3-Deoxy-galactosone does not have a defined pharmacological target but is a reactive electrophilic dicarbonyl compound that rapidly reacts with nucleophilic sites on biomolecules, particularly the amino groups of lysine and arginine residues in proteins. This reaction leads to the formation of advanced glycation end-products (AGEs) through a cascade of non-enzymatic modifications (glycation). The AGEs generated from 3-deoxy-galactosone can bind to the receptor for advanced glycation end-products (RAGE), triggering downstream pro-inflammatory and pro-oxidant signaling pathways. Through this indirect mechanism, 3-deoxy-galactosone contributes to the pathophysiology of galactosemia and diabetic complications, as well as food quality deterioration. The compound is also reactive with thiol groups, potentially depleting glutathione and other cellular antioxidants. 3-Deoxy-galactosone is less studied than its glucose-derived analog 3-deoxyglucosone, but it is recognized as a significant glycating agent in systems containing high galactose concentrations. In the context of galactosemia (an inborn error of galactose metabolism), elevated galactose leads to increased production of 3-deoxy-galactosone and other dicarbonyl compounds, which are implicated in the long-term complications of the disease, including cataracts, cognitive impairment, and ovarian failure. As a research tool, 3-deoxy-galactosone is used to study the chemical biology of dicarbonyl-mediated protein damage and to evaluate the efficacy of dicarbonyl scavengers as potential therapeutic agents for glycation-related diseases.

3-Deoxygalactosone has also been found in foods free of galactose, like beer and apple juice [1]. Through the intermediary 3,4-dideoxyglucosone-3-ene (3,4-DGE), 3-deoxyglucosone (3-DG) transforms into 3-deoxygalactosone in glucose-containing solutions [2].

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In vitro studies have demonstrated that 3-deoxy-galactosone reacts with proteins to form AGEs. Incubation of 3-deoxy-galactosone with model proteins such as bovine serum albumin (BSA) or human serum albumin (HSA) leads to the formation of AGE structures that can be detected by fluorescence spectroscopy (characteristic AGE fluorescence at excitation ~370 nm, emission ~440 nm), by ELISA using anti-AGE antibodies, or by LC-MS identification of specific AGE modifications such as imidazolone, pyrraline, and Nε-(carboxyethyl)lysine (CEL). The rate of AGE formation from 3-deoxy-galactosone is influenced by pH, temperature, and the presence of metal ions. Compared to glucose (which reacts very slowly with proteins), dicarbonyl compounds like 3-deoxy-galactosone are thousands of times more reactive and are considered the major precursors of AGEs under physiological conditions. 3-Deoxy-galactosone also reacts with reduced glutathione (GSH), leading to depletion of this important intracellular antioxidant and formation of glutathione conjugates. This reaction can be monitored spectrophotometrically or by LC-MS. In cell culture models (e.g., lens epithelial cells, endothelial cells, neuronal cells), exposure to 3-deoxy-galactosone (typically 0.1-10 mM) induces oxidative stress (increased ROS production, decreased GSH levels), activates NF-kappaB (nuclear factor-kappa B) signaling, increases expression of pro-inflammatory cytokines (e.g., TNF-alpha, IL-6), and induces apoptosis (caspase-3 activation, DNA fragmentation). Detailed in vitro activity data beyond these basic glycation and cytotoxicity studies are not consistently available in supplier datasheets, as 3-deoxy-galactosone is primarily used as an analytical reference standard rather than a pharmacological tool compound. The compound is recognized as a marker for galactose degradation during food processing and heat sterilization of medical solutions (e.g., peritoneal dialysis fluids, parenteral nutrition).

