Olsalazine
Based on 2 publication(s) in Google Scholar
Olsalazine is an orally active prodrug of 5-ASA (HY-15027). Olsalazine can inhibit cells proliferation and induce apoptosis. Olsalazine can reduce DAI and MPO activity and inhibit inflammatory cytokines levels. Olsalazine can be used for the researches of cancer, inflammation and metabolic disease, such as colorectal cancer, inflammatory bowel disease (IBD) and hyperuricemic.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 99.83%
- CAS. Nr.: 15722-48-2
- Formel: C14H10N2O6
- Molecular Weight:302.24
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Speicherung:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
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Lösungsmittel & Löslichkeit
- Protokoll
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
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HY-15027
5-Aminosalicylic AcidEndogenous Metabolite -
HY-14655
SulfasalazineAnti-rheumatic Agent -
HY-B0579
Cyclosporin ACalcineurin Inhibitor -
HY-B0290
PranlukastEndogenous Metabolite -
HY-13628
EtalocibLTB4 Receptor Antagonist -
HY-B0174AR
Olsalazine (Standard)Anticancer/Antiinflammation Agent -
HY-B0290R
Pranlukast (Standard)Endogenous Metabolite -
HY-107608
Leukotriene B4PROTAC linker -
HY-17492
ZafirlukastLeukotriene Receptor Antagonist -
HY-19989
MK-571ABCC1/MRP4 Inhibitor -
HY-19193
CP-105696LTB4 Receptor Antagonist -
HY-15744
LY255283LTB4 Receptor Antagonist
Publications Citing Use of MedChemExpress (MCE) Olsalazine
More
Biologische Aktivität
Beschreibung
IC50 & Target
IC50: 0.39 mM (LTB4)[1]
In Vitro
Olsalazine (0-30 μM, 48 h) reduces cell viability in canine lymphoid tumor cell[4].
Olsalazine (0.19-1.64 μM, 24 h) induces apoptosis in canine lymphoid tumor cell[4].
Olsalazine (0.03 μM, 48 h) increases 5-mC levels of genomic DNA in canine lymphoid tumor cell lines[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Olsalazine (50 mg/kg, p.o., daily for 11 days) ameliorates colitis companied with Cannabidiol in dextran sulphate sodium (DSS)-induced acute and chronic colitis mice models[2].
Olsalazine (Sodium) (5-20 mg/kg) decreases the levels of serum urate in hyperuricemic rats[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Colorectal cancer rats models[1]
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Dosage:25 mg/kg
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Administration:Orally gavage, daily for 3 weeks
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Result:Reduced the numbers of ACF and tumors.
Increased apoptotic cells and inhibited proliferation of tumor.
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Animal Model:Dextran sulphate sodium (DSS)-induced acute and chronic colitis mice models[2]
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Dosage:50 mg/kg, companied with Cannabidiol (10 mg/kg)
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Administration:Orally administration, daily for 11 days
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Result:Reduced DAI, MPO activity, and inflammatory cytokines.
Restored colon length and GLP-1 levels.
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Animal Model:Hyperuricemic rats[3]
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Dosage:5, 10 and 20 mg/kg (Olsalazine Sodium)
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Administration:Intraperitoneally injection
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Result:Reduced the levels of serum urate.
Reduced GLUT9, OAT3, OAT1 and NPT1 levels.
Chemical Information
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CAS. Nr. 15722-48-2
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Appearance Solid
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Molecular Weight 302.24
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Formel C14H10N2O6
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Color Light yellow to yellow
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SMILES
O=C(O)C1=C(O)C=CC(/N=N/C2=CC(C(O)=O)=C(O)C=C2)=C1
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Publications (2)
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Journal Impact Factor
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Most Recent
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Int J Biol Macromol
Reticuline isomerase AKR1B1 with aldo-keto reductase activity and detoxification function from the insect Blaps rhynchopetera. [Abstract]2026 Mar:352:151224. PMID: 41791543 -
Lösungsmittel & Löslichkeit
In Vitro:
DMSO : 20 mg/mL (66.17 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2 mg/mL (6.62 mM); Clear solution
This protocol yields a clear solution of ≥ 2 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protokoll
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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DSS-Induced Colitis
Dextran sulfate sodium (DSS)-induced colitis is generated by administering DSS in mouse drinking water, producing epithelial injury, barrier disruption, weight loss, diarrhea, fecal blood, colon shortening, histologic mucosal damage, and inflammatory mediator changes; the model is mainly used to study acute or chronic intestinal inflammation resembling selected features of ulcerative colitis. DSS injury is interpreted through clinical and tissue readouts rather than a single molecular endpoint: daily body weight, stool consistency, and bleeding are combined into a disease activity index, while colon length, histology, cytokines, myeloperoxidase activity, intestinal permeability, and tight-junction markers provide complementary measures of inflammation and barrier damage.
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TNBS-Induced Colitis
TNBS-induced colitis is produced by intrarectal delivery of 2,4,6-trinitrobenzene sulfonic acid in ethanol, where ethanol disrupts the mucosal barrier and TNBS haptenates colonic proteins, generating immune-mediated colonic inflammation with weight loss, diarrhea, ulceration, transmural injury, inflammatory-cell infiltration, and cytokine responses. The model is used as an experimental intestinal inflammation model with Crohn’s disease–like features, especially when Th1-type responses, IL-12–dependent inflammation, chronic relapsing inflammation, or fibrosis-related endpoints are studied.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Reinheit & Dokumentation
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Data Sheet (277 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Brown WA, et al. 5-aminosalicyclic acid and olsalazine inhibit tumor growth in a rodent model of colorectal cancer. Dig Dis Sci. 2000 Aug;45(8):1578-84. [Content Brief]
[2]. Thapa D, et al. Cannabidiol Enhances the Therapeutic Efficacy of Olsalazine and Cyclosporine in a Murine Model of Colitis. Int J Mol Sci. 2025 Aug 16;26(16):7913. [Content Brief]
[3]. Niu Y, et al. Olsalazine Sodium Increases Renal Urate Excretion by Modulating Urate Transporters in Hyperuricemic Animals. Biol Pharm Bull. 2020 Nov 1;43(11):1653-1659. [Content Brief]
[4]. Itoh S, et al. Olsalazine inhibits cell proliferation and DNA methylation in canine lymphoid tumor cell lines. Pol J Vet Sci. 2021 Dec;24(4):515-523. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
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| DMSO | 1 mM | 3.3086 mL | 16.5431 mL | 33.0863 mL | 82.7157 mL |
| 5 mM | 0.6617 mL | 3.3086 mL | 6.6173 mL | 16.5431 mL | |
| 10 mM | 0.3309 mL | 1.6543 mL | 3.3086 mL | 8.2716 mL | |
| 15 mM | 0.2206 mL | 1.1029 mL | 2.2058 mL | 5.5144 mL | |
| 20 mM | 0.1654 mL | 0.8272 mL | 1.6543 mL | 4.1358 mL | |
| 25 mM | 0.1323 mL | 0.6617 mL | 1.3235 mL | 3.3086 mL | |
| 30 mM | 0.1103 mL | 0.5514 mL | 1.1029 mL | 2.7572 mL | |
| 40 mM | 0.0827 mL | 0.4136 mL | 0.8272 mL | 2.0679 mL | |
| 50 mM | 0.0662 mL | 0.3309 mL | 0.6617 mL | 1.6543 mL | |
| 60 mM | 0.0551 mL | 0.2757 mL | 0.5514 mL | 1.3786 mL |
Olsalazine Related Classifications
HY-B0174A Related Classifications
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