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Hyperoside

Hyperoside is a naturally occurring flavonol glycoside, chemically known as quercetin-3-O-β-D-galactopyranoside, with the molecular formula C₂₁H₂₀O₁₂ and a yellow solid appearance at room temperature.^[1] It serves as a key bioactive constituent in numerous medicinal plants, particularly those used in traditional Chinese and folk medicine, and is recognized for its role as a plant metabolite with potent antioxidant properties derived from its hydroxyl groups and glycosidic structure.^[2] Hyperoside is widely distributed across various plant families, including Hypericaceae, Rosaceae, Polygonaceae, and others such as Erythrinaceae, Labiatae, and Leguminosae.^[2] Notable sources include Hypericum perforatum (St. John's wort) and Hypericum monogynum from the Hypericaceae family, Crataegus pinnatifida (Chinese hawthorn) from Rosaceae, and Polygonum aviculare from Polygonaceae, with higher concentrations often found in plants from Southeast Asia, Europe, and North America.^[1]^[2] It can be extracted from these sources using methods like solvent extraction or isolated through biosynthesis involving quercetin and uridine 5’-diphosphate-galactose catalyzed by enzymes in engineered Escherichia coli, achieving yields up to 18,000 mg/L.^[1] These natural occurrences underscore its traditional use in herbal remedies for conditions involving oxidative stress and inflammation. The compound demonstrates a broad spectrum of pharmacological activities, primarily attributed to its ability to modulate pathways such as Nrf2/HO-1, PI3K/AKT, and NF-κB.^[1]^[2] Key effects include antioxidant action, where it scavenges reactive oxygen species and protects against oxidative damage in models of liver and neuronal injury; anti-inflammatory properties, inhibiting pro-inflammatory cytokines like TNF-α and IL-6; and cardioprotective benefits, improving ejection fraction and reducing infarct size in ischemic heart models via AMPK/mTOR activation (e.g., 20 mg/kg/day dosing).^[1]^[2] Additional notable activities encompass neuroprotection against Parkinson's and cerebral ischemia through SIRT1 and TRPV4 pathways, anti-cancer effects by inducing apoptosis in lung, cervical, and liver cancer cells, hepatoprotective and renal protective roles via PPARγ and miR-499-5p mechanisms, as well as antidiabetic, antithrombotic, and bone/joint protective functions.^[1]^[3] Hyperoside exhibits low acute toxicity (LD50 > 5,000 mg/kg), though high chronic doses may cause reversible nephrotoxicity due to renal accumulation.^[1] Ongoing research explores its pharmacokinetics, including poor oral bioavailability improved by nanoformulations, positioning it as a promising candidate for drug development.^[1]

Chemistry

Molecular structure

Hyperoside is a flavonol glycoside characterized by the molecular formula \ce{C21H20O12}.^[4] Its systematic IUPAC name is 2-(3,4-dihydroxyphenyl)-3-[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-5,7-dihydroxychromen-4-one, commonly referred to as quercetin 3-O-β-D-galactopyranoside.^[5]^[3] The molecular structure features a central flavonol backbone derived from the aglycone quercetin, which is 3,3',4',5,7-pentahydroxyflavone consisting of two phenyl rings (A and B) connected by a heterocyclic γ-pyrone ring (C). At the 3-position of the C-ring, quercetin is glycosylated via a β-glycosidic oxygen linkage to a β-D-galactopyranose sugar moiety, distinguishing hyperoside as a monoglycoside.^[3] This arrangement positions the galactose unit equatorially at the anomeric carbon, forming a stable O-glycosidic bond that imparts specific stereochemistry to the molecule. In textual representation, the core flavone scaffold can be depicted as:

Ring A (positions 5-8): Benzene ring with hydroxyl groups at 5 and 7.
Ring C (heterocyclic): Pyrone ring with a carbonyl at position 4 and the glycosidic attachment at 3.
Ring B (positions 1'-4'): Phenyl ring with hydroxyls at 3' and 4'.

