Natural flavonoid
Morin monohydrate targets multiple cellular pathways involved in inflammation, oxidative stress, and apoptosis. The compound reduces the mRNA expression of pro-inflammatory cytokines including TNF-α, COX-2, IL-1β, and IL-6. It also downregulates the expression of caspases (caspase-1, caspase-3, and caspase-11) involved in the apoptosis pathway. Morin monohydrate functions as an antioxidant by reducing malondialdehyde (MDA) levels and increasing the activity of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-PX). The compound's flavonoid structure enables it to scavenge free radicals and chelate metal ions, contributing to its antioxidant and anti-inflammatory activities.

A reversed-phase high-performance liquid chromatographic method with fluorescence detection for the determination of labile monomeric aluminium has been developed through pre-column complexation using morin as the analytical reagent. The highly fluorescent aluminium-morin complex (excitation wavelength 418 nm, emission wavelength 490 nm) was separated on a Spherisorb ODS 2 column with an eluent consisting of 30% methanol and 70% water (pH 1.0 with perchloric acid). The most remarkable point of this protocol was that only the most toxic aluminium species, that is, free aqua-aluminium ion and its monomeric hydroxo complex ions, selectively respond among various aluminium complexes. This strategy has been successfully applied to direct fractionation of the toxic aluminium in natural waters and biological samples without any pretreatment.[2]
In vitro, Morin monohydrate exhibits anticancer, antioxidant, and anti-inflammatory activities. The compound reduces T-2 toxin-induced expression of pro-inflammatory cytokines including TNF-α, COX-2, IL-1β, and IL-6, as well as caspases (caspase-1, caspase-3, and caspase-11). It improves T-2 toxin-induced damage by reducing malondialdehyde (MDA) and increasing superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-PX). The compound also demonstrates low antioxidant activity in certain assays. Morin monohydrate is a fluorescing chelating agent used in aluminum speciation. Its flavonoid structure enables it to interact with various cellular targets and modulate signaling pathways involved in inflammation and oxidative stress.

Flavonoids are polyphenolic compounds with potential antioxidant activity via multiple reduction capacities. Oxidation of cellular lipids has been implicated in many diseases. Consequently, this study has assessed the ability of several dietary flavonoid aglycones to suppress lipid peroxidation of hepatic microsomes derived from rats deficient in the major lipid soluble antioxidant, dα-tocopherol. Antioxidant effectiveness was galangin > quercetin > kaempferol > fisetin > myricetin > morin > catechin > apigenin. However, none of the flavonoids were as effective as dα-tocopherol, particularly at the lowest concentrations used. In addition, there appears to be an important distinction between the in vitro antioxidant effectiveness of flavonoids and their ability to suppress indices of oxidation in vivo. Compared with dα-tocopherol, repletion of vitamin E deficient rats with quercetin, kaempferol, or myricetin did not significantly affect indices of lipid peroxidation and tissue damage. Direct antioxidant effect of flavonoids in vivo was not apparent probably due to low bioavailability although indirect redox effects through stimulation of the antioxidant response element cannot be excluded.[1]
In vivo, Morin monohydrate has been investigated for its potential therapeutic effects in various disease models. As a flavonoid with antioxidant and anti-inflammatory activities, it may protect against toxin-induced damage and oxidative stress. The compound's ability to reduce T-2 toxin-induced damage by modulating inflammatory cytokines and antioxidant enzymes suggests potential applications in mitigating toxin-induced toxicity. Morin monohydrate may also have anticancer properties, as flavonoids are known to inhibit tumor growth and metastasis through multiple mechanisms including apoptosis induction, cell cycle arrest, and angiogenesis inhibition. Further preclinical studies are needed to fully establish its in vivo efficacy and therapeutic potential.

Mindray Perfect Plus 400 was used to measure the activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), and alanine aminotransferase (ALT) in the serum. The results were given in units of U/L.
In vitro enzyme/receptor binding (non-cellular) assays for Morin monohydrate typically involve measuring its antioxidant activity using cell-free systems such as DPPH (2,2-diphenyl-1-picrylhydrazyl) radical scavenging, ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)) radical scavenging, and FRAP (ferric reducing antioxidant power) assays. In these assays, the compound is incubated with the radical-generating system or the ferric complex, and the reduction in absorbance is measured spectrophotometrically. The compound's metal-chelating activity can be assessed using ferrozine-based or other colorimetric assays that detect the formation of metal complexes. These assays help quantify the compound's antioxidant and metal-chelating properties and compare them to standard antioxidants.

MTT cell proliferation assay[3]
Morin’s effect on the proliferation of HCT116 and CT26 was determined using 3-(4,5-Dimethylthiazol-2-YI)-2,5-Diphenyltetrazolium Bromide (MTT) based colorimetric assay. Wells were seeded with 5000 cells/well and allowed to grow overnight. Cells were treated with different concentrations of morin (50 μM,100 μM,150 μM, 200 μM, and 400 μM) and incubated for 48 h. After the incubation time, MTT reagent was added and incubated in the incubator for 4 h. Later DMSO is added to dissolve the formazan crystals and incubated in dark for 30 min, absorbance at 570 nm is measured.

