2. JAK/STAT Signaling Stem Cell/Wnt Immunology/Inflammation Apoptosis
  3. STAT NOD-like Receptor (NLR) Apoptosis
  4. ODZ10117

ODZ10117 是一种 STAT3 和 NLRP3 抑制剂，其对人源 STAT3 SH2 结构域的 IC50 为 7.5 μM。ODZ10117 可结合 STAT3 SH2 结构域，抑制酪氨酸磷酸化、二聚化、核转位及转录活性。ODZ10117 可结合 NLRP3，破坏其与 NEK7 的相互作用，抑制炎症小体形成，并阻断 caspase-1 和 IL-1β 的切割。ODZ10117 可减少 MSU (HY-B2130A) 诱导的 IL-1β 释放，降低 LPS (HY-D1056) 诱导的脓毒症死亡率，具有抗炎作用。ODZ10117 可诱导细胞凋亡 (apoptosis)，抑制乳腺癌细胞的迁移与侵袭，减少肿瘤生长及肺转移，并延长乳腺癌模型小鼠的生存期。ODZ10117 可用于 MSU 诱导的腹膜炎、LPS 诱导的脓毒症、乳腺癌、胶质母细胞瘤及阿尔茨海默病的相关研究。

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ODZ10117

ODZ10117 Chemical Structure

CAS No. : 1632152-27-2

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ODZ10117 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

ODZ10117 is a STAT3 and NLRP3 inhibitor with a human STAT3 SH2 domain IC50 of 7.5 μM. ODZ10117 binds to the STAT3 SH2 domain, suppressing tyrosine phosphorylation, dimerization, nuclear translocation, and transcriptional activity. ODZ10117 binds to NLRP3, impairs NEK7 interaction, prevents inflammasome formation, and inhibits caspase-1 and IL-1β cleavage.ODZ10117 reduces MSU (HY-B2130A)-induced IL-1β release, lowers LPS (HY-D1056)-induced sepsis mortality, and exhibits anti-inflammatory effects. ODZ10117 induces apoptosis, suppresses breast cancer cell migration and invasion, reduces tumor growth and lung metastasis, and extends survival in breast cancer models. ODZ10117 can be used for the research of Monosodium urate (HY-B2130A)-induced peritonitis, LPS-induced sepsis, breast cancer, glioblastoma, and Alzheimer's disease[1][2][3][4].

IC50 & Target[1][3]

NLRP3

 

STAT3

7.5 μM (IC50)

体外研究
(In Vitro)