In vivo, 3-deoxy-galactosone is produced endogenously in conditions of elevated galactose, such as galactosemia (genetic deficiency of galactose-1-phosphate uridyltransferase, galactokinase, or UDP-galactose-4-epimerase). In rodent models of galactosemia (e.g., rats or mice fed a high-galactose diet), elevated tissue and plasma levels of 3-deoxy-galactosone have been detected. Chronic galactose feeding in animals leads to the development of cataracts (opacification of the lens), learning and memory deficits, ovarian dysfunction, and liver damage, similar to the complications seen in human galactosemia. The administration of dicarbonyl scavengers (e.g., aminoguanidine, pyridoxamine, metformin) in these models has been shown to reduce AGE levels and ameliorate some of the complications, indirectly implicating dicarbonyl compounds including 3-deoxy-galactosone as pathogenic mediators. However, direct administration of 3-deoxy-galactosone to animals to study its in vivo effects is less commonly reported, as the compound is highly reactive and would be rapidly cleared or bound to plasma proteins. The compound is a known glucose degradation product (GDP) in peritoneal dialysis (PD) solutions. During heat sterilization of PD fluids, galactose (present as a component of the solution) degrades to form 3-deoxy-galactosone and other GDPs, which have been shown to cause cytotoxicity to peritoneal mesothelial cells and contribute to the long-term complications of PD, such as peritoneal fibrosis and membrane failure. Studies in animal models of PD have demonstrated that PD solutions containing high levels of GDPs induce more peritoneal damage (thickening of the submesothelial layer, inflammation, fibrosis, angiogenesis) than solutions with low GDP content. Therefore, 3-deoxy-galactosone is used as a marker of PD solution quality and as a tool to study GDP-induced peritoneal injury. The detection and quantification of 3-deoxy-galactosone in plasma, urine, tissues, and pharmaceutical solutions are performed by HPLC with UV detection, LC-MS, or GC-MS after derivatization. The compound is not a therapeutic agent and is not used for pharmacological intervention in vivo; its relevance is in pathophysiology and analytical chemistry rather than drug discovery.

For in vitro protein glycation assays with 3-deoxy-galactosone, similar protocols to those described for 3-deoxyglucosone are used but substituting galactose-derived dicarbonyl. Bovine serum albumin (BSA, 10 mg/mL) is dissolved in 0.2 M phosphate buffer (pH 7.4) containing 0.02% sodium azide as a bacteriostatic agent. 3-Deoxy-galactosone (1-50 mM) is added to the BSA solution, and the mixture is incubated at 37degC for up to 14 days under sterile conditions. At various time points (days 1, 3, 7, 14), aliquots are collected. Glycation is monitored by fluorescence spectroscopy (ex 370 nm/em 440 nm), by SDS-PAGE to visualize crosslinking, by Western blotting using specific antibodies against imidazolone or CEL (carboxyethyl lysine) AGEs, or by LC-MS after protein hydrolysis. For LC-MS quantification of specific AGEs, the protein samples are hydrolyzed in 6 M HCl at 110degC for 18-24 hours under nitrogen. The hydrolysate is dried, reconstituted in mobile phase, and analyzed by LC-MS/MS using stable isotope-labeled internal standards for CEL, imidazolone, and other AGEs. To study the reaction kinetics, the decrease in free amino groups (using the OPA or TNBS assay) or the increase in protein-bound AGEs can be measured over time. To test dicarbonyl scavengers (e.g., aminoguanidine, pyridoxamine, metformin, quercetin, carnosine), these compounds (at various concentrations, e.g., 0.1-10 mM) are co-incubated with 3-deoxy-galactosone and BSA, and AGE formation is compared to control incubations without the scavenger. The percentage of inhibition of AGE formation is calculated. For glutathione (GSH) depletion assays, 3-deoxy-galactosone (0.1-10 mM) is incubated with 1 mM GSH in 0.1 M phosphate buffer (pH 7.4) at 37degC for 0-60 minutes. At each time point, an aliquot is mixed with 5% metaphosphoric acid to precipitate proteins, and after centrifugation, the supernatant is analyzed for GSH content using a colorimetric assay (Ellman‘s reagent, DTNB) or by HPLC with electrochemical detection. The kinetics of GSH depletion (pseudo-first-order rate constant) are determined. To identify glutathione conjugates of 3-deoxy-galactosone, the reaction mixture is analyzed by LC-MS.

