| Size | Price | |
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| 500mg | ||
| 1g | ||
| Other Sizes |
| ln Vitro |
ODZ10117 (5-40 μM; 6 h) showed no significant cytotoxicity to mouse bone marrow-derived macrophages after incubation at concentrations up to 40 μM for 6 hours [1]. ODZ10117 (5-20 μM; 1 h pretreatment) dose-dependently inhibited NLRP3 inflammasome-mediated IL-1β release and pyroptosis in LPS-pretreated mouse bone marrow-derived macrophages treated with ATP, nigra, silica crystals, or imiquimod, with the strongest inhibitory effect at 20 μM [1]. ODZ10117 (5-20 μM; 1 h pretreatment) inhibited the activation of the NLRP3 inflammasome in LPS-pretreated mouse bone marrow-derived macrophages by inhibiting the cleavage of caspase-1, IL-1β, and GSDMD, without altering the expression levels of core inflammasome components [1]. ODZ10117 (5-20 μM; 1 h pretreatment) did not inhibit the activation of AIM2 or NLRC4 inflammasomes in LPS-pretreated mouse bone marrow-derived macrophages, indicating its specificity for NLRP3 inflammasomes [1]. ODZ10117 (5-20 μM; 1 h pretreatment) dose-dependently inhibited NLRP3 inflammasome-mediated ASC translocation, oligomerization, and speckle formation in LPS-pretreated mouse bone marrow-derived macrophages without affecting ASC dynamics during AIM2 or NLRC4 inflammasome activation [1]. ODZ10117 (20 μM) inhibited the interaction between NLRP3 and NEK7 in HEK293T cells overexpressing NLRP3 and NEK7 [1]. ODZ10117 (300-900 μM; incubated with cell lysate for 30 min) directly binds to NLRP3 and STAT3 in LPS-pretreated J774A.1 cell lysates, showing dose-dependent protection against protease degradation, but does not bind to NEK7 or caspase-1 [1]. ODZ10117 binds to the ADP binding pocket of the NLRP3 NACHT domain through multiple stable interactions, with a binding energy of -7.7 kcal/mol [1]. ODZ10117 binds tightly to the phosphotyrosine binding pocket of the STAT3 SH2 domain, with a Glide docking score of -6.17 kcal/mol, indicating that its binding affinity is higher than that of the known STAT3 inhibitors S3I-201 and STA-21 [2]. ODZ10117 (40 μM; 24 h) inhibited tyrosine phosphorylation of STAT3 in a variety of constitutively STAT3-activated human cancer cell lines, including HDLM-2, MDA-MB-231, HepG2, and U87MG[2]. ODZ10117 (40 μM; 24 h) inhibited IL-6-induced STAT3 tyrosine phosphorylation, which has been found in a variety of human cancer cell lines, including RPMI8226, MCF-7, and U251MG[2]. ODZ10117 (40 μM; 24 h) inhibited STAT3 homodimerization and tyrosine phosphorylation in transfected MDA-MB-231 breast cancer cells[2]. ODZ10117 (40 μM; 24 h) can induce apoptosis in MDA-MB-231 breast cancer cells by activating caspase-3 and PARP cleavage and downregulating anti-apoptotic proteins Bcl-2, Bcl-xL, Mcl-1 and survivin [2]. ODZ10117 (40 μM; 24 h) inhibits nuclear translocation of tyrosine phosphorylated STAT3 in MDA-MB-231 breast cancer cells [2]. ODZ10117 (2.5-40 μM; 24 h) inhibits the transcriptional activity of STAT3 in MDA-MB-231/STAT3-Luc breast cancer cells, with an IC50 of 7.5 μM after 24 hours of incubation [2]. ODZ10117 (40 μM; 0.5–12 h) inhibited tyrosine phosphorylation of STAT3 in MDA-MB-231 and MDA-MB-468 breast cancer cells, with the inhibition beginning 2 h after treatment [2]. ODZ10117 (10–40 μM; 9 h) inhibited tyrosine phosphorylation of STAT3 in MDA-MB-231 and MDA-MB-468 breast cancer cells in a concentration-dependent manner, and significantly inhibited tyrosine phosphorylation of STAT3 after incubation at concentrations ≥20 μM for 9 h [2]. ODZ10117 (40 μM; 16 h) specifically inhibited tyrosine phosphorylation of STAT3 without affecting other STAT family proteins, JAK kinases, or upstream signaling regulators Akt, Src, and ERK1/2 in MDA-MB-231 and MDA-MB-468 breast cancer cells [2]. After 24 hours of incubation, ODZ10117 (10-100 μM; 24 hours) reduced the viability of MDA-MB-231, MDA-MB-468, ZR-75-1 and 4T1 breast cancer cells in a concentration-dependent manner [2]. ODZ10117 (40 μM; 24 hours) increased apoptosis in MDA-MB-231 breast cancer cells, showing a 5-fold increase in Annexin V positive cells and a 3-fold increase in PI positive cells [2]. ODZ10117 (40 μM; 24 hours) downregulated the mRNA expression of STAT3-dependent anti-apoptotic genes Bcl-2, Bcl-xL, Mcl-1 and Survivin in MDA-MB-231 breast cancer cells [2]. ODZ10117 (40 μM; 24 hours) reduced the migration ability of MDA-MB-231 breast cancer cells in wound healing experiments [2]. ODZ10117 effectively and selectively inhibits the transcriptional activity of STAT3 in breast cancer cells, with an IC50 value of 7.5 μM[3]. ODZ10117 exerts its anticancer