Category: 106392-48-7

《Erbstatin blocks platelet activating factor-induced protein-tyrosine phosphorylation, polyphosphoinositide hydrolysis, protein kinase C activation, serotonin secretion and aggregation of rabbit platelets》 was written by Salari, Hassan; Duronio, Vincent; Howard, Sandra L.; Demos, Michelle; Jones, Kelvin; Reany, Anne; Hudson, Alan T.; Pelech, Steven L.. Application of 106392-48-7 And the article was included in FEBS Letters on April 9 ,1990. The article conveys some information:

The role of protein-tyrosine phosphorylation in the signal transduction of platelet activating factor (PAF) was investigated in rabbit platelets with a range of synthetic compounds that inhibit protein-tyrosine kinases. In particular, erbstatin (IC50 ∼ 20 μg/mL) abrogated a wide range of platelet responses to PAF, including tyrosine phosphorylation of cellular proteins, polyphosphoinositide turnover, activation of membranous protein kinase C, platelet aggregation, and serotonin secretion. With about a third of the potency of erbstatin, compound RG50864 also inhibited many of these responses, whereas at 100 μg/mL, genistein, 670C88 and ST271 were without effect. Finally, the ability of thrombin to cause platelet aggregation and serotonin secretion was also compromised by erbstatin.2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Application of 106392-48-7) was used in this study.

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides.Application of 106392-48-7 The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Recommanded Product: 106392-48-7On March 28, 1994, Blake, Robert A.; Asselin, Judith; Walker, Trevor; Watson, Steve P. published an article in FEBS Letters. The article was 《Fcγ receptor II stimulated formation of inositol phosphates in human platelets is blocked by tyrosine kinase inhibitors and associated with tyrosine phosphorylation of the receptor》. The article mentions the following:

The authors report that activation of phospholipase C (PLC) by crosslinking of the platelet low-affinity Fcγ receptor II (FcγRII) is inhibited by two structurally distinct tyrosine kinase inhibitors, staurosporine and ST 271. This contrasts with PLC activation induced by thrombin and U 46619, a thromboxane mimetic, whose receptors have seven transmembrane domains characteristic of G-protein coupled receptors. Several proteins undergo phosphorylation on tyrosine on FcγRII crosslinking upstream of protein kinase C (PKC), Ca2+ and aggregation, including the FcγRII itself. The role of FcγRII phosphorylation in the regulation of PLC is discussed. The experimental part of the paper was very detailed, including the reaction process of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Recommanded Product: 106392-48-7)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides.Recommanded Product: 106392-48-7 The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Computed Properties of C16H20N2O2On March 22, 1993, Young, Stephen W.; Poole, Robert C.; Hudson, Alan T.; Halestrap, Andrew P.; Denton, Richard M.; Tavare, Jeremy M. published an article in FEBS Letters. The article was 《Effects of tyrosine kinase inhibitors on protein kinase-independent systems. [Erratum to document cited in CA119(1):3745h]》. The article mentions the following:

The omission of the title and legend to Table I has been corrected The error was not reflected in the abstract or the index entries. In the part of experimental materials, we found many familiar compounds, such as 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Computed Properties of C16H20N2O2)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides.Computed Properties of C16H20N2O2 Amides include many other important biological compounds, as well as many drugs like paracetamol, penicillin and LSD. Low-molecular-weight amides, such as dimethylformamide, are common solvents.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Quality Control of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamideOn March 1, 1994, Laneuville, Pierre; Timm, Martina; Hudson, Alan T. published an article in Cancer Research. The article was 《Bcr/abl expression in 32D cl3(G) cells inhibits apoptosis induced by protein tyrosine kinase inhibitors》. The article mentions the following:

