Alexidine dihydrochloridePTPMT1 inhibitor CAS# 1715-30-6 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 1715-30-6 | SDF | Download SDF |
PubChem ID | 102678 | Appearance | Powder |
Formula | C26H58Cl2N10 | M.Wt | 581.71 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 250 mg/mL (429.77 mM; Need ultrasonic) | ||
Chemical Name | 1-[N'-[6-[[amino-[[N'-(2-ethylhexyl)carbamimidoyl]amino]methylidene]amino]hexyl]carbamimidoyl]-2-(2-ethylhexyl)guanidine;dihydrochloride | ||
SMILES | CCCCC(CC)CN=C(N)NC(=NCCCCCCN=C(N)NC(=NCC(CC)CCCC)N)N.Cl.Cl | ||
Standard InChIKey | BRJJFBHTDVWTCJ-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C26H56N10.2ClH/c1-5-9-15-21(7-3)19-33-25(29)35-23(27)31-17-13-11-12-14-18-32-24(28)36-26(30)34-20-22(8-4)16-10-6-2;;/h21-22H,5-20H2,1-4H3,(H5,27,29,31,33,35)(H5,28,30,32,34,36);2*1H | ||
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 | Selective inhibitor of protein tyrosine phosphatases localized to mitochondrion 1 (PTPMT1) (IC50 = 1.08 μM in vitro). Stimulates increased insulin secretion by β-cells in rat pancreatic islets. Displays antitcancer properties in FaDu cells. Also preserves functional hematopoietic stem cells ex vivo. |
Alexidine dihydrochloride Dilution Calculator
Alexidine dihydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.7191 mL | 8.5953 mL | 17.1907 mL | 34.3814 mL | 42.9767 mL |
5 mM | 0.3438 mL | 1.7191 mL | 3.4381 mL | 6.8763 mL | 8.5953 mL |
10 mM | 0.1719 mL | 0.8595 mL | 1.7191 mL | 3.4381 mL | 4.2977 mL |
50 mM | 0.0344 mL | 0.1719 mL | 0.3438 mL | 0.6876 mL | 0.8595 mL |
100 mM | 0.0172 mL | 0.086 mL | 0.1719 mL | 0.3438 mL | 0.4298 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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Selective inhibitor of protein tyrosine phosphatases localized to mitochondrion 1 (PTPMT1) (IC50 = 1.08 μM in vitro). Stimulates increased insulin secretion by β-cells in rat pancreatic islets. Displays antitcancer properties in FaDu cells.
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Alexidine Dihydrochloride Attenuates Osteoclast Formation and Bone Resorption and Protects Against LPS-Induced Osteolysis.[Pubmed:26363136]
J Bone Miner Res. 2016 Mar;31(3):560-72.
Aseptic loosening and periprosthetic infection leading to inflammatory osteolysis is a major complication associated with total joint arthroplasty (TJA). The liberation of bacterial products and/or implant-derived wear particles activates immune cells that produce pro-osteoclastogenic cytokines that enhance osteoclast recruitment and activity, leading to bone destruction and osteolysis. Therefore, agents that prevent the inflammatory response and/or attenuate excessive osteoclast (OC) formation and bone resorption offer therapeutic potential by prolonging the life of TJA implants. Alexidine dihydrochloride (AD) is a bisbiguanide compound commonly used as an oral disinfectant and in contact lens solutions. It possesses antimicrobial, anti-inflammatory and anticancer properties; however, its effects on OC biology are poorly described. Here, we demonstrate that AD inhibits OC formation and bone resorption in vitro and exert prophylatic protection against LPS-induced osteolysis in vivo. Biochemical analysis demonstrated that AD suppressed receptor activator of NF-kappaB ligand (RANKL)-induced activation of mitogen-activated protein kinases (ERK, p38, and JNK), leading to the downregulation of NFATc1. Furthermore, AD disrupted F-actin ring formation and attenuated the ability of mature OC to resorb bone. Collectively, our findings suggest that AD may be a promising prophylactic anti-osteoclastic/resorptive agent for the treatment of osteolytic diseases caused by excessive OC formation and function.
Potential use of alexidine dihydrochloride as an apoptosis-promoting anticancer agent.[Pubmed:16985057]
Mol Cancer Ther. 2006 Sep;5(9):2234-40.
