360AG-quadruplex structures inhibitor CAS# 794458-56-3 |
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Quality Control & MSDS
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| Cas No. | 794458-56-3 | SDF | Download SDF |
| PubChem ID | 11430774 | Appearance | Powder |
| Formula | C27H23N5O2+2 | M.Wt | 99.1 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | 25℃: DMSO | ||
| Chemical Name | 2-N,6-N-bis(1-methylquinolin-1-ium-3-yl)pyridine-2,6-dicarboxamide | ||
| SMILES | C[N+]1=CC(=CC2=CC=CC=C21)NC(=O)C3=NC(=CC=C3)C(=O)NC4=CC5=CC=CC=C5[N+](=C4)C | ||
| Standard InChIKey | KPOOEJJPTYXNTN-UHFFFAOYSA-P | ||
| Standard InChI | InChI=1S/C27H21N5O2/c1-31-16-20(14-18-8-3-5-12-24(18)31)28-26(33)22-10-7-11-23(30-22)27(34)29-21-15-19-9-4-6-13-25(19)32(2)17-21/h3-17H,1-2H3/p+2 | ||
| 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. |
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| 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. |
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| 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. | ||
| Description | 360A is a selective stabilizer of G-quadruplex, and also inhibits telomerase activity with an IC50 of 300 nM for telomerase in TRAP-G4 assay.In Vitro:360A inhibits telomerase activity and stabilizes G-quadruplex, with an IC50 of 300 nM for telomerase in TRAP-G4 assay. 360A reduces the viability of glioma cell lines, such as T98G, CB193, U118-MG, SAOS-2 and Primary astrocytes, with IC50s of 4.8 ± 1.1 μM, 3.9 ± 0.4 μM, 8.4 ± 0.5 μM, >15 μM and 17.4 ± 1.2 μM, respectively[1]. 360A causes Rad51-dependent telomere aberrations preferentially involving the lagging strand telomeres, including telomere losses or telomere doublets, and induces DNA-PKcs-dependent sister telomere fusions[2]. References: | |||||
360A Dilution Calculator
360A Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 10.0908 mL | 50.4541 mL | 100.9082 mL | 201.8163 mL | 252.2704 mL |
| 5 mM | 2.0182 mL | 10.0908 mL | 20.1816 mL | 40.3633 mL | 50.4541 mL |
| 10 mM | 1.0091 mL | 5.0454 mL | 10.0908 mL | 20.1816 mL | 25.227 mL |
| 50 mM | 0.2018 mL | 1.0091 mL | 2.0182 mL | 4.0363 mL | 5.0454 mL |
| 100 mM | 0.1009 mL | 0.5045 mL | 1.0091 mL | 2.0182 mL | 2.5227 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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Description: IC50 Value: N/A 360A is a 2,6-pyridine-dicarboxamide derivative displaying strong affinity and selectivity for G-quadruplex structures and selective telomerase inhibition in vitro assays. 360A is a G-quadruplex ligand, which can influence the consequence of G-quadruplex formation and/or stabilization. in vitro: We found a S-phase accumulation in ATM-proficient, but not in ATM-deficient EBV-lymphocytes treated with 360A before induction of cell death. However, ATM status did not modify cell cycle distribution in 360A-treated SV40-fibroblasts and HeLa cells compared to DMSO treated controls [1]. DNA-PKcs-dependent NHEJ was responsible for sister telomere fusions as a direct consequence of G-quadruplex formation and/or stabilization induced by 360A on parental telomere G strands. NHEJ and HR activation at telomeres altered mitotic progression in treated cells [2]. This compound was shown to display a potent affinity and selectivity for telomeric G-quadruplex DNA over duplex DNA and to induce delayed growth inhibition in HT1080 tumor cell line [3]. in vivo: N/A Clinical trial: N/A
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Rad51 and DNA-PKcs are involved in the generation of specific telomere aberrations induced by the quadruplex ligand 360A that impair mitotic cell progression and lead to cell death.[Pubmed:21773671]
Cell Mol Life Sci. 2012 Feb;69(4):629-40.
