1032350-13-2 | 8-(4-(1-Aminocyclobutyl)phenyl)-9-phenyl-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3(2h)-one dihydrochloride

Packsize	Purity	Availability	Price	Discounted Price
5mg	95%	in stock	$22.00	$15.00
50mg	95%	in stock	$188.00	$132.00
100mg	95%	in stock	$201.00	$141.00
250mg	95%	in stock	$339.00	$237.00
1g	95%	in stock	$836.00	$585.00

Description

• Catalog Number: AE11280
• Chemical Name: 8-(4-(1-Aminocyclobutyl)phenyl)-9-phenyl-[1,2,4]triazolo[3,4-f][1,6]naphthyridin-3(2h)-one dihydrochloride
• CAS Number: 1032350-13-2
• Molecular Formula: C25H23Cl2N5O
• Molecular Weight: 480.389
• MDL Number: MFCD14584463
• SMILES: O=c1[nH]nc2n1ccc1c2cc(c(n1)c1ccc(cc1)C1(N)CCC1)c1ccccc1.Cl.Cl

Computed Properties

• Complexity: 760
• Covalently-Bonded Unit Count: 3
• Heavy Atom Count: 33
• Hydrogen Bond Acceptor Count: 4
• Hydrogen Bond Donor Count: 4
• Rotatable Bond Count: 3

Upstream Synthesis Route

MK-2206 Dihydrochloride is a potent and selective allosteric inhibitor of Akt (protein kinase B) that plays a crucial role in various signaling pathways within cells. This compound is widely utilized in chemical synthesis for its ability to specifically target and modulate Akt activity, a key regulator of cell growth, survival, and metabolism.In chemical synthesis, MK-2206 Dihydrochloride is employed as a valuable tool for studying the downstream effects of Akt inhibition on cellular processes. By selectively blocking the activation of Akt, researchers can investigate the impact of this inhibition on signaling cascades, protein expression, and cell proliferation. This provides valuable insights into the molecular mechanisms underlying diseases such as cancer, where aberrant Akt signaling is commonly observed.Furthermore, MK-2206 Dihydrochloride's unique mechanism of action makes it a versatile compound for designing novel strategies in drug development and chemical biology. Its specificity towards Akt distinguishes it as a valuable resource for exploring the intricate interplay between signaling pathways and identifying potential therapeutic targets for various disease conditions.Overall, the application of MK-2206 Dihydrochloride in chemical synthesis offers a sophisticated approach to unraveling the complexities of cellular signaling and opens up new possibilities for innovative research in understanding and treating diseases at the molecular level.

Literature

• Plasticizer Di-(2-Ethylhexyl)Phthalate Induces Epithelial-to-Mesenchymal Transition and Renal Fibrosis In Vitro and In Vivo.

  Toxicological sciences : an official journal of the Society of Toxicology 20180701

• Gap junctional intercellular communication and endoplasmic reticulum stress regulate chronic cadmium exposure induced apoptosis in HK-2 cells.

  Toxicology letters 20180515

• Airborne nitro-PAHs induce Nrf2/ARE defense system against oxidative stress and promote inflammatory process by activating PI3K/Akt pathway in A549 cells.

  Toxicology in vitro : an international journal published in association with BIBRA 20171001

• Akt activation by Ca(2+)/calmodulin-dependent protein kinase kinase 2 (CaMKK2) in ovarian cancer cells.

  The Journal of biological chemistry 20170825

• Role of Exchange Protein Directly Activated by Cyclic AMP Isoform 1 in Energy Homeostasis: Regulation of Leptin Expression and Secretion in White Adipose Tissue.

  Molecular and cellular biology 20161001

• Taurocholate Induces Cyclooxygenase-2 Expression via the Sphingosine 1-phosphate Receptor 2 in a Human Cholangiocarcinoma Cell Line.

  The Journal of biological chemistry 20151225

• Utilization of human nuclear receptors as an early counter screen for off-target activity: a case study with a compendium of 615 known drugs.

  Toxicological sciences : an official journal of the Society of Toxicology 20150601

• Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines.

  Journal of cancer research and clinical oncology 20150401

• S6 inhibition contributes to isoflurane neurotoxicity in the developing brain.