Eight protein tyrosine kinase inhibitors with in vitro epidermal growth factor receptor kinase 50% inhibitory concentration values ranging from 0.043 to 22 μM were studied for their ability to inhibit the growth of the murine interleukin-3 (IL-3) dependent myeloid 32D cl3(G) cell line, and a subclone (LG7) transformed to IL-3 independent growth by retroviral transduction and expression of the chronic myelogenous leukemia-associated protein tyrosine kinase p210bcr/abl. Cell proliferation 50% inhibitory concentration values ranged from 4 to 250 μM, and one compound was not inhibitory at 500 μM. The dose-cell proliferation curves were remarkably similar for parental 32D cl3(G) cells + IL-3 and LG7 ± IL-3, and reversion of LG7 cells to IL-3 dependence was not observed, suggesting that none of the compounds tested could selectively inhibit p21bcr/abl. However, 6 compounds induced the appearance of a 200-base pair nucleosomal DNA ladder characteristic of apoptosis at 24 h in parental 32D cl3(G) cells + IL-3, which mimicked the effects of IL-3 withdrawal alone, but not in similarly growth arrested LG7 cells that eventually developed a necrotic pattern of DNA fragmentation. These studies suggest that the expression of p210bcr/abl can suppress apoptotic signal transduction and that this may contribute to the development of the myeloid hyperplasia that occurs in chronic phase chronic myelogenous leukemia.2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Quality Control of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide) was used in this study.

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole. The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors.“,” In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Quality Control of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

COA of Formula: C16H20N2O2On May 1, 1989 ,《Specific inhibitors of tyrosine-specific protein kinases: properties of 4-hydroxycinnamamide derivatives in vitro》 appeared in Cancer Research. The author of the article were Shiraishi, Tadayoshi; Owada, M. Koji; Tatsuka, Masaaki; Yamashita, Takashi; Watanabe, Kiyoshi; Kakunaga, Takeo. The article conveys some information:

Inhibition by 7 synthetic 4-hydroxycinnamamide derivatives, ST 271, ST 280, ST 458, ST 494, ST 633, ST 638, and ST 642, of tyrosine-specific protein kinases (tyrosine kinase) of oncogene or proto-oncogene products (p130gag-v-fps, p70gag-actin-v-fgr, pp60v-src, pp60c-src) and epidermal growth factor (EGF) receptor kinase were investigated. ST 638 (α-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamide) strongly inhibited more of the tyrosine kinases than any of the other compounds The susceptibilities of these tyrosine kinases to ST 638 increased in the following order: EGF receptor > p70gag-actin-v-fgr > pp60c-src > p130gag-v-fps, pp60v-src, with 50% inhibitory concentration values of 1.1, 4.2, 18, 70, and 87 μM, resp. The phosphorylation of the tyrosine residues in particulate fractions from RR1022 cells expressing pp60v-src was inhibited by ST 638 in a dose-dependent way, while it had a negligible effect on the phosphorylations of threonine and serine residues. Kinetic anal. showed that ST 638 competitively inhibited the phosphorylation of an exogenous substrate by the EGF receptor kinase with a Ki of 2.1 μM. ST 638 noncompetitively inhibited autophosphorylation by EGF receptor kinase. Thus, ST 638 is a potent and specific inhibitor of tyrosine kinases in vitro, and its inhibitory activity is caused by competing with the substrate protein for the tyrosine kinase binding site. In the experiment, the researchers used 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7COA of Formula: C16H20N2O2)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole.COA of Formula: C16H20N2O2 The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

HPLC of Formula: 106392-48-7On October 3, 1994 ,《Phosphorylation of JAK2 in thrombin-stimulated human platelets》 was published in FEBS Letters. The article was written by Rodriguez-Linares, Belen; Watson, Steve P.. The article contains the following contents:

We show the presence of the tyrosine kinase JAK2 in human platelets and demonstrate that it undergoes phosphorylation on tyrosine residues on challenge with the G protein receptor stimulus, thrombin, or the tyrosine phosphatase inhibitor, peroxovanadate. Thrombin-induced phosphorylation of JAK2 is inhibited by two structurally distinct inhibitors of tyrosine kinases, staurosporine and the tyrphostin ST271. The protein kinase C (PKC) inhibitor, Ro 31-8220, and intracellular Ca2+ chelator, BAPTA-AM, also inhibit thrombin-induced phosphorylation of JAK2, while the phorbol ester, phorbol dibutyrate (PDBu), and Ca2+ ionophore, A23187, induce tyrosine phosphorylation of JAK2. These results suggest that tyrosine phosphorylation of JAK2 stimulated by thrombin may be mediated downstream of phosphoinositide metabolism In the experiment, the researchers used many compounds, for example, 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7HPLC of Formula: 106392-48-7)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides.HPLC of Formula: 106392-48-7Amides are pervasive in nature and technology. Proteins and important plastics like Nylons, Aramid, Twaron, and Kevlar are polymers whose units are connected by amide groups (polyamides); these linkages are easily formed, confer structural rigidity, and resist hydrolysis.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