Functional telomeres are protected from non-homologous end-joining (NHEJ) and homologous recombination (HR) DNA repair pathways. Replication is a critical period for telomeres because of the requirement for reconstitution of functional protected telomere conformations, a process that involves DNA repair proteins. Using knockdown of DNA-PKcs and Rad51 expression in three different cell lines, we demonstrate the respective involvement of NHEJ and HR in the formation of telomere aberrations induced by the G-quadruplex ligand 360A during or after replication. HR contributed to specific chromatid-type aberrations (telomere losses and doublets) affecting the lagging strand telomeres, whereas DNA-PKcs-dependent NHEJ was responsible for sister telomere fusions as a direct consequence of G-quadruplex formation and/or stabilization induced by 360A on parental telomere G strands. NHEJ and HR activation at telomeres altered mitotic progression in treated cells. In particular, NHEJ-mediated sister telomere fusions were associated with altered metaphase-anaphase transition and anaphase bridges and resulted in cell death during mitosis or early G1. Collectively, these data elucidate specific molecular and cellular mechanisms triggered by telomere targeting by the G-quadruplex ligand 360A, leading to cancer cell death.
Long-term results of 360A degrees scleral buckling and vitrectomy with silicone oil tamponade for management of gunshot-perforating ocular injury.[Pubmed:22863820]
Eye (Lond). 2012 Oct;26(10):1318-23.
PURPOSE: This is a retrospective consecutive study to assess the long-term results of combined scleral buckling and pars plana vitrectomy (PPV) with silicone oil for the management of perforating ocular injury caused by gunshots. METHODS: Data were gathered from medical records of patients who underwent scleral buckling and PPV with silicone oil 2 weeks after primary repair elsewhere, in Magrabi eye center (Tanta, Egypt), from June 2005 to May 2010. RESULTS: The evaluated group consisted of 49 cases, out of which 26 cases presented with gunshot injury. Twenty-two were male (84.62%) and four were female (15.38%), with a mean age of 27.19+12.7 years. The follow-up ranged from 12 to 72 months, with a mean period of 32.04+8.9 months. The t-test was used to determine the visual outcome and main prognostic factors. Visual acuity improved in 22 of 26 eyes (76.92%), was unchanged in 4 eyes (15.38%), and worsened in 2 eyes (6.69%). Ten eyes (38.46%) achieved visual acuity between (20/40) and (20/100), and eight eyes (30.76%) had visual acuity between (20/200) and (20/400). The 18 eyes (69.23%) with visual acuity better than counting fingers (CF) had an attached retina with no signs of active proliferation after removal of the silicone oil. CONCLUSION: POI due to gunshot is usually a terminal event for the eye. Eyes with perforating injury can be saved and may attain useful vision after performance of combined scleral buckling and PPV with silicone oil tamponade. The final visual outcome depends on the macular or the optic nerve involvement and the final retinal stability, and phthisis bulbi can also be prevented.
Role of ATM in the telomere response to the G-quadruplex ligand 360A.[Pubmed:18263609]
Nucleic Acids Res. 2008 Mar;36(5):1741-54.
Telomeres are known to prevent chromosome ends from being recognized as DNA double-strand breaks. Conversely, many DNA damage response proteins, including ATM, are thought to participate to telomere maintenance. However, the precise roles of ATM at telomeres remain unclear due to its multiple functions in cell checkpoints and apoptosis. To gain more insights into the role of ATM in telomere maintenance, we determined the effects of the G-quadruplex ligand 360A in various cell lines lacking functional ATM. We showed, by using Fluorescence in situ hybridization (FISH) and Chromosome Orientation-FISH using telomere PNA probes, that 360A induced specific telomere aberrations occurring during or after replication, mainly consisting in sister telomere fusions and also recombinations that involved preferentially the lagging strand telomeres. We demonstrate that ATM reduced telomere instability independently of apoptosis induction. Our results suggest thus that ATM has a direct role in preventing inappropriate DNA repair at telomeres, which could be related to its possible participation to the formation of protected structures at telomeres.
