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| Licochalcone A - Licorice-Derived Chalcone Type: Natural chalcone / flavonoid-related phytochemical Sources: Found primarily in licorice species including Glycyrrhiza inflata and related Glycyrrhiza plants. Function: Licochalcone A is a bioactive chalcone with anticancer, anti-inflammatory, antioxidant, antimicrobial, and metabolic effects. Reported mechanisms include modulation of PI3K/AKT, MAPK, NF-κB, STAT3, ROS, apoptosis, autophagy, and cell-cycle regulatory pathways. Cancer: Preclinical studies demonstrate inhibition of cancer-cell proliferation, migration, invasion, and metastasis, together with induction of apoptosis, autophagy, oxidative stress, and cell-cycle arrest. LCA has shown anticancer activity in breast, lung, gastric, colorectal, prostate, liver, ovarian, and other experimental cancer models. Alzheimer's Disease: Preclinical evidence suggests neuroprotective and anti-inflammatory effects relevant to neurodegeneration, including suppression of oxidative stress and inflammatory signaling, although the Alzheimer's-specific evidence is less developed than the cancer literature. Licochalcone A — a naturally occurring prenylated chalcone and phenolic phytochemical found principally in licorice species, especially Glycyrrhiza inflata. It is classified as a natural chalcone/flavonoid-related small molecule and is commonly abbreviated LCA, LicA, or Lico A. Its experimental pharmacology is strongly context-dependent: in many cancer models LCA promotes oxidative stress, mitochondrial dysfunction, apoptosis, autophagy, cell-cycle arrest, and suppression of proliferative and inflammatory signaling, whereas in non-malignant injury models it can activate NRF2-dependent antioxidant defenses. Anticancer development remains preclinical. Primary mechanisms (ranked):
Bioavailability / PK relevance: Free oral LCA has poor systemic exposure; a rat pharmacokinetic study reported absolute oral bioavailability of approximately 3.3%. Poor aqueous solubility, limited permeability, intestinal first-pass metabolism, glucuronidation, and other metabolic pathways constrain exposure. Formulation materially changes PK: a self-microemulsifying drug-delivery system increased oral bioavailability approximately 2.36-fold in rats, while nanoparticle approaches have produced still larger increases experimentally. LCA also inhibits P-glycoprotein and several CYP enzymes, particularly CYP3A and CYP2C9 in experimental systems, creating a potential drug-interaction concern. In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 μM LCA, with several reported IC50 values in the tens of micromolar range. These concentrations are difficult to reconcile with the low systemic exposure of unformulated oral LCA, so direct translation of conventional cell-culture concentrations to achievable human systemic exposure is uncertain. Delivery systems, local exposure, metabolites, and combination strategies may alter this limitation. Clinical evidence status: Cancer: preclinical only, with cell-culture and animal xenograft evidence but no established anticancer efficacy in humans. Human exposure evidence is substantially stronger for topical dermatologic/cosmetic use: randomized or prospective studies have evaluated LCA-containing formulations for acne, dermatitis, erythema, and rosacea. LCA is not an established systemic oncology drug. Current translational priorities are exposure optimization, human PK, dose-limiting safety characterization, and controlled oncology trials. Licochalcone A Cancer Mechanisms
P: 0–30 min R: 30 min–3 hr G: >3 hr Alzheimer's disease relevance: Licochalcone A now has meaningful disease-specific preclinical evidence rather than only general neuroprotective plausibility. Studies in transgenic AD mouse models report improved cognition together with reduced Aβ burden, reduced neuroinflammation, improved insulin/glucose signaling, inhibition of ER-stress-mediated neuronal apoptosis, and NRF2-associated protection. A 2026 APP/PS1 study reported improved memory, increased synaptic markers, reduced Aβ42 and plaque burden, improved glucose handling, and reduced glial activation after 15 mg/kg/day intraperitoneal LCA for four weeks. A separate transgenic mouse study found inhibition of PERK/eIF2α/ATF4/CHOP ER-stress signaling and neuronal apoptosis. Evidence remains preclinical; there is no established human AD efficacy. Primary AD mechanisms (ranked):
Clinical evidence status: Preclinical. Evidence includes cell studies and multiple transgenic mouse AD models, including disease-specific studies published in 2025 and 2026. Human efficacy, optimal systemic dose, CNS pharmacokinetics, and long-term safety have not been established. Licochalcone A Alzheimer Mechanisms
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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 8235- | LCA, | Anticancer effects of licochalcones: A review of the mechanisms |
| - | Review, | Var, | NA |
| 8237- | LCA, | Role of Licochalcone A in Potential Pharmacological Therapy: A Review |
| - | Review, | Var, | NA |
| 8261- | LCA, | Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels |
| - | in-vitro, | CRC, | T24/HTB-9 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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