Boc-Lys(Tfa)-AMC
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Boc-Lys(Tfa)-AMC

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Boc-Lys(Tfa)-AMC is a fluorogenic substrate for the assaying of histone deacetylase (HDAC) 4, 5 and 7 activity in a protease-coupled assay.

Category
BOC-Amino Acids
Catalog number
BAT-007637
CAS number
97885-44-4
Molecular Formula
C23H28F3N3O6
Molecular Weight
499.49
Boc-Lys(Tfa)-AMC
IUPAC Name
tert-butyl N-[(2S)-1-[(4-methyl-2-oxochromen-7-yl)amino]-1-oxo-6-[(2,2,2-trifluoroacetyl)amino]hexan-2-yl]carbamate
Synonyms
tert-butyl N-[(2S)-1-[(4-methyl-2-oxochromen-7-yl)amino]-1-oxo-6-[(2,2,2-trifluoroacetyl)amino]hexan-2-yl]carbamate; (S)-tert-Butyl (1-((4-methyl-2-oxo-2H-chromen-7-yl)amino)-1-oxo-6-(2,2,2-trifluoroacetamido)hexan-2-yl)carbamate; Boc-L-Lys-MCA; Boc L Lys MCA
Purity
98%
Storage
Store at 2-8 °C
InChI
InChI=1S/C23H28F3N3O6/c1-13-11-18(30)34-17-12-14(8-9-15(13)17)28-19(31)16(29-21(33)35-22(2,3)4)7-5-6-10-27-20(32)23(24,25)26/h8-9,11-12,16H,5-7,10H2,1-4H3,(H,27,32)(H,28,31)(H,29,33)/t16-/m0/s1
InChI Key
UFFVNATYYXBMGO-INIZCTEOSA-N
Canonical SMILES
CC1=CC(=O)OC2=C1C=CC(=C2)NC(=O)C(CCCCNC(=O)C(F)(F)F)NC(=O)OC(C)(C)C
1. Changes in Class I and IIb HDACs by δ-Opioid in Chronic Rat Glaucoma Model
Syed A H Zaidi, Wendy Guzman, Sudha Singh, Shikhar Mehrotra, Shahid Husain Invest Ophthalmol Vis Sci. 2020 Dec 1;61(14):4. doi: 10.1167/iovs.61.14.4.
Purpose: This study determines if δ-opioid receptor agonist (i.e. SNC-121)-induced epigenetic changes via regulation of histone deacetylases (HDACs) for retinal ganglion cell (RGC) neuroprotection in glaucoma model. Methods: Intraocular pressure was raised in rat eyes by injecting 2M hypertonic saline into the limbal veins. SNC-121 (1 mg/kg; i.p.) was administered to the animals for 7 days. Retinas were collected at days 7 and 42, post-injury followed by measurement of HDAC activities, mRNA, and protein expression by enzyme assay, quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemistry. Results: The visual acuity, contrast sensitivity, and pattern electroretinograms (ERGs) were declined in ocular hypertensive animals, which were significantly improved by SNC-121 treatment. Class I and IIb HDACs activities were significantly increased at days 7 and 42 in ocular hypertensive animals. The mRNA and protein expression of HDAC 1 was increased by 1.33 ± 0.07-fold and 20.2 ± 2.7%, HDAC 2 by 1.4 ± 0.05-fold and 17.0 ± 2.4%, HDAC 3 by 1.4 ± 0.06-fold and 17.4 ± 3.4%, and HDAC 6 by 1.5 ± 0.09-fold and 15.1 ± 3.3% at day 7, post-injury. Both the mRNA and protein expression of HDACs were potentiated further at day 42 in ocular hypertensive animals. HDAC activities, mRNA, and protein expression were blocked by SNC-121 treatment at days 7 and 42 in ocular hypertensive animals. Conclusions: Data suggests that class I and IIb HDACs are activated and upregulated during early stages of glaucoma. Early intervention with δ-opioid receptor activation resulted in the prolonged suppression of class I and IIb HDACs activities and expression, which may, in part, play a crucial role in RGC neuroprotection.
2. PI3K/Akt Pathway: A Role in δ-Opioid Receptor-Mediated RGC Neuroprotection
Shahid Husain, Anis Ahmad, Sudha Singh, Carolyn Peterseim, Yasir Abdul, Matthew J Nutaitis Invest Ophthalmol Vis Sci. 2017 Dec 1;58(14):6489-6499. doi: 10.1167/iovs.16-20673.
