Licochalcone B

Licochalcone B at a Glance

Licochalcone B is a prenylated retrochalcone from licorice root — one of the family of “licochalcones” (A, B, C, D and relatives) that are characteristic of Glycyrrhiza and, in particular, of Xinjiang licorice (Glycyrrhiza inflata). Like all the licochalcones it is a retrochalcone, lacking the usual oxygen function at the 2′-position that ordinary chalcones carry ^{2,18Reference 2Furusawa J et al. · 2009Glycyrrhiza inflata-derived chalcones, licochalcone A, licochalcone B and licochalcone D, inhibit phosphorylation of NF-κB p65 in LPS signaling pathwayView study →Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}.

It is a close sibling of licochalcone A, and much of its broad preclinical activity — anti-inflammatory, antioxidant, antitumour, hepatoprotective — overlaps the wider chalcone story. What sets licochalcone B apart is one unusually clean, well-defined mechanism: it is a selective inhibitor of the NLRP3 inflammasome that acts by disrupting the NEK7–NLRP3 interaction ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}. That is its signature, and it is the reason the molecule has its own page rather than sitting inside the licorice monograph.

The honest headline is that essentially all of this is preclinical — cell-culture and rodent work on the isolated molecule. There are no human trials of licochalcone B, and its own toxicology is only lightly characterised, though as an isolated chalcone it carries a low toxicity flag ^{18Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}.

Selective NLRP3-Inflammasome Inhibition (NEK7 Disruption)

This is licochalcone B’s most distinctive finding and the mechanism that separates it from its siblings. In macrophages, licochalcone B specifically inhibits activation of the NLRP3 inflammasome — the sensor complex whose assembly drives caspase-1 activation and the release of interleukin-1β — while leaving the related AIM2 and NLRC4 inflammasomes untouched ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}. That selectivity is unusual for a natural product.

The mechanism is molecularly resolved: licochalcone B binds directly to NEK7 (NIMA-related kinase 7) and blocks the NEK7–NLRP3 interaction that is required for the inflammasome to oligomerise and fire ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}. Because NEK7 is the licensing partner that NLRP3 specifically depends on, disrupting that single contact switches off NLRP3 without hitting the other inflammasome sensors.

Downstream, this translated into protection in mouse models of NLRP3-driven disease — lipopolysaccharide-induced septic shock, monosodium-urate-induced peritonitis (a gout-flare model), and non-alcoholic steatohepatitis (NASH) ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}. It is the cleanest link in the whole file between a defined molecular target and an in-vivo outcome.

Gap: the evidence is the isolated molecule in cells and mice ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}; there is no human data, and this NEK7-binding selectivity has not been reproduced against the whole-plant extract, where licochalcone B is only a minor constituent.

What It's Used For

Beyond the NLRP3 signature, licochalcone B has been tested across inflammation, cancer, liver injury, oxidative stress and the nervous system. The pattern is consistent: a genuine, mechanistically-detailed preclinical signal, almost always on the isolated molecule in vitro or in rodents, with no human confirmation.

A selective NLRP3-inflammasome brake:licochalcone B binds NEK7 and disrupts the NEK7–NLRP3 interaction, inhibiting NLRP3 (but not AIM2 or NLRC4) and protecting mice from septic shock, MSU peritonitis and NASH ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}. This is the load-bearing, target-defined result.

A broad but preclinical anti-inflammatory / antioxidant chalcone:it suppresses NF-κB p65 phosphorylation in LPS-stimulated macrophages ^{2Reference 2Furusawa J et al. · 2009Glycyrrhiza inflata-derived chalcones, licochalcone A, licochalcone B and licochalcone D, inhibit phosphorylation of NF-κB p65 in LPS signaling pathwayView study →}, inhibits 15-lipoxygenase ^{3Reference 3Li H et al. · 2021Discovery of natural 15-LOX small-molecule inhibitors from Chinese herbal medicine using virtual screening, biological evaluation and molecular dynamics studiesView study →}, scavenges radicals and activates the Nrf2/HO-1 antioxidant axis in liver, lung and neuronal models ^{4,12,13,15Reference 4Fu Y et al. · 2013Antioxidant and anti-inflammatory activities of six flavonoids separated from licoriceView study →Reference 12Gao XP et al. · 2017Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of ERK signalingView study →Reference 13Zhou Y et al. · 2021AnimalLicochalcone B attenuates neuronal injury through anti-oxidant effect and enhancement of Nrf2 pathway in an MCAO rat model of strokeView study →Reference 15Huang X et al. · 2023AnimalLicochalcone B confers protective effects against LPS-induced acute lung injury in cells and mice through the Keap1/Nrf2 pathwayView study →}.