For in vitro cellular assays to evaluate the cytotoxic and pro-inflammatory effects of 3-deoxy-galactosone, human lens epithelial cells (HLECs), human peritoneal mesothelial cells (HPMCs), human umbilical vein endothelial cells (HUVECs), or neuronal cell lines (e.g., PC12, SH-SY5Y) are used. Cells are cultured in appropriate media (e.g., DMEM, M199, RPMI-1640) supplemented with 10% fetal bovine serum, penicillin (100 U/mL), and streptomycin (100 microg/mL) at 37degC in 5% CO2. Cells are seeded in 6-well, 12-well, or 96-well plates at densities appropriate for the endpoint and allowed to attach overnight. 3-Deoxy-galactosone is added to the culture medium at concentrations ranging from 0.1 mM to 20 mM (or lower, e.g., 10-500 microM, if studying chronic effects or using sensitive cells). The compound is water-soluble, and the pH of the medium should be checked (dicarbonyl compounds can slightly acidify the medium). Control cells receive medium alone or vehicle (water). Incubation times vary from 4 hours to 7 days depending on the endpoint. For acute toxicity and oxidative stress endpoints, 4-24 hours are typical; for chronic effects on cell proliferation and function, 3-7 days may be used. Endpoints measured include: (1) Cell viability - MTT assay (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), WST-1 assay, or CellTiter-Glo luminescent assay. (2) Oxidative stress - intracellular reactive oxygen species (ROS) production measured by DCFH-DA (2‘,7‘-dichlorofluorescin diacetate) fluorescence; lipid peroxidation measured by TBARS (thiobarbituric acid reactive substances) assay or by measuring malondialdehyde (MDA) by HPLC; reduced glutathione (GSH) levels measured by a fluorometric or colorimetric assay; activity of antioxidant enzymes (superoxide dismutase, SOD; catalase; glutathione peroxidase, GPx). (3) AGE formation - immunocytochemistry using an anti-AGE antibody (e.g., anti-imidazolone) followed by fluorescent secondary antibody; visualization by fluorescence microscopy; quantification by image analysis. Alternatively, Western blotting of cell lysates using anti-AGE antibodies. (4) Activation of RAGE and downstream signaling - Western blotting for total and phosphorylated NF-kappaB p65; and for phosphorylated ERK1/2, p38 MAPK, and JNK. (5) Inflammatory response - ELISA or qRT-PCR for TNF-alpha (tumor necrosis factor-alpha), IL-1beta (interleukin-1 beta), IL-6, MCP-1 (monocyte chemoattractant protein-1), ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1). (6) Apoptosis - Annexin V-FITC/propidium iodide staining measured by flow cytometry; caspase-3/7 activity using fluorogenic substrates (e.g., DEVD-AMC) by fluorometry; TUNEL assay (terminal deoxynucleotidyl transferase dUTP nick end labeling) by fluorescence microscopy or flow cytometry; Western blotting for cleaved PARP (poly ADP-ribose polymerase) and cleaved caspase-3. (7) Cell migration and wound healing - scratch-wound closure assay in confluent monolayers. (8) Proliferation - BrdU (5-bromo-2‘-deoxyuridine) incorporation or Ki67 immunostaining. For peritoneal mesothelial cells specifically (HPMCs), the effect of 3-deoxy-galactosone on cell morphology (rounding, detachment), epithelial-to-mesenchymal transition (EMT) markers (E-cadherin, vimentin, alpha-SMA, fibronectin) by Western blotting or immunofluorescence, and the production of extracellular matrix components (collagen I, collagen III, fibronectin) by ELISA can be studied, as these are relevant to peritoneal fibrosis in patients on peritoneal dialysis. To mimic the clinical scenario of peritoneal dialysis fluid exposure, HPMCs can be treated with 3-deoxy-galactosone-containing solutions (similar to PD fluid composition) for 6-24 hours.

