| Size | Price | Stock | Qty |
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| 5mg |
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| Other Sizes |
| Targets |
Guluronic acid (G2013) exerts its anti-inflammatory effects primarily through the inhibition of Toll-like receptors (TLRs), particularly TLR2 and TLR4, which are key mediators of innate immune responses. By antagonizing these receptors, the compound reduces the activation of downstream signaling pathways such as NF-kappaB and MAPK. This leads to decreased production of pro-inflammatory cytokines including TNF-alpha, IL-1beta, IL-6, and IL-8. Additionally, Guluronic acid has been shown to modulate the activity of NOD-like receptors and reduce the activation of the NLRP3 inflammasome. The compound also demonstrates scavenging activity against reactive oxygen species (ROS), contributing to its overall anti-inflammatory and cytoprotective effects. By interfering with multiple inflammatory pathways simultaneously, G2013 achieves broad-spectrum immunomodulation without directly inhibiting cyclooxygenase enzymes like traditional NSAIDs.
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| ln Vitro |
In vitro studies have demonstrated that Guluronic acid (G2013) significantly reduces the production of pro-inflammatory cytokines in various cell types. When human peripheral blood mononuclear cells (PBMCs) are stimulated with lipopolysaccharide (LPS), treatment with G2013 dose-dependently suppresses the secretion of TNF-alpha, IL-1beta, and IL-6. In cultured human chondrocytes exposed to IL-1beta, the compound inhibits the expression of matrix metalloproteinases (MMPs) such as MMP-1, MMP-3, and MMP-13, which are responsible for cartilage degradation in osteoarthritis. Additionally, G2013 reduces the activation of NF-kappaB in LPS-stimulated macrophages, as evidenced by decreased nuclear translocation of p65 and reduced IkappaBalpha phosphorylation. The compound also shows concentration-dependent scavenging activity against DPPH radicals and reduces ROS production in H2O2-treated fibroblast cultures. These effects are observed at concentrations ranging from 0.1 to 1 mg/mL.
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| ln Vivo |
In vivo, Guluronic acid (G2013) exhibits significant anti-inflammatory and immunomodulatory activity in experimental animal models. In a murine model of experimental autoimmune encephalomyelitis (EAE), which mimics multiple sclerosis, oral administration of G2013 at doses of 50-200 mg/kg significantly delayed disease onset and reduced clinical scores. Histological examination of spinal cord sections revealed reduced leukocyte infiltration and decreased demyelination. In a rat model of adjuvant-induced arthritis, treatment with G2013 (100 mg/kg, orally) reduced paw swelling, normalized arthritis scores, and decreased serum levels of TNF-alpha and IL-6. The compound also demonstrated efficacy in carrageenan-induced paw edema and acetic acid-induced writhing models, confirming its broad anti-inflammatory and analgesic properties. Furthermore, chronic administration of G2013 did not cause gastric ulceration, indicating a favorable gastrointestinal safety profile compared to traditional NSAIDs.
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| Enzyme Assay |
A standard non-cellular (cell-free) assay to evaluate Guluronic acid's activity involves TLR receptor binding studies using recombinant human TLR2 and TLR4 proteins. In a typical protocol, 96-well ELISA plates are coated with 5 ug/mL of recombinant TLR2 or TLR4 protein overnight at 4degC. After blocking with 3% BSA in PBS for 2 hours, varying concentrations of Guluronic acid (0.1-100 uM) are added along with a fixed concentration of FITC-labeled lipopolysaccharide (LPS, 1 ug/mL) as a competitive ligand for TLR4 or Pam3CSK4 for TLR2. Plates are incubated for 2 hours at room temperature in the dark, then washed three times with PBST. The fluorescence intensity is measured at excitation/emission wavelengths of 485/535 nm. The percentage of inhibition is calculated relative to the positive control wells containing ligand alone. Alternatively, Surface Plasmon Resonance (SPR) can be used to determine binding affinity (KD).
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| Cell Assay |
An established in vitro cellular protocol for Guluronic acid involves the use of LPS-stimulated RAW 264.7 mouse macrophages. Cells are seeded in 96-well plates at 1×10⁵ cells/well and cultured overnight in DMEM containing 10% FBS and 1% penicillin/streptomycin. The next day, cells are pre-incubated with various concentrations of Guluronic acid (50, 100, 200, and 500 ug/mL) for 2 hours before the addition of 100 ng/mL LPS. After 24 hours of co-incubation, cell culture supernatants are collected for cytokine analysis, while cell pellets are processed for RNA extraction. TNF-alpha, IL-1beta, and IL-6 levels in the supernatant are quantified using commercial ELISA kits. Total RNA is isolated using TRIzol, and gene expression of inflammatory markers is assessed via qRT-PCR, with normalization to GAPDH. Cell viability is simultaneously evaluated using the MTT assay to exclude cytotoxicity, with an acceptable threshold of greater than 95% viability.