Wide in-vitro antitumour activity, one molecule at a time:apoptosis and cell-cycle arrest across hepatoma, esophageal, osteosarcoma and bladder cancer cells through PI3K/AKT/mTOR, JAK2/STAT3, p53 and MAPK routes ^{5,6,7,8,9Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →Reference 6Zhang X et al. · 2022Licochalcone B induces DNA damage, cell-cycle arrest, apoptosis, and enhances TRAIL sensitivity in hepatocellular carcinoma cellsView study →Reference 7Huang WC · 2022Licochalcone B induced apoptosis and autophagy in osteosarcoma tumor cells via the inactivation of the PI3K/AKT/mTOR pathwayView study →Reference 8Song Y et al. · 2020Janus kinase 2 inhibition by licochalcone B suppresses esophageal squamous-cell-carcinoma growthView study →Reference 9Yuan X et al. · 2014Licochalcone B inhibits growth of bladder cancer cells by arresting cell-cycle progression and inducing apoptosisView study →}.

The honest headline:every one of these is the isolated compound in cells or rodents — there are no human trials, pharmacokinetics are barely characterised, and licochalcone B is only a minor retrochalcone in the whole root ^{1,18Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini 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. Every row here is preclinical (no human data), so scores stay modest by design and reward the applications with an in-vivo mechanism.

A wide but uniformly in-vitro picture: licochalcone B triggers apoptosis and cell-cycle arrest across several cancer cell types, each through a somewhat different route. In hepatoma (HepG2) cells it caused G2/M arrest, ROS generation and caspase-dependent apoptosis (IC50 ≈ 110 µM) ^{5Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →}, and in a separate study induced DNA damage and sensitised cells to TRAIL via AKT/mTOR inhibition and ER stress ^{6Reference 6Zhang X et al. · 2022Licochalcone B induces DNA damage, cell-cycle arrest, apoptosis, and enhances TRAIL sensitivity in hepatocellular carcinoma cellsView study →}.

It inhibited JAK2 directly to suppress STAT3 signalling and esophageal squamous-cell-carcinoma growth ^{8Reference 8Song Y et al. · 2020Janus kinase 2 inhibition by licochalcone B suppresses esophageal squamous-cell-carcinoma growthView study →}, drove PI3K/AKT/mTOR-dependent apoptosis and autophagy in osteosarcoma cells ^{7Reference 7Huang WC · 2022Licochalcone B induced apoptosis and autophagy in osteosarcoma tumor cells via the inactivation of the PI3K/AKT/mTOR pathwayView study →}, and arrested bladder cancer cells with apoptosis in vitro and in an animal model ^{9Reference 9Yuan X et al. · 2014Licochalcone B inhibits growth of bladder cancer cells by arresting cell-cycle progression and inducing apoptosisView study →}.

Gap: overwhelmingly cell-line data on the isolate; the effective concentrations (tens to >100 µM) are high, in-vivo confirmation is limited, and there is no clinical work ^{5,6,7,8,9Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →Reference 6Zhang X et al. · 2022Licochalcone B induces DNA damage, cell-cycle arrest, apoptosis, and enhances TRAIL sensitivity in hepatocellular carcinoma cellsView study →Reference 7Huang WC · 2022Licochalcone B induced apoptosis and autophagy in osteosarcoma tumor cells via the inactivation of the PI3K/AKT/mTOR pathwayView study →Reference 8Song Y et al. · 2020Janus kinase 2 inhibition by licochalcone B suppresses esophageal squamous-cell-carcinoma growthView study →Reference 9Yuan X et al. · 2014Licochalcone B inhibits growth of bladder cancer cells by arresting cell-cycle progression and inducing apoptosisView study →}.

