Search Site
Home >> Research Area >>PI3K/Akt/mTOR Signaling>>Akt >> 10-DEBC hydrochloride
10-DEBC hydrochlorideAkt inhibitor

10-DEBC hydrochloride

Catalog No. BCC7409
Size Price Stock
10mg $142.00 Ship Within 7 Days
50mg $600.00 Ship Within 7 Days
Related Products

Organizitions Citing Our Products recently


Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris

Quality Control of 10-DEBC hydrochloride

Chemical structure

10-DEBC hydrochloride

Biological Activity of 10-DEBC hydrochloride

Selective inhibitor of Akt/PKB. Inhibits IGF-1-stimulated phosphorylation and activation of Akt (complete inhibition at 2.5 μM), suppressing downstream activation of mTOR, p70 S6 kinase and S6 ribosomal protein. Shows no activity at PDK1, SGK1 or PI 3-kinase. Inhibits cell growth (IC50 ~ 2-6 μM) and induces apoptosis in rhabdomyosarcoma cells.

10-DEBC hydrochloride Dilution Calculator

Concentration (start)
Volume (start)
Concentration (final)
Volume (final)


10-DEBC hydrochloride Molarity Calculator



Chemical Properties of 10-DEBC hydrochloride

Cas No. 925681-41-0 SDF Download SDF
Chemical Name 10-[4'-(N,N-Diethylamino)butyl]-2-chlorophenoxazine hydrochloride
Standard InChI InChI=1S/C20H25ClN2O.ClH/c1-3-22(4-2)13-7-8-14-23-17-9-5-6-10-19(17)24-20-12-11-16(21)15-18(20)23;/h5-6,9-12,15H,3-4,7-8,13-14H2,1-2H3;1H
Formula C20H25N2OCl.HCl M.Wt 381.34
Solubility Soluble to 100 mM in water and to 100 mM in DMSO
Storage Desiccate at +4°C
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.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 10-DEBC hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.6223 mL 13.1117 mL 26.2233 mL 52.4466 mL 65.5583 mL
5 mM 0.5245 mL 2.6223 mL 5.2447 mL 10.4893 mL 13.1117 mL
10 mM 0.2622 mL 1.3112 mL 2.6223 mL 5.2447 mL 6.5558 mL
50 mM 0.0524 mL 0.2622 mL 0.5245 mL 1.0489 mL 1.3112 mL
100 mM 0.0262 mL 0.1311 mL 0.2622 mL 0.5245 mL 0.6556 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.

Background on 10-DEBC hydrochloride

10-DEBC hydrochloride is a selective inhibitor of Akt (or termed PKB) [1], with an IC50 value of approximate 48 μM [2].

Akt is a type of serine/threonine kinase. It phosphorylates and inactivates components in the apoptotic machinery, including Caspase 9 and BAD. Akt phosphorylates and inhibits a Forkhead transcription factor, and hence promotes cell survival [3].

As demonstrated by LDH and MTT tests, 10-DEBC dihydrochloride at 10 μM did not affect cell viability when it was applied alone. 10-DEBC dihydrochloride at this concentration in cisplatin-treated U251 cells abrogated the cytoprotective effect of metformin. 10-DEBC dihydrochloride showed neutralization effect on the antiapoptotic activity of metformin, increasing the cell membrane phosphatidylserine exposure and DNA fragmentation to the levels observed with cisplatin alone. In U251 cells, 10-DEBC dihydrochloride significantly induced the production of reactive oxygen species. In cisplatin-treated cells, 10-DEBC dihydrochloride consequently reduced the antioxidative effect of metformin [1].

Studies in effects of 10-DEBC hydrochloride on BAT explants incubated with phentolamine were carried out. Without any effect on total Akt protein, 10-DEBC hydrochloride inhibited the phosphorylation of Akt Ser473 by ~40%. In WT explants, the 10-DEBC hydrochloride alone had no effect on the phosphorylation of Ser485/491 of AMPK, and did not affect the phentolamine effect. However, in β-AR KO explants, 10-DEBC hydrochloride blunted the AMPK Ser485/491 phosphorylation increased by phentolamine [4].

