NSC 405020

MT1-MMP inhibitor CAS# 7497-07-6

NSC 405020

Catalog No. BCC2120----Order now to get a substantial discount!

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Quality Control of NSC 405020

Number of papers citing our products

Chemical structure

NSC 405020

3D structure

Chemical Properties of NSC 405020

Cas No. 7497-07-6 SDF Download SDF
PubChem ID 346721 Appearance Powder
Formula C12H15Cl2NO M.Wt 260.16
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : ≥ 260 mg/mL (999.38 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 3,4-dichloro-N-pentan-2-ylbenzamide
SMILES CCCC(C)NC(=O)C1=CC(=C(C=C1)Cl)Cl
Standard InChIKey ARDYECYBETXQFD-UHFFFAOYSA-N
Standard InChI InChI=1S/C12H15Cl2NO/c1-3-4-8(2)15-12(16)9-5-6-10(13)11(14)7-9/h5-8H,3-4H2,1-2H3,(H,15,16)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of NSC 405020

DescriptionMembrane type-1 matrix metalloproteinase (MT1-MMP) inhibitor (IC50 > 100 μmol/L). Directly interacts with the hemopexin domain (PEX) of MT1-MMP, affecting homodimerization and repressing its pro-tumorigenic activity in vivo. Displays no effect on the catalytic activity of MT1-MMP or MMP-2.

NSC 405020 Dilution Calculator

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NSC 405020 Molarity Calculator

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Preparing Stock Solutions of NSC 405020

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.8438 mL 19.2189 mL 38.4379 mL 76.8758 mL 96.0947 mL
5 mM 0.7688 mL 3.8438 mL 7.6876 mL 15.3752 mL 19.2189 mL
10 mM 0.3844 mL 1.9219 mL 3.8438 mL 7.6876 mL 9.6095 mL
50 mM 0.0769 mL 0.3844 mL 0.7688 mL 1.5375 mL 1.9219 mL
100 mM 0.0384 mL 0.1922 mL 0.3844 mL 0.7688 mL 0.9609 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on NSC 405020

NSC-405020 is a novel small molecule inhibitor of membrane type-I matrix metalloproteinase (MT1-MMP) that specifically targets the hemopexin (PEX) domain rather than the catalytic domain of MT1-MMP with 50% inhibition concentration IC50 value larger than 100 μmol/L and does not inhibit the catalytic activity of MT1-MMP or MMP-2. NSC-405020 directly interacts with and binds to PEX in a vicinity of Met-328, Arg-330, Asp-376, Met-22 and Ser-470 of the druggable pocket in the full-length MT1-MMP structure, which affects the conformation and flexibility of blades I to IV of the β-propeller resulting in the decrease of the PEX-dependent homodimerization of cellular MT1-MMP. NSC-405020 dose not affect the ability of MT1-MMP to activate MMP-2 but its ability to degrade COL-I.

Reference

Remacle AG, Golubkov VS, Shiryaev SA, Dahl R, Stebbins JL, Chernov AV, Cheltsov AV, Pellecchia M, Strongin AY. Novel MT1-MMP small-molecule inhibitors based on insights into hemopexin domain function in tumor growth. Cancer Res. 2012 May 1;72(9):2339-49. doi: 10.1158/0008-5472.CAN-11-4149. Epub 2012 Mar 9.

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References on NSC 405020

VEGF alleviates ALS-CSF induced cytoplasmic accumulations of TDP-43 and FUS/TLS in NSC-34 cells.[Pubmed:28163215]

J Chem Neuroanat. 2017 Apr;81:48-52.

Cytoplasmic mislocalisation and aggregation of TDP-43 and FUS/TLS proteins in spinal motor neurons contribute to the pathogenesis of the highly fatal disorder amyotrophic lateral sclerosis (ALS). We investigated the neuroprotective effect of VEGF on expression of these proteins in the motor neuronal cell line NSC-34 modelled to reminisce sporadic form of ALS. We studied the expression of TDP-43 and FUS/TLS proteins after exposure to ALS-CSF and following VEGF supplementation by quantitative confocal microscopy and electron microscopy. ALS-CSF caused cytoplasmic overexpression of both the proteins and stress-granule formation in the cells. These alterations were alleviated by VEGF supplementation. The related ultrastructural changes like nuclear membrane dysmorphism and p-bodies associated changes were also reversed. However the protein expression did not completely translocate to the nucleus, as some cells continued to show to cytoplasmic mislocalisation. Thus, the present findings indicate that VEGF alleviates TDP43 and FUS pathology by complimenting its role in controlling apoptosis and reversing choline acetyl transferase expression. Hence, VEGF appears to target multiple pathogenic processes in the neurodegenerative cascade of ALS.

Important modifications by sugammadex, a modified gamma-cyclodextrin, of ion currents in differentiated NSC-34 neuronal cells.[Pubmed:28049438]

BMC Neurosci. 2017 Jan 3;18(1):6.

