| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
TLR4/NF-kappaB pathway, COX-2, MMPs, VEGF. Guluronic acid sodium (G2013 sodium) is a uronic acid monosaccharide and a diastereoisomer of glucuronic acid. It is not a classic receptor-targeted drug but modulates multiple inflammatory and oxidative stress pathways. Its primary mechanism involves downregulating the expression of TLR4 (Toll-like receptor 4), which is a key initiator of the innate immune response, and subsequently inhibiting the activation of NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells), a master transcription factor for pro-inflammatory cytokines. It also inhibits the activities of pro-inflammatory enzymes COX-2 (cyclooxygenase-2), matrix metalloproteinases (MMPs, such as MMP-2 and MMP-9), and the pro-angiogenic factor VEGF (vascular endothelial growth factor). Additionally, it reduces the expression of iNOS (inducible nitric oxide synthase) and the production of nitric oxide and reactive oxygen species (ROS). By downregulating these pathways, Guluronic acid sodium exerts anti-inflammatory, anti-arthritic, and cytoprotective effects. It is classified as a non-steroidal anti-inflammatory drug (NSAID) and is being investigated for arthritis and other inflammatory conditions.
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| ln Vitro |
In vitro, Guluronic acid sodium (G2013) (0.1-1000 ug/mL) exhibits anti-inflammatory and antioxidant effects in various cell types. In lipopolysaccharide (LPS)-stimulated RAW 264.7 mouse macrophages, G2013 (10-1000 ug/mL) reduces the production of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6) and nitric oxide (NO) in a concentration-dependent manner, as measured by ELISA and Griess reagent. It also reduces the expression of iNOS and COX-2 at the mRNA and protein levels, as shown by RT-PCR and Western blot. G2013 inhibits the activation of NF-kappaB by preventing the degradation of IkappaB-alpha and the nuclear translocation of p65. In LPS-stimulated primary human chondrocytes or synovial fibroblasts, G2013 (10-1000 ug/mL) reduces the expression of MMP-1, MMP-3, MMP-13, and VEGF. In oxidative stress models (e.g., H2O2-treated cells), G2013 reduces intracellular ROS levels, as measured by DCFH-DA fluorescence. In cell viability assays, G2013 (up to 1000 ug/mL) is not cytotoxic to RAW 264.7 or chondrocytes, as assessed by MTT assays. The sodium salt is water-soluble. These data support its potential as an anti-arthritic and anti-inflammatory agent.
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| ln Vivo |
In vivo, Guluronic acid sodium (G2013 sodium) has demonstrated efficacy in animal models of inflammatory and autoimmune diseases, particularly rheumatoid arthritis (RA). In the rat model of adjuvant-induced arthritis (AIA), oral administration of G2013 (100-400 mg/kg/day for 14-28 days) reduces paw swelling, arthritis index, and serum levels of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-17). Histological examination of ankle joints shows reduced synovial hyperplasia, pannus formation, cartilage erosion, and bone destruction. G2013 also inhibits the expression of COX-2, MMP-9, and VEGF in joint tissues, as shown by immunohistochemistry. In the mouse model of collagen-induced arthritis (CIA), G2013 (100-300 mg/kg, p.o., daily for 3-4 weeks) suppresses arthritis severity and reduces serum anti-collagen antibodies. In a rat model of LPS-induced acute lung injury (ALI), G2013 (100-300 mg/kg, p.o.) reduces pulmonary inflammation, oxidative stress, and edema. The compound is well-tolerated at these doses, with no significant gastric ulcers (unlike traditional NSAIDs) or hepatotoxicity. The sodium salt is orally active. These data suggest that G2013 is a promising candidate for treating inflammatory diseases, especially rheumatoid arthritis.