Despite advances in surgery, radiation, and chemotherapy, novel therapeutics are needed for head and neck cancer treatment. The objective of this current study was to evaluate Alexidine dihydrochloride as a novel compound lead for head and neck cancers. Using a tetrazolium-based assay, the dose required to reduce cell viability by 50% (ED50) was found to be approximately 1.8 micromol/L in FaDu (human hypopharyngeal squamous cancer) and approximately 2.6 micromol/L in C666-1 (human undifferentiated nasopharyngeal cancer) cells. In contrast, the ED50 values were much higher in untransformed cells, specifically at approximately 8.8 micromol/L in GM05757 (primary normal human fibroblast), approximately 8.9 micromol/L in HNEpC (primary normal human nasal epithelial), and approximately 19.6 micromol/L in NIH/3T3 (mouse embryonic fibroblast) cells. Alexidine dihydrochloride did not interfere with the activities of cisplatin, 5-fluorouracil, or radiation, and interacted in a less-than-additive manner. DNA content analyses and Hoechst 33342 staining revealed that this compound induced apoptosis. Alexidine dihydrochloride-induced mitochondrial damage was visualized using transmission electron microscopy. Mitochondrial membrane potential (DeltaPsiM) depolarization was detectable after only 3 hours of treatment, and was followed by cytosolic Ca2+ increase along with loss of membrane integrity/cell death. Caspase-2 and caspase-9 activities were detectable at 12 hours, caspase-8 at 24 hours, and caspase-3 at 48 hours. FaDu cell clonogenic survival was reduced to < 5% with 1 micromol/L Alexidine dihydrochloride, and, correspondingly, this compound decreased the in vivo tumor-forming potential of FaDu cells. Thus, we have identified Alexidine dihydrochloride as the first bisbiguanide compound with anticancer specificity.
Maintenance of mouse hematopoietic stem cells ex vivo by reprogramming cellular metabolism.[Pubmed:25593337]
Blood. 2015 Mar 5;125(10):1562-5.
The difficulty in maintaining the reconstituting capabilities of hematopoietic stem cells (HSCs) in culture outside of the bone marrow microenvironment has severely limited their utilization for clinical therapy. This hurdle is largely due to the differentiation of long-term stem cells. Emerging evidence suggests that energy metabolism plays an important role in coordinating HSC self-renewal and differentiation. Here, we show that treatment with Alexidine dihydrochloride, an antibiotic and a selective inhibitor of the mitochondrial phosphatase Ptpmt1, which is crucial for the differentiation of HSCs, reprogrammed cellular metabolism from mitochondrial aerobic metabolism to glycolysis, resulting in a remarkable preservation of long-term HSCs ex vivo in part through hyperactivation of adenosine 5'-monophosphate-activated protein kinase (AMPK). In addition, inhibition of mitochondrial metabolism and activation of AMPK by metformin, a diabetes drug, also decreased differentiation and helped maintain stem cells in culture. Thus, manipulating metabolic pathways represents an effective new strategy for ex vivo maintenance of HSCs.
Pharmacological targeting of the mitochondrial phosphatase PTPMT1.[Pubmed:20167843]
J Pharmacol Exp Ther. 2010 May;333(2):584-92.
The dual-specificity protein tyrosine phosphatases (PTPs) play integral roles in the regulation of cell signaling. There is a need for new tools to study these phosphatases, and the identification of inhibitors potentially affords not only new means for their study, but also possible therapeutics for the treatment of diseases caused by their dysregulation. However, the identification of selective inhibitors of the protein phosphatases has proven somewhat difficult. PTP localized to mitochondrion 1 (PTPMT1) is a recently discovered dual-specificity phosphatase that has been implicated in the regulation of insulin secretion. Screening of a commercially available small-molecule library yielded Alexidine dihydrochloride, a dibiguanide compound, as an effective and selective inhibitor of PTPMT1 with an in vitro concentration that inhibits response by 50% of 1.08 microM. A related dibiguanide analog, chlorhexidine dihydrochloride, also significantly inhibited PTPMT1, albeit with lower potency, while a monobiguanide analog showed very weak inhibition. Treatment of isolated rat pancreatic islets with Alexidine dihydrochloride resulted in a dose-dependent increase in insulin secretion, whereas treatment of a pancreatic beta-cell line with the drug affected the phosphorylation of mitochondrial proteins in a manner similar to genetic inhibition of PTPMT1. Furthermore, knockdown of PTPMT1 in rat islets rendered them insensitive to Alexidine dihydrochloride treatment, providing evidence for mechanism-based activity of the inhibitor. Taken together, these studies establish Alexidine dihydrochloride as an effective inhibitor of PTPMT1, both in vitro and in cells, and support the notion that PTPMT1 could serve as a pharmacological target in the treatment of type II diabetes.