Mechanisms

Target / pathway	Effect	Relevant to
NEK7 → NEK7–NLRP3 interaction	direct NEK7 binding, disrupting the NEK7–NLRP3 contact → selective NLRP3-inflammasome inhibition (AIM2/NLRC4 spared)	anti-inflammatory (the signature)
NF-κB p65	reduced phosphorylation in LPS-stimulated macrophages	anti-inflammatory
15-lipoxygenase	enzyme inhibition (IC50 ≈ 9.67 µM), ↓ TNF-α	anti-inflammatory
Nrf2 / HO-1 (Keap1/Nrf2)	antioxidant-response activation across liver, lung, neuronal tissue	antioxidant / hepatoprotective / neuroprotective
ERK signalling	ERK–Nrf2 activation protecting hepatocytes	hepatoprotective
PI3K / AKT / mTOR	inhibition → apoptosis + autophagy	antitumour (osteosarcomahepatoma)
JAK2 / STAT3	direct JAK2 inhibition → ↓ STAT3 phosphorylation	antitumour (esophageal SCC)
p53 / Bax / Bcl-2 / caspases	pro-apoptotic shift, cell-cycle arrest, ROS	antitumour (multiple lines)
11β-hydroxysteroid dehydrogenase 2 (11β-HSD2)	enzyme inhibition (IC50 ≈ 31.85 µM, human)	toxicity (chalcone-class off-target)

The load-bearing row is NEK7: a defined, selective molecular target with a matching in-vivo phenotype is what makes this molecule more than “another anti-inflammatory chalcone” ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}. The remaining pathways are the familiar chalcone repertoire — Nrf2 upregulation and pro-apoptotic MAPK/PI3K signalling — shared with licochalcone A and other licorice flavonoids.

Pharmacokinetics

Human pharmacokinetics for licochalcone B are essentially uncharacterised — no reliable absorption, oral-bioavailability, half-life or metabolite data are established, which is a real limitation given that most of the efficacy work is in-vitro at low-to-mid-micromolar (and, for hepatoma cytotoxicity, ~110 µM) concentrations ^{5Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →}. As a lipophilic prenylated chalcone it would be expected to be poorly water-soluble, and the in-vivo studies dose it directly in rodents rather than model realistic human exposure. Until proper ADME work exists, the gap between the concentrations that act in a dish and anything achievable from eating licorice or taking an extract should be read conservatively.

Clinical Trials

There are no clinical trials of isolated licochalcone B. The entire evidence base is preclinical — cell culture and rodent disease models.

Completed	Planned	Terminated	Preclinical
—	—	—	NLRP3/NEK7(mouse); antitumour (multiple cell lines); hepatoprotective, neuroprotective, anti-lung-injury (rodent) ^{1,5,6,7,8,9,10,11,12,13,14,15Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →Reference 6Zhang X et al. · 2022Licochalcone B induces DNA damage, cell-cycle arrest, apoptosis, and enhances TRAIL sensitivity in hepatocellular carcinoma cellsView study →Reference 7Huang WC · 2022Licochalcone B induced apoptosis and autophagy in osteosarcoma tumor cells via the inactivation of the PI3K/AKT/mTOR pathwayView study →Reference 8Song Y et al. · 2020Janus kinase 2 inhibition by licochalcone B suppresses esophageal squamous-cell-carcinoma growthView study →Reference 9Yuan X et al. · 2014Licochalcone B inhibits growth of bladder cancer cells by arresting cell-cycle progression and inducing apoptosisView study →Reference 10Teng H et al. · 2016AnimalHepatoprotective effects of licochalcone B on carbon-tetrachloride-induced liver toxicity in miceView study →Reference 11Lin Y et al. · 2017AnimalNrf2 activators from Glycyrrhiza inflata and their hepatoprotective activities against CCl₄-induced liver injury in miceView study →Reference 12Gao XP et al. · 2017Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of ERK signalingView study →Reference 13Zhou Y et al. · 2021AnimalLicochalcone B attenuates neuronal injury through anti-oxidant effect and enhancement of Nrf2 pathway in an MCAO rat model of strokeView study →Reference 14Cao G et al. · 2020Licochalcone B, a chalcone derivative from Glycyrrhiza inflata, as a multifunctional agent for the treatment of Alzheimer’s diseaseView study →Reference 15Huang X et al. · 2023AnimalLicochalcone B confers protective effects against LPS-induced acute lung injury in cells and mice through the Keap1/Nrf2 pathwayView study →}

Last checked: July 2026.