For in vivo studies of dicarbonyl-induced tissue damage using 3-deoxy-galactosone, two primary approaches are used: (1) galactose-fed animal models, which endogenously produce elevated 3-deoxy-galactosone; (2) direct administration of 3-deoxy-galactosone to animals (less common, due to its high reactivity and instability). Approach 1 - Galactose-fed rat model of galactosemia: Male or female weanling rats (50-100 g, or 6-8 week old rats for older models) are fed a diet containing 30-50% D-galactose (by weight) for 4-8 weeks. Control animals receive a standard chow diet without galactose supplementation. At the end of the feeding period, animals are euthanized, and blood, lens, liver, kidney, brain, and ovary tissues are collected. 3-Deoxy-galactosone levels in plasma and tissues are measured by LC-MS/MS. AGE levels (e.g., imidazolone, CEL, pentosidine) in tissues are quantified by ELISA or immunohistochemistry. Biomarkers of oxidative stress (MDA, GSH, SOD, catalase) are measured in tissue homogenates. To assess cataracts (lens opacification), animals are examined weekly using a slit-lamp biomicroscope, and cataract severity is graded on a scale (0 = clear lens, 1 = minimal opacity, 2 = mild opacity, 3 = moderate opacity, 4 = severe opacity). After the animals are euthanized, lenses are dissected, photographed, and processed for histology (H&E staining) and for measurement of lens opacity (measuring light transmission). To assess cognitive function (learning and memory), the Morris water maze test (spatial learning and memory) or novel object recognition test is performed during the final week of feeding. To assess ovarian function, ovarian tissue is examined histologically for follicle counts (primordial, primary, secondary, antral follicles), corpora lutea, and signs of apoptosis. To assess liver function, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels are measured, and liver tissue is examined histologically. To test the efficacy of dicarbonyl scavengers (e.g., aminoguanidine, 50-100 mg/kg intraperitoneally or orally; pyridoxamine, 50-200 mg/kg; metformin, 100-300 mg/kg orally; or other AGE inhibitors), these compounds are administered daily (by oral gavage, intraperitoneal injection, or mixed in drinking water) starting at the same time as the galactose diet. The outcomes (cataract formation, AGE levels, cognitive deficits, ovarian damage, liver injury) are compared between the galactose-only group, the galactose + scavenger group, and the control group. Approach 2 - Direct intraperitoneal administration of 3-deoxy-galactosone in rats for peritoneal dialysis (PD) model: Male Sprague-Dawley rats (250-350 g) are used. A peritoneal catheter is surgically implanted under anesthesia. After recovery (3-5 days), the rats receive daily intraperitoneal infusions (2-3 times per day) of 25-50 mL of a solution containing 3-deoxy-galactosone at concentrations mimicking those found in commercial PD fluids (e.g., 5-50 microM, but higher concentrations, 100-500 microM, may be used to accelerate damage). Control animals receive PD fluid without the added dicarbonyl (or standard commercial PD fluid). After 4-8 weeks of daily infusions, animals are euthanized. The peritoneum (parietal and visceral) is examined histologically (H&E, Masson‘s trichrome for collagen/fibrosis, immunohistochemistry for alpha-SMA, TGF-beta1, VEGF). The thickness of the submesothelial compact zone is measured as a marker of peritoneal fibrosis. The degree of angiogenesis (CD31 or von Willebrand factor immunostaining to count microvessels) and inflammation (infiltration of macrophages/monocytes, measured by ED-1 staining) are assessed. Ex vivo peritoneal function can be assessed by measuring the dialysate-to-plasma ratio of creatinine (D/P Cr) and ultrafiltration volume during a peritoneal equilibration test (PET) before euthanasia. This model is used to study the role of glucose degradation products (GDPs), including 3-deoxy-galactosone, in PD-related peritoneal damage and to test potential protective interventions. Approach 3 - Direct intravenous or intraperitoneal injection of 3-deoxy-galactosone in mice to study acute effects: 6-8 week old male mice (20-25 g) are injected intraperitoneally with a single dose of 3-deoxy-galactosone (e.g., 50-500 mg/kg) or vehicle (saline). Blood and tissue samples are collected 1-24 hours post-injection. The compound‘s very short half-life due to rapid reaction with plasma proteins makes it difficult to detect the parent compound, but downstream markers (oxidative stress, AGE formation, inflammatory cytokines) can be measured as endpoints. Given the lack of detailed published in vivo study protocols specifically optimized for 3-deoxy-galactosone in standard supplier datasheets, the above approaches are based on established protocols for the study of dicarbonyl compounds and GDPs in the published literature. 3-Deoxy-galactosone is not itself a therapeutic agent, and these in vivo applications are for research purposes only, aimed at understanding the pathophysiology of galactosemia, peritoneal dialysis complications, and glycation-related diseases.

