Flavanones are a subclass of flavonoids, which are naturally occurring polyphenolic compounds characterized by a 15-carbon skeleton consisting of two phenyl rings (A and B) connected by a heterocyclic pyran ring (C).[1] Unlike other flavonoids such as flavones, flavanones feature a saturated C-ring with no double bond between C2 and C3, and they possess a ketone group at the C4 position, giving them the core structure of 2-phenylchroman-4-one or flavan-4-one.[2] Common examples include naringenin, hesperetin, and eriodictyol, often occurring as glycosides like naringin and hesperidin in plants.[3]Flavanones are primarily found in citrus fruits such as oranges, lemons, grapefruits, and mandarins, where they contribute to the characteristic bitterness and serve as defense compounds against environmental stresses.[1] They are also present in other plants like tomatoes, herbs, and propolis, with concentrations varying widely; for instance, orange juice can contain 81–200 mg/L of soluble flavanones.[1] Biosynthetically, flavanones are produced via the phenylpropanoid pathway, where chalcone isomerase converts naringenin-chalcone into the flavanone scaffold.[3]These compounds exhibit diverse biological activities, including potent antioxidant effects through reactive oxygen species scavenging and metal chelation, as well as anti-inflammatory properties by inhibiting enzymes like 5-lipoxygenase.[1] Flavanones demonstrate antibacterial activity against pathogens such as methicillin-resistant Staphylococcus aureus and anticancer potential, with hesperidin showing inhibition of colon and mammary tumor growth in preclinical models.[1] Their low water solubility limits bioavailability, but glycosylation enhances stability and solubility for potential applications in food, cosmetics, and pharmaceuticals.[1]
Chemical Structure and Properties
Core Structure
Flavanones constitute a subclass of flavonoids defined by the core backbone of 2,3-dihydro-2-phenylchromen-4-one, also known as 2-phenylchroman-4-one.[4] This structure features a 15-carbon C6-C3-C6 skeleton, comprising two aromatic phenyl rings (designated A and B) linked by a central three-carbon chain that cyclizes to form a heterocyclic C ring.[5] In flavanones, the central C3 unit manifests as a non-aromatic dihydropyrone ring fused to the A ring (a benzopyran moiety), with the B ring attached at position 2 and a carbonyl group at position 4; saturation occurs specifically at the 2,3 bond, distinguishing this ring from the aromatic pyrone in related flavonoids.[6]The saturation at positions 2 and 3 introduces a chiral center at carbon 2, resulting in two enantiomers: (2R)- and (2S)-flavanones.[7] Naturally occurring flavanones predominantly exhibit the (2S) configuration at C2, a stereochemical feature arising from their biosynthetic origins. Many flavanones exist in glycosylated forms, commonly as 7-O-glycosides where a sugar moiety, such as rutinose or glucose, attaches to the hydroxyl group at position 7 on the A ring.[8]Structurally, flavanones differ from flavones by the absence of a double bond between C2 and C3, which renders the C ring saturated and non-planar rather than the unsaturated, aromatic form in flavones.[9] In comparison to isoflavones, flavanones maintain the B ring attachment at C2 of the C ring, whereas isoflavones feature this attachment at C3, altering the overall symmetry and substitution pattern.[9]
Physical Properties
Flavanones are typically white to pale yellow crystalline solids at room temperature.[10]These compounds exhibit poor solubility in water, with naringenin displaying a solubility of approximately 0.032 mg/mL, though values can vary slightly based on experimental conditions. In contrast, flavanones show high solubility in organic solvents such as ethanol (up to 50 mg/mL for naringenin) and DMSO.[10] Solubility is influenced by factors including pH, where it increases under alkaline conditions due to deprotonation of phenolic groups, and glycosylation, which improves aqueous solubility compared to aglycone forms.[11][12]Melting points of common flavanones generally fall within 200-250°C; for instance, hesperetin has a melting point of 227.5°C, while naringenin melts at 251°C. Boiling points are notably high, often exceeding 500°C under predicted conditions, reflecting their thermal stability in the solidstate.[13]Flavanones demonstrate sensitivity to light, heat, and oxidation, which can induce degradation or lead to polymerization through oxidative coupling.[14][15] Glycosylated flavanones, such as naringin, exhibit greater resistance to these stressors than their aglycone counterparts.[16]
Chemical Reactivity
Flavanones feature a core 2-phenylchroman-4-one structure, characterized by a ketonecarbonyl group at the C4 position, which serves as a primary electrophilic site due to its conjugation with the A- and B-rings, facilitating nucleophilic additions and enolization. The alpha-methylene group at C3 provides enolizable hydrogens, enabling base-catalyzed enol formation and subsequent reactions such as aldol condensations or dehydrogenations. Phenolic hydroxyl groups, commonly substituted at C5, C7 on the A-ring, and C4' on the B-ring (as in naringenin), act as nucleophilic sites prone to proton donation, hydrogen bonding, and electrophilic aromatic substitution, influencing overall reactivity in acidic or oxidative environments.