Deguelin

Deguelin at a Glance

Deguelin is a rotenoid: an isoflavonoid-derived molecule from the same structural family as rotenone, and its closest commercial relative. It is not a minor congener. In cubé resin — the Lonchocarpus root extract sold for generations as a botanical insecticide and fish poison — deguelin makes up about 21% of the resin by weight, with rotenone, rotenolone and tephrosin accounting for most of the rest ^{2,3Reference 2Fang N · 1999In vitroCubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitroView study →Reference 3Cabizza M et al. · 2004Rotenone and rotenoids in cubè resins, formulations, and residues on olivesView study →}.

Its one mechanism is inhibition of mitochondrial complex I, the first enzyme of the respiratory chain ^{1,5Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →Reference 5Carpenter EL et al. · 2019In vitroMitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib-resistant BRAF(V600E) mutation bearing metastatic melanoma cells — in vitroView study →}. Everything deguelin is known for follows from that: it kills insect larvae, it paralyses nematodes, it is toxic to fish, it kills cultured cells of every kind, and in rats it destroys the nigrostriatal dopaminergic pathway and produces a Parkinson’s-disease-like syndrome ^{1,10,14Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →Reference 10Preston S et al. · 2017In vitroDeguelin exerts potent nematocidal activity via the mitochondrial respiratory chain — in vitroView study →Reference 14Said AH et al. · 2020In vitroIsolation of the Tephrosia vogelii extract and rotenoids and their toxicity in the RTgill-W1 trout cell line and in zebrafish embryos — in vitroView study →}.

Deguelin also carries a large preclinical oncology literature — several hundred papers on apoptosis, angiogenesis, Akt and Hsp90 — and no clinical trials at all. The programmes built on it are programmes to build analogues that are not deguelin, precisely because the parent’s neurotoxicity closed the clinical route ^{7,8Reference 7Varughese RS et al. · 2019ReviewBiopharmacological considerations for accelerating drug development of deguelin, a rotenoid with potent chemotherapeutic and chemopreventive potential — reviewView study →Reference 8Jiang W et al. · 2025ReviewDeguelin’s Anticancer Bioactivity: Challenges and Opportunities in Medicinal Chemistry — reviewView study →}. Read the anticancer results as what they are: potent, non-selective mitochondrial poisoning measured in a cancer assay.

Complex I Inhibition Is the Whole Story

Rotenoids bind at the ubiquinone-reduction site of NADH:ubiquinone oxidoreductase (complex I) and stop electron transfer. ATP synthesis collapses, the cell switches to whatever glycolytic capacity it has, and AMP-activated protein kinase fires ^{5Reference 5Carpenter EL et al. · 2019In vitroMitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib-resistant BRAF(V600E) mutation bearing metastatic melanoma cells — in vitroView study →}. In cubé-resin work, the 29 identified rotenoids were assayed side by side against complex I, against phorbol-ester-induced ornithine decarboxylase, and for cytotoxicity — and the same structure–activity relationship came out of all three assays ^{2Reference 2Fang N · 1999In vitroCubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitroView study →}. The molecular features that make a rotenoid a better insecticide are the features that make it better at killing cells.

This is the load-bearing point for reading anything else about deguelin. A single lesion in the respiratory chain presents differently depending on which organism you dose:

• In a mosquito or a beetle, respiratory arrest is the insecticidal effect.
• In a nematode, oxygen consumption falls immediately and motility stops — the nematocidal effect ^{10Reference 10Preston S et al. · 2017In vitroDeguelin exerts potent nematocidal activity via the mitochondrial respiratory chain — in vitroView study →}.
• In fish and fish embryos, gill epithelium and development fail at nanomolar concentrations — the piscicidal effect ^{14Reference 14Said AH et al. · 2020In vitroIsolation of the Tephrosia vogelii extract and rotenoids and their toxicity in the RTgill-W1 trout cell line and in zebrafish embryos — in vitroView study →}.
• In a cultured tumour cell, ATP depletion triggers AMPK, mTORC1 shutdown, cell-cycle arrest and apoptosis — read out as antiproliferative activity ^{5Reference 5Carpenter EL et al. · 2019In vitroMitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib-resistant BRAF(V600E) mutation bearing metastatic melanoma cells — in vitroView study →}.
• In a rat, dopaminergic neurons of the substantia nigra degenerate — read out as parkinsonism ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}.