Isolate vs. Plant Studies

Licochalcone B sits firmly on the isolate side of the ledger, and unusually so — nearly every result cited here used the purified molecule, not a licorice extract. The NEK7–NLRP3 work ^{1Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →}, the antitumour cell-line studies ^{5,6,7,8,9Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →Reference 6Zhang X et al. · 2022Licochalcone B induces DNA damage, cell-cycle arrest, apoptosis, and enhances TRAIL sensitivity in hepatocellular carcinoma cellsView study →Reference 7Huang WC · 2022Licochalcone B induced apoptosis and autophagy in osteosarcoma tumor cells via the inactivation of the PI3K/AKT/mTOR pathwayView study →Reference 8Song Y et al. · 2020Janus kinase 2 inhibition by licochalcone B suppresses esophageal squamous-cell-carcinoma growthView study →Reference 9Yuan X et al. · 2014Licochalcone B inhibits growth of bladder cancer cells by arresting cell-cycle progression and inducing apoptosisView study →} and the hepatoprotective rodent models ^{10,11,12Reference 10Teng H et al. · 2016AnimalHepatoprotective effects of licochalcone B on carbon-tetrachloride-induced liver toxicity in miceView study →Reference 11Lin Y et al. · 2017AnimalNrf2 activators from Glycyrrhiza inflata and their hepatoprotective activities against CCl₄-induced liver injury in miceView study →Reference 12Gao XP et al. · 2017Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of ERK signalingView study →} all test isolated licochalcone B. That is a genuine strength for mechanistic clarity: when the compound acts, we know it is the compound.

The weakness is the mirror image. Because licochalcone B is only a minor retrochalcone in the root — and because whole-licorice pharmacology is dominated by glycyrrhizin, glabridin and the far more abundant flavonoids — none of these isolate findings can be assumed to occur when someone consumes licorice or a standardised extract. The one whole-plant-adjacent result is the COPD study, and even that is a two-compound combination (licochalcone B + liquiritin), not the extract ^{16Reference 16Dong Y et al. · 2024A synergistic mechanism of liquiritin and licochalcone B from Glycyrrhiza uralensis against COPDView study →}. The correct reading: strong isolate mechanism, no human data, and no demonstrated bridge from the molecule back to the herb.

Prevalence in Nature

Licochalcone B is a retrochalcone of Glycyrrhiza (licorice) and is most closely associated with Xinjiang licorice, Glycyrrhiza inflata — the species from which the licochalcones were first isolated and whose chalcones are, distinctively, all retrochalcones ^{2,18Reference 2Furusawa J et al. · 2009Glycyrrhiza inflata-derived chalcones, licochalcone A, licochalcone B and licochalcone D, inhibit phosphorylation of NF-κB p65 in LPS signaling pathwayView study →Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}. It is also reported from Chinese licorice (G. uralensis) ^{5Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →} and common licorice (G. glabra).

Within the root it is a minor constituent: the licochalcones as a group sit inside the prenylated-flavonoid fraction, well below the dominant saponin (glycyrrhizin) and the bulk flavonoids such as the chalcone glycoside isoliquiritin. Its quantitative abundance is not well documented in the literature, and it varies with species and chemotype — the same species discipline that governs all of licorice phytochemistry, where G. inflata, G. uralensis and G. glabra differ chemically and cannot be treated as interchangeable. Licochalcone B typically co-occurs with its sibling licochalcone A and with the other retrochalcones (C, D) of G. inflata ^{18Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}.

Discovery & Synthesis

The licochalcones entered the literature in the mid-1970s: licochalcones A and B were among the first “new-type” chalcones isolated from licorice root by Saitoh and Shibata (1975), who recognised the family’s unusual retrochalcone skeleton — a chalcone lacking the 2′-oxygen function of ordinary chalcones ^{2,18Reference 2Furusawa J et al. · 2009Glycyrrhiza inflata-derived chalcones, licochalcone A, licochalcone B and licochalcone D, inhibit phosphorylation of NF-κB p65 in LPS signaling pathwayView study →Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}. Later phytochemical work established Glycyrrhiza inflata as the characteristic source and extended the series to licochalcones C, D and beyond. Structurally, licochalcone B is a chalcone — two aromatic rings bridged by an α,β-unsaturated ketone — carrying the prenylation and hydroxylation pattern typical of the licorice retrochalcones ^{18Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}.