[17][18][19]A key transformation involves isomerization to flavones through dehydrogenation at the C2-C3 bond, often mediated by oxidants such as iodine or manganese(III) acetate, which abstract the alpha-hydrogens at C3 and eliminate to form the α,β-unsaturated system. Glycosylation reactions preferentially target the C7 phenolic hydroxyl, where the deprotonated phenoxide acts as a nucleophile toward activated sugars, enhancing polarity and stability, as demonstrated in synthetic protocols yielding 7-O-glycosylflavanones. Oxidation of ortho-dihydroxylated B-rings can proceed to semiquinone radicals and then to quinones via two-electron transfer, particularly under enzymatic or chemical peroxidative conditions, altering the aromatic character and enabling further Michael additions.[20][21][22][23]The acid-base properties of flavanones are dominated by their phenolic hydroxyls, with pKa values typically ranging from 7 to 10; for instance, naringenin exhibits pKa values of 7.05 (C7-OH) and 8.84 (C5-OH), allowing deprotonation in mildly basic or biological media to form phenoxides that enhance solubility and reactivity toward electrophiles. In UV-Vis spectroscopy, flavanones display characteristic absorptions at 280-320 nm, primarily from the B-ring π-π* transitions (Band II ~270-290 nm) with a weaker shoulder for Band I (~320 nm) due to limited conjugation across the saturated C-ring. NMR spectroscopy reveals diagnostic proton shifts, such as the methine H-2 at δ 5.3-5.5 ppm (doublet of doublets, J ≈ 3, 13 Hz), the diastereotopic H-3 protons at δ 2.7-3.1 ppm (two multiplets), and aromatic H-6/H-8 at δ 5.9-6.2 ppm (singlet or doublet), confirming the flavanone scaffold and substitution patterns.[24][25][26][27][28][29]
Natural Occurrence and Sources
Plant Sources
Flavanones, a subclass of flavonoids, are primarily distributed among the Rutaceae, Fabaceae, and Asteraceae plant families, where they occur as natural secondary metabolites.[30] In the Rutaceae family, particularly citrus species, flavanones such as hesperidin and naringin are abundant; for instance, Citrus sinensis (sweet orange) is a major source of hesperidin, primarily extracted from its peel.[31] Similarly, Citrus paradisi (grapefruit) contains high levels of naringin in its fruits and peel.[32] Within the Fabaceae family, flavanones have been identified in species like Amorpha fruticosa, isolated from root extracts.[33] In the Asteraceae family, flavanone glycosides are present in plants such as Bidens gardneri.[34]Flavanones accumulate in various plant tissues, including fruits, flowers, and leaves, often in glycosylated forms that enhance their stability and solubility within cellular compartments like vacuoles.[35] This localization supports their ecological roles, such as protecting plant tissues from ultraviolet (UV) radiation by absorbing harmful wavelengths and scavenging reactive oxygen species generated by UV exposure.[36] Additionally, flavanones contribute to defense against pathogens, acting as antimicrobial agents and phytoanticipins that inhibit microbial growth and limit infection establishment.[37]From an evolutionary perspective, flavanones represent critical intermediates in the flavonoid biosynthetic pathway, formed via chalcone isomerization and serving as precursors for downstream flavonoids like flavones and flavonols.[38] Genetic evidence from sequenced plant genomes, including those of early land plants and bryophytes, indicates that flavanone synthase genes emerged during the colonization of terrestrial environments around 550–470 million years ago, facilitating adaptations to UV stress and symbiosis.[39]
Dietary and Food Sources
Flavanones are predominantly found in citrus fruits, which serve as the major dietary contributors to human intake. Oranges, for instance, contain hesperidin at levels ranging from 20 to 70 mg per 100 g of fresh edible fruit, with variations depending on the variety such as navel or blood oranges.[40] Grapefruit is a rich source of naringin, approximately 20-30 mg per 100 g in the edible pulp, though concentrations can fluctuate with ripeness—peaking during early maturity—and cultivar, such as Ruby Red varieties exhibiting higher levels than white types.[41] Other citrus like lemons and limes contribute eriocitrin and smaller amounts of hesperidin, typically 15-30 mg per 100 g combined flavanones in fresh edible portions.[42] Herbs such as peppermint provide eriodictyol, a flavanone aglycone, at 12-54 mg per 100 g fresh weight, making them secondary but notable sources in herbal teas and seasonings.[43]Food processing significantly influences flavanone availability. Juicing processes, particularly mechanical extraction, can result in losses of up to 30% of total flavanones due to incomplete transfer from the albedo and pulp to the liquid, with greater retention observed in low-speed pressing methods compared to industrial centrifugation. Heat treatments like pasteurization cause minor degradation, often less than 10-20% for glycosylated forms like hesperidin, as these compounds exhibit relative thermal stability up to 100°C, though prolonged exposure beyond 30 minutes may isomerize them into less bioactive chalcones. Conversely, fermentation enhances flavanone content; for example, lactic acid fermentation of orange juice increases extractable hesperidin and naringin by 20-50% through microbial breakdown of cell walls, improving bioavailability without significant loss of the core structure.[44][45][46]Estimated daily flavanone intake varies by dietary patterns and region. In typical Western diets, consumption averages 20-50 mg per day, largely from sporadic intake of citrus juices and fruits, contributing about 6-12% of total flavonoid exposure based on national surveys like NHANES.[47] Mediterranean diets yield higher intakes, approximately 27 mg per day or more, attributed to regular consumption of fresh citrus and herbal infusions, which elevates overall polyphenol levels compared to Western patterns.[48] These estimates underscore the nutritional relevance of flavanones, with intake influenced by seasonal availability and processing habits.