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Colony formation assay[3]
HCT116 and CT26 cells (500 cells/well) were seeded on a 6-well plate and allowed to grow overnight. The next day the plates were treated with IC50 concentration of morin for respective cell lines. After 48 h of incubation, the medium was changed and incubated for 10 days. Colonies were fixed with 10% formalin and stained with 1% crystal violet in 10% ethanol. Images were documented and colonies were counted using ImageJ software and graphs were plotted using GraphPad Prism.

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Wound healing assay[3]
For wound healing assay, 1 × 105 cells were seeded in each well of a 6-well plate and cultured until it reaches 75–80% confluency. A wound was made using a 100 μl pipette tip, washed the detached cells with PBS, and cells were overlayed with reduced serum medium. Images were captured at 0 h, 24 h, and 48 h, the wound area was quantitatively measured using ImageJ software.
In vitro cellular experiments with Morin monohydrate are performed using various cell lines to assess its anticancer, antioxidant, and anti-inflammatory activities. Cells such as RAW 264.7 macrophages, HepG2 hepatoma cells, or cancer cell lines are cultured in appropriate media and treated with varying concentrations of the compound for 24-72 hours. Inflammatory responses are induced using lipopolysaccharide (LPS) or other stimuli, and the expression of inflammatory cytokines (TNF-α, COX-2, IL-1β, IL-6) and caspases is measured by RT-qPCR or ELISA. Oxidative stress markers such as MDA, SOD, CAT, GSH, and GSH-PX are measured using biochemical assays. Cell viability and proliferation are assessed using MTT or CellTiter-Glo assays.

35 male Wistar albino rats (weighing between 280 and 300 g, 11–12 weeks old) were separated into five groups of 7 male rats each at random:[4]
Control group: The animals received 0.9% saline via oral gavage for 10 days and a single intraperitoneal injection of saline on day 5 only.
Morin group: The animals were given 100 mg/kg morin hydrate orally for 10 days and intraperitoneal saline injection was given on the 5th day of the experiment.
MTX group: The animals were administered saline orally for 10 days and on the 5th day of the experiment, a single dose of 20 mg/kg MTX was injected intraperitoneally.
MTX + Morin 50 group: Rats were given 50 mg/kg morin hydrate orally for 10 days and a single dose of 20 mg/kg MTX was injected intraperitoneally on the 5th day of the experiment.
MTX + Morin 100 group: Rats were given 100 mg/kg morin hydrate orally for 10 days and a single dose of 20 mg/kg MTX was injected intraperitoneally on the 5th day of the experiment.
Following day, the rats were sacrificed under mild sevoflurane anesthesia. Blood serum was separated by centrifugation at 3000×g for 10 min, and the serum samples were then tested for liver function analysis. Livers were immediately removed and washed with ice-cold physiological saline solution for biochemical and molecular analysis and then stored at -20 °C.
Mol Biol Rep. 2023 Apr;50(4):3479-3488.
In vivo animal studies with Morin monohydrate have been conducted in models of toxin-induced damage to assess its protective effects. Rodents are administered T-2 toxin or other toxins to induce oxidative stress and inflammation, followed by treatment with Morin monohydrate via oral or intraperitoneal administration. Efficacy is assessed by measuring inflammatory cytokine levels, oxidative stress markers, and histopathological examination of affected tissues. The compound's ability to reduce MDA and increase SOD, CAT, GSH, and GSH-PX is evaluated. Morin monohydrate has also been studied in cancer models, where tumor growth inhibition and survival rates are assessed. Further studies are needed to fully establish its in vivo efficacy and therapeutic potential.

Metabolites/Metabolites
Known metabolites of Morin include (2S,3S,4S,5R)-6-[2-(2,4-dihydroxyphenyl)-5,7-dihydroxy-4-oxochromen-3-yl]oxy-3,4,5-trihydroxyoxacyclohexane-2-carboxylic acid.
Pharmacokinetic properties of Morin monohydrate are not extensively characterized. The compound has molecular formula C₁₅H₁₂O₈ and molecular weight 320.25. As a flavonoid, it is expected to have moderate oral bioavailability, with absorption and metabolism influenced by gut microbiota and intestinal transporters. Flavonoids are typically metabolized by phase II enzymes (glucuronidation, sulfation) and excreted in urine and bile. The compound is soluble in DMSO at concentrations suitable for in vitro studies. Storage recommendations: powder at -20°C for up to 3 years. Detailed pharmacokinetic parameters including half-life, clearance, and bioavailability require further investigation from primary research publications.