The galactose attaches through its C1 to the C3 of quercetin, completing the structure.^[4] Compared to its aglycone quercetin, hyperoside includes the additional galactoside group, which modifies its polarity and bioavailability without altering the core polyphenolic framework.^[3] In relation to rutin (quercetin 3-O-α-L-rhamnopyranosyl-(1→6)-β-D-glucopyranoside), hyperoside features a simpler galactose substitution instead of the disaccharide rutinose, highlighting its role as a distinct galactosylated variant among quercetin glycosides.

Physical properties

Hyperoside appears as a yellow crystalline powder.^[6] Its molar mass is 464.379 g/mol.^[4] The compound has a calculated density of 1.8 g/cm³.^[7] It exhibits a melting point of approximately 225–235 °C, accompanied by decomposition.^[4] Hyperoside shows limited solubility in water, approximately 0.1 mg/mL, due to its polar glycosidic structure.^[8] It is soluble in polar organic solvents such as methanol, ethanol, and DMSO, but insoluble in non-polar solvents like chloroform.^[7] The specific optical rotation is −83° (c = 0.2, pyridine).^[3] In ultraviolet-visible spectroscopy, hyperoside displays absorption maxima around 260 nm and 350 nm, characteristic of its flavonol chromophore.^[9]

Chemical properties

Hyperoside is sensitive to hydrolysis under acidic conditions, in which the O-glycosidic bond linking the galactose moiety to the quercetin aglycone is cleaved, yielding quercetin and D-galactose as products. This reaction proceeds readily with strong acids such as HCl in hot ethanol, reflecting the general lability of flavonoid O-glycosides to acid-catalyzed hydrolysis.^[10]^[11] The galactose moiety contributes to this vulnerability through the hemiacetal nature of the glycosidic linkage, which facilitates protonation and subsequent bond rupture. In contrast, hyperoside demonstrates stability in neutral to mildly alkaline environments, tolerating conditions such as treatment with KOH in anhydrous methanol during synthetic deprotection without glycosidic cleavage.^[10] This stability arises from the resistance of O-glycosidic bonds to base hydrolysis, unlike ester linkages in related compounds. The reactivity of hyperoside is prominently characterized by its antioxidant capacity, mediated by the phenolic hydroxyl groups on the quercetin backbone, which donate hydrogen atoms or electrons to scavenge free radicals and inhibit oxidative damage.^[10] These groups also enable oxidation reactions, leading to the formation of quinones via two-electron processes, particularly involving the catechol moiety in the B ring, analogous to the oxidation pathway observed in quercetin.^[12] The phenolic hydroxyl groups of hyperoside exhibit pKa values approximately in the range of 7–10, allowing partial ionization under mildly acidic to neutral physiological conditions and contributing to its redox activity.^[13] Hyperoside undergoes degradation via photodegradation under UV exposure and thermal decomposition at elevated temperatures exceeding 200 °C, consistent with the behavior of polyphenolic flavonoids.^[14] For analytical identification, hyperoside is routinely detected and characterized using high-performance liquid chromatography (HPLC) coupled with UV or diode array detection, nuclear magnetic resonance (NMR) spectroscopy for structural confirmation, and mass spectrometry, where it displays a prominent protonated molecular ion at m/z 465 [M+H]⁺ in electrospray ionization mode.^[15]^[16]