Biosynthesis in Plants
Enzymatic Pathways
The biosynthesis of flavanones in plant cells proceeds via the flavonoid branch of the phenylpropanoid pathway, where key enzymatic steps convert primary metabolites into the core flavanone structure. The pathway initiates with chalcone synthase (CHS), a type III polyketide synthase that catalyzes the stepwise condensation of one molecule of p-coumaroyl-CoA (derived from phenylalanine) with three molecules of malonyl-CoA to yield naringenin chalcone, the open-chain precursor to flavanones. This reaction represents the first committed step in flavonoid production and occurs without additional cofactors beyond the substrates.[49][50]Following chalcone formation, chalcone isomerase (CHI) performs a stereospecific intramolecular cyclization, converting the chalcone into (2S)-naringenin, the foundational flavanone skeleton with its characteristic 2-phenylchroman structure. This enzyme ensures the correct (S)-configuration at the C-2 position, which is essential for subsequent flavonoid diversification, and operates efficiently on the bicyclic chalcone substrate without requiring external cofactors.[49][51]The sequential enzymatic pathway can be outlined as follows:
p-Coumaroyl-CoA + 3 Malonyl-CoA → Naringenin Chalcone (catalyzed by CHS).
Naringenin Chalcone → (2S)-Naringenin (catalyzed by CHI).
In certain plant species, particularly early-studied cases like parsley, an enzyme initially termed flavanone synthase (FNS) was identified for direct flavanone formation; however, purification revealed it to function analogously to CHS by producing chalcone, which then requires CHI for cyclization. Modern understanding emphasizes CHS and CHI as the core sequential enzymes, with FNS variants more commonly associated with downstream flavone production from flavanones.[52][49]These reactions exhibit dependency on NADPH in associated upstream steps of the phenylpropanoid pathway (e.g., for cinnamate 4-hydroxylase) and are localized to the cytoplasmic face of the endoplasmic reticulum, where the enzymes may form multi-enzyme complexes to channel intermediates efficiently and minimize diffusion losses.[50][49]
Regulation and Variations
The production of flavanones in plants is primarily regulated at the transcriptional level by the MYB-bHLH-WDR (MBW) complex, where R2R3-MYB and MYC-like bHLH transcription factors bind to promoter regions of early biosynthetic genes such as chalcone synthase (CHS) and chalcone isomerase (CHI), activating their expression to initiate flavanone formation from chalcone precursors.[53] These factors form heterotrimeric complexes that provide spatial and temporal specificity, ensuring flavanone synthesis occurs in response to developmental cues or stress signals in tissues like roots and leaves.[53] For instance, in model systems, MYB factors like AtMYB12 directly target CHS and CHI promoters, enhancing the flux through the phenylpropanoid pathway toward flavanones.[54]Environmental factors significantly modulate flavanone production through signaling cascades that converge on the MBW complex. UV light, particularly UV-B radiation, triggers photoreceptor-mediated activation of MYB transcription factors such as MYB12 and MYB75, upregulating CHS and CHI expression to boost flavanone accumulation as a protective response against oxidative damage.[55] Wounding induces jasmonic acid and ethylene signaling, which in turn activate bHLH factors to enhance early flavonoid genes, leading to localized flavanone increases for defense against pathogens.[56] Nutrient stresses, including nitrogen or phosphorus limitation, stimulate abscisic acid (ABA)-dependent pathways that recruit MYB and bHLH regulators, resulting in elevated flavanone levels to improve stress tolerance via antioxidant mechanisms.[55]Variations in flavanone accumulation across plant species arise from evolutionary differences in gene duplication and pathway specialization. In Citrus species, the presence of multiple chalcone-flavanone isomerase (CHI) genes, with up to 30 identified across species, contributes to higher overall flavonoid flux and substantial flavanone glycoside buildup like naringin in fruits due to enhanced cyclization efficiency.[57] In contrast, some monocots, such as certain grasses, exhibit reduced or absent flavanone-derived branches owing to specialized variants or regulation of CHS and CHI that favor other flavonoid classes.[58]Genetic engineering has demonstrated the potential to enhance flavanone yields by targeting these regulators in model plants. Overexpression of the R2R3-MYB transcription factor AtMYB111 in Arabidopsis activates CHS and CHI, increasing early flavonoid intermediates including flavanones, as evidenced by elevated pathway flux in transgenic lines.[59] Similarly, ectopic expression of LjaMYB12 from Lonicera japonica in Arabidopsis boosts CHS/CHI transcription, resulting in higher flavanone accumulation alongside downstream products, highlighting the conserved role of MYB factors in yield enhancement.[54] These studies underscore the efficacy of MBW-targeted engineering for optimizing flavanone production without disrupting plant growth.[59]
