Need Assistance?

US & Canada:
+
UK: +

FAQs

Resources

Our Highlights

GMP Grade Efficient workshop for GMP production.
Optimal Prices Buying products on this site guarantees the best price!
Commercial Batches Independent GMP manufacturing suites that handle commercial batches
Prompt Delivery Warehouses in multiple cities to ensure timely delivery
Flexible Quantity Quantities available from milligrams to ton

Application Area

γ-(2-Thienyl)-D-β-homoalanine hydrochloride

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

Category

β−Amino Acids

Catalog number

BAT-007541

CAS number

270065-91-3

Molecular Formula

C8H12ClNO2S

Molecular Weight

221.70

γ-(2-Thienyl)-D-β-homoalanine hydrochloride

IUPAC Name

(3S)-3-amino-4-thiophen-2-ylbutanoic acid;hydrochloride

Alternative CAS

332061-90-2

Synonyms

H-D-Ala(2-Thienyl)-(C#CH2)OH HCl; (S)-3-Amino-4-(2-thienyl)butanoic acid hydrochloride; (3S)-3-amino-4-thiophen-2-ylbutanoic acid,hydrochloride; (S)-3-AMINO-4-(2-THIENYL)BUTANOIC ACID HYDROCHLORIDE; (S)-3-Amino-4-(thiophen-2-yl)butanoic acid hydrochloride; (S)-3-Amino-4-(2-thienyl)-butyric acid HCl; (2-Thienyl)-L-ss-homoalanine hydrochloride; (2-Thienyl)-L-β-homoalanine hydrochloride; L-β-HomoAla(2-thienyl)-OH HCl

Appearance

Off-white powder

Purity

≥ 98% (HPLC)

Density

1.291 g/cm3 (Predicted)

Melting Point

176-182 °C

Boiling Point

336.9 °C at 760 mmHg

Storage

Store at 2-8 °C

InChI

InChI=1S/C8H11NO2S.ClH/c9-6(5-8(10)11)4-7-2-1-3-12-7;/h1-3,6H,4-5,9H2,(H,10,11);1H/t6-;/m1./s1

InChI Key

DPMHHGFSWLCCBH-FYZOBXCZSA-N

Canonical SMILES

C1=CSC(=C1)CC(CC(=O)O)N.Cl

γ-(2-Thienyl)-D-β-homoalanine hydrochloride, an amino acid derivative with applications in pharmaceuticals and biochemical research, offers a myriad of opportunities for innovation. Here are the key applications portrayed with high perplexity and burstiness:

Drug Development: Positioned at the forefront of pharmaceutical innovation, γ-(2-Thienyl)-D-β-homoalanine hydrochloride serves as a foundational element in crafting novel drug entities. Its distinct chemical architecture seamlessly integrates into drug structures, elevating their efficacy, durability, and specificity. Through the strategic incorporation of this compound, researchers can customize medications for optimal therapeutic outcomes, pushing the boundaries of pharmaceutical excellence.

Peptide Synthesis: Embraced across diverse biological and medical research domains, this compound plays a pivotal role in peptide synthesis, a cornerstone of scientific exploration. By embedding γ-(2-Thienyl)-D-β-homoalanine into peptides, scientists embark on an intricate journey to decipher the impact of specific amino acid alterations on peptide functionality and reactivity. This application is indispensable for the development of peptide-centered therapeutics and the unraveling of complex protein interactions, paving the way for groundbreaking advancements in medicine.

Enzyme Inhibition Studies: Serving as a fundamental tool in the realm of enzyme inhibition investigations, γ-(2-Thienyl)-D-β-homoalanine hydrochloride unravels the intricacies of enzyme mechanics and kinetics. Researchers harness the power of this compound to engineer inhibitors that target precise enzyme pathways, potentially birthing novel therapeutic modalities. This strategic approach aids in identifying critical metabolic routes and cellular regulatory nodal points, heralding a new era of therapeutic innovation and scientific enlightenment.

Neurochemical Research: Nestled within the realm of neurochemistry, γ-(2-Thienyl)-D-β-homoalanine hydrochloride emerges as a pioneering agent in unraveling the enigmatic world of neurotransmitter systems. By reshaping the landscape of neurotransmitter-associated amino acids, scientists embark on a quest to probe the intricate roles of these compounds in neural signaling pathways and neurological disorder etiology. This groundbreaking research holds the key to unlocking revolutionary treatments for neurological ailments, heralding a transformative era in neuroscience and medical therapeutics.