Isolation from licorice root remains the usual laboratory route to the compound; no dominant commercial total synthesis is documented here, and the molecule is handled as a research-grade natural-product isolate rather than a manufactured ingredient.

Patents: not yet researched.

Toxicity & Safety

Licochalcone B carries a low toxicity flag: it is an isolated plant chalcone with no reported acute-toxicity signal at the doses used in its rodent studies, and the mini-review that collates its pharmacology notes that its toxicology is, frankly, poorly characterised ^{18Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}. The flag reflects the absence of alarming findings rather than a thorough safety dossier — “not much studied” is not the same as “shown to be safe.”

The one concrete safety-relevant off-target is a chalcone-class effect: licochalcone B inhibits 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in vitro (human enzyme IC50 ≈ 31.85 µM) ^{17Reference 17Lin S et al. · 2024AnimalChalcones from plants cause toxicity by inhibiting human and rat 11β-hydroxysteroid dehydrogenase 2View study →}. 11β-HSD2 protects the mineralocorticoid receptor from cortisol, so its inhibition is the same category of mechanism (though a different enzyme step) that underlies licorice’s well-known tendency to raise blood pressure and cause potassium loss via glycyrrhetinic acid. This is a plausible mechanistic caution for concentrated chalcone exposure, characterised only in enzyme assays ^{17Reference 17Lin S et al. · 2024AnimalChalcones from plants cause toxicity by inhibiting human and rat 11β-hydroxysteroid dehydrogenase 2View study →}.

Safety at a Glance

Low / no toxicity

An isolated plant chalcone with no acute-toxicity signal in the rodent studies conducted to date ^{18Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}.
Toxicology is barely characterised. There are no human safety data and no repeat-dose or reproductive dataset for the isolate — absence of findings is not evidence of safety ^{18Reference 18Shaikh S et al. · 2024ReviewTherapeutic potential and action mechanisms of licochalcone B: a mini reviewView study →}.
Chalcone-class 11β-HSD2 inhibition in vitro (IC50 ≈ 32 µM, human enzyme) — the enzyme family behind licorice’s blood-pressure/potassium effects; a mechanistic caution for concentrated exposure, not a demonstrated clinical harm ^{17Reference 17Lin S et al. · 2024AnimalChalcones from plants cause toxicity by inhibiting human and rat 11β-hydroxysteroid dehydrogenase 2View study →}.
Everything is preclinical. Effects are shown for the isolated molecule in cells and animals, often at concentrations far above anything achievable from licorice in the diet.

Dosage

There is no established or recommended human dose for licochalcone B — it has never been given to people as an isolated compound. The figures in the literature are entirely preclinical:

Setting	Model	Reported figure
15-Lipoxygenase inhibition	Enzyme / macrophage assay	IC50 ≈ 9.67 µM ^{3Reference 3Li H et al. · 2021Discovery of natural 15-LOX small-molecule inhibitors from Chinese herbal medicine using virtual screening, biological evaluation and molecular dynamics studiesView study →}
Nitric-oxide inhibition	LPS-stimulated RAW264.7	IC50 ≈ 8.78 µM
Hepatoma cytotoxicity	HepG2 cells	IC50 ≈ 110 µM ^{5Reference 5Wang J et al. · 2019Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2View study →}
11β-HSD2 inhibition	Human enzyme assay	IC50 ≈ 31.85 µM ^{17Reference 17Lin S et al. · 2024AnimalChalcones from plants cause toxicity by inhibiting human and rat 11β-hydroxysteroid dehydrogenase 2View study →}
Anti-inflammatory / hepatoprotective / stroke	Mouse & rat disease models	Dosed directly in animals ^{1,10,13Reference 1Li Q et al. · 2022Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interactionView study →Reference 10Teng H et al. · 2016AnimalHepatoprotective effects of licochalcone B on carbon-tetrachloride-induced liver toxicity in miceView study →Reference 13Zhou Y et al. · 2021AnimalLicochalcone B attenuates neuronal injury through anti-oxidant effect and enhancement of Nrf2 pathway in an MCAO rat model of strokeView study →}

The spread — from single-digit-micromolar enzyme inhibition to ~110 µM for cancer-cell cytotoxicity — is itself worth noting: the concentrations that act in a dish vary widely by target, and none has been shown to be reachable in humans. These are research figures and are not a personal recommendation.