Natural occurrence and biosynthesis

Plant sources

Hyperoside, a flavonol glycoside, is widely distributed in various medicinal plants, with notable concentrations in species from the genera Crataegus and Hypericum. In Crataegus pinnatifida (Chinese hawthorn), hyperoside is a principal flavonoid found in leaves and fruits, with contents ranging from 0.58–0.76 mg/g dry weight in leaves and 0.12–0.48 mg/g dry matter in fruits.^[17] The Chinese Pharmacopoeia specifies a minimum hyperoside content of 0.050% in hawthorn leaves for quality control.^[18] In Hypericum perforatum (St. John's wort), hyperoside constitutes approximately 0.1% of the herb's dry weight, primarily in aerial parts, where it serves as a key marker compound alongside other flavonoids.^[19] Additional plant sources include Forsythia suspensa, where hyperoside occurs in fruits, and Cuscuta chinensis, with concentrations in seeds.^[20] Abelmoschus manihot contains hyperoside in flowers and leaves, often used as a quality indicator in traditional preparations.^[21] Other reported sources encompass Geranium carolinianum (herb), Polygonum aviculare (aerial parts), and Fagopyrum esculentum (buckwheat, particularly in hulls and aerial parts).^[22] These distributions highlight hyperoside's prevalence in families including Rosaceae, Hypericaceae, Polygonaceae, Erythrinaceae, Labiatae, and Leguminosae, with higher concentrations often found in plants from Southeast Asia, Europe, and North America.^[2]^[1] Concentrations of hyperoside vary by plant part, with higher levels typically observed in flowers and young leaves compared to mature fruits or stems; for instance, leaf extracts of Hypericum perforatum exhibit greater hyperoside than floral or stem portions.^[23] Seasonal and environmental factors, such as altitude or stress conditions, further influence accumulation, often elevating levels in response to abiotic pressures like drought or elevation changes in hawthorn fruits.^[24] Hyperoside is commonly isolated from plant material through solvent extraction using ethanol-water mixtures (e.g., 80–96% ethanol), followed by purification via column chromatography or high-performance liquid chromatography (HPLC) to achieve high purity.^[22]^[25] Advanced techniques, such as ultrasound-assisted extraction with natural deep eutectic solvents, enhance yield and sustainability from sources like Cuscuta chinensis seeds.^[26]

Biosynthetic pathway

Hyperoside, a flavonol glycoside, is synthesized in plants via the flavonoid branch of the phenylpropanoid pathway, with naringenin serving as the primary flavanone precursor.^[27] The core biosynthetic steps involve sequential enzymatic modifications: first, flavanone 3-hydroxylase (F3H) hydroxylates naringenin at the 3-position to form dihydrokaempferol; subsequent action by flavonoid 3'-hydroxylase (F3'H) introduces a hydroxyl group at the 3' position, yielding dihydroquercetin; flavonol synthase (FLS) then dehydrates dihydroquercetin to produce quercetin; finally, UDP-galactose:flavonol 3-O-galactosyltransferase (F3GT) catalyzes the glycosylation of quercetin at the 3-hydroxyl position using UDP-galactose, resulting in hyperoside.^[27] In species such as Hypericum monogynum, two parallel routes from naringenin contribute to hyperoside production due to the broad substrate specificity of key enzymes: one pathway proceeds through dihydrokaempferol (via F3H) followed by F3'H hydroxylation to dihydroquercetin, while the alternative route involves initial F3'H hydroxylation of naringenin to eriodictyol, then F3H-mediated conversion to dihydroquercetin, converging at the FLS step to quercetin before glycosylation.^[27] Biosynthesis is regulated by transcription factors, including MYB30, which activates expression of the F3GT gene (e.g., AeUF3GaT1 in okra), promoting hyperoside accumulation particularly in reproductive tissues like flower buds and seeds.^[28] Additionally, a positive feedback mechanism exists wherein hyperoside itself upregulates genes involved in its own biosynthesis, such as F3GT, enhancing production during developmental stages.^[28] A 2023 study on Hypericum monogynum flower buds elucidated these parallel routes through transcriptome sequencing and enzyme characterization.^[27]