  Toxicology letters 20150304

• The Akt inhibitor MK-2206 enhances the cytotoxicity of paclitaxel (Taxol) and cisplatin in ovarian cancer cells.

  Naunyn-Schmiedeberg's archives of pharmacology 20150101

• Elucidating mechanisms of toxicity using phenotypic data from primary human cell systems--a chemical biology approach for thrombosis-related side effects.

  International journal of molecular sciences 20150101

• Detection of key enzymes, free radical reaction products and activated signaling molecules as biomarkers of cell damage induced by benzo[a]pyrene in human keratinocytes.

  Toxicology in vitro : an international journal published in association with BIBRA 20140801

• PI3K signaling mediates diverse regulation of ATF4 expression for the survival of HK-2 cells exposed to cadmium.

  Archives of toxicology 20140201

• Preventing the calorie restriction-induced increase in insulin-stimulated Akt2 phosphorylation eliminates calorie restriction's effect on glucose uptake in skeletal muscle.

  Biochimica et biophysica acta 20121101

• A novel PKB/Akt inhibitor, MK-2206, effectively inhibits insulin-stimulated glucose metabolism and protein synthesis in isolated rat skeletal muscle.

  The Biochemical journal 20121001

• Phosphatidylinositol 3-kinase/Akt signaling pathway activates the WNK-OSR1/SPAK-NCC phosphorylation cascade in hyperinsulinemic db/db mice.

  Hypertension (Dallas, Tex. : 1979) 20121001

• Dual targeting of the Akt/mTOR signaling pathway inhibits castration-resistant prostate cancer in a genetically engineered mouse model.

  Cancer research 20120901

• Harnessing the PI3K/Akt/mTOR pathway in T-cell acute lymphoblastic leukemia: eliminating activity by targeting at different levels.

  Oncotarget 20120801

• Combination of an allosteric Akt Inhibitor MK-2206 with etoposide or rapamycin enhances the antitumor growth effect in neuroblastoma.

  Clinical cancer research : an official journal of the American Association for Cancer Research 20120701

• Akt inhibitors MK-2206 and nelfinavir overcome mTOR inhibitor resistance in diffuse large B-cell lymphoma.

  Clinical cancer research : an official journal of the American Association for Cancer Research 20120501

• The Akt inhibitor MK2206 synergizes, but perifosine antagonizes, the BRAF(V600E) inhibitor PLX4032 and the MEK1/2 inhibitor AZD6244 in the inhibition of thyroid cancer cells.

  The Journal of clinical endocrinology and metabolism 20120201

• MK-2206, a novel allosteric inhibitor of Akt, synergizes with gefitinib against malignant glioma via modulating both autophagy and apoptosis.

  Molecular cancer therapeutics 20120101

• Inhibition of AKT with the orally active allosteric AKT inhibitor, MK-2206, sensitizes endometrial cancer cells to progestin.

  PloS one 20120101

• First-in-man clinical trial of the oral pan-AKT inhibitor MK-2206 in patients with advanced solid tumors.

  Journal of clinical oncology : official journal of the American Society of Clinical Oncology 20111210

• IKBKE protein activates Akt independent of phosphatidylinositol 3-kinase/PDK1/mTORC2 and the pleckstrin homology domain to sustain malignant transformation.

  The Journal of biological chemistry 20111028

• The insulin-like growth factor 1 pathway is a potential therapeutic target for low-grade serous ovarian carcinoma.

  Gynecologic oncology 20111001

• Next-generation Akt inhibitors provide greater specificity: effects on glucose metabolism in adipocytes.

  The Biochemical journal 20110415

• The Akt-specific inhibitor MK2206 selectively inhibits thyroid cancer cells harboring mutations that can activate the PI3K/Akt pathway.

  The Journal of clinical endocrinology and metabolism 20110401

• eEF-2 kinase dictates cross-talk between autophagy and apoptosis induced by Akt Inhibition, thereby modulating cytotoxicity of novel Akt inhibitor MK-2206.

  Cancer research 20110401

• MK-2206, an allosteric Akt inhibitor, enhances antitumor efficacy by standard chemotherapeutic agents or molecular targeted drugs in vitro and in vivo.

  Molecular cancer therapeutics 20100701

• Combination treatment with MEK and AKT inhibitors is more effective than each drug alone in human non-small cell lung cancer in vitro and in vivo.

  PloS one 20100101