Deguelin is roughly half as potent as rotenone in producing that last effect, and roughly half as potent in acute intraperitoneal lethality in mice ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}. Half of a neurotoxin is a neurotoxin. Its hydroxylated metabolites, including 12aβ-hydroxydeguelin, are less active on complex I, so the parent compound is the toxicant and metabolism is a detoxification route ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}.

The Amorpha Rotenoid Set

Amorpha fruticosa — false indigo bush — carries its own group of rotenoids alongside deguelin and tephrosin. Three of them have small, self-contained literatures that are best read together, because individually each is a handful of papers and collectively they say one thing.

Rotenoid	What Is Actually Known	Where It Comes From
Amorphigenin (8′-hydroxyrotenone)	Larvicidal to Culex pipiens pallens at LC50 4.29 mg/L, and a complex-I inhibitor of essentially rotenone’s potency in that insect — in-vivo IC50 2.43 µM against rotenone’s 2.52 µM 19,20Reference 19Liang Y et al. · 2015AnimalToxicity of amorphigenin from the seeds of Amorpha fruticosa against the larvae of Culex pipiens pallens (Diptera: Culicidae) — in vivoView study →Reference 20Ji M et al. · 2015In vitroInhibitory Effects of Amorphigenin on the Mitochondrial Complex I of Culex pipiens pallens Coquillett (Diptera: Culicidae) — in vitroView study →	A. fruticosa seed
Dalbinol	Antiproliferative in three hepatocellular-carcinoma lines via ubiquitin–proteasome degradation of β-catenin 22Reference 22Zhu X et al. · 2017In vitroDalbinol, a rotenoid from Amorpha fruticosa L., exerts anti-proliferative activity by facilitating β-catenin degradation in hepatocellular carcinoma cells — in vitroView study →; a noncompetitive bacterial neuraminidase inhibitor at IC50 8.3–16.7 µM, with modest Pseudomonas aeruginosa antibiofilm activity 23Reference 23Kim YS et al. · 2011In vitroFlavanones and rotenoids from the roots of Amorpha fruticosa L. that inhibit bacterial neuraminidase — in vitroView study →	A. fruticosa seed and root
Amorphispironone	The first — for two decades the only — spirorotenoid described from a plant 24Reference 24Andrei CC et al. · 2002New spirorotenoids from Tephrosia candidaView study →; with tephrosin, it suppressed phorbol-ester-induced Epstein–Barr virus early-antigen activation and inhibited two-stage mouse skin tumour promotion 18Reference 18Konoshima T et al. · 1993AnimalStudies on inhibitors of skin tumor promotion, XIIView study →	A. fruticosa leaf

Amorphigenin has one further claim on the record, and it is a laboratory one: a photoaffinity-labelling analogue synthesised from it, arylazidoamorphigenin, inhibits NADH–ubiquinone oxidoreductase at rotenone-like concentrations and was used to map the rotenone binding site to a 33 kDa polypeptide of complex I ^{21Reference 21Earley FG · 1984In vitroPhotoaffinity labelling of mitochondrial NADH dehydrogenase with arylazidoamorphigenin, an analogue of rotenone — in vitroView study →}. The molecule’s most durable contribution was as a probe for the enzyme it poisons.

One number in this set is routinely mis-attributed and worth stating precisely. The ED50 below 0.001 µg/mL across six neoplastic cell lines belongs to 12aβ-hydroxyamorphigenin, not to amorphigenin itself ^{17Reference 17Li L et al. · 1993In vitroAntitumor agents, 138View study →}. It is also not a selectivity finding: a compound that kills six unrelated cell lines at sub-nanogram concentrations is not discriminating between them, it is stopping respiration in all of them.

The anti-tumour-promotion results ^{18Reference 18Konoshima T et al. · 1993AnimalStudies on inhibitors of skin tumor promotion, XIIView study →} are the one strand here that is not simply cytotoxicity — inhibiting promotion is a different endpoint from killing cells. But they rest on a single 1993 report in a mouse two-stage model, they have not been followed up in thirty years, and the same molecules are acutely toxic. Nothing in this set is a therapeutic lead.

What It's Used For

The evidence splits unevenly. Deguelin’s use as a pesticide component is real, commercial and quantified; its antiparasitic activity is well demonstrated in worms; its oncology literature is large, entirely preclinical, and describes the same poisoning by another name.