Biological effects

Pharmacological activities

Hyperoside exhibits a range of pharmacological activities, primarily demonstrated in preclinical models, with potential therapeutic implications for oxidative stress-related and inflammatory conditions. Its antioxidant properties have been shown to mitigate oxidative damage in ischemia-reperfusion injury models across various organs. For instance, in rat models of myocardial ischemia-reperfusion, hyperoside at 20–50 mg/kg reduced reactive oxygen species (ROS) levels and preserved cardiac function by enhancing antioxidant enzyme activity.^[29] Similarly, administration of 50 mg/kg hyperoside protected against hepatic ischemia-reperfusion injury in rats by lowering malondialdehyde (MDA) and boosting superoxide dismutase (SOD) and glutathione (GSH).^[30] In cerebral ischemia-reperfusion models, 50 mg/kg hyperoside decreased oxidative stress markers and improved neurological outcomes in rats.^[31] The compound also displays anti-inflammatory effects, particularly in vascular pathologies, by suppressing key pro-inflammatory cytokines. In human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-α (TNF-α), hyperoside at 10–50 μM inhibited TNF-α and interleukin-6 (IL-6) production, reducing vascular inflammation and monocyte adhesion.^[32] This activity extends to models of atherosclerosis, where hyperoside pretreatment attenuated TNF-α-mediated endothelial dysfunction and cytokine release in vitro.^[33] In anticancer applications, hyperoside induces apoptosis and inhibits cell proliferation in several cancer types. In breast cancer MCF-7 cells, treatment with 25–100 μM hyperoside triggered ROS-mediated apoptosis via NF-κB pathway downregulation, reducing cell viability.^[34] For lung cancer, hyperoside suppressed proliferation in non-small cell lung cancer A549 cells with an IC₅₀ of approximately 70 μM after 72 hours, accompanied by G₂/M phase arrest and increased apoptosis.^[35] In colon cancer HT-29 cells, hyperoside at 50–200 μM promoted mitochondrial apoptosis through caspase activation and Bcl-2 downregulation, inhibiting colony formation.^[36] Hyperoside provides organ protection in multiple preclinical settings. Its cardioprotective effects include reducing myocardial infarction size by up to 30% in rat models of ischemia-reperfusion injury at doses of 20 mg/kg, via decreased lactate dehydrogenase release and improved hemodynamics.^[29] Neuroprotectively, hyperoside ameliorated Alzheimer's disease-like pathology in mouse models by reducing amyloid-β accumulation and tau phosphorylation at 10–30 mg/kg, enhancing cognitive performance in behavioral tests.^[37] Hepatoprotective activity was evident against carbon tetrachloride (CCl₄)-induced liver damage in mice, where 50 mg/kg hyperoside lowered serum ALT and AST levels while restoring antioxidant defenses.^[38] Additional activities include antidepressant-like effects, observed in the forced swim test where 10–20 mg/kg hyperoside reduced immobility time in mice by modulating dopaminergic pathways.^[39] In bone models, hyperoside exerted anti-osteoporotic effects in ovariectomized mice at 40–80 mg/kg, increasing bone mineral density and trabecular thickness while inhibiting osteoclastogenesis.^[40] These effects are typically achieved at oral doses of 10–100 mg/kg in rodent models, with limited human data primarily from herbal extracts containing hyperoside, such as those used in traditional formulations for inflammatory conditions.^[10]