The intraperitoneal LD50 in mice was 555 mg/kg. Behavior: somnolence (overall activity inhibition); Behavior: muscle weakness; Lung, pleural, or respiratory: respiratory depression. Archives of Pharmacodynamics and Therapeutics, 123(395), 1960 [PMID:13796312]

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Adverse Reactions
Occupational Hepatotoxicity - Secondary Hepatotoxicity: Potential toxic effects in occupational settings based on cases of human ingestion or animal experimental poisoning.
Toxicological information for Morin monohydrate indicates that the compound is a natural flavonoid with a favorable safety profile. It is extracted from edible plants including mulberry, Osage orange, and guava. The compound exhibits low toxicity in cell-based assays and is generally considered safe for research use. Standard safety precautions for handling research chemicals apply, including use of personal protective equipment (gloves, safety goggles, lab coat) and working in a well-ventilated area. The compound should be stored in a cool, dry place. Morin monohydrate is for research use only and is not approved for clinical use.

[1]. Antioxidant capacity of flavonoids in hepatic microsomes is not reflected by antioxidant effects in vivo. Oxid Med Cell Longev. 2012;2012:165127.

[2]. Morin applied in speciation of aluminium in natural waters and biological samples by reversed-phase high-performance liquid chromatography with fluorescence detection. Anal Bioanal Chem. 2003 Jun;376(4):542-8.

[3]. Morin inhibits colon cancer stem cells by inhibiting PUM1 expression in vitro. Med Oncol. 2022 Oct 12;39(12):251.

[4]. Morin ameliorates methotrexate-induced hepatotoxicity via targeting Nrf2/HO-1 and Bax/Bcl2/Caspase-3 signaling pathways. Mol Biol Rep. 2023 Apr;50(4):3479-3488.

Morin is a pentahydroxyflavonoid, a derivative of 7-hydroxyflavone alcohol, with three hydroxyl substituents at the 2', 4', and 5 positions. It possesses a variety of activities, including antioxidant, metabolic, antihypertensive, hepatoprotective, neuroprotective, anti-inflammatory, antitumor, antibacterial, EC 5.99.1.2 (DNA topoisomerase) inhibitor, and angiogenesis regulator. It is a pentahydroxyflavonoid and a 7-hydroxyflavone alcohol. Morin has been reported in apple wood (Maclura pomifera), Taiwan coltsfoot (Petasites formosanus), and other organisms with relevant data. See also: Apple wood (note moved here). Flavonoids are polyphenolic compounds with various reducing abilities and potential antioxidant activity. Cellular lipid peroxidation is associated with a variety of diseases. Therefore, this study evaluated the ability of several dietary flavonoid aglycones to inhibit lipid peroxidation in rat liver microsomes lacking the major lipid-soluble antioxidant dα-tocopherol. The antioxidant effects were in the following order: galangin > quercetin > kaempferol > fisetin > myricetin > morin > catechin > apigenin. However, the antioxidant effects of all flavonoids were inferior to dα-tocopherol, especially at the lowest concentrations. In addition, there appeared to be a significant difference between the in vitro antioxidant effects of flavonoids and their ability to inhibit oxidative indicators in vivo. Compared with dα-tocopherol, supplementation of vitamin E-deficient rats with quercetin, kaempferol or myricetin did not significantly affect lipid peroxidation and tissue damage indicators. The direct antioxidant effects of flavonoids in vivo may be less obvious due to low bioavailability, but indirect redox effects through stimulation of antioxidant response elements cannot be ruled out. [1]
Morin monohydrate (CAS 6202-27-3) is a flavonoid extracted from Morus alba (mulberry) plants, as well as from Maclura pomifera (Osage orange), Maclura tinctoria (old fustic), and leaves of Psidium guajava (common guava). It has molecular formula C₁₅H₁₂O₈ and molecular weight 320.25. Morin monohydrate exhibits anticancer, antioxidant, and anti-inflammatory activities. It reduces T-2 toxin-induced TNF-α, COX-2, IL-1β, IL-6, caspase-1, caspase-3, and caspase-11 mRNA expression, and improves T-2 toxin-induced damage by reducing malondialdehyde (MDA) and increasing superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GSH-PX). The compound is a fluorescing chelating agent used in aluminum speciation. Purity is typically ≥97%.

C15H12O8

320.250985145569

320.053

6202-27-3

Morin;480-16-0; 654055-01-3 (hydrate)

16219651

Typically exists as solid at room temperature

Originated from plants: other families

1.923

6

8

1

23

488

0

C1=CC(=C(C=C1O)O)C2=C(C(=O)C3=C(C=C(C=C3O2)O)O)O.O

MYUBTSPIIFYCIU-UHFFFAOYSA-N

InChI=1S/C15H10O7.H2O/c16-6-1-2-8(9(18)3-6)15-14(21)13(20)12-10(19)4-7(17)5-11(12)22-15;/h1-5,16-19,21H;1H2

2-(2,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate

Morin hydrate; 654055-01-3; 6202-27-3; Morin (monohydrate); 2-(2,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one hydrate; MFCD00217054; 2-(2,4-dihydroxyphenyl)-3,5,7-trihydroxychromen-4-one;hydrate; Morin Hydrate (>85% purity);

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)