As a reactive dicarbonyl compound, 3-deoxy-galactosone is rapidly cleared from the circulation due to its high reactivity with plasma proteins (primarily albumin), thiols (such as glutathione), and other nucleophiles. Following injection or absorption, the compound is quickly eliminated through these covalent adduction reactions, resulting in a very short half-life (likely on the order of minutes). The pharmacokinetic behavior of 3-deoxy-galactosone is characterized by its instability in biological matrices rather than by conventional PK parameters (Cmax, Tmax, AUC, t½) as typically defined for drug molecules. In vitro, the compound‘s stability in buffer and biological fluids (plasma, serum, tissue homogenates) can be measured by spiking a known concentration (e.g., 10-100 microM) and incubating at 37degC, with aliquots withdrawn at various times (0, 5, 15, 30, 60, 120 minutes) and analyzed by LC-MS after derivatization with O-(2,3,4,5,6-pentafluorobenzyl)hydroxylamine (PFBHA) or other carbonyl-reactive derivatizing agents. The half-life is calculated from the exponential decay curve. 3-Deoxy-galactosone is primarily eliminated by covalent adduction to proteins and reaction with glutathione (forming conjugates that are further metabolized and excreted in urine or bile). The compound is also reduced by aldo-keto reductases to 3-deoxy-galactitol. In the context of galactosemia, the metabolism of 3-deoxy-galactosone may be partially dependent on the aldo-keto reductase pathway. For analytical purposes, 3-deoxy-galactosone is used as a reference standard to quantify its concentration in biological samples (plasma, urine, tissue) and pharmaceutical formulations (peritoneal dialysis solutions, parenteral nutrition solutions). Detection is typically performed by HPLC-UV (after derivatization with agents such as 2,4-dinitrophenylhydrazine, DNPH, forming hydrazone derivatives with strong UV absorbance) or by LC-MS/MS (more sensitive and specific). In peritoneal dialysis (PD) solutions, 3-deoxy-galactosone is measured as part of the GDP profile to ensure product quality and safety. The compound is not administered as a therapeutic, and its own ADME (absorption, distribution, metabolism, excretion) is not studied in the same sense as for a drug candidate. However, its formation, reactivity, and elimination are studied in the context of chemical toxicology and food science. Detailed PK parameters are not available in standard supplier datasheets; the primary focus is on the compound‘s stability, reactivity, and analytical quantitation.

3-Deoxy-galactosone is a reactive dicarbonyl compound that can cause cellular damage through glycation and oxidative stress, and prolonged exposure is associated with cytotoxicity and tissue injury. The compound is not a drug, and formal toxicity studies (e.g., LD₅0, repeat-dose toxicity, genotoxicity, carcinogenicity) have not been conducted for 3-deoxy-galactosone itself. However, its toxicity is inferred from the known pathogenicity of elevated dicarbonyl compounds in conditions such as galactosemia and from studies using galactose-fed animals or GDP-containing peritoneal dialysis solutions. In galactose-fed rodents (a model of galactosemia), elevated 3-deoxy-galactosone levels are associated with development of cataracts (due to glycation of lens crystallins), cognitive impairment (due to AGE accumulation in brain and RAGE-mediated neuroinflammation), liver damage (steatosis, inflammation, fibrosis), and ovarian dysfunction (reduced follicle numbers, impaired oocyte quality). These toxic effects are mediated by 3-deoxy-galactosone through AGE/RAGE and oxidative stress pathways rather than by direct acute toxicity. In vitro, 3-deoxy-galactosone is cytotoxic to various cell types at millimolar concentrations (LC₅0 values typically in the range of 1-10 mM, depending on cell type and exposure duration), but lower concentrations (100-500 microM) induce sub-lethal effects such as oxidative stress, inflammation, and apoptosis over extended periods. The compound is known to deplete cellular glutathione, making cells more vulnerable to oxidative damage. In the context of peritoneal dialysis (PD), 3-deoxy-galactosone is present in conventional PD fluids at concentrations that, while low (micromolar), contribute over years of treatment to cumulative peritoneal damage, including loss of ultrafiltration capacity, peritoneal fibrosis, and angiogenesis. Therefore, efforts are made by PD solution manufacturers to minimize GDP formation (including 3-deoxy-galactosone) through the use of improved sterilization methods (e.g., heat sterilization at lower temperatures, use of multi-chamber bags, or filtration sterilization) or by using alternative buffer systems (e.g., bicarbonate/lactate-buffered solutions). 3-Deoxy-galactosone is not intended for human consumption, and as a research chemical, appropriate safety precautions should be taken during handling to avoid skin contact, eye contact, and inhalation, as the compound may cause irritation and has the potential to react with biomolecules in exposed tissues. The Material Safety Data Sheet (MSDS) for 3-deoxy-galactosone should be consulted for specific hazard information, but based on its chemical reactivity, it should be handled as a potential health hazard. In research applications, appropriate personal protective equipment (PPE - gloves, lab coat, eye protection) should be used, and the compound should be handled in a fume hood or well-ventilated area to avoid inhalation of dust (if in solid form) or aerosols (if in solution).