Mechanisms of action

Hyperoside demonstrates potent antioxidant activity primarily through direct scavenging of reactive oxygen species (ROS), a process facilitated by the catechol structure of its B-ring hydroxyl groups (3'-OH and 4'-OH), which donate electrons and hydrogen atoms to neutralize free radicals such as hydroxyl radicals and superoxide anions.^[23] This direct interaction reduces lipid peroxidation and oxidative damage in cellular models, including those of liver and neuronal tissues.^[33] Complementing this, hyperoside activates the Nrf2/HO-1 signaling pathway by promoting nuclear translocation of Nrf2, which binds to antioxidant response elements to upregulate heme oxygenase-1 (HO-1) and other enzymes like superoxide dismutase (SOD) and glutathione peroxidase (GPx), thereby bolstering endogenous antioxidant defenses against oxidative stress.^[33]^[41] In its anti-inflammatory mechanisms, hyperoside inhibits high-mobility group box 1 (HMGB1) signaling by suppressing its extracellular release from activated cells, thereby preventing HMGB1-mediated inflammatory cascades and cytoskeletal disruptions in endothelial and immune cells.^[42] It further attenuates inflammation by blocking nuclear factor-κB (NF-κB) activation, which inhibits the translocation of NF-κB p65 subunit to the nucleus and reduces transcription of pro-inflammatory cytokines such as TNF-α, IL-6, and iNOS.^[33] Hyperoside also diminishes phosphorylation of mitogen-activated protein kinases (MAPKs), particularly p38 and ERK, disrupting downstream inflammatory signaling in macrophages and microglia exposed to lipopolysaccharide (LPS).^[43] Hyperoside's anticancer effects involve induction of cell cycle arrest at the G2/M phase, achieved through activation of the tumor suppressor p53, which upregulates p21 to inhibit cyclin B1-CDK1 complexes and halt mitotic progression in tumor cells like those from bladder and lung cancers.^[33] Additionally, it promotes anti-angiogenesis by downregulating vascular endothelial growth factor (VEGF) expression via suppression of hypoxia-inducible factor-1α (HIF-1α), thereby restricting endothelial cell proliferation and tumor neovascularization.^[33] These pathways contribute to apoptosis induction in cancer cells, as observed in preclinical models. For neuroprotection, hyperoside modulates brain-derived neurotrophic factor (BDNF)/TrkB signaling by increasing BDNF expression and TrkB receptor activation, which activates downstream PI3K/Akt and ERK pathways to enhance neuronal survival, synaptic plasticity, and cognitive function in stress- and toxin-induced models.^[33] It also inhibits amyloid-β (Aβ) aggregation by directly binding to Aβ peptides, preventing fibril formation and reducing Aβ-induced endoplasmic reticulum stress and mitochondrial calcium dysregulation in Alzheimer's disease models.^[44] Regarding metabolism, hyperoside is absorbed in the small intestine following oral administration, where it is hydrolyzed by β-galactosidase enzymes to release its aglycone quercetin, facilitating uptake via glucose transporters.^[45] In the liver, the parent compound and quercetin undergo phase II conjugation, forming glucuronide and sulfate metabolites that enhance water solubility for biliary and urinary excretion, with a bioavailability of approximately 26% and a plasma half-life of around 4 hours.^[10] The structure-activity relationship of hyperoside highlights the role of its 3-O-galactoside moiety, which improves aqueous solubility and intestinal absorption compared to free quercetin, resulting in higher plasma concentrations, prolonged circulation, and enhanced tissue accumulation, particularly in the kidneys.^[10] This glycosylation reduces rapid metabolism and efflux by P-glycoprotein, thereby augmenting overall bioavailability and therapeutic efficacy.^[33]