ODZ10117 (5-40 μM；6 小时) 在孵育 6 小时后，浓度高达 40 μM 时对小鼠骨髓来源巨噬细胞无显著细胞毒性[1]。
ODZ10117 (5-20 μM；1 小时预处理) 可剂量依赖性地抑制经 ATP、尼日利亚菌素、二氧化硅晶体或咪喹莫特处理的 LPS 预刺激小鼠骨髓来源巨噬细胞中 NLRP3 炎症小体介导的 IL-1β 释放和细胞焦亡，在 20 μM 时抑制作用达到最强[1]。
ODZ10117 (5-20 μM；1 小时预处理) 可通过抑制 caspase-1、IL-1β 和 GSDMD 的切割，在经 LPS 预处理的小鼠骨髓来源巨噬细胞中抑制 NLRP3 炎性小体的活化，且不会改变炎性小体核心组分的表达水平[1]。
ODZ10117 (5-20 μM；1 小时预处理) 不会抑制经 LPS 预处理的小鼠骨髓来源巨噬细胞中 AIM2 或 NLRC4 炎症小体的激活，表明其对 NLRP3 炎症小体具有特异性[1]。
ODZ10117 (5-20 μM；1 小时预处理) 可剂量依赖性地抑制 LPS 预刺激的小鼠骨髓来源巨噬细胞中 NLRP3 炎症小体介导的 ASC 转位、寡聚化及斑点形成，且不影响 AIM2 或 NLRC4 炎症小体激活过程中的 ASC 动力学[1]。
ODZ10117 (20 μM) 可在过表达 NLRP3 与 NEK7 的 HEK293T 细胞中抑制二者的相互作用[1]。
ODZ10117 (300-900 μM；30 min incubation with lysates) 可直接与 LPS 预处理的 J774A.1 细胞裂解物中的 NLRP3 和 STAT3 结合，这一点可通过其对链霉蛋白酶降解的剂量依赖性保护作用得到证实，且该化合物不与 NEK7 或 caspase-1 结合[1]。
ODZ10117 通过多种稳定相互作用结合于 NLRP3 NACHT 结构域的 ADP 结合口袋，结合能为 -7.7 kcal/mol[1]。
ODZ10117 可紧密结合至 STAT3 SH2 结构域的磷酸酪氨酸结合口袋，其 Glide 对接得分为 −6.17 kcal/mol，结合亲和力高于已知 STAT3 抑制剂 S3I-201 (HY-15146) 和 STA-21 (HY-121482)[2]。
ODZ10117 (40 μM；24 小时) 可抑制多种组成型激活 STAT3 的人类癌细胞系 (包括 HDLM-2、MDA-MB-231、HepG2 和 U87MG) 中 STAT3 的酪氨酸磷酸化[2]。
ODZ10117 (40 μM；24 小时) 可抑制 IL-6 诱导的人癌细胞系 (包括 RPMI8226、MCF-7 和 U251MG) 中 STAT3 的酪氨酸磷酸化[2]。
ODZ10117 (40 μM；24 小时) 可抑制转染的 MDA-MB-231 乳腺癌细胞中 STAT3 的同源二聚化及酪氨酸磷酸化[2]。
ODZ10117 (40 μM；24 小时) 可通过激活 caspase-3、切割 PARP 并下调抗凋亡蛋白 Bcl-2、Bcl-xL、Mcl-1 和 survivin，诱导 MDA-MB-231 乳腺癌细胞发生凋亡[2]。
ODZ10117 (40 μM；24 小时) 可抑制 MDA-MB-231 乳腺癌细胞中酪氨酸磷酸化 STAT3 的核转位[2]。
ODZ10117 (2.5-40 μM；24 小时) 可抑制 MDA-MB-231/STAT3-Luc 乳腺癌细胞中 STAT3 的转录活性，孵育 24 小时后的 IC50 为 7.5 μM[2]。
ODZ10117 (40 μM；0.5-12 小时) 可在处理后 2 小时开始抑制 MDA-MB-231 和 MDA-MB-468 乳腺癌细胞中 STAT3 的酪氨酸磷酸化[2]。
ODZ10117 (10-40 μM；9 小时) 以浓度依赖的方式抑制 MDA-MB-231 和 MDA-MB-468 乳腺癌细胞中 STAT3 的酪氨酸磷酸化，孵育 9 小时后在 ≥20 μM 浓度下可产生显著抑制作用[2]。
ODZ10117 (40 μM；16 小时) 可在 MDA-MB-231 和 MDA-MB-468 乳腺癌细胞中特异性抑制 STAT3 的酪氨酸磷酸化，而不影响其他 STAT 家族蛋白、JAK 激酶或上游信号调节因子 Akt、Src 及 ERK1/2[2]。
ODZ10117 (10-100 μM；24 小时) 以浓度依赖的方式降低 MDA-MB-231、MDA-MB-468、ZR-75-1 和 4T1 乳腺癌细胞的活力[2]。
ODZ10117 (40 μM；24 小时) 可增加 MDA-MB-231 乳腺癌细胞的凋亡性细胞死亡，Annexin V 阳性细胞数量增加 5 倍、PI 阳性细胞数量增加 3 倍可证明这一点[2]。
ODZ10117 (40 μM；24 小时) 可下调 MDA-MB-231 乳腺癌细胞中 STAT3 依赖性抗凋亡基因 Bcl-2、Bcl-xL、Mcl-1 和 Survivin 的 mRNA 表达[2]。
ODZ10117 (40 μM；24 小时) 可在伤口愈合实验中降低 MDA-MB-231 乳腺癌细胞的迁移能力[2]。
ODZ10117 可强效且选择性地抑制乳腺癌细胞中 STAT3 的转录活性，其 IC50 为 7.5 μM[3]。
ODZ10117 通过直接阻断 STAT3 SH2 结构域、抑制同源二聚化与转录活性、诱导细胞凋亡并降低迁移及侵袭能力，对 MDA-MB-231 乳腺癌细胞发挥抗癌作用[3]。
ODZ10117 (10 μM；12 小时预处理) 可通过减轻氧化应激诱导的细胞损伤，提高经 H2O2 处理的人神经母细胞瘤 SH-SY5Y 细胞的存活率[4]。
ODZ10117 (10 μM；12 小时预处理) 可抑制 H2O2 诱导的人神经母细胞瘤 SH-SY5Y 细胞中 caspase 依赖性凋亡[4]。
ODZ10117 (10 μM；12 小时预处理) 可抑制人神经母细胞瘤 SH-SY5Y 细胞中 STAT3 的磷酸化，并诱导 ERK 和 CREB 的短暂磷酸化，其作用峰值出现在 1 小时[4]。
ODZ10117 (10 μM；1-12 小时) 可上调人神经母细胞瘤 SH-SY5Y 细胞中记忆相关 IEGs 和 BDNF 的蛋白表达，且在 6 小时时即可检测到表达水平升高[4]。
ODZ10117 (10 μM；3 小时) 诱导人神经母细胞瘤 SH-SY5Y 细胞中 CREB 磷酸化的过程依赖于 ERK 信号通路[4]。
ODZ10117 (10 μM；3-6 小时) 可上调人神经母细胞瘤 SH-SY5Y 细胞中与记忆相关的 IEGs 的 mRNA 表达，在 3 小时时效应达到峰值[4]。
ODZ10117 (10 μM；12 小时) 诱导人神经母细胞瘤 SH-SY5Y 细胞中记忆相关 IEG 和 BDNF 蛋白上调的作用依赖于 ERK 信号通路[4]。
ODZ10117 (10 μM；12 小时预处理) 在人神经母细胞瘤 SH-SY5Y 细胞中缓解 H2O2 诱导的氧化应激和 caspase 依赖性凋亡的能力依赖于 ERK 信号通路[4]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