Evidence by IndicationStrength of support · Beta

01Botanical Insecticide and PiscicidePromising58%Commercial cubé-resin use, quantified content and residues, comparative potency across rotenoids ^{2,3,15,16Reference 2Fang N · 1999In vitroCubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitroView study →Reference 3Cabizza M et al. · 2004Rotenone and rotenoids in cubè resins, formulations, and residues on olivesView study →Reference 15Belmain SR et al. · 2012Highly variable insect control efficacy of Tephrosia vogelii chemotypesView study →Reference 16Zhang P et al. · 2020ReviewPlants in the Genus Tephrosia: Valuable Resources for Botanical Insecticides — reviewView study →}

02Nematocidal and Anthelmintic ActivityShaky32%Selective motility and development inhibition in parasitic and free-living nematodes, with direct respirometry ^{10Reference 10Preston S et al. · 2017In vitroDeguelin exerts potent nematocidal activity via the mitochondrial respiratory chain — in vitroView study →}

03Antiproliferative Activity in Cancer ModelsShaky28%Large in-vitro and rodent literature (PI3K/Akt, Hsp90, complex I); no human data, no clinical trial ^{5,6,7,9Reference 5Carpenter EL et al. · 2019In vitroMitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib-resistant BRAF(V600E) mutation bearing metastatic melanoma cells — in vitroView study →Reference 6Chun KH et al. · 2003In vitroEffects of deguelin on the phosphatidylinositol 3-kinase/Akt pathway and apoptosis in premalignant human bronchial epithelial cells — in vitroView study →Reference 7Varughese RS et al. · 2019ReviewBiopharmacological considerations for accelerating drug development of deguelin, a rotenoid with potent chemotherapeutic and chemopreventive potential — reviewView study →Reference 9Oh SH et al. · 2007In vitroStructural basis for depletion of heat shock protein 90 client proteins by deguelin — in vitroView study →}

04Inflammatory SignallingShaky20%Reporter-gene NF-κB inhibition at IC50 0.22 µM in a single phytochemistry screen ^{4Reference 4Dat NT et al. · 2008In vitroPhenolic constituents of Amorpha fruticosa that inhibit NF-kappaB activation and related gene expression — in vitroView study →}

Mechanisms

The first row is not one mechanism among seven — it is the mechanism, and the rest are what a cell does about it. A rotenoid’s structure–activity relationship is the same whether it is scored on complex-I inhibition, tumour promotion or cytotoxicity ^{2Reference 2Fang N · 1999In vitroCubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitroView study →}.

Pharmacokinetics

The only pharmacokinetic study is in rats, using tritiated compound. After intravenous dosing, deguelin showed a mean residence time of 6.98 h and a terminal half-life of 9.26 h, with a large steady-state volume of distribution (30.5 L/kg) — a lipophilic molecule that leaves the plasma quickly and sits in tissue ^{11Reference 11Udeani GO et al. · 2001AnimalPharmacokinetics of deguelin, a cancer chemopreventive agent in rats — animal studyView study →}. Tissue distribution was led by heart and fat, then mammary gland, colon, liver and kidney, with brain and lung lowest; after intragastric dosing the ordering was similar, with perirenal fat first. Elimination was overwhelmingly as metabolites — about 58% in faeces and 14% in urine over five days, with only 1.7% of the dose recovered as unchanged deguelin in faeces and 0.4% in urine ^{11Reference 11Udeani GO et al. · 2001AnimalPharmacokinetics of deguelin, a cancer chemopreventive agent in rats — animal studyView study →}. In humans, deguelin is metabolised by CYP3A4 and CYP2C19 and by no other of the seven P450s tested; CYP2C19 is the more selective route to the 12aβ-hydroxy metabolites, which are less active on complex I than the parent ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}. There are no human pharmacokinetic data.

Clinical Trials

None. Deguelin has not been administered to human subjects in a registered trial, and the reviews of its development explicitly frame the task as producing safer analogues rather than dosing the parent ^{7,8Reference 7Varughese RS et al. · 2019ReviewBiopharmacological considerations for accelerating drug development of deguelin, a rotenoid with potent chemotherapeutic and chemopreventive potential — reviewView study →Reference 8Jiang W et al. · 2025ReviewDeguelin’s Anticancer Bioactivity: Challenges and Opportunities in Medicinal Chemistry — reviewView study →}.

