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β-(2-Anthryl)-L-alanine

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β-(2-Anthryl)-L-alanine is utilized in biological studies of non-natural amino acids for protein synthesis.

Category

L-Amino Acids

Catalog number

BAT-007513

CAS number

155760-00-2

Molecular Formula

C17H15NO2

Molecular Weight

265.31

IUPAC Name

(2S)-2-amino-3-anthracen-2-ylpropanoic acid

Synonyms

H-Ala(2-Anth)-OH; 3-(2-Anthryl)alanine; beta-(2-Anthryl)-L-alanine; 3-(2-ANTHRYL)-L-ALANINE; (S)-α-Amino-2-anthracenepropanoic Acid; (αS)-α-Amino-2-anthracenepropanoic Acid; H-L-Ala(2-Anth)-OH; (2S)-2-Amino-3-(anthracen-2-yl)propanoic Acid; β-(2-Anthryl)-L-alanine

Appearance

white crystalline powder

Purity

≥ 98%

InChI

InChI=1S/C17H15NO2/c18-16(17(19)20)8-11-5-6-14-9-12-3-1-2-4-13(12)10-15(14)7-11/h1-7,9-10,16H,8,18H2,(H,19,20)/t16-/m0/s1

InChI Key

IXSDAIHAHNXSEH-INIZCTEOSA-N

Canonical SMILES

C1=CC=C2C=C3C=C(C=CC3=CC2=C1)CC(C(=O)O)N

One of the key applications of β-(2-Anthryl)-L-alanine is in the field of analytical chemistry. This compound is prominently utilized as a fluorescent probe due to the intrinsic fluorescence properties of the anthracene moiety. When incorporated into peptide chains or used as a standalone reagent, β-(2-Anthryl)-L-alanine can help in the detection and quantification of peptide interactions, conformational changes, and other biochemical phenomena. Its sensitivity allows detecting even minute concentrations of target molecules in assays, making it a powerful tool in the analysis of complex biological samples. The high photostability of the anthryl group ensures that the fluorescent signals remain stable over time, which is crucial for long-term studies and high-throughput screening processes.

In the realm of pharmaceutical research, β-(2-Anthryl)-L-alanine has found significant use in the design and study of peptide-based drugs. Due to its unique structural features, this compound can be incorporated into peptides to increase their stability, bioavailability, and overall efficacy. The anthryl group’s bulky structure can protect peptides from enzymatic degradation, enhancing their therapeutic potential. Furthermore, the fluorescence property of β-(2-Anthryl)-L-alanine enables researchers to track the distribution and dynamics of these peptides within biological systems, facilitating a deeper understanding of their mechanisms of action. This dual role as both a structural modifier and a tracking agent makes β-(2-Anthryl)-L-alanine an invaluable tool in the development of novel peptide therapeutics.

β-(2-Anthryl)-L-alanine has pivotal applications in biochemical research, particularly in the study of protein dynamics and interactions. By incorporating this amino acid analog into protein sequences, scientists can employ fluorescence resonance energy transfer (FRET) techniques to examine intricate details of protein folding, conformational changes, and intermolecular interactions. This assists in elucidating mechanisms behind various cellular processes and disease states. Additionally, β-(2-Anthryl)-L-alanine can be used to create site-specific labels on proteins, providing precise data on the structural and functional aspects of proteins. This utility is especially important in the fields of structural biology and proteomics, where understanding protein behavior at the molecular level is essential.

Beyond its biological applications, β-(2-Anthryl)-L-alanine also proves useful in the field of material science. The incorporation of the anthracene moiety imparts distinct photophysical properties to materials, enabling the development of novel fluorescent materials and sensors. These materials can be deployed in various applications such as organic light-emitting diodes (OLEDs), photovoltaics, and environmental sensors. The ability to fine-tune the properties of materials by integrating β-(2-Anthryl)-L-alanine offers a versatile approach to designing advanced materials with specific desired characteristics. Additionally, these materials can be used to create light-responsive systems and devices, contributing to the advancement of smart materials and nanotechnology.