[1]. 3-Deoxygalactosone, a new glucose degradation product in peritoneal dialysis fluids: identification, quantification by HPLC/DAD/MSMS and its pathway of formation. Anal Bioanal Chem. 2011 Feb;399(4):1689-97.

[2]. 3-deoxygalactosone, a "new" 1,2-dicarbonyl compound in milk products. J Agric Food Chem. 2010 Oct 13;58(19):10752-60.

3-Deoxy-galactosone (CAS# 4134-97-8) is a research-grade analytical standard and a tool compound for the study of Maillard reaction intermediates, galactose degradation products, and the formation of advanced glycation end-products (AGEs). It is also known as 3-deoxy-D-galactosone and 3-deoxy-galacto-2-ulose. The compound has a molecular weight of 162.14 and a molecular formula of C₆H10O₅. It is a 1,2-dicarbonyl compound derived from galactose, and it is structurally analogous to 3-deoxyglucosone (3-DG) but with the epimer configuration at carbon 4 corresponding to D-galactose rather than D-glucose. 3-Deoxy-galactosone is formed in foods during Maillard reaction and caramelization, contributing to the color, flavor, and aroma development during cooking and food processing. It is also formed during heat sterilization of medical solutions such as peritoneal dialysis (PD) fluids and parenteral nutrition solutions, where it is considered a glucose (or galactose) degradation product (GDP). In research, 3-deoxy-galactosone is used for multiple applications: (1) as an analytical reference standard for the detection and quantification of GDPs in PD solutions, pharmaceutical formulations, and food products using HPLC-UV, GC-MS, or LC-MS/MS (after derivatization with agents such as O-(2,3,4,5,6-pentafluorobenzyl)hydroxylamine (PFBHA) or 2,4-dinitrophenylhydrazine (DNPH)); (2) as a model dicarbonyl compound to study the kinetics of glycation reactions and to evaluate the efficacy of AGE inhibitors and dicarbonyl scavengers; (3) as a tool to induce protein glycation in vitro for the production of AGE-modified proteins for use as antigens in immunoassays or for structural studies; (4) in cell culture studies to investigate the mechanisms of dicarbonyl-induced cellular damage (oxidative stress, inflammation, apoptosis) in the context of galactosemia, diabetic complications, and dialysis-related toxicity; (5) in animal models of galactosemia and peritoneal dialysis to study pathophysiology and to test potential protective interventions; (6) in food science to understand the role of galactose degradation in food quality and safety. The compound is typically stored as a solid at -20degC (or at -80degC for long-term storage) to maintain stability, as it is prone to decomposition (polymerization, further degradation) under ambient conditions. It is soluble in water and organic solvents such as methanol, ethanol, and DMSO. 3-Deoxy-galactosone is not an approved drug and has no therapeutic indications. It is intended for laboratory use only and is not for human consumption. Purity of commercially available reference standards is typically 90% or higher (e.g., 90%, 95%, 98%) depending on the supplier and batch. When using 3-deoxy-galactosone in cell culture or biological assays, it is important to note that the compound can react with media components (amino acids, serum proteins), potentially reducing its effective concentration over time, and the pH of the medium should be monitored. The compound‘s reactivity with thiols such as glutathione means that it can impact cellular redox status. For analytical method development, 3-deoxy-galactosone serves as an important marker compound for assessing the quality of galactose-containing products and for monitoring the degradation of galactose under various processing and storage conditions. In conclusion, 3-deoxy-galactosone is a valuable research standard in glycation chemistry, food science, and pharmaceutical analysis, but it is not a drug candidate and its research applications are primarily in the fields of biochemistry, toxicology, and pharmaceutical quality control.

C₆H₁₀O₅

162.14

162.052

4134-97-8

3513658

Typically exists as solid at room temperature

1.5±0.1 g/cm3

440.7±45.0 °C at 760 mmHg

191.9±22.2 °C

0.0±2.4 mmHg at 25°C

1.555

-1.76

3

5

1

11

157

0

C1[C@H](C(CO)OC(C1=O)O)O

UHPMJDGOAZMIID-UHFFFAOYSA-N

InChI=1S/C6H10O5/c7-2-5-3(8)1-4(9)6(10)11-5/h3,5-8,10H,1-2H2

2,5-dihydroxy-6-(hydroxymethyl)oxan-3-one

3Deoxygalactosone; 3 Deoxy galactosone

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.)