effect by directly blocking the SH2 domain of STAT3, inhibiting homodimerization and transcriptional activity, inducing apoptosis, and reducing cell migration and invasion[3]. ODZ10117 (10 μM; pretreatment for 12 hours) can enhance the survival rate of H2O2-treated SH-SY5Y human neuroblastoma cells by alleviating oxidative stress-induced cell damage[4]. ODZ10117 (10 μM; pretreatment for 12 hours) can inhibit H2O2-induced caspase-dependent apoptosis in SH-SY5Y human neuroblastoma cells[4]. ODZ10117 (10 μM; 1–12 h) inhibited STAT3 phosphorylation in SH-SY5Y human neuroblastoma cells and induced transient phosphorylation of ERK and CREB, with peak effects observed at 1 h [4]. ODZ10117 (10 μM; 1–12 h) upregulated the protein expression of memory-related IEG and BDNF in SH-SY5Y human neuroblastoma cells, with detectable increases beginning at 6 h [4]. ODZ10117 (10 μM; 3 h)-induced phosphorylation of CREB in SH-SY5Y human neuroblastoma cells was dependent on the ERK signaling pathway [4]. ODZ10117 (10 μM; 3–6 h) upregulated the mRNA expression of memory-related IEG in SH-SY5Y human neuroblastoma cells, peaking at 3 h [4]. The upregulation of memory-related IEG and BDNF proteins induced by ODZ10117 (10 μM; 12 h) in SH-SY5Y human neuroblastoma cells was dependent on the ERK signaling pathway [4]. ODZ10117 (10 μM; 12 h treatment) could alleviate H2O2-induced oxidative stress and caspase-dependent apoptosis in SH-SY5Y human neuroblastoma cells, a process dependent on the ERK signaling pathway [4].
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| ln Vivo |
ODZ10117 (5–20 mg/kg; intraperitoneal injection; single dose) dose-dependently reduced IL-1β release in a mouse model of monosodium urate (MSU)-induced peritonitis, with significant inhibitory effects observed at doses of 10 and 20 mg/kg [1]. ODZ10117 (5–20 mg/kg; intraperitoneal injection; two doses (12 hours and 2 hours before LPS administration, respectively)) dose-dependently reduced IL-1β release and improved survival in a mouse model of LPS-induced sepsis, with significant therapeutic effects observed at doses of 10 and 20 mg/kg [1]. ODZ10117 (1–10 mg/kg; intraperitoneal injection; 5 times weekly; for 23 days) dose-dependently inhibited the growth of orthotopic mammary tumors in BALB/c nude mice, with the 10 mg/kg dose group showing better tumor weight reduction than the 1 mg/kg dose group [2]. ODZ10117 (10 mg/kg; intratumoral injection; once every 2 days; for 2 weeks) inhibited the growth of subcutaneous mammary tumors in BALB/c nude mice and regulated STAT3-dependent apoptosis and metastasis markers in tumor tissue [2]. ODZ10117 (1-10 mg/kg; intraperitoneal injection; 5 times a week; for 3 weeks) inhibited the growth of primary tumors, reduced lung metastasis, and prolonged survival in a BALB/c mouse model of homologous breast cancer, with the 10 mg/kg dose showing better efficacy than the 1 mg/kg dose [2]. ODZ10117 (10 mg/kg; intratumoral injection) significantly reduced tumor growth and lung metastasis in BALB/c mice carrying MDA-MB-231 breast cancer xenografts [3].
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| Cell Assay |
Cytotoxicity assay [1]
Cell Types: Mouse bone marrow-derived macrophages (BMDM) Tested Concentrations: 5 μM; 10 μM; 20 μM; 40 μM Incubation Duration: 6 hours Experimental Results: At concentrations up to 40 μM, there was no significant cytotoxicity to BMDM, and cell viability was close to 100% at all test concentrations. Western Blot Analysis [1] Cell Types: LPS-pretreated mouse bone marrow-derived macrophages (BMDM) Tested Concentrations: 5 μM; 10 μM; 20 μM Incubation Duration: Pretreatment for 1 hour Experimental Results: Dose-dependently inhibited the cleavage of pro-caspase-1 to active caspase-1 (p20), pro-IL-1β to active IL-1β (p17), and full-length GSDMD to N-terminal GSDMD (N-GSDMD) in cell supernatant and lysis buffer. It had no effect on the steady-state protein levels of NLRP3, ASC, pro-caspase-1, pro-IL-1β, or full-length GSDMD in cell lysis buffer. Immunofluorescence [1] Cell Types: LPS-pretreated mouse bone marrow-derived macrophages (BMDM) Tested Concentrations: 5 μM; 10 μM; 20 μM Incubation Duration: Pretreatment for 1 hour Experimental Results: In BMDM treated with NLRP3 triggers (ATP, nigrain, silica crystals), ASC translocation to the Triton X-100 insoluble component, ASC oligomerization, and ASC spot formation were inhibited in a dose-dependent manner. At a concentration of 20 μM, ATP and nigrain triggers reduced ASC spot formation by approximately 50%. In BMDM treated with AIM2 or NLRC4 triggers, there was no effect on ASC translocation or spot formation.
