ACHP - CAS 406208-42-2
Category: Inhibitor
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Molecular Formula:
C21H24N4O2
Molecular Weight:
364.44
COA:
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Targets:
IKK
Description:
ACHP, an IkB kinase inhibitor, has been found to exhibit activities in inducing apoptosis in human myeloma cell lines.
Purity:
≥97% by HPLC
Appearance:
White Solid
Synonyms:
2-Amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-(4-piperidinyl)-3-pyridinecarbonitrile
MSDS:
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InChIKey:
DWQVGCQPWXKRKO-JZJYNLBNSA-N
InChI:
InChI=1S/C21H24N4O2/c22-11-16-15(14-6-8-24-9-7-14)10-17(25-21(16)23)20-18(26)2-1-3-19(20)27-12-13-4-5-13/h1-3,10,13-14,24-25H,4-9,12,23H2/b20-17-
Canonical SMILES:
C1CC1COC2=CC=CC(=O)C2=C3C=C(C(=C(N3)N)C#N)C4CCNCC4
1.Dry chemical processing and ensiling of rice straw to improve its quality for use as ruminant feed.
Ghasemi E;Khorvash M;Ghorbani GR;Emami MR;Karimi K Trop Anim Health Prod. 2013 Jun;45(5):1215-21. doi: 10.1007/s11250-012-0349-0. Epub 2013 Jan 20.
In this study, changes in the chemical composition, pH, cell wall and degradability of ensiled rice straw were investigated when treated with alkali, acid, oxidant agents (1-11 %, w/w) and a combination of an oxidant with either an alkali (ALHP) or an acid (ACHP). The findings of the study revealed that ALHP had a lower efficiency in enhancing fibre degradability compared to alkali alone. Oxidant treatment showed no detectable changes in pH, dry matter (DM) and phenolic compound (PC) solubility, or in silica and fibre content, but led to increased esterified groups formed within the cell wall constituents (hemicellulose and lignin). Increasing acid concentration led to an exponential change in both pH and solubility of DM and hemicelluloses while it quadratically increased PC and silica solubility. Moreover, crystallinity, hydrogen bonding and esterification were enhanced under high acid concentrations (11 %), but decreased under mild acid conditions (5 %). Increased alkalinity led to the linear enhancement of DM and PC solubility. Solubility of silica and hemicellulose did not exhibit any significant changes with alkali concentration above 7 %. A gradual enhancement (29 %) was observed in ruminal DM degradability with increasing oxidant concentration, whereas exponential (91 %) and quadratic (23 %) enhancements were observed with alkaline and acid treatments, respectively.
2.[The effect of TWP on the reactivity of AChR on the end-plate membrane of frog sartorius].
Li K;Lü G;Zhang Y;Wang T;Xu J Sichuan Da Xue Xue Bao Yi Xue Ban. 2003 Apr;34(2):286-8.
OBJECTIVE: ;To study the effect of Tripterygium Wilfordii Polyglycosidium (TWP) on the reactivity of n-Acetylcholine receptor (nAChR) on the end plate membrane.;METHODS: ;Using the microionophoretic method, we applied the exogenous acetylcholine chloride (AChCl) to the superficial end-plates of the isolated nonuniform stretched frog sartorius, and acetylcholine potential (AChP) recorded was taken as an indicator of the reactivity of the nAChR in the end plate.;RESULTS: ;1. After the addition of TWP, the apparent change of AChP was recorded at 20 min in the 20 mg/L group, and at 10 min in the 40 mg/L and 60 mg/L groups respectively. 2. Within the 20 mg/L and 40 mg/L TWP groups, the change in amplitude of AChP showed significant difference with the time (P < 0.05), the greatest being at 60 min. 3. In the 60 mg/L TWP group, action potential was recorded at 40 min, 60 min and 80 min. 4. There was significant difference in the percentage of AChP amplitude change between the three concentration groups (P < 0.05), and the highest percentage of change appeared in the 60 mg/L group.;CONCLUSION: ;TWP can increase the reactivity of nAChR in the end plate membrane, and there exist an apparent concentration-effect relationship and a certain time-effect relationship.
3.IL-8 regulates the doxorubicin resistance of colorectal cancer cells via modulation of multidrug resistance 1 (MDR1).
Du J;He Y;Li P;Wu W;Chen Y;Ruan H Cancer Chemother Pharmacol. 2018 Jun;81(6):1111-1119. doi: 10.1007/s00280-018-3584-x. Epub 2018 Apr 24.
Cytokines play important roles in tumorigenesis and progression of cancer cells, while their functions in drug resistance remain to be illustrated. We successfully generated doxorubicin (Dox)-resistant CRC HCT-116 and SW480 cells (namely HCT-116/Dox and SW480/Dox, respectively). Cytokine expression analysis revealed that IL-8, while not FGF-2, EGF, TGF-β, IL-6, or IL-10, was significantly increased in Dox-resistant CRC cells as compared with their corresponding parental cells. Targeted inhibition of IL-8 via siRNAs or its inhibitor reparixin can increase the Dox sensitivity of HCT-116/Dox and SW480/Dox cells. The si-IL-8 can decrease the mRNA and protein expression of multidrug resistance 1 (MDR1, encoded by ABCB1), while has no effect on the expression of multidrug resistance-associated protein 1 (ABCC1), in CRC Dox-resistant cells. IL-8 can increase the phosphorylation of p65 and then upregulate the binding between p65 and promoter of ABCB1. BAY 11-7082, the inhibitor of NF-κB, suppressed the recombination IL-8 (rIL-8) induced upregulation of ABCB1. It confirmed that NF-κB is involved in IL-8-induced upregulation of ABCB1. rIL-8 also increased the phosphorylation of IKK-β, which can further activate NF-κB, while specific inhibitor of IKK-β (ACHP) can reverse rIL-8-induced phosphorylation of p65 and upregulation of MDR1.
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CAS 406208-42-2 ACHP

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