, non-competitive inhibitor at the ATP site ^{1Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →}. That selectivity is why it became a standard laboratory tool compound for probing Lck biology.

Damnacanthal is not a single-target molecule, though. Later work makes it a multi-kinase inhibitor: it directly inhibits c-Met (the hepatocyte-growth-factor receptor) and lowers downstream Akt phosphorylation in liver-cancer cells ^{3Reference 3García-Vilas JA et al. · 2015Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cellsView study →}, and molecular and functional studies add VEGFR-2 and focal adhesion kinase (FAK) to the list ^{4Reference 4García-Vilas JA et al. · 2017The noni anthraquinone damnacanthal is a multi-kinase inhibitor with potent anti-angiogenic effectsView study →}. Separately, one of the earliest noni studies showed damnacanthal reverses the transformed phenotype of K-ras-transformed cells — restoring normal morphology and cytoskeleton reversibly, without changing Ras levels, and with no effect on src-transformed cells — marking it as an inhibitor of Ras function ^{2Reference 2Hiramatsu T et al. · 1993Induction of normal phenotypes in ras-transformed cells by damnacanthal from Morinda citrifoliaView study →}.

The load-bearing honesty point: this is biochemistry and cell biology, not clinical pharmacology. Damnacanthal’s identity as a “p56lck inhibitor” is a real, reproducible lab-reagent fact — but it has never been shown to inhibit these kinases usefully or safely in a person, and potent Lck inhibition also implies an immunosuppressive liability (Lck drives T-cell activation), not only an anticancer one.

The Noni Marker

Damnacanthal is noni’s signature anthraquinone — the compound most often named when noni products are promoted for cancer, immunity and “detox.” That marketing leans on the preclinical literature summarised here, and the gap between the two is the most important thing to understand about this molecule.

Three facts create the gap:

• The evidence is isolate-and-preclinical. Damnacanthal’s anticancer results come from purified compound applied to cultured cells or dosed into mice ^{3,4,5,6,7Reference 3García-Vilas JA et al. · 2015Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cellsView study →Reference 4García-Vilas JA et al. · 2017The noni anthraquinone damnacanthal is a multi-kinase inhibitor with potent anti-angiogenic effectsView study →Reference 5Aziz MYA et al. · 2014Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cellsView study →Reference 6Nualsanit T et al. · 2012Damnacanthal, a noni component, exhibits antitumorigenic activity in human colorectal cancer cellsView study →Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →}. None is a human result, and none used a noni beverage.
• The molecule lives in the root, not the juice. Damnacanthal is a root and root-bark anthraquinone ^{10Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}; noni fruit juice — the commonest consumer product — contains very little of it, so drinking noni juice is not a meaningful way to ingest damnacanthal.
• The human noni trial was negative for tumour response. The only phase I clinical study of noni in advanced-cancer patients used freeze-dried noni fruit capsules (tolerable up to ~12 g/day, with modest self-reported pain/fatigue signals) and reported no tumour regression ^{9Reference 9Issell BF et al. · 2009Clinical trialUsing quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II doseView study →} — and it tested the fruit, not isolated damnacanthal.

So “noni fights cancer because of damnacanthal” quietly splices together two different things: isolated-root-compound cell data and whole-fruit-juice human exposure that barely contains the compound. Damnacanthal is a genuinely interesting research molecule; that is not the same as evidence that a noni product does anything in people.

What It's Used For

The pharmacology is broad on paper and thin on translation. Damnacanthal has a coherent, well-documented set of anticancer and kinase-inhibitory activities in vitro and in rodents — but all of it is the isolate in preclinical models, its aqueous solubility and human pharmacokinetics are poorly characterised, and there is no clinical evidence ^{9,10Reference 9Issell BF et al. · 2009Clinical trialUsing quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II doseView study →Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}.

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. Damnacanthal’s evidence is entirely preclinical isolate work, so scores stay low by design. Each application links to its write-up.

