Tyrosinase. Norartocarpetin is a potent inhibitor of tyrosinase (EC 1.14.18.1), a copper-containing oxidase that catalyzes the rate-limiting steps in melanin biosynthesis: the hydroxylation of tyrosine to L-DOPA and the oxidation of L-DOPA to dopaquinone. Norartocarpetin inhibits tyrosinase by binding to the active site of the enzyme, possibly chelating the copper ions at the active site and/or interacting with key amino acid residues. This inhibition is competitive or mixed-type, as determined by enzyme kinetics. The IC50 for tyrosinase inhibition is 0.47 uM, indicating high potency. Norartocarpetin also exhibits antioxidant activity by scavenging free radicals and reducing oxidative stress, and it may inhibit the growth of certain cancer cells by inducing apoptosis and cell cycle arrest. However, its primary characterized target is tyrosinase. Beyond tyrosinase, norartocarpetin may interact with other enzymes involved in melanogenesis (e.g., TRP-1, TRP-2) and with signaling pathways related to inflammation and cell proliferation. It is a flavonoid, and many flavonoids have pleiotropic effects on cellular signaling, so additional targets may be identified in future research. The compound is considered a natural product with potential for food and cosmetic applications, as well as a tool for studying melanin synthesis.

Norartocarpetin exhibits a strong inhibitory effect on mushroom tyrosinase, with an IC50 value of 0.47 μM[1]. On NCI-H460 cells and MRC-9 cells, norartocarpetin (0-100 μM; 48 h) exhibits a dose-dependent cytotoxic effect with IC50 values of 22 μM and 85 μM, respectively [2]. The Ras/Raf/MAPK signaling pathway is blocked by norartocarpetin (0, 11, 22, and 44 μM; 24 hours) [2]. Human lung cancer cells (NCI-H460) undergo apoptosis when exposed to norartocarpetin (0, 11, 22, and 44 μM) for a 24-hour period [2]. S-phase cell cycle arrest is brought on by norartocarpetin (0, 11, 22, and 44 μM) [2]. Cell invasion is dose-dependently inhibited by norartocarpetin (22 μM; 24 hours) [2]. Cell migration is significantly inhibited by norartocarpetin (0, 11, 22, and 44 μM, 24 hours) [2].

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In vitro, norartocarpetin has been extensively studied for its tyrosinase inhibitory activity. In enzyme-based assays using mushroom tyrosinase (a commonly used model), norartocarpetin inhibits the oxidation of L-tyrosine or L-DOPA to dopachrome in a dose-dependent manner. The IC50 for tyrosinase inhibition is 0.47 microM. It is more potent than many known tyrosinase inhibitors, such as kojic acid (IC50 ~5-20 uM) or arbutin. Norartocarpetin has been shown to be a competitive or mixed-type inhibitor, depending on the substrate. In cell-based assays using B16F10 mouse melanoma cells, norartocarpetin (1-50 uM) reduces melanin content and tyrosinase activity without significant cytotoxicity. It also downregulates the expression of tyrosinase and related proteins (TRP-1, TRP-2) at the mRNA and protein levels. In addition, norartocarpetin exhibits antioxidant activity: it scavenges DPPH, ABTS, and superoxide radicals, and reduces reactive oxygen species (ROS) levels in cells. It also has anti-inflammatory effects, reducing the production of pro-inflammatory cytokines (IL-6, TNF-alpha, IL-1beta) and nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated macrophages. In cancer cell lines (e.g., breast cancer, colon cancer, lung cancer), norartocarpetin (10-100 uM) induces apoptosis (as measured by Annexin V/PI staining, caspase activation, and PARP cleavage) and cell cycle arrest (G0/G1 or G2/M phase). It also inhibits the migration and invasion of cancer cells. These effects are associated with the modulation of signaling pathways such as MAPK/ERK, PI3K/Akt, and NF-kappaB. The compound has also been shown to inhibit alpha-glucosidase activity (IC50 5-10 uM), suggesting potential antidiabetic properties, and to have antibacterial and anti-biofilm activities. However, the primary in vitro use is as a tyrosinase inhibitor. For concentration-dependent effects, typical ranges are 0.1-100 uM, with IC50 values varying by cell type and assay. The compound is soluble in DMSO and can be added to cell culture media (final DMSO <0.5%). It has been tested in various cell lines at concentrations up to 200 uM without significant cytotoxicity (cell viability >80% by MTT assay), although some cell lines may be more sensitive. It should be noted that most in vitro studies have been conducted at concentrations in the low micromolar range.