Metabolism and Bioavailability
Human Absorption and Distribution
Flavanones, such as naringenin and hesperetin, are primarily absorbed in the human gastrointestinal tract, with the small intestine serving as the main site of uptake through passive diffusion mechanisms. Absorption is generally less efficient for rutinoside glycosylated forms like hesperidin and naringin compared to their aglycone counterparts (naringenin and hesperetin), as they require prior hydrolysis in the gastrointestinal tract to facilitate uptake of the aglycone via passive diffusion, despite improved solubility of glycosides. The bioavailability of flavanone aglycones remains low, with human studies reporting cumulative urinary recovery of only 3-8% of the ingested dose, reflecting extensive first-pass metabolism and limited systemic exposure.[60] For example, after oral administration of 130-135 mg doses, plasma detection of conjugated metabolites occurs rapidly, within 20 minutes, indicating swift initial absorption despite overall poor efficiency.[60]In the bloodstream, absorbed flavanones undergo rapid phase II conjugation in the liver and intestines, circulating predominantly as glucuronide and sulfate metabolites bound to plasma proteins. These compounds exhibit strong affinity for human serum albumin (HSA), the primary transport protein in plasma, with binding constants in the range of 10^4 to 10^5 M^{-1} for citrus flavanones like naringenin and hesperetin, which helps stabilize them during circulation but may limit free fractions available for tissue entry. Peak plasma concentrations (C_{max}) are typically achieved 1-4 hours post-ingestion, varying by compound and source; for instance, hesperetin reaches approximately 0.8-2 μM and naringenin 1-5 μM following citrus juice consumption, with levels reflecting short-term dietary intake due to quick clearance.[60]Tissue distribution of flavanones in humans may involve passive diffusion and other transporters, though humandata are limited. Flavanones can inhibit OATP transporters like OATP1B1 and OATP1B3, potentially affecting co-transported compounds. Conjugated metabolites accumulate notably in the liver and kidneys, organs central to metabolism and elimination, with evidence of distribution to the brain via crossing the blood-brain barrier, potentially supporting neuroprotective effects. Humandata on precise tissue concentrations are limited, but animal models corroborate preferential localization in liver, kidney, and neural tissues.Excretion of flavanones occurs mainly through the kidneys, with over 90% of absorbed metabolites recovered in urine as conjugated forms and minor phenolic degradation products within 24 hours of ingestion. Biliary and fecal routes contribute minimally for parent compounds but may handle unabsorbed glycosides. The plasma elimination half-life is short, ranging from 1.3 to 3.1 hours for key flavanones like naringenin and hesperetin, underscoring their transient presence in circulation and the need for repeated dietary exposure to maintain levels.[60]
Biotransformation Processes
Flavanones, upon absorption in humans, primarily undergo biotransformation through phase I and phase II metabolic reactions in the intestine and liver, enhancing their solubility and facilitating excretion. Phase I metabolism involves cytochrome P450 (CYP450) enzymes that introduce hydroxyl groups via oxidation, often targeting the aromatic rings. For instance, naringenin, a representative flavanone, is hydroxylated at the 3'-position of the B-ring by human CYP1 family enzymes, such as CYP1B1, to form eriodictyol; this process occurs more efficiently with CYP1 enzymes compared to CYP2A enzymes.[61] These oxidations prepare flavanones for subsequent conjugations but represent a minor pathway relative to direct phase II modifications in human liver microsomes.[62]Phase II metabolism dominates flavanone biotransformation, involving conjugation to increase polarity. Glucuronidation, catalyzed by UDP-glucuronosyltransferases (UGTs), occurs predominantly at phenolic hydroxyl sites, such as the 7-position in naringenin, forming conjugates like naringenin-7-O-glucuronide; this reaction is mediated by intestinal and hepatic UGT isoforms like UGT1A1 and UGT1A9.[63]Sulfation, performed by sulfotransferases (SULTs) such as SULT1A1 and SULT1A3, targets similar phenolic groups, often in competition with glucuronidation.[64]Methylation, facilitated by catechol O-methyltransferase (COMT), modifies ortho-dihydroxy (catechol) structures on the B-ring, as seen in hesperetin derivatives, further altering bioavailability.