ODZ10117 相关抗体:

Cell Cytotoxicity Assay[1]

Cell Line: mouse bone marrow-derived macrophages (BMDMs)
Concentration: 5 μM; 10 μM; 20 μM; 40 μM
Incubation Time: 6 h
Result: Showed no significant cytotoxicity on BMDMs at concentrations up to 40 μM, with cell viability remaining near 100% across all tested concentrations.

Western Blot Analysis[1]

Cell Line: LPS-primed mouse bone marrow-derived macrophages (BMDMs)
Concentration: 5 μM; 10 μM; 20 μM
Incubation Time: 1 h pretreatment
Result: 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 supernatants and lysates.
Had no effect on the steady-state protein levels of NLRP3, ASC, pro-caspase-1, pro-IL-1β, or full-length GSDMD in cell lysates.

Immunofluorescence[1]

Cell Line: LPS-primed mouse bone marrow-derived macrophages (BMDMs)
Concentration: 5 μM; 10 μM; 20 μM
Incubation Time: 1 h pretreatment
Result: Dose-dependently suppressed ASC translocation to Triton X-100 insoluble fractions, ASC oligomerization, and ASC speck formation in BMDMs treated with NLRP3 triggers (ATP, nigericin, silica crystals).
Reduced ASC speck formation by ~50% for ATP and nigericin triggers at 20 μM.
Had no effect on ASC translocation or speck formation in BMDMs treated with AIM2 or NLRC4 triggers.

Western Blot Analysis[2]

Cell Line: HDLM-2, L540, K562, KCL22, LAMA84, DU145, MDA-MB-231, MDA-MB-468, SKOV3, PANC-1, A549, NCI-H460, HCT116, SW620, MKN-45, A431, A375, SK-MEL-146, HepG2, Huh7, A172, U87MG, U373MG, SH-SY5Y
Concentration: 40 μM
Incubation Time: 24 h
Result: Reduced the level of tyrosine-phosphorylated STAT3 in all tested constitutively STAT3-activated human cancer cell lines, without altering total STAT3 levels.