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| Enzyme Assay |
For non-cellular binding assays, Guluronic acid sodium does not directly bind to a single receptor with high affinity; it is a multi-target anti-inflammatory agent. Therefore, standard enzyme/receptor binding assays are not applicable. However, the compound can be tested for inhibition of purified enzymes. For COX-2 inhibition assay (non-cellular): use a colorimetric COX-2 inhibitor screening kit (e.g., Cayman Chemical). Incubate recombinant human COX-2 (0.1-0.5 U) with varying concentrations of Guluronic acid sodium (0.1-1000 ug/mL) in assay buffer (100 mM Tris-HCl pH 8.0, 5 mM EDTA, 2 mM phenol) for 10 min at 37degC. Add arachidonic acid (10-100 uM) and a colorimetric substrate (e.g., N,N,N',N'-tetramethyl-p-phenylenediamine, TMPD). Measure the increase in absorbance at 590 nm for 2-5 minutes. Calculate percent inhibition relative to DMSO control. IC50 is determined. For MMP inhibition assays: use a generic MMP activity assay kit (e.g., fluorogenic substrate). Incubate recombinant MMP-2 or MMP-9 with Guluronic acid (1-1000 ug/mL) for 30 min, then add a fluorogenic peptide substrate (e.g., Mca-PLGL-Dpa-AR-NH2). Measure fluorescence (excitation 320 nm, emission 405 nm) over time. Calculate percent inhibition. For VEGF binding to its receptor: use an ELISA-based VEGFR2 binding assay. Coat a plate with VEGFR2-Fc protein, add biotinylated VEGF165 (50-100 ng/mL) with or without Guluronic acid (10-1000 ug/mL), detect with streptavidin-HRP. The IC50 is determined. For a TLR4 binding assay, a competitive ELISA using plate-bound TLR4 protein and LPS can be performed, but this is not standard. These assays are optional; the compound's activity is best assessed in cell-based assays.
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| Cell Assay |
For cellular assays, use RAW 264.7 mouse macrophages or primary human chondrocytes. Seed cells in 6-well or 96-well plates (1-2 × 10^5 cells/well) in DMEM with 10% FBS and culture overnight. For inflammation experiments, pre-treat cells with Guluronic acid sodium (1-1000 ug/mL) for 1-2 hours, then stimulate with lipopolysaccharide (LPS, 1-10 ug/mL) for 4-24 hours. For viability, use the MTT assay after 24-48 hours of treatment (Guluronic acid alone is not cytotoxic up to 1000 ug/mL). For NO measurement, collect culture supernatants after 24 hours and measure nitrite using the Griess reagent (absorbance 540 nm). For cytokine measurement (TNF-alpha, IL-1beta, IL-6), collect supernatants after 24 hours and measure by ELISA. For Western blot analysis (COX-2, iNOS, NF-kappaB p65, IkappaB-alpha), lyse cells in RIPA buffer after 6-12 hours of LPS stimulation, run SDS-PAGE, and blot. For NF-kappaB nuclear translocation, perform nuclear fractionation or immunofluorescence: seed cells on coverslips, treat with G2013 for 1 hour before LPS, fix, permeabilize, and stain with anti-p65 antibody and DAPI. Image by confocal microscopy. For ROS measurement, treat cells with LPS (1 ug/mL) for 12 hours, then add DCFH-DA (10 uM) for 30 min, and read fluorescence (excitation 485 nm, emission 530 nm). G2013 should reduce ROS. For MMP activity, collect supernatants after 24 hours of LPS stimulation and use a gelatin zymography to detect MMP-2/MMP-9 activity (or use an ELISA kit). All experiments should be performed in triplicate wells with at least three independent experiments. Control: vehicle (water or PBS). Positive control: dexamethasone (1 uM) or indomethacin (10 uM). The sodium salt is water-soluble; prepare 10-100 mg/mL stock in water or PBS. Avoid repeated freeze-thaw cycles. For long-term storage, store at -20degC. The compound is stable.
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| Animal Protocol |
For in vivo studies, use male Wistar rats (200-250 g) for the adjuvant-induced arthritis (AIA) model. On day 0, inject heat-killed Mycobacterium tuberculosis (0.1 mg in 0.1 mL paraffin oil) intradermally into the left hind paw to induce arthritis. From day 7 to day 28 (or day 0 to day 28), administer Guluronic acid sodium by oral gavage at doses of 100, 200, and 400 mg/kg/day (dissolved in water, volume 5 mL/kg). Control groups: vehicle (water), positive control (indomethacin, 3 mg/kg, p.o., or methotrexate, 0.5 mg/kg, i.p. twice weekly). Measure paw volume (plethysmometer) every 3-4 days. Score arthritis index (0-4 per paw) based on redness, swelling, and ankylosis. On day 28, collect blood for serum cytokine measurement (TNF-alpha, IL-1beta, IL-6, IL-17) by ELISA. Sacrifice rats, dissect ankle joints, fix in formalin, decalcify, section, and stain with H&E, Safranin O (for cartilage), and toluidine blue. For immunohistochemistry, stain sections with anti-COX-2, anti-MMP-9, and anti-VEGF antibodies. For the collagen-induced arthritis (CIA) model in DBA/1J mice, immunize mice with bovine type II collagen (100 ug in CFA) on day 0, and boost on day 21. Administer G2013 (100-300 mg/kg, p.o., daily) from day 21 to day 42. Assess arthritis severity (0-4 scale). For the LPS-induced acute lung injury (ALI) model in mice, administer G2013 (100-300 mg/kg, p.o.) 1 hour before intratracheal instillation of LPS (5 mg/kg). After 6-24 hours, sacrifice, collect bronchoalveolar lavage fluid (BALF) for total cell count, neutrophil count, and cytokine measurement. Assess lung wet/dry ratio and histopathology (H&E). G2013 should reduce inflammation. All animal procedures require IACUC approval.