[1].  Janjetovic K, Vucicevic L, Misirkic M, et al. Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt. European journal of pharmacology, 2011, 651(1): 41-50.
[2].  De Abreu LA, Calixto C, Waltero CF, et al. The conserved role of the AKT/GSK3 axis in cell survival and glycogen metabolism in Rhipicephalus (Boophilus) microplus embryo tick cell line BME26. Biochimica et Biophysica Acta (BBA)-General Subjects, 2013, 1830(3): 2574-2582.
[3].  Brunet A, Bonni A, Zigmond MJ, et al. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. cell, 1999, 96(6): 857-868.
[4].  Pulinilkunnil T, He H, Kong D, et al. Adrenergic regulation of AMP-activated protein kinase in brown adipose tissue in vivo. Journal of Biological Chemistry, 2011, 286(11): 8798-8809.

References on 10-DEBC hydrochloride

Fabrication yields of serially harvested calf-fed Holstein steers fed zilpaterol hydrochloride.[Pubmed: 28380524]

Holstein steers ( = 110) were fed zilpaterol hydrochloride (ZH) for 0 or 20 d before slaughter during a 280-d serial harvest study. Cattle were harvested every 28 d beginning at 254 d on feed (DOF) and concluding at 534 DOF. After slaughter, carcasses were chilled for 48 h and then fabricated into boneless closely trimmed or denuded subprimals, lean trim, trimmable fat, and bone. Inclusion of ZH increased cold side weight (CSW) by 10.3 kg ( < 0.01; 212.7 vs. 202.4 kg [SEM 1.96]) and saleable yield by 10.4 kg ( < 0.01; 131.9 vs. 121.5 kg [SEM 1.16]) in calf-fed Holstein steer carcasses. Additionally, saleable yield as a percentage of CSW increased ( ≤ 0.01) by 2.19% (62.64 vs. 60.45% [SEM 0.22]) for cattle supplemented with ZH. Subprimal weights were heavier ( ≤ 0.05) from cattle that received ZH except for the bottom sirloin ball tip, back ribs, and outside skirt regardless of slaughter endpoint. Yield of top round, bottom round, and knuckle was increased ( ≤ 0.01) following ZH supplementation by 0.37, 0.24, and 0.18%, respectively. Yield of the top sirloin butt, strip loin, and tenderloin was increased ( ≤ 0.01) concurrent with ZH supplementation by 0.18, 0.11, and 0.09%, respectively. Regarding the rib primal, the rib eye roll tended ( = 0.08) to had increased yield (2.80 vs. 2.72% [SEM 0.03]) with ZH supplementation; both back ribs and blade meat exhibited increased ( ≤ 0.04) yields of 0.04%. Relative to the chuck primal, increased ( ≤ 0.03) yields of shoulder clod, pectoral meat, and mock tender were observed (0.13, 0.07, and 0.04%, respectively). Yield changes for subprimal brisket, plate, and flank were limited to increased ( < 0.01) proportion of flank steak and elephant ear (cutaneous trunci), 0.07 and 0.04%, respectively. Feeding duration notably altered ( ≤ 0.01) weights and percentages of all subprimals except the brisket. Saleable yield increased ( ≤ 0.01) by 0.192 kg/d with additional DOF. Moreover, trimmable fat and bone increased ( ≤ 0.01) by 0.146 and 0.050 kg/d, respectively. These data illustrate improved saleable meat yields for calf-fed Holstein steers supplemented with ZH and provide the beef industry knowledge of fabrication yield changes throughout a wide range of harvest endpoints.

Biophysical study on the interaction between eperisone hydrochloride and human serum albumin using spectroscopic, calorimetric, and molecular docking analysis.[Pubmed: 28380300]