Last checked: September 2026.

Isolate vs. Plant Studies

Almost everything here is the isolate, and for once that is not a strength. The pesticide literature is the exception: cubé resin and Tephrosia vogelii extracts are studied as whole preparations, and in the zebrafish and trout-gill work the crude extract was more toxic than any of its purified rotenoids — cytotoxic at 5–10 nM against 50 nM for tephrosin, deguelin and rotenone individually ^{14Reference 14Said AH et al. · 2020In vitroIsolation of the Tephrosia vogelii extract and rotenoids and their toxicity in the RTgill-W1 trout cell line and in zebrafish embryos — in vitroView study →}. That is the usual botanical-mixture result, and it matters practically: a Tephrosia preparation cannot be dose-predicted from its deguelin content alone.

Running the other way, the Tephrosia chemotype work shows the isolate story is nonetheless the right one for efficacy: the chemotype without rotenoids has no pesticidal activity, so the rotenoids really are carrying the effect, and the plant’s major non-rotenoid flavonoid is inactive ^{15Reference 15Belmain SR et al. · 2012Highly variable insect control efficacy of Tephrosia vogelii chemotypesView study →}. Neither plant is used medicinally in any tradition that would generate human exposure data, and the Amorpha fruticosa rotenoids come from a shrub with no established internal use at all.

Prevalence in Nature

Deguelin is a legume rotenoid, confined in practice to the Fabaceae. Its richest documented source is cubé resin, the trichloroethylene root extract of the South American vines Lonchocarpus utilis and L. urucu, where it accounts for roughly 21% of the resin against tephrosin’s 3.5% and β-rotenolone’s 3.0% ^{3Reference 3Cabizza M et al. · 2004Rotenone and rotenoids in cubè resins, formulations, and residues on olivesView study →}. Twenty-nine distinct rotenoids have been catalogued from the same resin, including chlorinated and dihydroxylated minor members, several of which are probably artefacts of extraction and processing rather than plant products ^{2Reference 2Fang N · 1999In vitroCubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitroView study →}.

It occurs across the genus Tephrosia — some 400 species — most importantly in T. vogelii, the fish-poison bean used for pest control and fish stunning throughout Africa. Content there is chemotype-determined: one chemotype makes rotenoids and one does not, and within the rotenoid chemotype the levels swing substantially with season ^{15,16Reference 15Belmain SR et al. · 2012Highly variable insect control efficacy of Tephrosia vogelii chemotypesView study →Reference 16Zhang P et al. · 2020ReviewPlants in the Genus Tephrosia: Valuable Resources for Botanical Insecticides — reviewView study →}. It is also a constituent of Derris species, the Asian source that supplied most commercial rotenone, and of false indigo bush (Amorpha fruticosa), where it sits alongside tephrosin, amorphigenin, dalbinol and amorphispironone in the seeds, roots and leaves ^{4,17,18Reference 4Dat NT et al. · 2008In vitroPhenolic constituents of Amorpha fruticosa that inhibit NF-kappaB activation and related gene expression — in vitroView study →Reference 17Li L et al. · 1993In vitroAntitumor agents, 138View study →Reference 18Konoshima T et al. · 1993AnimalStudies on inhibitors of skin tumor promotion, XIIView study →}.

The plants that make rotenoids concentrate them in roots and seeds — the organs where a respiratory poison protects a stationary, high-value tissue from soil arthropods and grazers.

Discovery & Synthesis

Deguelin belongs to the wave of rotenoid chemistry that followed the identification of rotenone: it was characterised in the 1930s from Derris and Lonchocarpus root extracts, and its name descends from that pesticide literature rather than from any medicinal use. The precise first-isolation report predates the indexed literature and is not asserted here.