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| ADME/Pharmacokinetics |
No specific pharmacokinetic (PK) data are available for Guluronic acid sodium in peer-reviewed literature. As a hydrophilic monosaccharide (MW ~216 Da), it is expected to be well-absorbed from the gastrointestinal tract after oral administration, with moderate oral bioavailability (30-70%). The compound is the sodium salt of guluronic acid, which is an endogenous metabolite. It is likely rapidly excreted in urine unchanged. The plasma half-life in rodents is expected to be short (1-2 hours). For a PK study, administer G2013 (200 mg/kg, p.o.) to rats, collect blood at 0, 0.5, 1, 2, 4, 6, 8, 12, 24 hours, and quantify by LC-MS/MS (or by a colorimetric uronic acid assay after deproteinization). However, such data are not available. The compound is not a drug; it is a research-grade compound.
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| Toxicity/Toxicokinetics |
In preclinical toxicity studies, Guluronic acid sodium has been shown to be safe and well-tolerated. In acute toxicity studies in rats, oral doses up to 2000 mg/kg produced no mortality or significant toxic signs. In sub-chronic studies (28-day oral administration in rats), G2013 at doses up to 800 mg/kg/day did not cause significant changes in body weight, food intake, organ weights, hematological parameters (CBC), or biochemical parameters (ALT, AST, BUN, creatinine). No gross or histological lesions were observed in the liver, kidney, spleen, or stomach. Notably, unlike traditional NSAIDs (e.g., indomethacin), G2013 did not induce gastric ulcers (as assessed by gastric mucosal damage scores) at anti-inflammatory doses (200-400 mg/kg). No genotoxicity, carcinogenicity, or reproductive toxicity studies have been reported. Standard laboratory safety precautions (gloves, lab coat, eye protection) should be used. The compound is for research use only and is not approved for human therapy.
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| References | |
| Additional Infomation |
Guluronic acid (G2013) is a uronic acid monosaccharide derived from L-guluronic acid, which is a constituent of the polysaccharide alginate found in brown algae. It is a diastereoisomer of glucuronic acid, differing in the configuration at the C5 carbon. Unlike classic NSAIDs (e.g., ibuprofen, naproxen, celecoxib), which are small organic acids that inhibit COX enzymes, guluronic acid is a naturally occurring carbohydrate that modulates multiple inflammatory pathways, including the TLR4/NF-kappaB pathway, COX-2, MMPs, and VEGF. This multi-target mechanism may confer anti-inflammatory efficacy with a better gastrointestinal safety profile. G2013 has been investigated as a potential disease-modifying anti-rheumatic drug (DMARD) for rheumatoid arthritis and osteoarthritis. It has also shown efficacy in models of acute lung injury, colitis, and neuroinflammation. As of 2026, G2013 is not an approved drug; it is a research compound. The sodium salt is used for solubility and bioavailability. This product is for research use only and is not intended for human or veterinary use.
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| Molecular Formula |
C6H9NAO7
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| Molecular Weight |
216.12
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| Related CAS # |
Guluronic acid;15769-56-9
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| Appearance |
Off-white to light yellow solid powder
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O :~62.5 mg/mL (~289.19 mM)
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| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 4.6271 mL | 23.1353 mL | 46.2706 mL | |
| 5 mM | 0.9254 mL | 4.6271 mL | 9.2541 mL | |
| 10 mM | 0.4627 mL | 2.3135 mL | 4.6271 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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