01Anticancer / ApoptosisShaky40%Isolated damnacanthal; multiple tumour cell lines + tumour-bearing mice; p53/p21, NAG-1, caspase ^{5,6,7Reference 5Aziz MYA et al. · 2014Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cellsView study →Reference 6Nualsanit T et al. · 2012Damnacanthal, a noni component, exhibits antitumorigenic activity in human colorectal cancer cellsView study →Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →}

02Tyrosine-Kinase / Ras InhibitionShaky38%Isolated damnacanthal; potent p56lck (IC₅₀ ~17 nM) + c-Met/Akt + Ras-phenotype reversal ^{1,2,3Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →Reference 2Hiramatsu T et al. · 1993Induction of normal phenotypes in ras-transformed cells by damnacanthal from Morinda citrifoliaView study →Reference 3García-Vilas JA et al. · 2015Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cellsView study →}

03Anti-AngiogenesisShaky30%Isolated damnacanthal; multi-kinase (VEGFR-2/c-Met/FAK), ex-vivo + in-vivo angiogenesis assays ^{4Reference 4García-Vilas JA et al. · 2017The noni anthraquinone damnacanthal is a multi-kinase inhibitor with potent anti-angiogenic effectsView study →}

04Antinociceptive / Anti-InflammatoryShaky22%Isolated damnacanthal from noni root; single rodent study, non-opioid, weak H₁ antagonism ^{8Reference 8Okusada K et al. · 2011The antinociceptive and anti-inflammatory action of the CHCl₃-soluble phase and its main active component, damnacanthal, isolated from the root of Morinda citrifoliaView study →}

Mechanisms

The kinase inhibition is the load-bearing biology; the apoptosis and anti-angiogenesis readouts largely flow downstream of it. The same potency that reads as “anticancer” against Lck also reads as “immunosuppressive.”

Pharmacokinetics

This is the weakest and most important part of the file. Damnacanthal is a lipophilic, poorly water-soluble anthraquinone aldehyde, and there is no robust human ADME data — no oral bioavailability figure, Cmax or half-life for the isolate. The active concentrations in its cell studies are micromolar (e.g. MCF-7 IC₅₀ in the ~8 µg/mL to ~13 µM range) ^{5,11Reference 5Aziz MYA et al. · 2014Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cellsView study →Reference 11Akhtar MN et al. · 2013Total synthesis, cytotoxic effects of damnacanthal, nordamnacanthal and related anthraquinone analoguesView study →}, and reaching and sustaining such levels systemically from an oral dose is exactly the unanswered question — which is why some groups have pursued nanoformulations to raise exposure. What limited in-vivo data exist come from acute rodent toxicology: oral damnacanthal is absorbed enough to cause hepatocellular necrosis at 2000 mg/kg in an acute-toxicity study ^{7Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →}. The practical upshot mirrors the other anthraquinones here (see emodin and chrysophanol): poor solubility and undocumented human kinetics discount the in-vitro potencies, and no in-vitro result should be read as a human dose.

Clinical Trials

There are no clinical trials of isolated damnacanthal — every study here is cell-culture or rodent. The only human evidence anywhere near it is a phase I trial of noni fruit (not the isolate): freeze-dried M. citrifolia fruit capsules in advanced-cancer patients, tolerable to about 12 g/day with modest self-reported pain/fatigue signals but no tumour response ^{9Reference 9Issell BF et al. · 2009Clinical trialUsing quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II doseView study →}. That tests the plant, and damnacanthal is a root compound scarce in the fruit.

Last checked: July 2026.

Isolate vs. Plant Studies

Damnacanthal’s evidence base is almost entirely the isolated molecule, and that cuts both ways. As a preclinical mechanism story it is a strength: the p56lck, c-Met, VEGFR-2/FAK, Ras-reversal and apoptosis results all test purified damnacanthal (or defined root fractions) directly, not a crude extract ^{1,2,3,4Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →Reference 2Hiramatsu T et al. · 1993Induction of normal phenotypes in ras-transformed cells by damnacanthal from Morinda citrifoliaView study →Reference 3García-Vilas JA et al. · 2015Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cellsView study →Reference 4García-Vilas JA et al. · 2017The noni anthraquinone damnacanthal is a multi-kinase inhibitor with potent anti-angiogenic effectsView study →}. But the human end is entirely plant, not molecule — and a mismatched plant at that. The one clinical noni study used whole noni fruit ^{9Reference 9Issell BF et al. · 2009Clinical trialUsing quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II doseView study →}, whereas damnacanthal is concentrated in noni root/root bark and is scarce in fruit and juice ^{10Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}. So there is no point at which the isolate’s activity and a human noni exposure meet: the compound with the data is not the compound most people ingest, and the product with the human data barely contains it. This is the cleanest example on the site of an isolate-vs-plant gap being used as a marketing bridge it cannot actually support.