References

Li Q, et al. (2022). Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7–NLRP3 interaction. EMBO Reports. https://pubmed.ncbi.nlm.nih.gov/34882936/
Furusawa J, et al. (2009). Glycyrrhiza inflata-derived chalcones, licochalcone A, licochalcone B and licochalcone D, inhibit phosphorylation of NF-κB p65 in LPS signaling pathway. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/19291859/
Li H, et al. (2021). Discovery of natural 15-LOX small-molecule inhibitors from Chinese herbal medicine using virtual screening, biological evaluation and molecular dynamics studies. Bioorganic Chemistry. https://pubmed.ncbi.nlm.nih.gov/34426159/
Fu Y, et al. (2013). Antioxidant and anti-inflammatory activities of six flavonoids separated from licorice. Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/23790887/
Wang J, et al. (2019). Licochalcone B extracted from Glycyrrhiza uralensis Fisch induces apoptotic effects in human hepatoma cell HepG2. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/30835110/
Zhang X, et al. (2022). Licochalcone B induces DNA damage, cell-cycle arrest, apoptosis, and enhances TRAIL sensitivity in hepatocellular carcinoma cells. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/35948134/
Huang WC, Jin H (2022). Licochalcone B induced apoptosis and autophagy in osteosarcoma tumor cells via the inactivation of the PI3K/AKT/mTOR pathway. Biological & Pharmaceutical Bulletin. https://pubmed.ncbi.nlm.nih.gov/35431285/
Song Y, et al. (2020). Janus kinase 2 inhibition by licochalcone B suppresses esophageal squamous-cell-carcinoma growth. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/32144852/
Yuan X, et al. (2014). Licochalcone B inhibits growth of bladder cancer cells by arresting cell-cycle progression and inducing apoptosis. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/24384411/
Teng H, et al. (2016). Hepatoprotective effects of licochalcone B on carbon-tetrachloride-induced liver toxicity in mice. Iranian Journal of Basic Medical Sciences. https://pubmed.ncbi.nlm.nih.gov/27746874/
Lin Y, et al. (2017). Nrf2 activators from Glycyrrhiza inflata and their hepatoprotective activities against CCl₄-induced liver injury in mice. Bioorganic & Medicinal Chemistry. https://pubmed.ncbi.nlm.nih.gov/28835349/
Gao XP, et al. (2017). Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of ERK signaling. Iranian Journal of Basic Medical Sciences. https://pubmed.ncbi.nlm.nih.gov/28293388/
Zhou Y, et al. (2021). Licochalcone B attenuates neuronal injury through anti-oxidant effect and enhancement of Nrf2 pathway in an MCAO rat model of stroke. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/34454290/
Cao G, et al. (2020). Licochalcone B, a chalcone derivative from Glycyrrhiza inflata, as a multifunctional agent for the treatment of Alzheimer’s disease. Natural Product Research. https://pubmed.ncbi.nlm.nih.gov/30345819/
Huang X, et al. (2023). Licochalcone B confers protective effects against LPS-induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway. Redox Report. https://pubmed.ncbi.nlm.nih.gov/37565601/
Dong Y, et al. (2024). A synergistic mechanism of liquiritin and licochalcone B from Glycyrrhiza uralensis against COPD. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/38870751/
Lin S, et al. (2024). Chalcones from plants cause toxicity by inhibiting human and rat 11β-hydroxysteroid dehydrogenase 2. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/38141941/
Shaikh S, Lee EJ, Ahmad K, et al. (2024). Therapeutic potential and action mechanisms of licochalcone B: a mini review. Frontiers in Molecular Biosciences. https://pubmed.ncbi.nlm.nih.gov/39021879/