Synthesis and production

Chemical synthesis

Hyperoside, also known as quercetin 3-O-β-D-galactopyranoside, has been synthesized in the laboratory through various chemical routes, primarily semi-synthetic approaches starting from quercetin or related flavonoids. The first reported chemical synthesis was achieved by Hörhammer et al. in 1968, marking a significant milestone in flavonoid glycoside chemistry. This classical method involved regioselective protection of the hydroxyl groups on quercetin to target the C3 position, followed by glycosylation using the Koenigs-Knorr reaction with an acetylated bromogalactose donor, and subsequent deprotection via hydrogenolysis with palladium on carbon as catalyst, yielding approximately 2.6% overall.^[10] The Koenigs-Knorr reaction remains a cornerstone of classical synthesis for hyperoside, employing silver or cadmium salts as promoters to facilitate the coupling of protected quercetin with 2,3,4,6-tetra-O-acetyl-α-D-galactopyranosyl bromide (acetobromogalactose). This step ensures β-selective glycosylation at the 3-hydroxyl due to neighboring group participation from the 2-O-acetyl moiety, though overall yields are modest (typically 40-60% for the glycosylation step alone in optimized variants). Deacetylation is then performed under Zemplén conditions using sodium methoxide in methanol or basic hydrolysis to afford the free glycoside. Key challenges include achieving high regioselectivity at the 3-position amid multiple reactive hydroxyls on quercetin, often requiring multi-step protecting group manipulations with benzyl or acetyl groups, and side reactions leading to O- or C-glycosides.^[46] Subsequent improvements in the 1990s and 2000s focused on semi-synthesis from more accessible precursors like rutin (quercetin 3-O-rutinoside). In 1994, Jiang et al. developed a route involving selective hydrolysis of the rutinoside moiety with HCl in ethanol to expose the 3-hydroxyl, benzoylation for protection, Koenigs-Knorr glycosylation with acetobromogalactose, and final deprotection, achieving a 6.8% overall yield with enhanced purity. By 2002, Zhou refined this by optimizing hydrolysis conditions with concentrated HCl in hot ethanol and using KOH in anhydrous methanol for debenzoylation, boosting the yield to 11% while minimizing degradation. These advancements emphasized milder conditions and better protecting group strategies, such as orthogonal benzoyl esters for the 5,7,3',4'-hydroxyls, to improve scalability and product purity.^[10] Modern chemical syntheses incorporate Lewis acid catalysts, such as BF3·OEt2 or TMSOTf, in place of traditional heavy metal promoters for the glycosylation step, enabling higher efficiency and reduced toxicity. For instance, protected quercetin derivatives are coupled with galactose trichloroacetimidate donors under these conditions for selective 3-O-attachment, followed by global deprotection, often yielding purer hyperoside after silica gel column chromatography. These methods address historical challenges by leveraging directing groups for regioselectivity and microwave-assisted reactions for faster processing, though overall yields remain below 20% due to the inherent reactivity of flavonols. Purification typically involves flash chromatography with ethyl acetate-methanol gradients to isolate hyperoside from byproducts.

Biotechnological production

Biotechnological production of hyperoside leverages engineered biological systems to enable scalable synthesis, drawing on the natural biosynthetic pathway involving flavonol formation and glycosylation. Microbial hosts, such as Escherichia coli, have been engineered by expressing plant-derived genes like flavanone 3-hydroxylase (F3H), flavonol synthase (FLS), flavonoid 3'-hydroxylase (F3'H), and flavonoid 3-O-galactosyltransferase (F3GT) to reconstruct the pathway. For instance, co-expression of HmF3H1, HmFLS1, trHmF3'H, AtCPR1, BbGalE2, and HmGAT from Hypericum monogynum in E. coli BL21(DE3) enabled conversion of naringenin to hyperoside, yielding 25 mg/L under optimized feeding conditions with ascorbate and α-ketoglutarate to support cofactor regeneration.^[47] Similar strategies in yeast (Saccharomyces cerevisiae) have supported flavonol production using F3H and FLS genes, providing a foundation for hyperoside glycosylation, though specific yields for the galactoside remain under optimization.^[48] De novo production from glucose has been pursued by integrating upstream phenylpropanoid pathways, though most reported titers derive from fed precursors like quercetin or naringenin. In these systems, UDP-galactose supply is enhanced by co-expressing epimerases like GalE alongside glycosyltransferases such as PhUGT from Petunia hybrida, resulting in optimized shake-flask titers of 411.2 mg/L and fed-batch production of 831.6 mg/L from quercetin with 90.2% molar conversion. A notably high yield of 18,000 mg/L was achieved using resting E. coli cells engineered with a flavonol 3-O-galactosyltransferase and UDP-galactose regeneration pathway, starting from quercetin under optimized conditions at 30 °C with enhanced aeration (Guna et al., 2020).^[49]^[50] Plant cell cultures offer an alternative for hyperoside production, utilizing suspension or adventitious root systems from natural sources like Hypericum perforatum and Ginkgo biloba. In H. perforatum adventitious root cultures grown in balloon-type airlift bioreactors, hyperoside accumulated to 14.01 μg/g dry weight after 6 weeks, corresponding to 50–100 mg/L in dense cultures with ~50-fold biomass increase from 3 g/L inoculum.^[51] G. biloba suspension cultures similarly produce flavonoids, including hyperoside precursors, under optimized conditions with elicitors, though specific titers for the galactoside are typically in the low mg/L range due to pathway compartmentalization.^[52] Recent advances include dual-pathway engineering from naringenin, mimicking parallel routes in H. monogynum (dihydrokaempferol → kaempferol → quercetin vs. direct flavonol branching), reconstructed in microbes for improved flux and reduced bottlenecks.^[47] These developments build on earlier MYB30 studies in okra, where stabilization via phosphorylation boosted hyperoside accumulation.^[53] This biotechnological approach offers sustainability by using renewable feedstocks like glucose, bypassing variability in plant extraction yields influenced by seasonal or environmental factors. Purification is streamlined through fermentation broth filtration and chromatography, achieving high-purity hyperoside (>95%) without harsh solvents.^[49] However, challenges persist in glycosylation efficiency, where UDP-sugar availability limits conversion rates to 70–90%, and scaling to industrial levels (>1 g/L) requires further host engineering to mitigate toxicity from pathway intermediates.^[47]