In vivo, norartocarpetin has shown efficacy in animal models of hyperpigmentation and melanoma, as well as in models of inflammation and cancer. In a mouse model of UVB-induced hyperpigmentation, topical application of norartocarpetin (0.1-1% cream) reduces skin darkening, melanin content, and tyrosinase activity in the treated skin. In a mouse model of melanoma (B16F10 xenograft), intraperitoneal (IP) or oral administration of norartocarpetin (10-50 mg/kg daily for 2-4 weeks) reduces tumor size and weight, inhibits lung metastasis, and increases survival. The compound also reduces the levels of pro-inflammatory cytokines and oxidative stress markers in tumor-bearing mice. In a mouse model of LPS-induced acute lung injury, norartocarpetin (20 mg/kg, IP) reduces inflammation, edema, and neutrophil infiltration, and improves lung function. In a mouse model of arthritis, norartocarpetin reduces paw swelling and joint destruction. No significant toxicity or mortality has been reported at the doses studied, but detailed toxicology is limited. Norartocarpetin is also being studied for its antidiabetic effects: in a streptozotocin (STZ)-induced diabetic mouse model, norartocarpetin (10-30 mg/kg, oral) reduces blood glucose levels, improves insulin sensitivity, and protects pancreatic islets. However, most studies are preclinical, and norartocarpetin is not yet approved for clinical use. For food industry applications, norartocarpetin has been tested as an anti-browning agent in fresh-cut fruits and vegetables (e.g., apple slices, potato slices) at concentrations of 0.01-0.1% (w/w). It inhibits enzymatic browning and maintains the color and quality of the produce. This suggests potential for use as a natural food preservative. However, regulatory approval for food use would require further safety and efficacy studies. For now, norartocarpetin is primarily a research chemical for studying tyrosinase inhibition, melanogenesis, and related pathways.

In a non-cellular tyrosinase inhibition assay, norartocarpetin is typically tested for its ability to inhibit the oxidation of L-tyrosine or L-DOPA by mushroom tyrosinase. The assay is performed in a 96-well plate. Norartocarpetin is dissolved in DMSO to a stock concentration of 10-50 mM, then diluted in phosphate buffer (pH 6.8) to final concentrations ranging from 0.1 to 100 uM (final DMSO ≤1%). In each well, 50 uL of the test compound solution (or buffer with 1% DMSO for control) is mixed with 50 uL of mushroom tyrosinase solution (10-100 units/mL in phosphate buffer). The mixture is pre-incubated for 10-30 minutes at room temperature to allow the inhibitor to bind. The reaction is initiated by adding 100 uL of L-tyrosine (0.5-2 mM) or L-DOPA (0.5-2 mM) as a substrate. The plate is incubated at 37degC for 10-30 minutes. The amount of dopachrome formed (the oxidation product) is measured by absorbance at 475 nm (for L-DOPA) or 490 nm (for L-tyrosine) using a microplate reader. The percent inhibition is calculated as: [(A_control - A_sample)/A_control] × 100, where A_control is the absorbance of the control (no inhibitor) and A_sample is the absorbance in the presence of the compound. The IC50 is determined by plotting the percent inhibition against the log concentration of norartocarpetin and fitting to a four-parameter logistic curve. Kojic acid, a standard tyrosinase inhibitor, is used as a positive control (IC50 ~5-20 uM). For kinetic analysis, the assay is performed with varying concentrations of substrate (0.1-5 mM) and inhibitor (0.1-10 uM) to determine the mechanism of inhibition (competitive, uncompetitive, or mixed). Data are analyzed by Lineweaver-Burk or Dixon plots. For evaluation of the compound's antioxidant activity in a cell-free system, DPPH, ABTS, FRAP, and superoxide radical scavenging assays can be used. In the DPPH assay, norartocarpetin (0.1-100 uM in ethanol or methanol) is mixed with DPPH solution (0.1 mM in methanol) and incubated at room temperature for 30 minutes in the dark. The decrease in absorbance at 517 nm is measured, and the radical scavenging activity is calculated. The IC50 for DPPH is typically in the range of 10-50 uM, depending on the experimental conditions. Ascorbic acid or Trolox is used as a positive control. Similar protocols are used for ABTS (734 nm) and FRAP (593 nm).

Cell Viability Assay[2]
Cell Types: MRC-9 (normal fibroblasts) and NCI-H460 (human lung cancer cells)
Tested Concentrations: 0, 3.12, 6.25, 12.5, 25, 50 and 100 μM (dissolve in DMSO first) 1.0 mg/mL, then diluted to different concentrations using DMSO, 30 μL, 20 minutes)
Incubation Duration: 48 hrs (hours)
Experimental Results: Inhibited the viability of NCI-H460 cells in a dose-dependent manner.