Western Blot Analysis[2]

Cell Line: RPMI8226, U266, U937, HL-60, HeLa, MCF-7, U251MG
Concentration: 40 μM
Incubation Time: 24 h
Result: Reduced the level of tyrosine-phosphorylated STAT3 induced by IL-6 stimulation in all tested human cancer cell lines, without altering total STAT3 levels.

Western Blot Analysis[2]

Cell Line: MDA-MB-231 breast cancer cells
Concentration: 40 μM
Incubation Time: 24 h
Result: Decreased the level of tyrosine-phosphorylated STAT3 without altering total STAT3 levels, and significantly reduced STAT3 homodimerization compared to vehicle-treated cells.\nIncreased the levels of cleaved PARP and cleaved caspase-3, and reduced the protein levels of anti-apoptotic genes Bcl-2, Bcl-xL, Mcl-1, and Survivin compared to vehicle-treated cells.

Immunofluorescence[2]

Cell Line: MDA-MB-231 breast cancer cells
Concentration: 40 μM
Incubation Time: 24 h
Result: Reduced the nuclear accumulation of tyrosine-phosphorylated STAT3 compared to vehicle-treated cells, where phosphorylated STAT3 was prominently localized in the nucleus.

Western Blot Analysis[2]

Cell Line: MDA-MB-231 and MDA-MB-468 breast cancer cells
Concentration: 40 μM
Incubation Time: 0.5 h; 1 h; 2 h; 4 h; 6 h; 9 h; 12 h
Result: Reduced tyrosine-phosphorylated STAT3 levels after 2 h of incubation, with the inhibitory effect sustained through 12 h of treatment, without altering total STAT3 levels.

Western Blot Analysis[2]

Cell Line: MDA-MB-231 and MDA-MB-468 breast cancer cells
Concentration: 10 μM; 20 μM; 30 μM; 40 μM
Incubation Time: 9 h
Result: Reduced tyrosine-phosphorylated STAT3 levels in a concentration-dependent manner, with significant inhibition observed at concentrations ≥20 μM, without altering total STAT3 levels.

Western Blot Analysis[2]

Cell Line: MDA-MB-231 and MDA-MB-468 breast cancer cells
Concentration: 40 μM
Incubation Time: 16 h
Result: Inhibited tyrosine phosphorylation of STAT3, but did not significantly affect phosphorylation levels of STAT1, STAT5, JAK1, JAK2, JAK3, Akt, Src, or ERK1/2, nor did it alter total levels of any of these proteins.

Cell Viability Assay[2]

Cell Line: MDA-MB-231, MDA-MB-468, ZR-75-1, and 4T1 breast cancer cells
Concentration: 10 μM; 20 μM; 40 μM; 60 μM; 80 μM; 100 μM
Incubation Time: 24 h
Result: Decreased cell viability in a concentration-dependent manner across all tested breast cancer cell lines.
At 100 μM, cell survival was reduced to 30-50% of vehicle-treated controls.

Apoptosis Analysis[2]

Cell Line: MDA-MB-231 breast cancer cells
Concentration: 40 μM
Incubation Time: 24 h
Result: Increased the population of PI-positive dead cells from 7.86% to 26.7% and Annexin V-positive apoptotic cells from 3.13% to 15.3% compared to vehicle-treated cells.

Real Time qPCR[2]

Cell Line: MDA-MB-231 breast cancer cells
Concentration: 40 μM
Incubation Time: 24 h
Result: Reduced the mRNA levels of Bcl-2, Bcl-xL, Mcl-1, and Survivin to 20-40% of vehicle-treated control levels.

Cell Migration Assay[2]

Cell Line: MDA-MB-231 breast cancer cells
Concentration: 40 μM
Incubation Time: 24 h
Result: Significantly reduced wound closure compared to vehicle-treated cells, indicating decreased cell migration.