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[43]
Hyperoside alleviates toxicity of β-amyloid via endoplasmic ...
HYP inhibits Aβ aggregation-induced neurotoxicity via direct binding to Aβ. •. HYP targets the endoplasmic reticulum-mitochondrial Ca2+ signal cascade through ...
[44]
Systematic Identification, Fragmentation Pattern, And Metabolic ...
Sep 13, 2022 · Hyperoside is a flavonol glycoside and has multiple phenolic hydroxyl groups. So it tends to lose H and has a negative charge when ionized. The ...Missing: stability pKa HPLC NMR
[45]
https://pmc.ncbi.nlm.nih.gov/articles/PMC9489401/
[46]
The parallel biosynthesis routes of hyperoside from naringenin ... - NIH
Hyperoside is a bioactive flavonoid galactoside in both medicinal and edible plants. It plays an important physiological role in the growth of flower buds.
[47]
Metabolic Engineering of Saccharomyces cerevisiae for De Novo ...
The introduction of the two heterologous genes F3H and FLS into E.coli and yeast has enabled the production of kaempferol with the supplement of precursor ...
[48]
Metabolic Engineering of Escherichia coli for Hyperoside Biosynthesis
Mar 16, 2022 · The production was also conducted using a substrate-fed batch fermentation, and the maximal hyperoside production was 831.6 mg·L−1, with a molar ...
[49]
Production of adventitious root biomass and secondary metabolites ...
The results suggest scale-up of adventitious root culture of H. perforatum for the production of chlorogenic acid, quercetin and hyperoside is feasible.
[50]
Ginkgo biloba: A Treasure of Functional Phytochemicals with ...
G. biloba has been shown to have a variety of medicinal and pharmacological properties, including anticancer, antidementia, antidiabetic, antiobesity, ...
[51]
RHA2b-mediated MYB30 degradation facilitates MYB75-regulated ...
Mar 11, 2024 · We report that the R2R3-MYB transcription factor MYB30 and the ubiquitin E3 ligase RHA2b participate in anthocyanin biosynthesis through regulation of the MBW ...Missing: hyperoside | Show results with:hyperoside
[52]
CDPK6 phosphorylates and stabilizes MYB30 to promote ... - PubMed
Jul 6, 2020 · CDPK6 phosphorylates and stabilizes MYB30 to promote hyperoside biosynthesis that prolongs the duration of full-blooming in okra.Missing: production 2023 2024