Purpose: This study examines the role of PI3K/Akt pathway in δ-opioid receptor agonist (SNC-121)-induced RGC neuroprotection in a chronic glaucoma rat model. Methods: Injecting hypertonic saline into the limbal veins of Brown Norway rats elevated IOP. Rats were treated either with 1 mg/kg SNC-121 or 3 mg/kg 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY-294002; PI3K/Akt inhibitor) plus SNC-121 once daily for 7 days. Pattern ERGs were recorded in response to contrast reversal of patterned visual stimuli. Retinal ganglion cells (RGC) were visualized by Fluorogold retrograde labeling. Optic nerve head (ONH) astrocytes were pretreated with PI3K/Akt inhibitors for 30 minutes followed by 1-μM SNC-121 treatment. Changes in matrix metalloproteinases (MMP-1, -2, and -3) production and PI3K/Akt activation in optic nerve and TNF-α treated ONH astrocytes were measured by immunohistochemistry and Western blotting. Results: SNC-121 activates the PI3K/Akt pathway in ONH astrocytes and the retina. In ONH astrocytes, SNC-121-induced Akt activation was fully inhibited by PI3K/Akt inhibitors. A sustained decline (7-42 days post injury) in Akt activation was seen in the ocular-hypertensive retina and optic nerve. This decline is reversed to normal levels by 1-mg/kg intraperitoneally (i.p.) SNC-121 treatment. Both pattern ERG amplitudes and RGC numbers were reduced in ocular hypertensive eyes, which were significantly increased in SNC-121-treated animals. Interestingly, SNC-121-induced increase in pattern-ERG amplitudes and RGC numbers were inhibited in LY-294002 pretreated animals. Additionally, SNC-121 treatment inhibited MMP-1, -2, and -3 production from the optic nerve of ocular hypertensive rats and TNF-α-treated ONH astrocytes. Conclusions: PI3K/Akt pathway plays a crucial role in SNC-121-mediated RGC neuroprotection against glaucomatous injury.
3. Delta-opioid receptors attenuate TNF-α-induced MMP-2 secretion from human ONH astrocytes
Naseem Akhter, Melissa Nix, Yasir Abdul, Sudha Singh, Shahid Husain Invest Ophthalmol Vis Sci. 2013 Oct 9;54(10):6605-11. doi: 10.1167/iovs.13-12196.
Purpose: We examined the signaling mechanisms involved in δ-opioid-receptor agonist, SNC-121-mediated attenuation of TNF-α-induced matrix metalloproteinase-2 (MMP-2) secretion from human optic nerve head (ONH) astrocytes. Methods: Human ONH astrocytes were treated with SNC-121 (1 μmol/L) for 15 minutes followed by TNF-α (25 ng/mL) treatment for 6 or 24 hours. Cells were pretreated with inhibitors of p38 mitogen-activated protein (MAP) kinase (SB-203580) or NF-κB (Helenalin) prior to TNF-α treatment. Changes in phosphorylation and expression of p38 MAP kinase, IκBα, NF-κB, and MMP-2 were measured by Western blotting. Translocation of NF-κB was determined by immunocytochemistry. Results: TNF-α treatment increased MMP-2 secretion from ONH astrocytes to 236% ± 17% and 142% ± 8% at 6 and 24 hours, respectively; while SNC-121 treatment reduced MMP-2 secretion to 149% ± 11% and 108% ± 7% at 6 and 24 hours, respectively. The SNC-121-mediated inhibitory response was blocked by the δ-opioid-receptor antagonist naltrindole. TNF-α treatment resulted in a sustained phosphorylation of p38 MAP kinase up to 24 hours (226% ± 15% over control levels), which was reduced to 150% ± 20% by SNC-121 treatment. TNF-α treatment increased the expression of NF-κB to 179% ± 21% and 139% ± 6% at 6 and 24 hours, respectively, which was significantly blocked by SNC-121 treatment. Furthermore, TNF-α-induced MMP-2 secretion was blocked by 100% and 78% in the presence of SB-203580 and Helenalin, respectively. Conclusions: Evidence is provided that SNC-121 attenuated TNF-α-induced MMP-2 secretion from ONH astrocytes. Data also supported the idea that p38 MAP kinase and NF-κB played central roles in TNF-α-induced MMP-2 secretion, and both were negatively regulated by SNC-121.
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