883886-67-7

Basic information

• Product Name: H-GLY-OME.HCL
• Synonyms: H-GLY-OME HCL;Methyl 2-aMinoacetate hydrochloride(2:1);NVFYYIKIOAQVBY-UHFFFAOYSA-N
• CAS NO: 883886-67-7
• Molecular Formula: C6H15ClN2O4
• Molecular Weight: 214.6473
• Mol File: 883886-67-7.mol
• Article Data: 127

Chemical Properties

• Appearance: /
• Storage Temp.: Sealed in dry,Room Temperature
• CAS DataBase Reference: H-GLY-OME.HCL(CAS DataBase Reference)
• NIST Chemistry Reference: H-GLY-OME.HCL(883886-67-7)
• EPA Substance Registry System: H-GLY-OME.HCL(883886-67-7)

Safety Data

• Hazardous Substances Data: 883886-67-7(Hazardous Substances Data)

Usage

General Description

H-GLY-OME.HCL is a chemical compound that consists of a hydrochloride salt form of H-GLY-OME, also known as N-(2-hydroxyethyl)glycine. It is a derivative of the amino acid glycine and is commonly used in organic synthesis and pharmaceutical research. H-GLY-OME.HCL is a white to off-white crystalline powder with a molecular weight of 151.60 g/mol. It is soluble in water and has a strong potential to act as a chelating agent due to its unique chemical structure. H-GLY-OME.HCL is often used in the development of new drugs and in the production of various pharmaceuticals.

Upstream product

• 67-56-1 methanol 
• 54930-24-4 (Z)-4-((carboxymethyl)amino)-4-oxobut-2-enoic acid 
• 4530-20-5 BOC-glycine 
• 13165-72-5 chlorosulfite de methyle 
• 56-40-6 glycine 
• 616-34-2 methoxycarbonylmethylamine 
• 298-12-4 Glyoxilic acid 
• 77-76-9 2,2-dimethoxy-propane 
• 74-88-4 methyl iodide 
• 4746-64-9 2-aminoacetyl chloride 
• 17136-35-5 N-benzyl glycine methyl ester hydrochloride 
• 7647-01-0 hydrogenchloride 
• 128666-05-7 2-phenyl-4-methoxyimidazole 
• 172912-98-0 methyl N-succinimidomethylglycinate 

Downstream Products

• 132221-25-1 [1-(4-Bromo-2-fluoro-benzyl)-2,4-dioxo-1,4-dihydro-2H-thieno[3,2-d]pyrimidin-3-yl]-acetic acid 
• 78399-59-4 N-(β-Benzoylethyl)-glycinmethylester-hydrochlorid 
• 171725-31-8 methyl-N'-[m-(2-propenyloxycarbonyl)phenyl]ureidoacetate 
• 1012796-05-2 5-O-benzyl-3-C-cyano-3-deoxy-1,2-O-isopropylidene-3-{[(methoxycarbonyl)methyl]amino}-α-D-ribofuranose 
• 132221-32-0 [1-(3,4-Dichloro-benzyl)-2,4-dioxo-1,4,5,6,7,8-hexahydro-2H-benzo[4,5]thieno[2,3-d]pyrimidin-3-yl]-acetic acid 
• 133166-77-5 [1-(3,4-Dichloro-benzyl)-5,6-dimethyl-2,4-dioxo-1,4-dihydro-2H-thieno[2,3-d]pyrimidin-3-yl]-acetic acid 
• 117196-03-9 [(S)-2-(2,3-Dichloro-quinoxaline-6-sulfonylamino)-3-(4-hydroxy-phenyl)-propionylamino]-acetic acid methyl ester 
• 146691-55-6 tert-Butyl N-(benzyloxycarbonyl)-2(RS)-<1-amino>ethyl>pipecolate 
• 112141-15-8 Z(OMe)-Gly-Lys(Z)-Gly₂-OMe 
• 159878-80-5 Boc Me Ant-Gly-OMe 
• 101055-29-2 methyl diphenylphosphorylglycinate 
• 101055-24-7 Z-Phe-ΔAla-Gly-OMe 
• 101055-35-0 [3-Azido-2-((S)-2-benzyloxycarbonylamino-3-phenyl-propionylamino)-propionylamino]-acetic acid methyl ester 

