CAS |
1416324-85-0 |
English Name |
CU-CPT22 |
Molecular Formula |
C19H22O7 |
Molecular Weight |
362.37 |
Solubility |
Soluble in DMSO ≥5mg/mL;Soluble in Water < 0.1mg/mL |
Purity |
≥98% |
Appearance |
Off-white to yellow Solid |
Storage |
Powder:2-8℃,2 years;Insolvent(Mother Liquid):-20℃,6 months;-80℃,1 year |
MDL |
MFCD26406409 |
SMILES |
O=C(C(C=C1O)=CC2=CC(OC)=C(O)C(O)=C2C1=O)OCCCCCC |
Target Point |
Toll-like Receptor (TLR) |
Passage |
Immunology & Inflammation |
Background |
CU-CPT22 is the first probe of the complex between Toll-like receptors TLR1 and TLR2. |
Biological Activity |
CU-CPT22抑制Pam3CSK4诱导的TLR1/2激活,IC50为0.58 ± 0.09 μM,而对TLR2/6没有显著抑制作用。它对PDGFRB, MET, DDR2, SRC, MAPK1, PAK1, AKT1, PKC-γ, CAMK1和PLK4仅具微弱的(或无)非特异性抑制作用。[1-3] |
IC50 |
TLR1/2(Cell-free):0.58μM [1] |
In Vitro |
CU-CPT22可与合成的三酰脂蛋白Pam3CSK4竞争结合TLR1/2,具有高度抑制活性和特异性,Ki值为0.41 ± 0.07 μM。CU-CPT22抑制TLR1/2信号,而不影响其他TLRs,说明它在完整细胞中具有高选择性。在RAW 264.7细胞中,浓度高达100 μM的CU-CPT22对细胞没有显著毒性作用。CU-CPT22对PDGFRB,MET,DDR2,SRC,MAPK1,PAK1,AKT1,PKC-γ,CAMK1和 PLK4仅具微弱的非特异性抑制作用,它能抑制TLR1/2介导的炎症反应。在RAW 264.7细胞中,8 μM CU-CPT22可抑制60% TNF-α和95% IL-1β[1]。 |
In Vivo |
在心肌梗塞(MI)前进行Cu-CPT22给药,可显著地抑制MI诱导的KIM-1、TLR2、TLR4、MyD88和chemokine(C-C motif)ligand 2水平的上调以及NF-κB的激活,而不改变NGAL、IL-6和TNF-α的表达水平[2]。[3] |
Cell Experiment |
将MUTZ-LCs接种于不含其它添加物的alpha培养基中(细胞密度为2.5 × 105 cells/ml),使其暴露于不同的微生物和促炎性刺激下24小时。通过Limulus Amebo-cyte Lysate(LAL)试验检测大肠杆菌E. coli产生的细胞因子(包含低浓度内毒素,≤1.0 EU/μg cytokine)。CU-CPT22在Pam3CSK4和Pam2CSK4刺激前1小时加入。[3] |
Animal Experiment |
Animal Models: Male LETO and OLETF rats; Dosages: 3 mg/kg; Administration: i.p.[2] |
Data Literature Source |
[1] Cheng K,et al. Angew Chem Int Ed Engl. 2012,51(49):12246-9. [2] Ohno K,et al. Am J Physiol Heart Circ Physiol. 2017,313(6):H1130-H1142. [3] Bock S,et al. Pharmacol Res. 2016,105:44-53 |
Unit |
Bottle |
Specification |
5mg 10mg |