| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg |
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| Other Sizes |
| Targets |
CUR5g targets the autophagy pathway, specifically blocking autophagosome-lysosome fusion. The compound inhibits the recruitment of STX17 (syntaxin 17) to autophagosomes through a UVRAG-dependent mechanism. STX17 is a SNARE protein that is essential for the fusion of autophagosomes with lysosomes. By blocking STX17 recruitment, CUR5g prevents autophagosome-lysosome fusion, leading to the accumulation of autophagosomes and inhibition of autophagy. This results in selective inhibition of autophagosome degradation in cancer cells.
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| ln Vitro |
In cancer cells, CUR5g (0–40 μM, 0–24 h) specifically causes autophagosome accumulation [1]. The levels of sequestosome 1 (SQSTM1) and LC3B-II are upregulated by CUR5g (0-40 μM, 0-24 hours) [1]. A549 cell migration and proliferation are inhibited by CUR5g (0–40 μM, 24 h), but neither necrosis nor apoptosis are brought on [1]. CUR5g Cell Autophagy Assay[1] Cell Line: A549 cells Concentration: 0, 1, 5, 10, 20, and 40 μM Incubation Time: 3, 6, 12, and 24 h Outcome: Decreased diffuse cytosolic staining of GFP-LC3B signal to a punctate pattern encircling autophagosomes. Induced widespread cytoplasmic vacuolization.
In vitro studies demonstrate that CUR5g is a potent autophagy inhibitor that selectively inhibits autophagosome degradation in cancer cells. The compound blocks the recruitment of STX17 to autophagosomes via a UVRAG-dependent mechanism. CUR5g inhibits migration and colony formation in A549 cells. The compound enhances the anticancer effects of cisplatin in A549 cells. No detailed IC50 values have been published in the available literature. |
| ln Vivo |
In vivo autophagic flux is inhibited by CUR5g (40 mg/kg, tail vein injection, once every two days for 15 days) and cisplatin (HY-17394) (1 mg/kg), which work in concert to combat cancer [1].
In vivo, CUR5g enhances the anticancer effects of cisplatin in A549 cells. The compound is an autophagy inhibitor that selectively inhibits autophagosome degradation in cancer cells. CUR5g is often used in combination with cisplatin for the study of cancer. Its ability to inhibit autophagy enhances the efficacy of chemotherapy in cancer models. |
| Enzyme Assay |
The autophagy inhibitory activity of CUR5g can be assessed using cell-based autophagy assays. In a typical assay, cells are treated with CUR5g and autophagy markers such as LC3-II and SQSTM1/p62 are assessed by Western blotting. The accumulation of autophagosomes can be visualized by fluorescence microscopy using GFP-LC3 or by staining with LysoTracker. The compound's ability to block autophagosome-lysosome fusion can be assessed by measuring the colocalization of autophagosomes and lysosomes.