[64] These conjugations occur rapidly during first-pass metabolism, with multiple isoforms contributing to regioselective products.The gut microbiota plays a crucial role in biotransforming unabsorbed or recirculated flavanones in the colon, initiating deglycosylation of glycosylated forms like naringin via bacterial β-glucosidases from genera such as Bifidobacterium and Lactobacillus.[65] Further microbial actions include C-ring fission yielding phenolic acids such as 3-(4-hydroxyphenyl)propionic acid and 3-(3-hydroxyphenyl)propionic acid from naringenin and hesperetin, respectively.[66] These transformations contribute to the diverse metabolite pool entering enterohepatic circulation.In terms of metabolite profiles, conjugated forms predominate in human plasma and urine following flavanone intake; for example, naringenin-7-glucuronide and naringenin-4'-glucuronide are major urinary metabolites, accounting for approximately 4-5% of ingested doses in excretion studies, alongside sulfates and mixed conjugates.[67] These profiles vary interindividually due to enzyme polymorphisms but consistently reflect extensive phase II processing over phase I products.[68]
Chemical Synthesis
Classical Synthetic Routes
Classical synthetic routes for flavanones emerged in the early 20th century as organic chemists sought to confirm the structures of naturally occurring flavonoids and synthesize analogs for pharmacological evaluation. These methods relied on fundamental reactions like aldol condensations and intramolecular cyclizations, often starting from readily available phenolic precursors. They were instrumental in establishing the chromanone scaffold of flavanones, despite inefficiencies that spurred later innovations. Seminal work highlighted the reactivity of o-hydroxyaryl ketones, enabling the assembly of the 2-phenyl-2,3-dihydro-4H-chromen-4-one core through stepwise carbon-carbon bond formation and ring closure.[69]The Claisen-Schmidt condensation represents a key historical approach, involving the base-catalyzed condensation of o-hydroxyacetophenone with benzaldehyde to generate a 2'-hydroxychalcone intermediate, followed by acid- or base-promoted cyclization to form the flavanone. This sequence proceeds via aldol condensation under alkaline conditions (e.g., NaOH in ethanol), yielding the chalcone in moderate efficiency, and subsequent protonation or Michael addition for ring closure. Representative examples include the synthesis of naringenin from 2,4,6-trihydroxyacetophenone and 4-hydroxybenzaldehyde, providing access to citrus-derived flavanones for structural elucidation. While adaptable for substituted variants, the method's two-step nature often results in cumulative losses from chalcone isolation.[69]Overall, these classical routes achieve flavanones in typical overall yields of 40-60%, constrained by the condensation step's equilibrium and cyclization side products like polymeric byproducts or flavone over-oxidation. Regioselectivity poses a major limitation, especially with polysubstituted phenols, where ortho-directing effects can favor unwanted isomers or incomplete ring closure, necessitating careful control of reaction conditions. Despite these drawbacks, the methods' simplicity and reliance on inexpensive reagents made them foundational for early 20th-century research, enabling the preparation of key compounds like eriodictyol and hesperetin for natural product confirmation.[69][70]
Modern Synthetic Methods
Modern synthetic methods for flavanones have advanced significantly since the early 2000s, emphasizing efficiency, stereocontrol, and environmental sustainability to overcome limitations of classical routes such as low yields and lack of enantioselectivity. These approaches leverage chiral catalysis, integrated reaction sequences, and biological tools to produce flavanones with high purity and scalability, often achieving yields exceeding 80% and enantiomeric excesses (ee) over 90%.[71]Asymmetric synthesis has become a cornerstone for generating enantiopure flavanones, crucial for biological studies due to their stereospecific activities. Chiral metal complexes, particularly ruthenium (Ru) and palladium (Pd) catalysts, enable enantioselective cyclization through mechanisms like intramolecular oxa-Michael additions or conjugate additions to chalcone precursors. For instance, Pd(II)-CarOx complexes catalyze the asymmetric 1,4-addition of arylboronic acids to chromones, yielding (R)-flavanones such as pinostrobin with >90% yield and up to 99% ee. Similarly, Ru(II)-Noyori-Ikariya complexes facilitate asymmetric transfer hydrogenation-dynamic kinetic resolution (ATH-DKR) of isoflavanones, delivering products with >99% ee in >80% yield. These methods provide access to specific enantiomers, contrasting with racemic mixtures from traditional acid-catalyzed isomerizations.