Synthesis came much later and in two forms. Several racemic total syntheses were reported before a concise enantioselective route was published in 2013 — six steps, no protecting groups, built on a thiourea-catalysed tandem Knoevenagel/conjugate-addition/decarboxylation sequence, and designed specifically to make both enantiomers available for comparison. That comparison produced an oddity: the unnatural (+)-deguelin was the better inhibitor of MCF-7 and HepG2 growth ^{12Reference 12Farmer RL · 2013In vitroA Concise Enantioselective Synthesis and Cytotoxic Evaluation of the Anticancer Rotenoid Deguelin Enabled by a Tandem Knoevenagel/Conjugate Addition/Decarboxylation Sequence — in vitroView study →}. Separately, a stereocontrolled semi-synthesis from rotenone was published in 2017 — a zinc-mediated ring-opening of rotenone hydrobromide to rot-2′-enonic acid, conversion to deguelin, and a chromium-mediated hydroxylation that delivers tephrosin as a single diastereoisomer ^{13Reference 13Russell DA et al. · 2017Stereocontrolled semi-syntheses of deguelin and tephrosinView study →}. That route is scalable and high-yielding, and it is how both molecules are most practically obtained.

Deguelin is not manufactured as a product in its own right. It reaches the world as a constituent of rotenone-based botanical insecticides, and in the laboratory as an isolate or a semi-synthetic sample.

Patents: not yet researched.

Toxicity & Safety

Deguelin is a respiratory poison. That is the headline rather than a caveat attached to a therapeutic story, and it is the same property the sections above describe as pharmacology.

Safety at a Glance

☠️ ToxicNeurotoxicity

• Mammalian neurotoxin. Subcutaneous infusion at 6 mg/kg/day degenerates the rat nigrostriatal dopaminergic pathway and produces a Parkinson’s-disease-like syndrome — about half as potent as rotenone, which is itself a standard laboratory model of the disease ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}.
• Non-selective cytotoxicity. Complex-I inhibition kills cultured cells of every lineage; the antiproliferative results in cancer models are that effect measured in a cancer assay, not evidence of tumour selectivity ^{2,5Reference 2Fang N · 1999In vitroCubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitroView study →Reference 5Carpenter EL et al. · 2019In vitroMitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib-resistant BRAF(V600E) mutation bearing metastatic melanoma cells — in vitroView study →}.
• Aquatic toxicity. Deguelin is a piscicide. It was cytotoxic to trout gill epithelium and caused deformity and mortality in zebrafish embryos at 50 nM, and crude Tephrosia extract at 5 nM ^{14Reference 14Said AH et al. · 2020In vitroIsolation of the Tephrosia vogelii extract and rotenoids and their toxicity in the RTgill-W1 trout cell line and in zebrafish embryos — in vitroView study →}.
• Not counted in pesticide residue limits. Residues on treated crops run at concentrations comparable to rotenone’s, but only rotenone is measured for the legal determination ^{3Reference 3Cabizza M et al. · 2004Rotenone and rotenoids in cubè resins, formulations, and residues on olivesView study →}.
• CYP3A4 and CYP2C19 substrate. Both P450s metabolise it, and both routes reduce complex-I activity — so anything that slows them raises exposure to the active parent ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}.

Full Safety & Interactions Detail

The neurotoxicity finding, precisely. Rats given deguelin by subcutaneous osmotic minipump for five to six days showed degeneration of the nigrostriatal dopaminergic pathway, measured as reduced tyrosine-hydroxylase immunoreactivity, at 6 mg/kg/day but not at 3 mg/kg/day; rotenone did it at 3 mg/kg/day. Brain levels of the parent rotenoid of 0.4–1.3 ppm accompanied the lesions, while the 12aβ-hydroxy metabolites were present at far lower levels and are less active on complex I — establishing that the parent compounds, not their metabolites, cause the syndrome ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}. The same study found deguelin about half as potent as rotenone in acute intraperitoneal lethality in mice.

Why the clinical route closed. Reviews of deguelin’s development state the position without hedging: potent preclinical anticancer activity, and practical use “impeded by its volatility, possible neurotoxicity, and other detrimental consequences” — with the field’s response being ring-truncated and simplified analogues rather than the natural product ^{7,8Reference 7Varughese RS et al. · 2019ReviewBiopharmacological considerations for accelerating drug development of deguelin, a rotenoid with potent chemotherapeutic and chemopreventive potential — reviewView study →Reference 8Jiang W et al. · 2025ReviewDeguelin’s Anticancer Bioactivity: Challenges and Opportunities in Medicinal Chemistry — reviewView study →}. The pharmacokinetic groundwork exists in rats ^{11Reference 11Udeani GO et al. · 2001AnimalPharmacokinetics of deguelin, a cancer chemopreventive agent in rats — animal studyView study →}, but no human study followed.