BACKGROUND: Sugammadex (SGX) is a modified gamma-cyclodextrin used for reversal of steroidal neuromuscular blocking agents during general anesthesia. Despite its application in clinical use, whether SGX treatment exerts any effects on membrane ion currents in neurons remains largely unclear. In this study, effects of SGX treatment on ion currents, particularly on delayed-rectifier K(+) current [I K(DR)], were extensively investigated in differentiated NSC-34 neuronal cells. RESULTS: After cells were exposed to SGX (30 muM), there was a reduction in the amplitude of I K(DR) followed by an apparent slowing in current activation in response to membrane depolarization. The challenge of cells with SGX produced a depolarized shift by 15 mV in the activation curve of I K(DR) accompanied by increased gating charge of this current. However, the inactivation curve of I K(DR) remained unchanged following SGX treatment, as compared with that in untreated cells. According to a minimal reaction scheme, the lengthening of activation time constant of I K(DR) caused by cell treatment with different SGX concentrations was quantitatively estimated with a dissociation constant of 17.5 muM, a value that is clinically achievable. Accumulative slowing in I K(DR) activation elicited by repetitive stimuli was enhanced in SGX-treated cells. SGX treatment did not alter the amplitude of voltage-gated Na(+) currents. In SGX-treated cells, dexamethasone (30 muM), a synthetic glucocorticoid, produced little or no effect on L-type Ca(2+) currents, although it effectively suppressed the amplitude of this current in untreated cells. CONCLUSIONS: The treatment of SGX may influence the amplitude and gating of I K(DR) and its actions could potentially contribute to functional activities of motor neurons if similar results were found in vivo.

Adult NSC diversity and plasticity: the role of the niche.[Pubmed:27978480]

Curr Opin Neurobiol. 2017 Feb;42:68-74.

Adult somatic stem cells are generally defined as cells with the ability to differentiate into multiple different lineages and to self-renew during long periods of time. These features were long presumed to be represented in one single tissue-specific stem cell. Recent development of single-cell technologies reveals the existence of diversity in fate and activation state of somatic stem cells within the blood, skin and intestinal compartments [1] but also in the adult brain. Here we review how recent advances have expanded our view of neural stem cells (NSCs) as a diverse pool of cells and how the specialized microenvironment in which they reside acts to maintain this diversity. In addition, we discuss the plasticity of the system in the injured brain.

c-Jun Amino-Terminal Kinase is Involved in Valproic Acid-Mediated Neuronal Differentiation of Mouse Embryonic NSCs and Neurite Outgrowth of NSC-Derived Neurons.[Pubmed:28321599]

Neurochem Res. 2017 Apr;42(4):1254-1266.

Valproic acid (VPA), an anticonvulsant and mood-stabilizing drug, can induce neuronal differentiation, promote neurite extension and exert a neuroprotective effect in central nervous system (CNS) injuries; however, comparatively little is known regarding its action on mouse embryonic neural stem cells (NSCs) and the underlying molecular mechanism. Recent studies suggested that c-Jun N-terminal kinase (JNK) is required for neurite outgrowth and neuronal differentiation during neuronal development. In the present study, we cultured mouse embryonic NSCs and treated the cells with 1 mM VPA for up to 7 days. The results indicate that VPA promotes the neuronal differentiation of mouse embryonic NSCs and neurite outgrowth of NSC-derived neurons; moreover, VPA induces the phosphorylation of c-Jun by JNK. In contrast, the specific JNK inhibitor SP600125 decreased the VPA-stimulated increase in neuronal differentiation of mouse embryonic NSCs and neurite outgrowth of NSC-derived neurons. Taken together, these results suggest that VPA promotes neuronal differentiation of mouse embryonic NSCs and neurite outgrowth of NSC-derived neurons. Moreover, JNK activation is involved in the effects of VPA stimulation.

Novel MT1-MMP small-molecule inhibitors based on insights into hemopexin domain function in tumor growth.[Pubmed:22406620]

Cancer Res. 2012 May 1;72(9):2339-49.

Membrane type-1 matrix metalloproteinase (MT1-MMP) is a promising drug target in malignancy. The structure of MT1-MMP includes the hemopexin domain (PEX) that is distinct from and additional to the catalytic domain. Current MMP inhibitors target the conserved active site in the catalytic domain and, as a result, repress the proteolytic activity of multiple MMPs instead of MT1-MMP alone. In our search for noncatalytic inhibitors of MT1-MMP, we compared the protumorigenic activity of wild-type MT1-MMP with an MT1-MMP mutant lacking PEX (DeltaPEX). In contrast to MT1-MMP, DeltaPEX did not support tumor growth in vivo, and its expression resulted in small fibrotic tumors that contained increased levels of collagen. Because these findings suggested an important role for PEX in tumor growth, we carried out an inhibitor screen to identify small molecules targeting the PEX domain of MT1-MMP. Using the Developmental Therapeutics Program (National Cancer Institute/NIH), virtual ligand screening compound library as a source and the X-ray crystal structure of PEX as a target, we identified and validated a novel PEX inhibitor. Low dosage, intratumoral injections of PEX inhibitor repressed tumor growth and caused a fibrotic, DeltaPEX-like tumor phenotype in vivo. Together, our findings provide a preclinical proof of principle rationale for the development of novel and selective MT1-MMP inhibitors that specifically target the PEX domain.

Description

NSC 405020 is a novel small molecule inhibitor of MT1-MMP that specifically targets PEX domain rather than the catalytic domain of MT1-MMP with IC50 >100 μM and does not inhibit the catalytic activity of MT1-MMP or MMP-2.

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