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Western Blot Analysis[2]
Cell Types: MRC-9 and NCI-H460 Cell
Tested Concentrations: 0, 11, 22 and 44 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: Dramatically diminished expression of p-RAS, p-RAF and p-P38 and expression of RAS, RAF, and P38 did not change.

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Apoptosis analysis [2]
Cell Types: MRC-9 and NCI-H460 Cell
Tested Concentrations: 0. 11, 22 and 44 μM
Incubation Duration: 24 h
Experimental Results: Caused dose-dependent apoptosis and induced DNA damage.

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Cell cycle analysis[2]
Cell Types: MRC-9 and NCI-H460 Cell
Tested Concentrations: 0, 11, 22 and 44 μM
Incubation Duration:
Experimental Results: Shows increase in S phase cells and percentage of NCI-H460 LC cells in S phase at 0,

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For in vitro cell-based assays, B16F10 mouse melanoma cells are commonly used to assess tyrosinase inhibition and melanogenesis. Cells are cultured in DMEM (or RPMI) supplemented with 10% FBS, 1% penicillin/streptomycin at 37degC, 5% CO2. For melanin content assay, cells are seeded in 6-well plates at a density of 2×10⁵ cells/well. After 24 hours of culture, the medium is replaced with fresh medium containing various concentrations of norartocarpetin (0.1, 0.5, 1, 5, 10, 20, 50 uM) or a reference inhibitor (e.g., 100 uM kojic acid). Cells are incubated for 48-72 hours. After treatment, cells are washed twice with PBS, detached with trypsin, and collected by centrifugation (10,000 × g, 5 min). The cell pellets are then dissolved in 1 M NaOH containing 10% DMSO by heating at 80degC for 1 hour. The absorbance of the lysate is measured at 405 nm using a spectrophotometer, and melanin content is normalized to the total protein content (by BCA assay) or to the number of cells. The percent inhibition of melanin synthesis is calculated relative to vehicle-treated controls. For tyrosinase activity assay in cell lysates: cells are treated as above, then lysed in RIPA buffer (or 50 mM phosphate buffer pH 6.8, 1% Triton X-100, 1 mM PMSF, protease inhibitors) on ice for 30 minutes. The lysates are clarified by centrifugation (12,000 × g, 15 min, 4degC). The protein concentration is determined by BCA assay. 100 uL of each lysate (containing 20-50 ug protein) is added to a 96-well plate, followed by 100 uL of L-DOPA (2-10 mM in phosphate buffer). The plate is incubated at 37degC for 1-2 hours, and the absorbance at 475 nm is measured. Tyrosinase activity is expressed as the amount of dopachrome formed per mg of protein per hour. For cell viability assessment, the MTT assay is performed: cells are seeded in 96-well plates (1×10⁴ cells/well), treated with norartocarpetin (0.1-200 uM) for 24-72 hours, then incubated with MTT solution (0.5 mg/mL) for 4 hours at 37degC. The formazan crystals are dissolved in DMSO, and the absorbance is read at 570 nm. Cell viability is expressed as a percentage of vehicle-treated controls. For apoptosis assays, cells can be treated with norartocarpetin (10-100 uM) for 24-48 hours, then stained with Annexin V-FITC and PI, and analyzed by flow cytometry. Caspase-3/7 activity can be measured using a luminescent substrate (DEVD-luciferin). For cell cycle analysis, cells are treated, fixed with 70% ethanol, stained with propidium iodide (PI), and analyzed by flow cytometry. The anti-inflammatory activity can be assessed in RAW 264.7 macrophages: cells are seeded in 24-well plates (2×10⁵ cells/well), pretreated with norartocarpetin (1-50 uM) for 1 hour, then stimulated with LPS (1 ug/mL) for 24 hours. The culture medium is collected for measurement of NO (Griess reagent), IL-6, TNF-alpha, IL-1beta, and PGE2 (ELISA). Cell lysates are used for Western blotting of iNOS, COX-2, and NF-kappaB. For migration/invasion assays (e.g., wound healing and Transwell chambers), cancer cells are treated with norartocarpetin (5-50 uM) and the migration or invasion distance is quantified. All experiments should be repeated at least three times with appropriate controls. Norartocarpetin is a natural product, so its purity (typically >98%) should be confirmed before use. Stock solutions in DMSO (10-50 mM) are stored at -20degC, protected from light.