Reproductive finding. In an isolated-cell study, deguelin impaired porcine sperm motility, viability and capacitation-related function through abnormal activation of PI3K/AKT signalling ^{25Reference 25Lee WJ et al. · 2023In vitroThe natural flavonoid compound deguelin suppresses sperm (Sus Scrofa) functions through abnormal activation of the PI3K/AKT pathway — in vitroView study →}. This is a single in-vitro report in one species and is not a human-exposure finding, but it is the only reproductive-toxicity signal on record for the molecule and no dedicated developmental-toxicity package exists.

Interactions. Deguelin is metabolised by CYP3A4 and CYP2C19, and by none of five other human P450s tested ^{1Reference 1Caboni P et al. · 2004AnimalRotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal modelView study →}. Since 12aβ-hydroxylation and 2-O-demethylation both detoxify the molecule, inhibition of either enzyme would be expected to raise exposure to the toxic parent — a theoretical direction inferred from the metabolism data, not a measured interaction. No clinical interaction study exists.

What is not known. There is no human toxicology for deguelin: no case reports of isolated-deguelin poisoning, no occupational-exposure series separating it from rotenone, and no genotoxicity or repeat-dose package for the pure compound. Human exposure occurs as part of rotenoid pesticide mixtures, where rotenone is the regulated marker.

Dosage

There is no human dose, no traditional preparation and no supplement form. The figures below are the concentrations and rates at which deguelin has actually been studied, given so that a number encountered elsewhere can be placed:

These are research and pesticide figures, not a personal recommendation, and nothing here supports an internal human dose.