Eperisone hydrochloride (EH) is a widely used as a muscle relaxant for patients with muscular contracture, low back pain, or spasticity. Human serum albumin (HSA), a highly soluble negatively charged, endogenous and abundant plasma protein ascribed with the ligand binding and transport properties. The current study was undertaken to explore the interaction between EH and the serum transport protein, HSA. Study of the interaction between HSA and EH was carried by UV-vis, fluorescence quenching, circular dichroism (CD) spectroscopy, FRET, and ITC. Tryptophan fluorescence intensity of HSA was strongly quenched by EH. The binding constants (Kb) were obtained by fluorescence quenching and results shows that the EH-HSA interaction revealed a static mode of quenching, with binding constant Kb ~104 reflecting high affinity of EH for HSA. The negative ΔGº value for binding indicated that HSA-EH interaction is a spontaneous process. Thermodynamic analysis shows HSA-EH complex formation occurs primarily due to hydrophobic interactions and hydrogen bonds were facilitate the binding of EH. EH binding induces α-helix of HSA as obtained by far-UV CD and FTIR spectroscopy. In addition, the distance between EH (acceptor) and Trp residue of HSA (donor) was calculated 2.18 nm using Förster's resonance energy transfer theory. Furthermore, molecular docking results revealed EH binds with HSA, and binding site is positioned in Sudlow Site I of HSA (subdomain IIA). This work provides a useful experimental strategy for studying the interaction of myorelaxant with HSA, helping to understand the activity and mechanism of drug binding.

Unusual 4-arsonoanilinium cationic species in the hydrochloride salt of (4-aminophenyl)arsonic acid and formed in the reaction of the acid with copper(II) sulfate, copper(II) chloride and cadmium chloride.[Pubmed: 28378716]

Structures having the unusual protonated 4-arsonoanilinium species, namely in the hydrochloride salt, C6H9AsNO3+·Cl-, (I), and the complex salts formed from the reaction of (4-aminophenyl)arsonic acid (p-arsanilic acid) with copper(II) sulfate, i.e. hexaaquacopper(II) bis(4-arsonoanilinium) disulfate dihydrate, (C6H9AsNO3)2[Cu(H2O)6](SO4)2·2H2O, (II), with copper(II) chloride, i.e. poly[bis(4-arsonoanilinium) [tetra-μ-chlorido-cuprate(II)]], {(C6H9AsNO3)2[CuCl4]}n, (III), and with cadmium chloride, i.e. poly[bis(4-arsonoanilinium) [tetra-μ-chlorido-cadmate(II)]], {(C6H9AsNO3)2[CdCl4]}n, (IV), have been determined. In (II), the two 4-arsonoanilinium cations are accompanied by [Cu(H2O)6]2+ cations with sulfate anions. In the isotypic complex salts (III) and (IV), they act as counter-cations to the {[CuCl4]2-}n or {[CdCl4]2-}n anionic polymer sheets, respectively. In (II), the [Cu(H2O)6]2+ ion sits on a crystallographic centre of symmetry and displays a slightly distorted octahedral coordination geometry. The asymmetric unit for (II) contains, in addition to half the [Cu(H2O)6]2+ ion, one 4-arsonoanilinium cation, a sulfate dianion and a solvent water molecule. Extensive O-H...O and N-H...O hydrogen bonds link all the species, giving an overall three-dimensional structure. In (III), four of the chloride ligands are related by inversion [Cu-Cl = 2.2826 (8) and 2.2990 (9) Å], with the other two sites of the tetragonally distorted octahedral CuCl6 unit occupied by symmetry-generated Cl-atom donors [Cu-Cl = 2.9833 (9) Å], forming a two-dimensional coordination polymer network substructure lying parallel to (001). In the crystal, the polymer layers are linked across [001] by a number of bridging hydrogen bonds involving N-H...Cl interactions from head-to-head-linked As-O-H...O 4-arsonoanilinium cations. A three-dimensional network structure is formed. CdII compound (IV) is isotypic with CuII complex (III), but with the central CdCl6 complex repeat unit having a more regular M-Cl bond-length range [2.5232 (12)-2.6931 (10) Å] compared to that in (III). This series of compounds represents the first reported crystal structures having the protonated 4-arsonoanilinium species.

Lens opacities in children using methylphenidate Hydrochloride.[Pubmed: 28376677]

To assess clinical findings of eye examination in children who is taking methylphenidate hydrochloride with Attention Deficit Hyperactivity Disorder.


10-DEBC hydrochloride,925681-41-0,PI3K/Akt/mTOR Signaling,Akt, supplier, inhibitor,Antagonist,Blocker,Modulator,Agonist, activators, activates, potent, BioCrick

Online Inquiry

Fill out the information below

* Required Fields