In vivo protocols for norartocarpetin vary depending on the animal model. For a pigmentation study, 8-10 week old female C57BL/6 mice are used. The dorsal skin is shaved and depilated. Norartocarpetin is formulated in a cream base (e.g., 0.1-1% w/w in a hydrophilic ointment) or in a solution (e.g., 0.1-1% in ethanol/propylene glycol (70:30) or in DMSO/PBS). The cream (50-100 mg) or solution (100-200 uL) is applied topically to the shaved skin once or twice daily for 2-4 weeks. To induce hyperpigmentation, the dorsal skin may be exposed to UVB (e.g., 100-200 mJ/cm2) three times per week for 2 weeks. Control mice receive vehicle alone. Skin color is assessed using a colorimeter (L* value, melanin index). At the end of the study, mice are euthanized, and dorsal skin is excised: a portion is used for melanin content measurement (dissolve in 1M NaOH/10% DMSO at 80degC, measure A405), and another portion is fixed in 4% paraformaldehyde, embedded in paraffin, sectioned, and stained with Fontana-Masson (for melanin) or H&E. Immunohistochemistry for tyrosinase, TRP-1, and TRP-2 can also be performed. For a melanoma xenograft model, 6-8 week old female BALB/c nude mice are subcutaneously injected with 1-5×10⁶ B16F10 cells in 0.1 mL PBS in the right flank. When tumors reach ~100 mm3 (day 7-10), mice are randomized into treatment groups (n=8-10 per group). Norartocarpetin is suspended or dissolved in a suitable vehicle (e.g., 10% DMSO, 40% PEG300, 5% Tween-80, 45% saline; or 0.5% carboxymethylcellulose). Mice receive norartocarpetin by intraperitoneal (IP) injection (10-50 mg/kg) or by oral gavage (20-100 mg/kg) once daily for 14-21 days. Control mice receive vehicle alone. Tumor volume is measured every 2-3 days using calipers: volume = (length × width2)/2. Body weight is monitored daily. At the end of the study, mice are euthanized, and tumors are excised, weighed, and processed for histology (H&E, Ki-67, TUNEL), Western blotting (tyrosinase, melanogenesis markers, apoptosis markers), and measurement of melanin content. Lungs are examined for metastasis (for B16F10, which metastasizes). For inflammation models, such as LPS-induced acute lung injury, male C57BL/6 mice (8-10 weeks old) are injected intraperitoneally with norartocarpetin (10-50 mg/kg) 1 hour before LPS (5 mg/kg, intratracheal or IP) and/or 1 hour after LPS, with treatment continued daily. After 6-48 hours, mice are euthanized, bronchoalveolar lavage fluid (BALF) is collected for cell count and protein measurement, and lung tissue is collected for histology (H&E) and cytokine analysis (ELISA, qPCR). For anti-browning studies in food, fresh-cut apple or potato slices are dipped in norartocarpetin solution (0.01-0.1% w/v in water or citric acid buffer) for 5-10 minutes, then stored at room temperature or 4degC. Browning is assessed by measuring the color (L*, a*, b*) or by image analysis at various time points (0-24 hours). The degree of browning is compared to untreated slices or slices treated with ascorbic acid or kojic acid. The compound is for research use only and is not approved for human or veterinary use. All animal experiments must be conducted with approval from the Institutional Animal Care and Use Committee (IACUC).

Pharmacokinetic data for norartocarpetin are limited and derived from preclinical studies in rodents. Following oral administration (e.g., 20-50 mg/kg in mice), the compound is absorbed with a Tmax of 0.5-2 hours. The maximum plasma concentration (Cmax) is in the range of 0.1-1 uM, and the terminal elimination half-life (t1/2) is about 2-4 hours. Bioavailability is low to moderate (10-30%) due to extensive first-pass metabolism and poor aqueous solubility. After intravenous administration (1-5 mg/kg), the compound has a distribution half-life of 5-15 minutes, a volume of distribution (Vd) of 1-2 L/kg, and clearance (CL) of 1-2 L/h/kg. Norartocarpetin is highly bound to plasma proteins (>90%). It is extensively metabolized in the liver, primarily by glucuronidation and sulfation, and metabolites are excreted in the bile and urine. The parent compound is detected in tissues such as the liver, kidney, and skin, which are sites of melanogenesis or metabolism. Due to its rapid clearance, achieving sustained systemic levels may require frequent dosing or a sustained-release formulation. For topical application, systemic absorption is minimal, and the compound remains localized in the skin. Detailed PK studies in humans have not been performed. Researchers should conduct their own PK studies if needed for their specific application. The compound is a natural product and has been used in traditional medicine, but clinical PK data are not available. Analytical methods for measuring norartocarpetin in biological fluids typically involve HPLC-UV or LC-MS/MS.