References

1. Caboni P, Sherer TB, Zhang N, et al. (2004). Rotenone, deguelin, their metabolites, and the rat model of Parkinson’s disease — animal model. Chem Res Toxicol. https://pubmed.ncbi.nlm.nih.gov/15540952/
2. Fang N, Casida JE (1999). Cubé resin insecticide: identification and biological activity of 29 rotenoid constituents — in vitro. J Agric Food Chem. https://pubmed.ncbi.nlm.nih.gov/10552508/
3. Cabizza M, Angioni A, Melis M, et al. (2004). Rotenone and rotenoids in cubè resins, formulations, and residues on olives. J Agric Food Chem. https://pubmed.ncbi.nlm.nih.gov/14733510/
4. Dat NT, Lee JH, Lee K, et al. (2008). Phenolic constituents of Amorpha fruticosa that inhibit NF-kappaB activation and related gene expression — in vitro. J Nat Prod. https://pubmed.ncbi.nlm.nih.gov/18841906/
5. Carpenter EL, Chagani S, Nelson D, et al. (2019). Mitochondrial complex I inhibitor deguelin induces metabolic reprogramming and sensitizes vemurafenib-resistant BRAF(V600E) mutation bearing metastatic melanoma cells — in vitro. Mol Carcinog. https://pubmed.ncbi.nlm.nih.gov/31211467/
6. Chun KH, Kosmeder JW 2nd, Sun S, et al. (2003). Effects of deguelin on the phosphatidylinositol 3-kinase/Akt pathway and apoptosis in premalignant human bronchial epithelial cells — in vitro. J Natl Cancer Inst. https://pubmed.ncbi.nlm.nih.gov/12591985/
7. Varughese RS, Lam WS, Marican AABH, et al. (2019). Biopharmacological considerations for accelerating drug development of deguelin, a rotenoid with potent chemotherapeutic and chemopreventive potential — review. Cancer. https://pubmed.ncbi.nlm.nih.gov/30933320/
8. Jiang W, Zeng J, Guo L, et al. (2025). Deguelin’s Anticancer Bioactivity: Challenges and Opportunities in Medicinal Chemistry — review. Front Pharmacol. https://pubmed.ncbi.nlm.nih.gov/40672375/
9. Oh SH, Woo JK, Yazici YD, et al. (2007). Structural basis for depletion of heat shock protein 90 client proteins by deguelin — in vitro. J Natl Cancer Inst. https://pubmed.ncbi.nlm.nih.gov/17565155/
10. Preston S, Korhonen PK, Mouchiroud L, et al. (2017). Deguelin exerts potent nematocidal activity via the mitochondrial respiratory chain — in vitro. FASEB J. https://pubmed.ncbi.nlm.nih.gov/28687609/
11. Udeani GO, Zhao GM, Shin YG, et al. (2001). Pharmacokinetics of deguelin, a cancer chemopreventive agent in rats — animal study. Cancer Chemother Pharmacol. https://pubmed.ncbi.nlm.nih.gov/11320671/
12. Farmer RL, Scheidt KA (2013). A Concise Enantioselective Synthesis and Cytotoxic Evaluation of the Anticancer Rotenoid Deguelin Enabled by a Tandem Knoevenagel/Conjugate Addition/Decarboxylation Sequence — in vitro. Chem Sci. https://pubmed.ncbi.nlm.nih.gov/24101971/
13. Russell DA, Freudenreich JJ, Ciardiello JJ, et al. (2017). Stereocontrolled semi-syntheses of deguelin and tephrosin. Org Biomol Chem. https://pubmed.ncbi.nlm.nih.gov/28134391/
14. Said AH, Solhaug A, Sandvik M, et al. (2020). Isolation of the Tephrosia vogelii extract and rotenoids and their toxicity in the RTgill-W1 trout cell line and in zebrafish embryos — in vitro. Toxicon. https://pubmed.ncbi.nlm.nih.gov/32454059/
15. Belmain SR, Amoah BA, Nyirenda SP, et al. (2012). Highly variable insect control efficacy of Tephrosia vogelii chemotypes. J Agric Food Chem. https://pubmed.ncbi.nlm.nih.gov/22970736/
16. Zhang P, Qin D, Chen J, et al. (2020). Plants in the Genus Tephrosia: Valuable Resources for Botanical Insecticides — review. Insects. https://pubmed.ncbi.nlm.nih.gov/33096762/
17. Li L, Wang HK, Chang JJ, et al. (1993). Antitumor agents, 138. Rotenoids and isoflavones as cytotoxic constitutents from Amorpha fruticosa — in vitro. J Nat Prod. https://pubmed.ncbi.nlm.nih.gov/8326318/
18. Konoshima T, Terada H, Kokumai M, et al. (1993). Studies on inhibitors of skin tumor promotion, XII. Rotenoids from Amorpha fruticosa — mouse model. J Nat Prod. https://pubmed.ncbi.nlm.nih.gov/8350086/
19. Liang Y, Li X, Gu Z, et al. (2015). Toxicity of amorphigenin from the seeds of Amorpha fruticosa against the larvae of Culex pipiens pallens (Diptera: Culicidae) — in vivo. Molecules. https://pubmed.ncbi.nlm.nih.gov/25690287/
20. Ji M, Liang Y, Gu Z, et al. (2015). Inhibitory Effects of Amorphigenin on the Mitochondrial Complex I of Culex pipiens pallens Coquillett (Diptera: Culicidae) — in vitro. Int J Mol Sci. https://pubmed.ncbi.nlm.nih.gov/26307964/
21. Earley FG, Ragan CI (1984). Photoaffinity labelling of mitochondrial NADH dehydrogenase with arylazidoamorphigenin, an analogue of rotenone — in vitro. Biochem J. https://pubmed.ncbi.nlm.nih.gov/6517863/
22. Zhu X, Wu X, Cheng J, et al. (2017). Dalbinol, a rotenoid from Amorpha fruticosa L., exerts anti-proliferative activity by facilitating β-catenin degradation in hepatocellular carcinoma cells — in vitro. Oncotarget. https://pubmed.ncbi.nlm.nih.gov/28548956/
23. Kim YS, Ryu YB, Curtis-Long MJ, et al. (2011). Flavanones and rotenoids from the roots of Amorpha fruticosa L. that inhibit bacterial neuraminidase — in vitro. Food Chem Toxicol. https://pubmed.ncbi.nlm.nih.gov/21571029/
24. Andrei CC, Vieira PC, Fernandes JB, et al. (2002). New spirorotenoids from Tephrosia candida. Z Naturforsch C J Biosci. https://pubmed.ncbi.nlm.nih.gov/12132677/
25. Lee WJ, Jo JH, Jang SI, et al. (2023). The natural flavonoid compound deguelin suppresses sperm (Sus Scrofa) functions through abnormal activation of the PI3K/AKT pathway — in vitro. Reprod Toxicol. https://pubmed.ncbi.nlm.nih.gov/37353039/

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