Nα-Z-L-2,4-diaminobutyric acid
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Nα-Z-L-2,4-diaminobutyric acid

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Category
CBZ-Amino Acids
Catalog number
BAT-005694
CAS number
62234-40-6
Molecular Formula
C12H16N2O4
Molecular Weight
252.48
Nα-Z-L-2,4-diaminobutyric acid
IUPAC Name
(2S)-4-amino-2-(phenylmethoxycarbonylamino)butanoic acid
Synonyms
Z-L-Dab-OH
Appearance
White crystalline powder
Purity
≥ 99% (HPLC)
Melting Point
182-190 °C
Storage
Store at 2-8°C
InChI
InChI=1S/C12H16N2O4/c13-7-6-10(11(15)16)14-12(17)18-8-9-4-2-1-3-5-9/h1-5,10H,6-8,13H2,(H,14,17)(H,15,16)/t10-/m0/s1
InChI Key
KXMSCBRTBLPGIN-JTQLQIEISA-N
Canonical SMILES
C1=CC=C(C=C1)COC(=O)NC(CCN)C(=O)O
1.Accelerating full thickness wound healing using Collagen Sponge of Mrigal Fish (Cirrhinus cirrhosus) scale Origin.
Pal P1, Srivas PK1, Dadhich P1, Das B1, Maity PP1, Moulik D2, Dhara S3. Int J Biol Macromol. 2016 Apr 13. pii: S0141-8130(16)30340-3. doi: 10.1016/j.ijbiomac.2016.04.032. [Epub ahead of print]
The potentiality of collagen sponge as a skin substitute, derived from mrigal (Cirrhinus cirrhosus) scale has been explored in this study. Acid soluble collagen (ASC) and pepsin soluble collagen (PSC) from the scale of mrigal were isolated and characterized. The yields of ASC and PSC were ∼3% and ∼7% based on the dry weight of scale while the hydroxyproline content was ∼90mg/g. Scanning electron microscope revealed progressive demineralization with EDTA on time dependent scale. Further, the D-Spacing in fibril bundles were calculated to be ∼67nm. Fourier transform infrared and circular dichroism spectra confirmed extracted protein to be collagen I, where both ASC and PSC comprised of two different α-chains (α1 and α2). The denaturation temperature (Td) of the collagen solution was 35°C closer to Td of mammalian collagen. In vitro cell culture studies on the extracted collagen sponge showed efficient cell growth and proliferation. Additionally, co-culture with fibroblast and keratinocyte cells showed development of stratified epidermal layer in vitro.
2.Lipoic Acid Exerts Antioxidant and Anti-inflammatory Effects in Response to Heat Shock in C2C12 Myotubes.
Lee CT1, Chang LC2, Wu PF3. Inflammation. 2016 Apr 16. [Epub ahead of print]
This study explored that lipoic acid treatment for 24 h significantly upregulated and promoted heat shock-induced catalase expression and downregulated GPx1 messenger RNA (mRNA) expression, indicating that lipoic acid exhibits antioxidant activity in the decomposition of hydrogen peroxide by upregulating catalase expression. Moreover, lipoic acid treatment for 3 h increased and promoted heat shock-induced interleukin (IL)-6 mRNA and protein levels and that for 24 h downregulated IL-6 mRNA expression, suggesting a dual effect of lipoic acid on IL-6 regulation. Lipoic acid alone failed to increase or reduce tumor necrosis factor (TNF)-α mRNA and protein levels, whereas heat shock alone downregulated TNF-α mRNA and protein expression. These data suggest that lipoic acid does not have a proinflammatory role and that heat shock acts as an anti-inflammatory agent by downregulating TNF-α expression in C2C12 myotubes. Moreover, lipoic acid or heat shock alone upregulated the IL-6 receptor (IL-6R-α) and glycoprotein 130 (gp130) mRNA expression followed by IL-6 expression; these data indicate that the regulation of lipoic acid or heat shock is mediated by IL-6R signaling, thus suggesting that C2C12 myotubes possesses a mechanism for regulating IL-6R and gp130 expression following lipoic acid treatment or heat shock.
3.Clinical Drug-Drug Pharmacokinetic Interaction Potential of Sucralfate with Other Drugs: Review and Perspectives.
Sulochana SP1, Syed M2, Chandrasekar DV1, Mullangi R1, Srinivas NR3. Eur J Drug Metab Pharmacokinet. 2016 Apr 16. [Epub ahead of print]
Sucralfate, a complex of aluminium hydroxide with sulfated sucrose, forms a strong gastrointestinal tract (GIT) mucosal barrier with excellent anti-ulcer property. Because sucralfate does not undergo any significant oral absorption, sucralfate resides in the GIT for a considerable length of time. The unabsorbed sucralfate may alter the pharmacokinetics of the oral drugs by impeding its absorption and reducing the oral bioavailability. Because of the increased use of sucralfate, it was important to provide a reappraisal of the published clinical drug-drug interaction studies of sucralfate with scores of drugs. This review covers several category of drugs such as non-steroidal anti-inflammatory drugs, fluoroquinolones, histamine H2-receptor blockers, macrolides, anti-fungals, anti-diabetics, salicylic acid derivatives, steroidal anti-inflammatory drugs and provides pharmacokinetic data summary along with study design, objectives and key remarks.
4.Crosstalk between liver antioxidant and the endocannabinoid systems after chronic administration of the FAAH inhibitor, URB597, to hypertensive rats.
Biernacki M1, Łuczaj W1, Gęgotek A1, Toczek M2, Bielawska K1, Skrzydlewska E3. Toxicol Appl Pharmacol. 2016 Apr 13. pii: S0041-008X(16)30076-X. doi: 10.1016/j.taap.2016.04.006. [Epub ahead of print]
Hypertension is accompanied by perturbations to the endocannabinoid and antioxidant systems. Thus, potential pharmacological treatments for hypertension should be examined as modulators of these two metabolic systems. The aim of this study was to evaluate the effects of chronic administration of the fatty acid amide hydrolase (FAAH) inhibitor [3-(3-carbamoylphenyl)phenyl]N-cyclohexylcarbamate (URB597) on the endocannabinoid system and on the redox balance in the livers of DOCA-salt hypertensive rats. Hypertension caused an increase in the levels of endocannabinoids [anandamide (AEA), 2-arachidonoyl-glycerol (2-AG) and N-arachidonoyl-dopamine (NADA)] and CB1 receptor and the activities of FAAH and monoacylglycerol lipase (MAGL). These effects were accompanied by an increase in the level of reactive oxygen species (ROS), a decrease in antioxidant activity/level, enhanced expression of transcription factor Nrf2 and changes to Nrf2 activators and inhibitors.
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