Its Role in Plants

Damnacanthal is a root anthraquinone pigment of noni and its Rubiaceae relatives, where anthraquinones function broadly as antimicrobial and defence compounds and as the coloured pigments of madder-family roots.

Critically for how it should be read alongside the other anthraquinones here, Rubiaceae anthraquinones are built by a different biosynthetic route than the emodin-type ones. The laxative anthraquinones (emodin, chrysophanol, rhein) are polyketide-derived. Rubiaceae anthraquinones like damnacanthal are made through the chorismate / o-succinylbenzoic-acid pathway instead: rings A and B derive from chorismate (via the shikimate pathway) and α-ketoglutarate through o-succinylbenzoic acid, while ring C is added from the terpenoid (isoprenoid) pathway. In Morinda citrifolia cell cultures the committed, rate-controlling step is isochorismate synthase, which channels chorismate toward anthraquinone production ^{12Reference 12Stalman M et al. · 2003Regulation of anthraquinone biosynthesis in cell cultures of Morinda citrifoliaView study →}.

That distinction is not academic: it is why damnacanthal, despite being an “anthraquinone,” is not a laxative anthraglycoside and should not be assumed to behave like the senna/rhubarb family.

Prevalence in Nature

Damnacanthal is a Rubiaceae root anthraquinone. Its best-known source is noni (Morinda citrifolia), where it concentrates in the roots and root bark; it is also reported across other Morinda species and in related genera including Damnacanthus (the genus it is named for), Prismatomeris, Heterophyllaea pustulata, Saprosma and Rennellia elliptica ^{10Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}.

Two occurrence facts matter. First, it is markedly a root compound — noni fruit and the fruit juice sold to consumers contain far less of it than the root does ^{10Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}. Second, quantitative content is poorly documented: reliable percent-dry-weight figures across noni tissues and across the other source plants are not well established in the accessible literature, so no comparative source chart is drawn here (this gap is tracked in the compound’s gaps file). Its close demethylated relative, nordamnacanthal (1,3-dihydroxy-2-formylanthraquinone), co-occurs in the same roots and is frequently studied alongside it.

Discovery & Synthesis

Damnacanthal takes its name from the genus Damnacanthus (Rubiaceae), from which this root anthraquinone was originally described, and it was long familiar as one of the coloured anthraquinones of madder-family roots. Its modern scientific profile, however, dates to 1995, when Faltynek and colleagues identified it as a highly potent, selective p56lck tyrosine-kinase inhibitor — the result that turned a plant pigment into a catalogued research reagent ^{1Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →}.

A practical total synthesis was reported by Akhtar and colleagues in 2013, using Friedel–Crafts acylation and a mild pyridinium-chlorochromate oxidation of a hydroxymethyl precursor to install the C-2 aldehyde in high yield; the same work confirmed by structure–activity comparison that the formyl group at C-2, methoxy at C-1 and hydroxyl at C-3 are the features that carry the cytotoxic activity ^{11Reference 11Akhtar MN et al. · 2013Total synthesis, cytotoxic effects of damnacanthal, nordamnacanthal and related anthraquinone analoguesView study →}. Today damnacanthal is obtained either by extraction from Morinda (and related Rubiaceae) roots or by synthesis, entirely at research scale — it is a reagent and a research compound, not a manufactured drug.

Patents: not yet researched.

Toxicity & Safety

Damnacanthal carries a moderate flag — not because it is acutely poisonous, but because it is a potent cytotoxic, apoptosis-inducing kinase inhibitor rather than a benign dietary molecule, and because it sits inside an anthraquinone class that carries a genuine genotoxicity concern.