Relevant articles and documents

Identification of a fluorescent small-molecule enhancer for therapeutic autophagy in colorectal cancer by targeting mitochondrial protein translocase TIM44

Objective As the modulation of autophagic processes can be therapeutically beneficial to cancer treatment, the identification of novel autophagic enhancers is highly anticipated. However, current autophagy-inducing anticancer agents exert undesired side effects owing to their non-specific biodistribution in off-target tissues. This study aims to develop a multifunctional agent to integrate cancer targeting, imaging and therapy and to investigate its mechanism. Design A series of mitochondria-targeting near-infrared (NIR) fluorophores were synthesised, screened and identified for their autophagy-enhancing activity. The optical properties and biological effects were tested both in vitro and in vivo. The underlying mechanism was investigated using inhibitors, small interfering RNA (siRNA), RNA sequencing, mass spectrometry and human samples. Results We have screened and identified a new NIR autophagy-enhancer, IR-58, which exhibits significant tumour-selective killing effects. IR-58 preferentially accumulates in the mitochondria of colorectal cancer (CRC) cells and xenografts, a process that is glycolysis-dependent and organic anion transporter polypeptide-dependent. IR-58 kills tumour cells and induces apoptosis via inducing excessive autophagy, which is mediated through the reactive oxygen species (ROS)-Akt-mammalian target of rapamycin (mTOR) pathway. RNA sequencing, mass spectrometry and siRNA interference studies demonstrate that translocase of inner mitochondrial membrane 44 (TIM44)-superoxide dismutase 2 (SOD2) pathway inhibition is responsible for the excessive ROS, autophagy and apoptosis induced by IR-58. TIM44 expression correlates positively with CRC development and poor prognosis in patients. Conclusions A novel NIR small-molecule autophagy-enhancer, IR-58, with mitochondria-targeted imaging and therapy capabilities was developed for CRC treatment. Additionally, TIM44 was identified for the first time as a potential oncogene, which plays an important role in autophagy through the TIM44-SOD2-ROS-mTOR pathway.

Translation of Mycobacterium Survival Strategy to Develop a Lipo-peptide based Fusion Inhibitor**

The entry of enveloped virus requires the fusion of viral and host cell membranes. An effective fusion inhibitor aiming at impeding such membrane fusion may emerge as a broad-spectrum antiviral agent against a wide range of viral infections. Mycobacterium survives inside the phagosome by inhibiting phagosome–lysosome fusion with the help of a coat protein coronin 1. Structural analysis of coronin 1 and other WD40-repeat protein suggest that the trp-asp (WD) sequence is placed at distorted β-meander motif (more exposed) in coronin 1. The unique structural feature of coronin 1 was explored to identify a simple lipo-peptide sequence (myr-WD), which effectively inhibits membrane fusion by modulating the interfacial order, water penetration, and surface potential. The mycobacterium inspired lipo-dipeptide was successfully tested to combat type 1 influenza virus (H1N1) and murine coronavirus infections as a potential broad-spectrum antiviral agent.

Silver-Mediated [3 + 2] Cycloaddition of Azomethine Ylides with Trifluoroacetimidoyl Chlorides for the Synthesis of 5-(Trifluoromethyl)imidazoles

A silver-mediated [3 + 2] cycloaddition of azomethine ylides with trifluoroacetimidoyl chlorides for the rapid assembly of 5-(trifluoromethyl)imidazoles has been developed. Notable features of the reaction include readily accessible reagents, a broad substrate scope, and high efficiency. The protocol can be successfully applied to construct the analogue of the specific allosteric modulator of GABAA receptors. The silver species could be recycled by a simple operation.