1. Determination of the active moiety of BX661A, a new therapeutic agent for ulcerative colitis, by studying its therapeutic effects on ulcerative colitis induced by dextran sulfate sodium in rats

I Kimura, M Kawasaki, S Nagahama, A Matsuda, M Kataoka, Y Kokuba Arzneimittelforschung. 1998 Nov;48(11):1091-6.

5-[4-(2-Carboxyethylcarbamoyl)phenylazo]salicylic acid disodium salt dihydrate (CAS 80573-04-2, BX661A) is being developed as a therapeutic drug for ulcerative colitis. To determine the active therapeutic moiety of BX661A, the therapeutic effects with single and combined administration of 5-aminosalicylic acid (5-ASA), 4-aminobenzoyl-beta-alanine (4-ABA) and 4-amino-N-2-pyridinyl-benzenesulfonamide (CAS 144-83-2, sulfapyridine, SP) on ulcerative colitis induced by dextran sulfate sodium (DSS) in rats were investigated, and the following results were obtained. 1. BX661A at doses of 30, 100 and 300 mg/kg (p.o.) dose-dependently decreased the erosion area (mm2) in the large intestine with % inhibition values of 28.7, 49.1 and 61.6%, and the shortening of the large intestine with % inhibition values of 17.1, 25.7 and 48.6%, respectively. Salazosulfapyridine (SASP) at doses of 30 and 100 mg/kg (p.o.) decreased the erosion area (mm2) in the large intestine with % inhibition values of 30.7 and 45.3%, respectively, but did not improve the shortening of the large intestine. However, at a dose of 300 mg/kg (p.o.) SASP, the % inhibition value of the erosion area in the large intestine was reduced. 2. A single intrarectal administration of 5-ASA (105 mg/kg, i.r.) significantly decreased the erosion area (mm2) in the large intestine, but a single administration of 4-ABA or SP did not show any significant effect on the erosion area. Combined administration with 5-ASA (105 mg/kg, i.r.) and 4-ABA (142.8 mg/kg, i.r.) significantly decreased the erosion area (mm2) in the large intestine with a % inhibition value of 63.8%. On the other hand, the efficacy of 5-ASA disappeared with combined administration with SP (% inhibition value of 7.3%). These results suggest that 5-ASA is the active moiety for the therapeutic effects of BX661A and indicate that the efficacy of 5-ASA disappears with the combined use of SP, but not of 4-ABA. Therefore, it seems that BX661A is clinically safe and more effective than SASP in the treatment of patients with ulcerative colitis.

2. Effects of BX661A, a new therapeutic agent for ulcerative colitis, on chemotaxis and reactive oxygen species production in polymorphonuclear leukocytes in comparison with salazosulfapyridine and its metabolite sulfapyridine

I Kimura, M Kawasaki, A Matsuda, M Kataoka, Y Kokurba Arzneimittelforschung. 1998 Dec;48(12):1163-7.

5-[4-(2-Carboxyethylcarbamoyl)phenylazo]salicylic acid disodium salt dihydrate (CAS 80573-04-2, BX661A) is developed as a therapeutic agent for ulcerative colitis. To clarify the mechanisms of action of BX661A, the effects of BX661A and its metabolites 5-aminosalicylic acid (5-ASA) and 4-aminobenzoyl-beta-aline (4-ABA) on polymorphonuclear (PMN) leukocyte chemotaxis and production of reactive oxygen species (ROS) from PMN cells were investigated and compared with the effects of 2-hydroxy-5-[[4-[(2-pyridinylamino)sulfonyl]phenyl]azo]-benzoic acid (CAS 599-79-1, SASP) and its metabolite 4-amino-N-2-pyridinyl-benzenesulfonamide (CAS 144-83-2, SP). 1. BX661A, SASP and SP concentration-dependently inhibited guinea pig PMN cell chemotaxis induced by zymosan-activated serum (IC50 = 1.39, 2.17 mmol/l, respectively) and by N-formyl-methionyl-leucyl-phenylalanine (FMLP) with IC50 values of 0.55, 0.06 and 0.66 mmol/l, respectively. 5-ASA and 4-ABA weakly affected the PMN cell chemotaxis induced by zymosan-activated serum (both IC50 values > or = 10 mmol/l) and by FMLP (IC50 > or = 10 and 8.05 mmol/l, respectively). 2. BX661A, SASP and SP concentration-dependently inhibited human PMN cell chemotaxis induced by FMLP with IC50 values of 0.68, 0.05 and 2.68 mmol/l, respectively, but both IC50 values of 5-ASA and 4-ABA were > 10 mmol/l. 3. BX661A, SASP, 5-ASA, 4-ABA and SP inhibited ROS production from rat PMN cells stimulated by FMLP in a concentration-dependent manner (IC50 = 58.4, 27.5, 0.61, 1242 and 13.9 mmol/l, respectively). 4. BX661A, SASP, 5-ASA, 4-ABA and SP inhibited ROS production from human PMN cells stimulated by FMLP in a concentration-dependent manner (IC50 = 67.4, 46.1, 0.69, 748 and 8.31 mumol/l, respectively). These results suggest that BX661A itself has inhibitory effects against PMN cell chemotaxis and ROS production from PMNs and that 5-ASA, which is the active moiety of BX661A, has a potent inhibitory effect against ROS production from PMNs. Therefore, these effects may be partially involved in the therapeutic effects of BX661A on ulcerative colitis.

