L-Tyrosine hydrochloride (BAT-004042)
* For research use only

Category
L-Amino Acids
Catalog number
BAT-004042
CAS number
16870-43-2
Molecular Formula
C9H11NO3·HCl
Molecular Weight
217.69
L-Tyrosine hydrochloride
Synonyms
L-Tyr-OH HCl; (S)-3-(4-Hydroxyphenyl)alanine hydrochloride; 3-(4-Hydroxyphenyl)-L-alanine hydrochloride; (3-(4-Hydroxyphenyl)-L-alanine; (2S)-2-amino-3-(4-hydroxyphenyl)propanoic acid hydrochloride; (S)-2-Amino-3-(4-hydroxyphenyl)propanoic acid hydrochloride
Appearance
White to off-white crystalline powder
Purity
≥ 99%
Melting Point
239 °C (dec.)(lit.)
Boiling Point
385.2 °C at 760 mmHg
Storage
Store at RT
1.Efficacy and safety of icotinib as first-line therapy in patients with advanced non-small-cell lung cancer.
Shen YW1, Zhang XM1, Li ST1, Lv M1, Yang J1, Wang F1, Chen ZL1, Wang BY1, Li P1, Chen L1, Yang J1. Onco Targets Ther. 2016 Feb 24;9:929-35. doi: 10.2147/OTT.S98363. eCollection 2016.
BACKGROUND AND OBJECTIVE: Several clinical trials have proven that icotinib hydrochloride, a novel epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor, exhibits encouraging efficacy and tolerability in patients with advanced non-small-cell lung cancer (NSCLC) who failed previous chemotherapy. This study was performed to assess the efficacy and toxicity of icotinib as first-line therapy for patients with advanced pulmonary adenocarcinoma with EGFR-sensitive mutation.
2.Potential of erlotinib cyclodextrin nanosponge complex to enhance solubility, dissolution rate, in vitro cytotoxicity and oral bioavailability.
Dora CP1, Trotta F2, Kushwah V3, Devasari N4, Singh C4, Suresh S5, Jain S6. Carbohydr Polym. 2016 Feb 10;137:339-49. doi: 10.1016/j.carbpol.2015.10.080. Epub 2015 Oct 28.
The present study was envisaged to evaluate the effect of erlotinib β-cyclodextrin nanosponge (ERL-NS) on the solubility, dissolution, in vitro cytotoxicity and oral bioavailability of erlotinib (ERL). Preliminary studies were conducted to select the optimized stoichiometry concentration of ERL and NS. The drug nanosponge complex comprising of 1:4 proportions of ERL and NS was prepared by freeze drying. ERL-NS formed nanoparticles of 372 ± 31 nm size with narrow size distribution (0.21 ± 0.07 PDI) and high zeta potential (-32.07 ± 4.58 mV). The complexation phenomenon was confirmed by DSC, SEM, PXRD, FTIR, and TEM studies. In vitro dissolution studies revealed an increased dissolution rate (2-folds) with an enhanced dissolution efficiency of the nanosponge complex in comparison to pure drug. In vitro cytotoxicity study and apoptosis assay in pancreatic cell lines (MIA PaCa-2 and PANC-1) indicates the increased toxicity of ERL-NS. Both, quantitative and qualitative cell uptake studies unveiled the higher uptake efficiency of ERL-NS than free drug.
3.Noradrenergic inputs from locus coeruleus to posterior ventral tegmental area are essential to support ethanol reinforcement.
Shelkar GP1, Kumar S2, Singru PS2, Subhedar NK3, Kokare DM1. Addict Biol. 2015 Nov 8. doi: 10.1111/adb.12321. [Epub ahead of print]
Although dysregulation of the dopaminergic mesolimbic system is generally considered central to addiction, the involvement of other circuits is increasingly being appreciated. An interaction between locus coeruleus (LC) noradrenergic neurons and the posterior ventral tegmental area (pVTA) dopaminergic system, in the processing of drug-triggered reward, has been suggested, but not demonstrated in behaving animals. Herein, we try to tease out the precise role of noradrenergic neurons in the LC-VTA circuit in mediating reward and reinforcement behavior associated with ethanol. In the standard two-lever (active/inactive) operant paradigm, the rats were trained to self-administer ethanol in pVTA and subjected to pharmacological intervention. Intra-pVTA administration of phenylephrine (alpha-1 adrenoceptor agonist) increased ethanol self-administration, while prazosin and disulfiram (agents that reduce noradrenergic tone) produced opposite effects.
4.Genetic Association of Curative and Adverse Reactions to Tyrosine Kinase Inhibitors in Chinese advanced Non-Small Cell Lung Cancer patients.
Ruan Y1, Jiang J1, Guo L2, Li Y3, Huang H4,5, Shen L1, Luan M1, Li M1, Du H1, Ma C1, He L1, Zhang X6, Qin S1,7. Sci Rep. 2016 Mar 18;6:23368. doi: 10.1038/srep23368.
Epidermal growth factor receptor (EGFR) Tyrosine kinase inhibitor (TKI) is an effective targeted therapy for advanced non-small cell lung cancer (NSCLC) but also causes adverse drug reactions (ADRs) e.g., skin rash and diarrhea. SNPs in the EGFR signal pathway, drug metabolism/ transport pathways and miRNA might contribute to the interpersonal difference in ADRs but biomarkers for therapeutic responses and ADRs to TKIs in Chinese population are yet to be fully investigated. We recruited 226 Chinese advanced NSCLC patients who received TKIs erlotinib, gefitinib and icotinib hydrochloride and systematically studied the genetic factors associated with therapeutic responses and ADRs. Rs884225 (T > C) in EGFR 3' UTR was significantly associated with lower risk of ADRs to erlotinib (p value = 0.0010, adjusted p value = 0.042). A multivariant interaction four-SNP model (rs884225 in EGFR 3'UTR, rs7787082 in ABCB1 intron, rs38845 in MET intron and rs3803300 in AKT1 5'UTR) was associated with ADRs in general and the more specific drug induced skin injury.
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