1. Tiagabine, SK&F 89976-A, CI-966, and NNC-711 are selective for the cloned GABA transporter GAT-1

L A Borden, T G Murali Dhar, K E Smith, R L Weinshank, T A Branchek, C Gluchowski Eur J Pharmacol. 1994 Oct 14;269(2):219-24. doi: 10.1016/0922-4106(94)90089-2.

gamma-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian brain. The synaptic action of GABA is terminated by rapid uptake into presynaptic terminals and surrounding glial cells. Molecular cloning has revealed the existence of four distinct GABA transporters termed GAT-1, GAT-2, GAT-3, and BGT-1. Pharmacological inhibition of transport provides a mechanism for increasing GABA-ergic transmission, which may be useful in the treatment of various neuropsychiatric disorders. Recently, a number of lipophilic GABA transport inhibitors have been designed and synthesized, which are capable of crossing the blood brain barrier, and which display anticonvulsive activity. We have now determined the potency of four of these compounds, SK&F 89976-A (N-(4,4-diphenyl-3-butenyl)-3-piperidinecarboxylic acid), tiagabine ((R)-1-[4,4-bis(3-methyl-2-thienyl)-3-butenyl]-3- piperidencarboxylic acid), CI-966 ([1-[2-[bis 4-(trifluoromethyl)phenyl]methoxy]ethyl]-1,2,5,6-tetrahydro-3- pyridinecarboxylic acid), and NNC-711 (1-(2-(((diphenylmethylene)amino)oxy)ethyl)-1,2,4,6-tetrahydro-3- pyridinecarboxylic acid hydrochloride), at each of the four cloned GABA transporters, and find them to be highly selective for GAT-1. These data suggest that the anticonvulsant activity of these compounds is mediated via inhibition of uptake by GAT-1.

2. Design, synthesis, and biological evaluation of the N-diarylalkenyl-piperidinecarboxylic acid derivatives as GABA uptake inhibitors (I)

Jianbin Zheng, Ren Wen, Xiaomin Luo, Guoqiang Lin, Jiange Zhang, Linfeng Xu, Lihe Guo, Hualiang Jiang Bioorg Med Chem Lett. 2006 Jan 1;16(1):225-7. doi: 10.1016/j.bmcl.2005.09.004. Epub 2005 Oct 21.

Twenty novel N-diarylalkenyl-piperidinecarboxylic acid derivatives were synthesized and evaluated as gamma-aminobutyric acid uptake inhibitors. The biological assay showed that (R)-1-[4,4-bis(3-phenoxymethyl-2-thienyl)-3-butenyl]-3-piperidinecarboxylic hydrochloride possessed almost as strong GAT1 inhibitory activity as tiagabine. The synthesis and structure-activity relationships are discussed.

3. Methyl CpG Binding Protein 2 Gene Disruption Augments Tonic Currents of γ-Aminobutyric Acid Receptors in Locus Coeruleus Neurons: IMPACT ON NEURONAL EXCITABILITY AND BREATHING

Weiwei Zhong, Ningren Cui, Xin Jin, Max F Oginsky, Yang Wu, Shuang Zhang, Brian Bondy, Christopher M Johnson, Chun Jiang J Biol Chem. 2015 Jul 24;290(30):18400-11. doi: 10.1074/jbc.M115.650465. Epub 2015 May 15.

People with Rett syndrome and mouse models show autonomic dysfunction involving the brain stem locus coeruleus (LC). Neurons in the LC of Mecp2-null mice are overly excited, likely resulting from a defect in neuronal intrinsic membrane properties and a deficiency in GABA synaptic inhibition. In addition to the synaptic GABA receptors, there is a group of GABAA receptors (GABAARs) that is located extrasynaptically and mediates tonic inhibition. Here we show evidence for augmentation of the extrasynaptic GABAARs in Mecp2-null mice. In brain slices, exposure of LC neurons to GABAAR agonists increased tonic currents that were blocked by GABAAR antagonists. With 10 μm GABA, the bicuculline-sensitive tonic currents were ~4-fold larger in Mecp2-null LC neurons than in the WT. Single-cell PCR analysis showed that the δ subunit, the principal subunit of extrasynaptic GABAARs, was present in LC neurons. Expression levels of the δ subunit were ~50% higher in Mecp2-null neurons than in the WT. Also increased in expression in Mecp2-null mice was another extrasynaptic GABAAR subunit, α6, by ~4-fold. The δ subunit-selective agonists 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol hydrochloride and 4-chloro-N-[2-(2-thienyl)imidazo[1,2-a]pyridin-3-yl]]benzamide activated the tonic GABAA currents in LC neurons and reduced neuronal excitability to a greater degree in Mecp2-null mice than in the WT. Consistent with these findings, in vivo application of 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol hydrochloride alleviated breathing abnormalities of conscious Mecp2-null mice. These results suggest that extrasynaptic GABAARs seem to be augmented with Mecp2 disruption, which may be a compensatory response to the deficiency in GABAergic synaptic inhibition and allows control of neuronal excitability and breathing abnormalities.