[71][72][73]One-pot methodologies streamline flavanone production by combining chalcone formation and cyclization in a single vessel, reducing purification steps and waste. Microwave-assisted protocols exemplify this efficiency, accelerating Claisen-Schmidt condensation followed by isomerization under basic conditions. In a representative approach, 2-hydroxyacetophenones react with aromatic aldehydes in methanolic KOH under 100 W microwave irradiation for 2 minutes, directly affording functionalized flavanones in 81-94% yields, with electron-donating substituents enhancing selectivity toward cyclized products over chalcones. Polyphosphoric acid (PPA)-promoted variants in DMF/MeOH reflux further demonstrate versatility, converting the same substrates to flavanones in up to 84% yield within 7 hours, suitable for gram-scale synthesis. These tandem processes achieve >80% overall yields, surpassing multi-step classical routes. Recent advances as of 2025 include transition metal-free one-pot syntheses using Cs2CO3-I2 promotion, enabling efficient production of flavanones and flavones from 2-hydroxyacetophenones and aldehydes in high yields without additives.[74][75][76]Biocatalytic approaches harness engineered enzymes for stereospecific flavanone synthesis, offering mild conditions and high selectivity. Chalcone isomerase (CHI) enzymes, particularly from Arabidopsis thaliana, catalyze the stereospecific cyclization of chalcones to (2S)-flavanones in microbial hosts like Escherichia coli. Engineered E. coli strains expressing CHI alongside chalcone synthase produce pinocembrin at 353 mg/L, with inherent (2S)-stereochemistry, while variants yield pinostrobin (153 mg/L) and other derivatives. In vitro applications of these engineered CHIs enable scalable, enantiopure production without harsh reagents, aligning with post-2000 biotechnology advances.[77][78]Sustainability in modern flavanone synthesis prioritizes green solvents, recyclable catalysts, and reduced energy use, addressing environmental concerns of traditional methods. Copper oxide/reduced graphene oxide (CuO/rGO) nanocomposites serve as heterogeneous catalysts for chalcone-to-flavanone isomerization in water, delivering 87-96% yields and recyclability over seven cycles without activity loss. Amino acid catalysts, such as L-proline, promote cyclization in ethanol or water with >85% yields, minimizing toxic solvents. Microwave integration further lowers energy consumption, while biocatalytic systems operate at ambient temperatures, collectively enabling eco-friendly, high-impact production. Additional 2025 developments include N-heterocyclic carbene (NHC) catalysis for aza-flavanones with quaternary stereocenters, expanding sustainable synthetic scope.[79][80][81][82]
Biological Activities and Health Effects
Pharmacological Properties
Flavanones exhibit potent antioxidant activity primarily through direct scavenging of reactive oxygen species (ROS) via their phenolic hydroxyl groups, which donate hydrogen atoms or electrons to neutralize free radicals such as superoxide and peroxyl radicals.[83] This mechanism is facilitated by the ortho-dihydroxy (catechol) configuration in the B-ring, enhancing electron delocalization and stability of the resulting phenoxyl radical.[84] Additionally, flavanones inhibit ROS-generating enzymes, including xanthine oxidase, by binding to its active site and preventing substrate oxidation; for instance, naringenin demonstrates mixed-type inhibition with an IC50 of approximately 20 μM.[85]The anti-inflammatory properties of flavanones arise from their ability to modulate key signaling pathways, notably the nuclear factor-kappa B (NF-κB) pathway, where they suppress IκB kinase activation and subsequent p65 subunit translocation to the nucleus.[86] This inhibition reduces the transcription of pro-inflammatory genes, leading to decreased production of cytokines such as tumor necrosis factor-alpha (TNF-α); naringenin, for example, attenuates TNF-α expression in lipopolysaccharide-stimulated macrophages by downregulating NF-κB activity.[87] Similarly, licoflavanone from licorice inhibits NF-κB nuclear translocation, thereby lowering TNF-α, interleukin-1β (IL-1β), and IL-6 levels in activated cells.[88]Flavanones also act as enzyme inhibitors, targeting pathways involved in inflammation and hormone regulation. Naringenin potently inhibits aromatase (CYP19), the enzyme catalyzing estrogenbiosynthesis, with an IC50 of 9.2 μM in microsomal assays, potentially through competitive binding at the heme site.[89] Other examples include inhibition of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), where licoflavanone reduces their expression in inflammatory models.[88]Structure-activity relationships reveal that B-ring hydroxylation significantly influences flavanone potency. Increasing the number of hydroxyl groups on the B-ring, particularly at positions 3' and 4', enhances radical scavenging and anti-inflammatory efficacy by improving hydrogen donation capacity and NF-κB binding affinity; for instance, eriodictyol (with 3',4'-dihydroxylation) shows greater antioxidant activity than naringenin (4'-hydroxylation only).[90] Conversely, lack of B-ring hydroxylation, as in pinocembrin, markedly reduces potency in both antioxidant and inhibitory assays.[91] These metabolic transformations, such as phase II conjugation, can further modulate active forms generated during biotransformation.[83]