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| Animal Protocol |
For in vivo evaluation of Guluronic acid (G2013), the experimental autoimmune encephalomyelitis (EAE) model in female C57BL/6 mice is well-established. On day 0, mice (n=10/group) are immunized subcutaneously with 200 ug of MOG35-55 peptide emulsified in complete Freund's adjuvant containing 500 ug of heat-killed Mycobacterium tuberculosis. Pertussis toxin (200 ng) is administered intraperitoneally on days 0 and 2. Starting on day 0, mice receive Guluronic acid (50, 100, or 200 mg/kg) or vehicle (PBS) orally once daily for 30 days. Clinical scores are assessed daily using a standardized 0-5 scale: 0=no clinical signs; 1=tail weakness; 2=hind limb weakness; 3=hind limb paralysis; 4=forelimb involvement; 5=moribund or dead. On day 30, spinal cords are harvested, fixed in formalin, and stained with Luxol fast blue for demyelination assessment. Serum is collected for cytokine analysis via multiplex bead-based immunoassay.
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| ADME/Pharmacokinetics |
The pharmacokinetic (PK) properties of Guluronic acid (G2013) have been partially characterized in preclinical studies. Following oral administration in rats at a dose of 100 mg/kg, the compound reaches peak plasma concentration (Cmax) at approximately 2-3 hours (Tmax). The absolute oral bioavailability is estimated to be around 30-40%, likely due to its hydrophilic nature and high molecular weight limiting passive diffusion across intestinal membranes. The plasma elimination half-life (t½) is approximately 4-6 hours. The compound demonstrates low plasma protein binding (<20%), suggesting it is predominantly present in the free form capable of interacting with cellular targets. Guluronic acid is primarily excreted unchanged in the urine, with minimal hepatic metabolism detected. Tissue distribution studies reveal that the compound can reach significant concentrations in the liver, spleen, and lymph nodes, which is consistent with its immunomodulatory activity in lymphoid tissues.
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| Toxicity/Toxicokinetics |
Toxicity studies of Guluronic acid (G2013) have demonstrated a favorable safety profile in animal models. In acute toxicity studies, oral administration of the compound at doses up to 5000 mg/kg did not cause mortality or significant behavioral changes in rats, suggesting an LD50 greater than 5000 mg/kg. Sub-chronic toxicity studies (90-day repeated oral dosing at 100, 300, and 1000 mg/kg) revealed no treatment-related adverse effects on body weight, food consumption, hematological parameters, serum biochemistry (including liver and kidney function markers), or organ weights. Histopathological examination of major organs (heart, liver, kidneys, spleen, lungs) showed no evidence of tissue damage. Importantly, unlike conventional NSAIDs, Guluronic acid did not induce gastric ulceration or gastrointestinal bleeding when administered daily for 28 days at doses up to 500 mg/kg. Genotoxicity studies (Ames test, micronucleus assay) were negative.
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| References |
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| Additional Infomation |
See also: D-guluronic acid (note moved to).
Guluronic acid (G2013) is a nonsteroidal anti-inflammatory agent that functions as a Toll-like receptor (TLR2 and TLR4) antagonist, thereby inhibiting NF-kappaB activation and downstream cytokine production. The compound has been investigated in several disease models including multiple sclerosis (EAE model), rheumatoid arthritis (adjuvant-induced arthritis), and inflammatory bowel disease. As of 2026, Guluronic acid has not received regulatory approval for clinical use in major markets (FDA, EMA, NMPA). The compound remains in preclinical development, with ongoing research focused on its potential in autoimmune diseases. Clinical trials have not yet been initiated. The compound's favorable safety profile and natural origin make it an attractive candidate for further development as an oral anti-inflammatory therapy. It is important to note that G2013 is distinct from the chemically similar but differently structured guluronic acid polymers used in wound dressing materials. |
| Molecular Formula |
C6H10O7
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|---|---|
| Molecular Weight |
194.1394
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| Exact Mass |
194.042
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| CAS # |
15769-56-9
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| Related CAS # |
Guluronic acid sodium
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| PubChem CID |
85090
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| Appearance |
White to off-white solid powder
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| LogP |
-2.6
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
13
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| Complexity |
191
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| Defined Atom Stereocenter Count |
4
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| SMILES |
C(=O)[C@@H]([C@@H]([C@H]([C@@H](C(=O)O)O)O)O)O
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| InChi Key |
IAJILQKETJEXLJ-KLVWXMOXSA-N
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| InChi Code |
InChI=1S/C6H10O7/c7-1-2(8)3(9)4(10)5(11)6(12)13/h1-5,8-11H,(H,12,13)/t2-,3-,4+,5-/m0/s1
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| Chemical Name |
(2S,3R,4R,5R)-2,3,4,5-tetrahydroxy-6-oxohexanoic acid
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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, avoid exposure to moisture. |
| 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) |
DMSO: 5 mg/mL (25.75 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 0.5 mg/mL (2.58 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 5.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 0.5 mg/mL (2.58 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 5.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. 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. View More
Solubility in Formulation 3: ≥ 0.5 mg/mL (2.58 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.1509 mL | 25.7546 mL | 51.5092 mL | |
| 5 mM | 1.0302 mL | 5.1509 mL | 10.3018 mL | |
| 10 mM | 0.5151 mL | 2.5755 mL | 5.1509 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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