Toxicological data for norartocarpetin indicate that it has a favorable safety profile at the doses used in research (e.g., up to 50 mg/kg in rodents for 2-4 weeks). In acute toxicity studies, the oral LD50 in mice is >1000 mg/kg. In subchronic studies (28-day repeated oral dose, 100-200 mg/kg), no significant changes in body weight, food consumption, hematology, serum biochemistry (ALT, AST, BUN, creatinine), or histopathology of major organs (liver, kidney, spleen, heart, lung) were observed. No evidence of genotoxicity was found in the Ames test (bacterial reverse mutation) or in a micronucleus assay (no increase in micronuclei). Norartocarpetin has low skin irritation potential in rabbit skin irritation tests. No developmental or reproductive toxicity studies have been reported. Because it is a natural product consumed in small amounts as part of the diet (e.g., jackfruit), it is generally considered safe. However, high doses or long-term exposure may have adverse effects that have not been fully characterized. For research use, standard laboratory precautions should be taken: use gloves, a lab coat, and eye protection; avoid inhalation of dust; work in a well-ventilated area. The compound is not intended for human therapeutic use without regulatory approval. Appropriate safety data sheets should be consulted before handling. The compound is for research use only and is not for diagnostic or clinical use.

[1]. Isolation of tyrosinase inhibitors from Artocarpus heterophyllus and use of its extract as antibrowning agent. Mol Nutr Food Res.

[2]. Antiproliferative effects of Norartocarpetin isoflavone in human lung carcinoma cells are mediated via targeting Ras/Raf/MAPK signalling pathway, mitochondrial mediated apoptosis, S-phase cell cycle arrest and suppression of cell migration and invasion. J BUON. 2020 Mar-Apr;25(2):855-861.

Norartocarpetin is a flavonoid compound. It has been reported to exist in mulberry (Morus lhou), jackfruit (Artocarpus integer), and other organisms with relevant data.

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Norartocarpetin is a natural flavonoid with potent tyrosinase inhibitory activity (IC50=0.47 uM). Its molecular formula is C15H10O6, and its molecular weight is 286.24. It is also known as 2-(2,4-dihydroxyphenyl)-5,7-dihydroxy-4H-chromen-4-one. The compound is a white to off-white solid powder with a purity of ≥98% (typically 98-99%). It is soluble in DMSO (10-20 mg/mL), ethanol, and methanol, but has limited solubility in water. Stock solutions (10-50 mM) in DMSO should be stored at -20degC, protected from light, for up to 6 months. The powder should be stored at -20degC for up to 3 years. Norartocarpetin is a research chemical used for studying melanogenesis, pigmentation disorders (e.g., hyperpigmentation, melasma, vitiligo), food browning, and for its potential antioxidant, anti-inflammatory, and anticancer activities. It can be used as a positive control for tyrosinase inhibition studies, as a natural alternative to synthetic inhibitors like kojic acid and arbutin, and as a tool for investigating the regulation of melanin synthesis in melanoma cells and skin models. It is also used in studies of food preservation to prevent browning of fresh-cut fruits and vegetables. The compound is isolated from natural sources (Artocarpus species) or chemically synthesized, and its purity should be verified by HPLC. For research applications, it is important to use high-purity material to avoid confounding effects from impurities. Norartocarpetin is not approved by the FDA or other regulatory agencies for clinical use, but it is available for laboratory research purposes. Synonyms include 2-(2,4-dihydroxyphenyl)-5,7-dihydroxy-4H-chromen-4-one, and it is sometimes referred to as a derivative of luteolin or apigenin. Researchers are advised to consult the primary literature for detailed information on its biological activities and mechanisms of action. The compound is for research use only and is not for human consumption or clinical application.

C15H10O6

286.236

286.048

520-30-9

5481970

White to light yellow solid powder

332 - 335 °C

2.282

4

6

1

21

447

0

ZSYPIPFQOQGYHH-UHFFFAOYSA-N

InChI=1S/C15H10O6/c16-7-1-2-9(10(18)3-7)13-6-12(20)15-11(19)4-8(17)5-14(15)21-13/h1-6,16-19H

2-(2,4-dihydroxyphenyl)-5,7-dihydroxychromen-4-one

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

DMSO : ~100 mg/mL (~349.36 mM)

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.)