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| Cell Assay |
Western Blot Analysis[1]
Cell Types: A549 cells Tested Concentrations: 0, 1, 5, 10, 20, and 40 μM Incubation Duration: 0, 1, 3, 6, 12, and 24 h Experimental Results: Up-regulated LC3B-II and sequestosome 1 (SQSTM1) levels time- and dose-dependently. This increase was not the result of enhanced transcription, as mRNA expression of SQSTM1 and LC3B were not increased within CUR5g-exposed cells, suggesting that CUR5g might block autophagic flux rather than increase autophagosome formation. Cell Proliferation Assay[1] Cell Types: A549 cells Tested Concentrations: 0, 1, 5, 10, 20, and 40 μM Incubation Duration: 24 h Experimental Results: demonstrated great toxicity to A549 cells at 20 μM. Slightly diminished A549 cell number at 10 μM, while diminished the number of A549 cells Dramatically at 20 μM. demonstrated no discernable activity in healthy human umbilical vein endothelial cell (HUVEC) viability at 40 µM. The cellular activity of CUR5g is assessed using A549 cells or other cancer cell lines. Cells are treated with varying concentrations of CUR5g. Cell migration is assessed using wound healing or Transwell assays. Colony formation is assessed using clonogenic assays. Cell viability is measured using MTT or CellTiter-Glo assays. The compound's ability to enhance cisplatin-induced cell death is assessed by combining CUR5g with cisplatin. Autophagy markers are assessed by Western blotting. |
| Animal Protocol |
Animal/Disease Models: BALB/c nude mice (4weeks old, A549 cells were subcutaneously (sc) injected into the right scapula of each nude mouse)[1]
Doses: 40 mg/kg, CUR5g (40 mg/kg) and Cisplatin (1 mg/kg) Route of Administration: Injected via caudal vein, once every 2 days for up to 15 days Experimental Results: Retarded the growth of xenografted tumors, whereas the combination treatment with Cisplatin almost completely inhibited tumor growth. Promoted the cisplatin sensitivity of A549 cells by inhibiting autophagic flux. CUR5g has been evaluated in animal models of cancer in combination with cisplatin. In these studies, the compound enhances the anticancer effects of cisplatin in A549 xenograft tumors. The compound is an autophagy inhibitor that selectively inhibits autophagosome degradation in cancer cells. Further studies would be needed to fully characterize its in vivo efficacy. |
| ADME/Pharmacokinetics |
No detailed pharmacokinetic data has been published for CUR5g. The compound has a molecular weight of 344.41 and a molecular formula of C22H20N2O2. Further studies would be needed to characterize its absorption, distribution, metabolism, and excretion properties, including oral bioavailability, plasma protein binding, clearance, and half-life.
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| Toxicity/Toxicokinetics |
No detailed toxicity data has been published for CUR5g. As an autophagy inhibitor, the compound may have on-target effects on autophagy in normal tissues. Comprehensive toxicology studies would be required to evaluate its safety profile for potential therapeutic development. The compound is intended for research use only.
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| References |
[1]. Chen J, et al. CUR5g, a novel autophagy inhibitor, exhibits potent synergistic anticancer effects with cisplatin against non-small-cell lung cancer. Cell Death Discov. 2022 Oct 31;8(1):435.
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| Additional Infomation |
CUR5g (CAS# 1370032-20-4) is a potent autophagy inhibitor that selectively inhibits autophagosome degradation in cancer cells by blocking autophagosome-lysosome fusion. It blocks STX17 recruitment to autophagosomes via a UVRAG-dependent mechanism. CUR5g inhibits migration and colony formation in A549 cells and enhances the anticancer effects of cisplatin. The molecular formula is C22H20N2O2 and molecular weight is 344.41. CUR5g is a research tool for studying autophagy and cancer therapy.
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| Molecular Formula |
C22H20N2O2
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| Molecular Weight |
344.406405448914
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| Exact Mass |
344.152
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| CAS # |
1370032-20-4
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| PubChem CID |
57341149
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| Appearance |
Yellow to brown solid powder
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| LogP |
3.4
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
26
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| Complexity |
589
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CN1C/C(=C\C2=CC=C(C=C2)O)/C(=O)/C(=C/C3=CNC4=CC=CC=C43)/C1
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| InChi Key |
JMVVTYLZZDOERS-ODPUSEOTSA-N
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| InChi Code |
InChI=1S/C22H20N2O2/c1-24-13-17(10-15-6-8-19(25)9-7-15)22(26)18(14-24)11-16-12-23-21-5-3-2-4-20(16)21/h2-12,23,25H,13-14H2,1H3/b17-10+,18-11+
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| Chemical Name |
(3E,5E)-3-[(4-hydroxyphenyl)methylidene]-5-(1H-indol-3-ylmethylidene)-1-methylpiperidin-4-one
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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) |
DMSO : 41.67 mg/mL (120.99 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.26 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 + to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.9035 mL | 14.5176 mL | 29.0352 mL | |
| 5 mM | 0.5807 mL | 2.9035 mL | 5.8070 mL | |
| 10 mM | 0.2904 mL | 1.4518 mL | 2.9035 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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