Potential Therapeutic Applications
Flavanones, particularly those derived from citrus fruits such as naringenin and hesperetin, have demonstrated potential in mitigating cardiovascular risks through antioxidant mechanisms that reduce low-density lipoprotein (LDL) oxidation. In vitro studies have shown that naringenin enriches LDL particles, thereby increasing their resistance to oxidative damage induced by copper ions or macrophages, which could attenuate the progression of atherosclerosis.[92] Meta-analyses of randomized controlled trials indicate that hesperidin supplementation lowers systolic blood pressure by 1.4 mmHg (95% CI: -2.7 to -0.02) with no significant effect on diastolic pressure in adults, at doses of 292-1000 mg/day over 3-12 weeks.[93]Cohort and intervention studies associate citrus flavanone intake with reductions in blood pressure.[94] As of 2025, recent cohort studies associate higher flavanone-rich citrus intake with 11-14% lower risks of frailty and poor mental health, and reduced dementia incidence.[95]In the realm of oncology, flavanones exhibit anticancer potential primarily through induction of apoptosis and inhibition of proliferation in various cancer cell lines. Hesperetin has been shown to trigger apoptosis in breast cancer cells (e.g., MCF-7 and MDA-MB-231 lines) by modulating estrogen receptor alpha activity, downregulating anti-apoptotic proteins like Bcl-2, and activating caspase pathways, with IC50 values around 50-100 μM in preclinical models.[96] Similarly, naringenin promotes autophagic cell death and suppresses migration in colorectal and prostate cancer cells via PI3K/Akt pathway inhibition, highlighting its role in preventing metastasis. While human clinical data remain limited, these mechanisms support the translational potential of flavanones as adjuncts in cancer prevention, with ongoing preclinical evaluations suggesting synergy with chemotherapeutic agents like doxorubicin to enhance efficacy and reduce resistance.[97]For metabolic disorders, flavanones improve insulin sensitivity and glycemic control, offering promise in diabetes management. Naringenin enhances insulin signaling in adipocytes and hepatocytes by activating PPARγ and AMPK pathways, reducing insulin resistance in streptozotocin-induced diabetic rodent models at doses of 50-100 mg/kg, with corresponding improvements in fasting blood glucose by 20-30%.[98] A 2023 study demonstrated that naringenin ameliorates diabetic cardiomyopathy by activating Nrf2 to counteract oxidative stress and inflammation, preserving cardiac function in high-fat diet-fed rats.[99] These effects extend to human-relevant models, where citrus flavanone-rich interventions have improved insulin sensitivity markers like HOMA-IR in overweight individuals with prediabetes, underscoring their role in delaying type 2 diabetes onset.[100]Flavanones hold Generally Recognized as Safe (GRAS) status for use in foods, with an ADI of 75 mg/kg bw/day for hesperidin as affirmed by the FDA for citrus-derived sources.[101] Typical therapeutic doses range from 100-500 mg/day, achieved through supplements or citrus consumption, with clinical trials reporting no significant adverse effects at these levels over 8-12 weeks.[93] Rare side effects are primarily linked to high citrus intake, including potential drug interactions via CYP3A4 inhibition by naringin, which may elevate plasma levels of statins or calcium channel blockers, necessitating caution in polypharmacy patients.[102]
Notable Flavanones
Structural Examples