• Acute toxicity is relatively low, but not clean. An acute oral study placed the LD₅₀ cut-off at 2500 mg/kg (OECD Guideline 423) — a low-acute-toxicity band — yet at the top dose (2000 mg/kg) it produced hepatocellular necrosis in the liver and minimal single-cell necrosis in kidney tubules ^{7Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →}. So even the “reassuring” acute study shows organ damage at high oral doses.
• It is a cytotoxic bioactive by design. The compound’s whole reputation is inducing apoptosis and arresting cell growth ^{3,5,6Reference 3García-Vilas JA et al. · 2015Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cellsView study →Reference 5Aziz MYA et al. · 2014Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cellsView study →Reference 6Nualsanit T et al. · 2012Damnacanthal, a noni component, exhibits antitumorigenic activity in human colorectal cancer cellsView study →}; a molecule selected for cytotoxicity toward dividing cells is not a molecule to treat as a food-grade constituent.
• Rubiaceae-anthraquinone genotoxicity context. Several anthraquinones from the madder/Rubiaceae family are genotoxic and animal-carcinogenic — lucidin forms DNA adducts, and 1-hydroxyanthraquinone is classified IARC Group 2B (possibly carcinogenic), with madder-root colour withdrawn from food use on these grounds ^{13Reference 13IARC Working Group · 2002ReviewRubia tinctorum, Morinda officinalis and anthraquinonesView study →}. Damnacanthal itself is not classified and its own genotoxicity is not well characterised, but its structural class means the concern must be flagged, not assumed away.
• Immunosuppression signal. Potent inhibition of p56lck, a kinase essential for T-cell activation, implies an immunosuppressive liability alongside the anticancer one ^{1Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →}; the immune consequences of meaningful systemic exposure are unstudied.
• No human isolate data. There is no human safety dataset for isolated damnacanthal, and no interaction, reproductive or repeat-dose package for the pure compound beyond the acute rodent study and the class context above ^{7,13Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →Reference 13IARC Working Group · 2002ReviewRubia tinctorum, Morinda officinalis and anthraquinonesView study →}. Reproductive and pregnancy/lactation questions are decided at the herb or product level, not on this molecule page; no isolate-specific verdict is issued here.

Safety at a Glance

⚠️ Moderate toxicity

• Low acute oral toxicity in the one study. An acute rodent study put the LD₅₀ cut-off at 2500 mg/kg (OECD 423) — a low-acute-toxicity band ^{7Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →}.
• It is a cytotoxic, apoptosis-inducing kinase inhibitor. This is a potent bioactive research compound, not a dietary constituent, and it caused hepatocellular necrosis at high oral doses ^{5,7Reference 5Aziz MYA et al. · 2014Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cellsView study →Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →}.
• Rubiaceae-anthraquinone genotoxicity class. Related madder/Rubiaceae anthraquinones are genotoxic/carcinogenic (lucidin DNA adducts; 1-hydroxyanthraquinone IARC 2B); damnacanthal’s own genotoxicity is uncharacterised ^{13Reference 13IARC Working Group · 2002ReviewRubia tinctorum, Morinda officinalis and anthraquinonesView study →}.
• Immunosuppression is plausible. Strong p56lck inhibition could blunt T-cell activation; the effect of real systemic exposure is unstudied ^{1Reference 1Faltynek CR et al. · 1995Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activityView study →}.
• No human isolate data at all — safety, interactions, pregnancy and repeat-dose exposure for the pure compound are unknown.

Dosage

There is no established or safe human dose for isolated damnacanthal, and nothing here is a recommendation. Its research figures are cell-culture concentrations (IC₅₀ roughly 8 µg/mL to ~13 µM against tumour lines) ^{5,11Reference 5Aziz MYA et al. · 2014Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cellsView study →Reference 11Akhtar MN et al. · 2013Total synthesis, cytotoxic effects of damnacanthal, nordamnacanthal and related anthraquinone analoguesView study →} and rodent oral doses in the tens-to-hundreds of milligrams per kilogram ^{7,8Reference 7Woradulayapinij W et al. · 2022Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesisView study →Reference 8Okusada K et al. · 2011The antinociceptive and anti-inflammatory action of the CHCl₃-soluble phase and its main active component, damnacanthal, isolated from the root of Morinda citrifoliaView study →} — values chosen to demonstrate an effect in a model, not to guide human intake, and inflated by the compound’s poor solubility. Human exposure occurs only indirectly through noni products, and even there the relevant human study used noni fruit capsules (maximum tolerated ~12 g/day of dried fruit) rather than the isolate, which is a root compound largely absent from the fruit ^{9,10Reference 9Issell BF et al. · 2009Clinical trialUsing quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II doseView study →Reference 10Abu N et al. · 2014ReviewDamnacanthal: a promising compound as a medicinal anthraquinone — reviewView study →}. These are doses studied in research and are not a personal recommendation.