Cell Viability Assay[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h pretreatment
Result: Significantly increased cell viability in SH-SY5Y cells exposed to H2O2, reversing the ~50% reduction in viability caused by H2O2 alone (statistically significant compared to the H2O2-treated group, p<0.005).

Cell Cytotoxicity Assay[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h pretreatment
Result: Significantly reduced the total green object area (a measure of dead cell cytotoxicity) in SH-SY5Y cells exposed to H2O2, compared to the H2O2-only group (p<0.005).

Apoptosis Analysis[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h (pretreatment); 12 h (H2O2 exposure)
Result: Significantly reduced the percentage of Annexin V-positive apoptotic SH-SY5Y cells exposed to H2O2, compared to the H2O2-only group (p<0.005).

Western Blot Analysis[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h pretreatment
Result: Reduced H2O2-induced cleavage of caspase-3, caspase-9, and PARP in SH-SY5Y cells, indicating inhibition of caspase-dependent apoptosis.

Western Blot Analysis[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 1 h; 3 h; 6 h; 12 h
Result: Induced peak p-STAT3 suppression at 1 h (persisting until 6 h), peak p-CREB levels at 1 h (gradually declining thereafter), and peak p-ERK levels at 1 or 3 h (gradually declining until 12 h) in SH-SY5Y cells.\nSignificantly increased protein levels of c-Fos, c-Jun, and BDNF in SH-SY5Y cells starting at 6 h.

Western Blot Analysis[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 3 h
Result: Pretreatment with PD98059 significantly reduced ODZ10117-induced p-ERK and p-CREB levels in SH-SY5Y cells.

Real Time qPCR[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 3 h; 6 h
Result: Significantly increased mRNA levels of all tested immediate early genes (c-Fos, c-Jun, Arc, Egr-1, NR4A1, and Homer1a) in SH-SY5Y cells, with a more pronounced response observed at 3 h compared to 6 h.

Western Blot Analysis[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h
Result: Induced increases in c-Fos, c-Jun, and BDNF protein levels in SH-SY5Y cells were abolished with PD98059 pretreatment.

Cell Viability Assay[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h
Result: Reduction of cell viability was reversed in H2O2-treated SH-SY5Y cells with PD98059 pretreatment.

Cell Cytotoxicity Assay[4]

Cell Line: human neuroblastoma SH-SY5Y cells
Concentration: 10 μM
Incubation Time: 12 h
Result: Reduction in cytotoxicity, caspase-3, caspase-9, PARP cleavage and apoptotic cell rate was reversed in H2O2-treated SH-SY5Y cells with PD98059 pretreatment.
体内研究
(In Vivo)

