CU-T12-9
目录号 : GC39285
CU-T12-9是一种特异性Toll样受体TLR1/TLR2异二聚体的小分子激动剂，其EC50为52.9nM，CU-T12-9通过促进TLR1和TLR2二聚化，进而激活NF-κB信号通路
Cas No.:1821387-73-8
Sample solution is provided at 25 µL, 10mM.
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CU-T12-9 is a small-molecule agonist that specifically targets the Toll-like receptor TLR1/TLR2 heterodimer, with an EC50 of 52.9nM. CU-T12-9 promotes the dimerization of TLR1 and TLR2, thereby activating the NF-κB signaling pathway[1-2]. CU-T12-9 is primarily used in research related to immune regulation, vaccine adjuvants, anti-tumor agents, and the development of therapeutics for inflammatory and infectious diseases[3-4].
In vitro, treatment of TREM1-knockdown human hepatocellular carcinoma Huh-7 and MHCC-97H cells with CU-T12-9 (1μM) activated the TLR2 signaling pathway and promoted the phosphorylation of PI3K-p85α and AKT, thereby rescuing the impairment in cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) caused by TREM1 downregulation[5]. Treatment of LPS (100ng/mL) and IFN-γ (10ng/mL)-induced M1-type bone marrow-derived macrophages with CU-T12-9 (1μM) for 2 hours reversed the inhibitory effect of photobiomodulation (PBM) on the TLR2/NLRP3/Caspase-1/IL-1β signaling pathway, significantly suppressed the expression of autophagy-related proteins LC3B and Beclin-1, and enhanced inflammasome activity and pro-inflammatory cytokine secretion[6].
In vivo, intramuscular injection of CU-T12-9 (10mg/kg) in a diabetic hindlimb ischemia mouse model twice a week for six weeks (total of six injections), specifically activated the NF-κB signaling pathway and significantly inhibited the formation of new blood vessels from endothelial cells and smooth muscle cells in the ischemic muscle tissue[7].
References:
[1] Cheng K, Gao M, Godfroy JI, et al. Specific activation of the TLR1-TLR2 heterodimer by small-molecule agonists. Sci Adv. 2015;1(3):e1400139.
[2] Wang Z, Zhu D, Yang F, et al. POSTN knockdown suppresses IL-1β-induced inflammation and apoptosis of nucleus pulposus cells via inhibiting the NF-κB pathway and alleviates intervertebral disc degeneration. J Cell Commun Signal. 2024 May 7;18(2):e12030.
[3] Chen Y, Guo Y, Song Z, et al. Luteolin restricts ASFV replication by regulating the NF-κB/STAT3/ATF6 signaling pathway. Vet Microbiol. 2022 Oct;273:109527.
[4] Zhang W, Liu W, Hu X. Robinin inhibits pancreatic cancer cell proliferation, EMT and inflammation via regulating TLR2-PI3k-AKT signaling pathway. Cancer Cell Int. 2023 Dec 18;23(1):328.
[5] Ren L, Qiao GL, Zhang SX, et al. Pharmacological Inhibition or Silencing of TREM1 Restrains HCC Cell Metastasis by Inactivating TLR/PI3K/AKT Signaling. Cell Biochem Biophys. 2024 Sep;82(3):2673-2685.
[6] Zuo X, Ju C, Zhang Z, et al. Photobiomodulation regulates inflammation and autophagy in spinal cord injury through NLRP3/Caspase-1/IL-1β pathway by targeting TLR2. Mol Immunol. 2025 Jun;182:1-10.
[7] Wang J, Zhang L, Duan W, et al. Salidroside analogue C-30 promotes neovascularization in diabetic hindlimb ischemic mice by inducing macrophage M2 polarization. Int Immunopharmacol. 2025 Oct 22;167:115708.
CU-T12-9是一种特异性Toll样受体TLR1/TLR2异二聚体的小分子激动剂，其EC50为52.9nM，CU-T12-9通过促进TLR1和TLR2二聚化，进而激活NF-κB信号通路[1-2]。CU-T12-9主要被用于免疫调节、疫苗佐剂、抗肿瘤制剂以及治疗炎症和传染病药物开发相关研究中[3-4]。
在体外，CU-T12-9（1μM）处理敲低TREM1的人肝癌Huh-7和MHCC-97H细胞，CU-T12-9激活了TLR2信号通路，促进PI3K-p85α和AKT的磷酸化水平，从而挽救了因TREM1下调导致的细胞增殖、侵袭和上皮-间质转化（EMT）过程受阻[5]。CU-T12-9（1μM）处理经LPS（100ng/mL）和IFN-γ（10ng/mL）诱导的M1型骨髓源性巨噬细胞2小时，CU-T12-9逆转了光生物调节（PBM）对TLR2/NLRP3/Caspase-1/IL-1β信号通路的抑制作用，并显著抑制自噬相关蛋白LC3B和Beclin-1的表达，同时增强炎症小体活性及促炎因子分泌[6]。
在体内，CU-T12-9（10mg/kg）肌肉注射处理糖尿病后肢缺血小鼠，每周两次，一共注射6周，通过特异性激活NF-κB信号通路，显著抑制缺血肌肉组织中内皮细胞和平滑肌细胞的新生血管形成[7]。
| Cell experiment [1]: | |
Cell lines | Huh-7 and MHCC-97H cells (human hepatocellular carcinoma cell lines) |
Preparation Method | Huh-7 and MHCC-97H cells were maintained in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS) at 37°C, 5% CO₂. Cells were transfected with si-TREM1 or control siRNA (si-Con) for 48 hours and subsequently treated with the TLR2-specific agonist CU-T12-9 (1µM). |
Reaction Conditions | 1μM; 48h |
Applications | CU-T12-9 treatment significantly reversed the si-TREM1-induced suppression of cell proliferation, invasion, and epithelial-mesenchymal transition (EMT). CU-T12-9 also restored the protein expression levels of TLR2/4, MyD88, and the phosphorylation of PI3K/AKT, which were downregulated by TREM1 knockdown. |
| Animal experiment [2]: | |
Animal models | Diabetic C57BL/6 mice with hindlimb ischemia (HLI) |
Preparation Method | Diabetic HLI mice were intramuscularly administered CU-T12-9 (10mg/kg body weight) alone or in combination with C-30 (30mg/kg body weight) at indicated time points after femoral artery excision. Mice were sacrificed at day 21 after surgery for analysis. |
Dosage form | 10mg/kg; intramuscular injection; twice a week for three weeks, total of six injections. |
Applications | CU-T12-9 administration abolished C-30-mediated blood perfusion recovery and neovascularization in diabetic HLI mice. CU-T12-9 significantly reversed C-30-induced M2 macrophage polarization and suppressed therapeutic angiogenesis by activating the NF-κB signaling pathway. |
References: | |
| Cas No. | 1821387-73-8 | SDF | |
| Canonical SMILES | CNC1=CC=C(C=C1N2C=C(N=C2)C3=CC=C(C=C3)C(F)(F)F)[N+]([O-])=O | ||
| 分子式 | C17H13F3N4O2 | 分子量 | 362.31 |
| 溶解度 | DMSO: 250 mg/mL (690.02 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7601 mL | 13.8003 mL | 27.6007 mL |
| 5 mM | 552 μL | 2.7601 mL | 5.5201 mL |
| 10 mM | 276 μL | 1.38 mL | 2.7601 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
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- Purity: >98.00%
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