References

1. Faltynek CR, Schroeder J, Mauvais P, et al. (1995). Damnacanthal is a highly potent, selective inhibitor of p56lck tyrosine kinase activity. Biochemistry. https://pubmed.ncbi.nlm.nih.gov/7547985/
2. Hiramatsu T, Imoto M, Koyano T, Umezawa K (1993). Induction of normal phenotypes in ras-transformed cells by damnacanthal from Morinda citrifolia. Cancer Letters. https://pubmed.ncbi.nlm.nih.gov/7693328/
3. García-Vilas JA, Quesada AR, Medina MA (2015). Damnacanthal, a noni anthraquinone, inhibits c-Met and is a potent antitumor compound against Hep G2 human hepatocellular carcinoma cells. Scientific Reports. https://pubmed.ncbi.nlm.nih.gov/25620570/
4. García-Vilas JA, Pino-Ángeles A, Martínez-Poveda B, Quesada AR, Medina MÁ (2017). The noni anthraquinone damnacanthal is a multi-kinase inhibitor with potent anti-angiogenic effects. Cancer Letters. https://pubmed.ncbi.nlm.nih.gov/27816491/
5. Aziz MYA, Omar AR, Subramani T, et al. (2014). Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells. Oncology Letters. https://pubmed.ncbi.nlm.nih.gov/24765160/
6. Nualsanit T, Rojanapanthu P, Gritsanapan W, Lee SH, Lawson D, Baek SJ (2012). Damnacanthal, a noni component, exhibits antitumorigenic activity in human colorectal cancer cells. Journal of Nutritional Biochemistry. https://pubmed.ncbi.nlm.nih.gov/21852088/
7. Woradulayapinij W, Pothiluk A, Nualsanit T, et al. (2022). Acute oral toxicity of damnacanthal and its anticancer activity against colorectal tumorigenesis. Toxicology Reports. https://pubmed.ncbi.nlm.nih.gov/36518435/
8. Okusada K, Nakamoto K, Nishida M, et al. (2011). The antinociceptive and anti-inflammatory action of the CHCl₃-soluble phase and its main active component, damnacanthal, isolated from the root of Morinda citrifolia. Biological & Pharmaceutical Bulletin. https://pubmed.ncbi.nlm.nih.gov/21212526/
9. Issell BF, Gotay CC, Pagano I, Franke AA (2009). Using quality of life measures in a phase I clinical trial of noni in patients with advanced cancer to select a phase II dose. Journal of Dietary Supplements. https://pubmed.ncbi.nlm.nih.gov/22435516/
10. Abu N, Ali NM, Ho WY, Yeap SK, Aziz MY, Alitheen NB (2014). Damnacanthal: a promising compound as a medicinal anthraquinone — review. Anti-Cancer Agents in Medicinal Chemistry. https://pubmed.ncbi.nlm.nih.gov/24164045/
11. Akhtar MN, Zareen S, Yeap SK, et al. (2013). Total synthesis, cytotoxic effects of damnacanthal, nordamnacanthal and related anthraquinone analogues. Molecules. https://pubmed.ncbi.nlm.nih.gov/23966087/
12. Stalman M, Koskamp AM, Luderer R, et al. (2003). Regulation of anthraquinone biosynthesis in cell cultures of Morinda citrifolia. Journal of Plant Physiology. https://pubmed.ncbi.nlm.nih.gov/12872482/
13. IARC Working Group (2002). Rubia tinctorum, Morinda officinalis and anthraquinones. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 82. https://www.ncbi.nlm.nih.gov/books/NBK326613/

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