3. Effects of BX661A, a new therapeutic agent for ulcerative colitis, on reactive oxygen species in comparison with salazosulfapyridine and its metabolite sulfapyridine

I Kimura, T Kumamoto, A Matsuda, M Kataoka, Y Kokuba Arzneimittelforschung. 1998 Oct;48(10):1007-11.

5-[4-(2-Carboxyethylcarbamoyl)phenylazo]salicylic acid disodium salt dihydrate (CAS 80573-04-2, BX661A) is developed as a therapeutic agent for ulcerative colitis. To clarify its mechanism of action, the effects of BX661A and its metabolites 5-aminosalicylic acid (5-ASA) and 4-aminobenzoyl-beta-alanine (4-ABA) on reactive oxygen species: superoxide radicals (O2-) generated by hypoxanthine and xanthine oxidase, hydrogen peroxide (H2O2), hypochlorite radicals (OCl-) and hydroxyl radicals (OH.), were investigated and compared with the effects of 2-hydroxy-5-[[4-[(2-pyridinylamino)sulfonyl]phenyl]azo]-benzoic acid (CAS 599-79-1, salazosulfapyridine, SASP) and its metabolite 4-amino-N-2-pyridinyl-benzenesulfonamide (CAS 144-83-2, sulfapyridine, SP). 1. BX661A, SASP and 5-ASA inhibited O2- radical production in a concentration-dependent manner (IC50 = 0.14, 0.13 and 0.19 mmol/l, respectively). The effects of 4-ABA and SP on O2- radical production were weak (IC50 = > 10 and > 3 mmol/l, respectively). In contrast, superoxide dismutase inhibited O2- radical production in a concentration-dependent manner (IC50 = 1.7 U/ml). 2. BX661A, SASP, 4-ABA and SP had no H2O2 scavenging effects. 5-ASA scavenged H2O2, but its maximal scavenging action was 51.3%. In contrast, catalase scavenged H2O2 in a concentration-dependent manner (IC50 = 0.47 U/ml). 3. BX661A, SASP and 5-ASA scavenged OCl- radicals in a concentration-dependent manner (IC50 = 69.5, 73.8 and 21.7 mumol/l, respectively). 4-ABA and SP had no OCl- radical scavenging effects. In contrast, nordihydroguaiaretic acid (NDGA) scavenged OCl- radicals in a concentration-dependent manner (IC50 = 8.7 mumol/l). 4. BX661A and SASP scavenged OH. radicals in a concentration-dependent manner; the maximal scavenging values were 39.5 (10 mmol/l) and 48.6% (3 mmol/l), respectively. 4-ABA and SP had no OH. radical scavenging effects. In contrast, 5-ASA scavenged OH. radical in a concentration-dependent manner (IC50 = 1.46 mmol/l). These results suggest that BX661A has O2- and OCl- radical scavenging effects and that 5-ASA has O2-, OCl- and OH. radical scavenging effects. Therefore, these effects may be partially involved in the therapeutic effects of BX661A on ulcerative colitis.