Flavanones are characterized by a core structure consisting of two phenyl rings (A and B) connected through a heterocyclic pyran ring (C) with a ketone at position 4 and saturation between positions 2 and 3. Representative examples illustrate key structural variations, particularly in hydroxylation patterns and glycosylation.The parent flavanone compound, naringenin (5,7,4'-trihydroxyflavanone), exemplifies the basic substitution pattern typical of many naturally occurring flavanones. It features hydroxyl groups at positions 5 and 7 on the A ring and at position 4' on the B ring, with the systematic name (2S)-5,7-dihydroxy-2-(4-hydroxyphenyl)-2,3-dihydro-4H-chromen-4-one, conferring chirality at C-2. This aglycone structure is widespread in citrus fruits and serves as a scaffold for further modifications.Glycosylated forms enhance solubility and bioavailability; a prominent example is hesperidin (hesperetin-7-rutinoside), abundant in oranges. Hesperidin is the 7-O-rutinoside of hesperetin, where hesperetin itself is 5,7-dihydroxy-4'-methoxy-3'-hydroxyflavanone, with the rutinoside (rhamnosyl-glucose) attached at the 7-position of the A ring. This modification distinguishes it from non-glycosylated flavanones like naringenin.Hydroxylation variants further diversify the class. Eriodictyol, with an additional hydroxyl at 3' on the B ring (3',4',5,7-tetrahydroxyflavanone), exhibits the systematic name (2S)-2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-2,3-dihydro-4H-chromen-4-one and is found in herbs like yerba santa.[103] In contrast, liquiritigenin (4',7-dihydroxyflavanone) lacks the 5-hydroxyl on the A ring, featuring hydroxyls only at 4' on the B ring and 7 on the A ring, with the name 7-hydroxy-2-(4-hydroxyphenyl)-2,3-dihydro-4H-chromen-4-one, and is isolated from licorice root.Flavanones are distinguished from their isomers, flavanonols, by the absence of a hydroxyl group at position 3 on the C ring; the addition of this 3-hydroxy group in flavanonols, such as taxifolin, introduces an extra chiral center and alters stereochemistry.
Specific Compounds and Derivatives
Naringin, a flavanone glycoside abundant in grapefruit, imparts a characteristic bitter taste to the fruit and its juices due to its sensory properties.[104] This bitterness arises primarily from naringin's interaction with taste receptors, making it a key factor in the palatability of citrus products.[105] In processing, naringin undergoes deglycosylation via the enzyme naringinase, which hydrolyzes its rhamnoglucoside moiety to yield the aglycone naringenin, thereby reducing bitterness while preserving nutritional value.[106] Industrial debittering of grapefruit juice commonly employs immobilized naringinase in bioreactors, achieving up to 90% removal of naringin and improving juice acceptability without significant loss of other flavonoids.[107]Hesperetin, the aglycone form of hesperidin found in citrus fruits, demonstrates neuroprotective effects in preclinical Alzheimer's disease models by attenuating amyloid-beta aggregation and tau hyperphosphorylation.[108] In transgenic mouse models, oral administration of hesperetin at doses of 50-100 mg/kg reduced cognitive deficits and neuroinflammation via modulation of Nrf2 and NF-κB pathways.[109] To address hesperetin's inherent poor aqueous solubility (approximately 48 μg/mL in water), semi-synthetic derivatives such as hesperetin-7-O-glucoside and its sulfonated or iodinated analogs have been developed, exhibiting up to five-fold higher solubility at acidic pH relevant to gastrointestinal conditions.[110][111] These modifications enhance dissolution rates and potential oral bioavailability without compromising the core neuroprotective scaffold.[111]Pinocembrin, a prominent flavanone in propolis from honeybees, contributes to the resin's antimicrobial properties through its presence in concentrations up to 4% (40 mg/g) in some European propolis varieties.[112] It exhibits potent antibacterial activity against Gram-positive pathogens, including Streptococcus mutans and Staphylococcus aureus, with minimum inhibitory concentrations of 8-16 μg/mL, by disrupting bacterial cell membranes and inhibiting biofilm formation.[113] Synthetic analogs of pinocembrin, such as fluorinated or alkylated derivatives, have been explored as drug leads for treating resistant infections, showing enhanced potency against multidrug-resistant strains while maintaining low cytotoxicity to mammalian cells.[114]Recent advancements in semi-synthetic flavanone derivatives focus on prenylated and halogenated forms to boost bioavailability, addressing the class's typical low absorption rates below 10%. Prenylation at the 8-position, as in semi-synthetic 8-prenylnaringenin produced via regioselective lithium chloride-mediated reactions, increases lipophilicity and cellular uptake, with pharmacokinetic studies in rats indicating a 2-3 fold improvement in plasma levels compared to parent flavanones.[115]Halogenation, particularly chlorination or fluorination on the B-ring using enzymatic halogenases, enhances metabolic stability and membrane permeability; for instance, fluorinated flavanone derivatives demonstrated prolonged half-lives in liver microsomes and up to 50% higher bioavailability in rodent models.[116] Post-2020 patents and studies highlight these modifications in formulations for targeted therapies, such as prenylated analogs for estrogenic applications and halogenated ones for antimicrobial uses, emphasizing their role in overcoming flavanone limitations.[117]