ODZ10117 (5-20 mg/kg；腹腔注射；单次给药) 可剂量依赖性地降低尿酸钠 (MSU) 诱导的腹膜炎小鼠的 IL-1β 释放量，在 10 和 20 mg/kg 剂量下可观察到显著的抑制作用[1]。
ODZ10117 (5-20 mg/kg；腹腔注射；LPS 给药前 12 h 和 2 h 分两次给药) 可剂量依赖性地降低 LPS 诱导脓毒症小鼠的 IL-1β 释放并提高其存活率，在 10 和 20 mg/kg 剂量下观察到显著疗效[1]。
ODZ10117 (1-10 mg/kg；腹腔注射；每周 5 次；持续 23 天) 以剂量依赖方式抑制 BALB/c 裸鼠的原位乳腺肿瘤生长，其中 10 mg/kg 剂量的肿瘤减重效果优于 1 mg/kg 剂量[2]。
ODZ10117 (10 mg/kg；瘤内注射；每 2 天 1 次；持续 2 周) 可抑制 BALB/c 裸鼠的皮下乳腺肿瘤生长，并调控肿瘤组织中 STAT3 依赖的凋亡及转移标志物[2]。
ODZ10117 (1-10 mg/kg；腹腔注射；每周 5 次；持续 3 周) 可抑制 BALB/c 小鼠同源乳腺癌模型中的原发肿瘤生长、减少肺转移并延长生存期，且 10 mg/kg 剂量的疗效优于 1 mg/kg 剂量[2]。
ODZ10117 (10 mg/kg；瘤内注射) 可显著抑制携带 MDA-MB-231 乳腺癌异种移植物的 BALB/c 小鼠的肿瘤生长与肺转移[3]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (female, 6-8 weeks old, intraperitoneal injection of MSU crystals at 50 mg/kg)[1]
Dosage: 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: i.p.; single dose
Result: Suppressed MSU-induced IL-1β release in a dose-dependent manner.
Achieved statistically significant reductions in IL-1β levels at 10 mg/kg and 20 mg/kg (p < 0.01) compared to the MSU-only group.
Animal Model: C57BL/6 (female, 6-8 weeks old, intraperitoneal injection of LPS at 20 mg/kg)[1]
Dosage: 5 mg/kg; 10 mg/kg; 20 mg/kg
Administration: i.p.; two doses (12 h and 2 h prior to LPS)
Result: Suppressed LPS-induced IL-1β release in a dose-dependent manner.
Achieved statistically significant reductions in IL-1β levels at 10 mg/kg and 20 mg/kg (p < 0.05) compared to the LPS-only group.
Improved survival rate: maintained 60% survival through 80 hours at 20 mg/kg, compared to 0% survival for the LPS-only group by 36 hours, with a statistically significant difference (p < 0.05).
Animal Model: BALB/c nude (6-week-old female, orthotopic xenograft via MDA-MB-231 cell injection into right fourth mammary fat pad)[2]
Dosage: 1 mg/kg; 10 mg/kg
Administration: i.p.; 5 times per week; 23 days
Result: Reduced final tumor weight to ~1.8 g (1 mg/kg dose) compared to vehicle control ~2.4 g.
Suppressed tumor volume growth over 22 days (1 mg/kg dose).
Reduced final tumor weight to ~1.4 g (10 mg/kg dose).
Suppressed tumor volume growth to a greater degree than the 1 mg/kg dose (10 mg/kg dose).
Did not affect mouse body weight (both doses).
Animal Model: BALB/c nude (6-week-old female, subcutaneous xenograft via MDA-MB-231 cell injection into neck)[2]
Dosage: 10 mg/kg
Administration: intratumoral injection; every 2 days; 2 weeks
Result: Significantly suppressed relative tumor volume growth over 14 days, with final relative volume ~2 compared to vehicle control ~5.
Reduced tumor cell population in treated tumors.
Decreased levels of pY705-STAT3, Bcl-xL, and pro-MMP-2 in treated tumors.
Increased levels of active caspase-3 in treated tumors.
Animal Model: BALB/c (6-week-old female, syngeneic xenograft via 4T1-Luc cell injection into right fourth mammary fat pad, spontaneous lung metastasis)[2]
Dosage: 1 mg/kg; 10 mg/kg
Administration: i.p.; 5 times per week; 3 weeks
Result: Reduced primary tumor volume at 21 days (1 mg/kg dose).
Increased median mouse survival from 12 days to 20 days (1 mg/kg dose).
Reduced visible lung metastatic nodules to ~22 compared to vehicle control ~30 (1 mg/kg dose).
Reduced primary tumor volume to a greater degree than the 1 mg/kg dose (10 mg/kg dose).
Increased median survival to 21 days (10 mg/kg dose).
Reduced visible lung metastatic nodules to ~17 (10 mg/kg dose).
Did not affect mouse body weight (both doses).
Animal Model: BALB/c[3]
Dosage: 10 mg/kg
Administration: intratumoral injection
Result: Significantly reduced tumor growth and lung metastasis.
分子量

362.42

Formula

C10H5Cl5N2O2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

ODZ10117 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

ODZ101171632152-27-2ODZ 10117ODZ-10117STATNOD-like Receptor (NLR)ApoptosisNLRP3breast cancerHEK293T cellsLPS-induced sepsisSTAT3mouse bone marrow-derived macrophagesJ774A.1 cellsMDA-MB-231 cellsSH-SY5Y human neuroblastoma cellshuman STAT3 SH2 domainInhibitorinhibitorinhibit

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