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| Animal Protocol |
Animal/Disease Models:C57BL/6 (female, 6-8 weeks old, intraperitoneal injection of monosodium urate crystals at a dose of 50 mg/kg) [1]
Doses: 5 mg/kg; 10 mg/kg; 20 mg/kg Route of Administration: Intraperitoneal injection; single dose Experimental Results: Inhibited monosodium urate-induced IL-1β release in a dose-dependent manner. Compared with the monosodium urate injection group, the 10 mg/kg and 20 mg/kg dose groups showed significantly lower IL-1β levels (p < 0.01). Animal/Disease Models:C57BL/6 (female, 6-8 weeks old, intraperitoneal injection of LPS at a dose of 20 mg/kg)[1] Doses: 5 mg/kg; 10 mg/kg; 20 mg/kg Route of Administration: Intraperitoneal injection; two administrations (12 hours and 2 hours before LPS injection) Experimental Results: LPS-induced IL-1β release was inhibited in a dose-dependent manner. IL-1β levels were significantly lower in the 10 mg/kg and 20 mg/kg dose groups compared with the LPS-only group (p < 0.05). Improved Survival: At the 20 mg/kg dose, the survival rate remained at 60% within 80 hours, while the survival rate in the LPS-only group was 0% within 36 hours, a statistically significant difference (p < 0.05). Animal/Disease Models:BALB/c nude mice (6-week-old females, orthotopic xenografted by injecting MDA-MB-231 cells into the right fourth mammary fat pad) [2] Doses: 1 mg/kg; 10 mg/kg Route of Administration: Intraperitoneal injection; 5 times a week; for 23 days Experimental Results: Compared with the vector control group (approximately 2.4 g), the final tumor weight in the 1 mg/kg dose group was reduced to approximately 1.8 g. The 1 mg/kg dose group inhibited tumor growth over 22 days. The final tumor weight in the 10 mg/kg dose group was reduced to approximately 1.4 g. The 10 mg/kg dose group had a stronger inhibitory effect on tumor growth than the 1 mg/kg dose group. Neither dose affected mouse body weight. Animal/Disease Models:BALB/c nude mice (6-week-old females, xenograft tumors established by subcutaneous injection of MDA-MB-231 cells in the neck) [2] Doses: 10 mg/kg Route of Administration: Intratumoral injection; once every 2 days; for 2 weeks Experimental Results: The relative volume of the tumor was significantly inhibited within 14 days, with a final relative volume of approximately 2, while that of the vector control group was approximately 5. The number of tumor cells in the tumors of the treatment group was reduced. The levels of pY705-STAT3, Bcl-xL and pro-MMP-2 in the tumors of the treatment group were reduced. The level of active caspase-3 in the tumors of the treatment group was increased. Animal/Disease Models:BALB/c (6-week-old female mice, allogeneic transplantation, established by injection of 4T1-Luc cells into the right fourth mammary fat pad, spontaneous lung metastasis) [2] Doses: 1 mg/kg; 10 mg/kg Route of Administration: Intraperitoneal injection; 5 times a week; for 3 weeks Experimental Results: Primary tumor volume decreased at 21 days (1 mg/kg dose). Median survival in mice increased from 12 days to 20 days (1 mg/kg dose). The number of visible lung metastatic nodules decreased to approximately 22, compared to approximately 30 in the vector control group (1 mg/kg dose). The reduction in primary tumor volume was greater than that of 1 mg/kg dose (10 mg/kg dose). Median survival increased to 21 days (10 mg/kg dose). The number of visible lung metastatic nodules decreased to approximately 17 (10 mg/kg dose). No effect on mouse body weight (both doses). Animal/Disease Models:BALB/c[3] Doses: 10 mg/kg Route of Administration: Intratumoral injection Experimental Results: Significantly reduced tumor growth and lung metastasis. |
| References |
|
| Molecular Formula |
C10H5CL5N2O2
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|---|---|
| Molecular Weight |
362.42
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| CAS # |
1632152-27-2
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| Appearance |
Typically exists as solids at room temperature
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| SMILES |
ClC1=CC=C(C(Cl)=C1)OCC2=NOC(C(Cl)(Cl)Cl)=N2
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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 |
| 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) |
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
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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 | 2.7592 mL | 13.7961 mL | 27.5923 mL | |
| 5 mM | 0.5518 mL | 2.7592 mL | 5.5185 mL | |
| 10 mM | 0.2759 mL | 1.3796 mL | 2.7592 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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