《Derivatives of cinnamic acid interact with the nucleotide binding site of mitochondrial aldehyde dehydrogenase: effects on the dehydrogenase reaction and stimulation of esterase activity by nucleotides》 was written by Poole, Robert C.; Bowden, Nicola J.; Halestrap, Andrew P.. Reference of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide And the article was included in Biochemical Pharmacology on April 22 ,1993. The article conveys some information:

A wide variety of cinnamic acid derivatives are inhibitors of the low Km mitochondrial aldehyde dehydrogenase. Two of the most potent inhibitors are α-cyano-3,4-dihydroxythiocinnamamide (Ki 0.6 μM) and α-cyano-3,4,5-trihydroxycinnamonitrile (Ki 2.6 μM). With propionaldehyde as substrate the inhibition by these compounds was competitive with respect to NAD+. α-Fluorocinnamate was a much less effective inhibitor of the enzyme, with mixed behavior toward NAD+, but with a major competitive component. These cinnamic acid derivatives were ineffective as inhibitors of the aldehyde dehydrogenase-catalyzed hydrolysis of p-nitrophenyl acetate, but inhibited the ability of NAD+ and NADH to activate this activity. Inhibition of the stimulation of esterase activity was competitive with respect to NAD+ and NADH, and the derived Ki values were the same as for inhibition of dehydrogenase activity. NAD+, but not acetaldehyde, could elute the low Km aldehyde dehydrogenase from α-cyanocinnamate-Sepharose, to which the enzyme binds specifically. The cinnamic acid derivatives have little effect on lactate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase or a high Km aldehyde dehydrogenase present in rat liver mitochondria. Thus, some cinnamic acid derivatives are potent inhibitors of the low Km aldehyde dehydrogenase, by competing with NAD+/NADH for binding to the enzyme. They are much less effective as inhibitors of other NAD+-dependent dehydrogenases. The experimental part of the paper was very detailed, including the reaction process of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Reference of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole. The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors.“,” In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Reference of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

《Protein tyrosine kinases regulate agonist-stimulated prostacyclin release but not von Willebrand factor secretion from human umbilical vein endothelial cells》 was written by Wheeler-Jones, Caroline P. D.; May, Michael J.; Morgan, Anthony J.; Pearson, Jeremy D.. HPLC of Formula: 106392-48-7 And the article was included in Biochemical Journal on April 15 ,1996. The article conveys some information:

The rapid synthesis and release of prostacyclin (PGI2) and the exocytotic secretion of von Willebrand Factor (vWF) elicited by activation of G-protein-coupled receptors on endothelium occur via signaling mechanisms which are incompletely defined. Activation of protein tyrosine kinases (PTKs) and modulation of the tyrosine-phosphorylation state of endogenous proteins have been implicated in several cellular processes including arachidonate release and exocytosis. In the present study we have examined the regulatory role of PTKs in agonist-stimulated release of PGI2 and vWF from human umbilical vein endothelial cells (HUVECs) using two chem. and mechanistically dissimilar PTK inhibitors (genistein and ST271). Genistein, but not the less active analog daidzein, dose-dependently attenuated PGI2 release in response to thrombin and histamine (IC50approx. 20 μM), and to the thrombin-receptor-activating peptide. A more potent inhibition of thrombin- and histamine-induced PGI2 synthesis was observed in cells exposed to ST271. In contrast, neither genistein nor ST271 modulated agonist-drive vWF secretion. At concentrations that abolished PGI2 release, genistein blocked thrombin- or histamine-evoked tyrosine phosphorylation of a 42 kDa protein. Ca2+ ionophore-induced PGI2 generation, but not vWF secretion, was also inhibited by both genistein and ST271, suggesting that these agents modulate PGI2 synthesis by acting at, or distal to, agonist-induced changes in intracellular Ca2+ ([Ca2+]i). In fura-2-loaded HUVECs genistein partially reduced the histamine-induced peak [Ca2+]i but had no effect on the thrombin response. Ca2+-induced PGI2 release from elec. permeabilized HUVECs was abolished in the presence of ST271 or genistein, but not daidzein. The generation of PGI2 in response to exogenous arachidonic acid was not modulated by genistein or ST271, suggesting that PTK inhibitors do not directly inhibit cyclo-oxygenase activity. Taken together, these results suggest that PTKs regulate PGI2 synthesis and release in HUVECs by modulating, directly or indirectly, a Ca2+-sensitive step upstream of cyclo-oxygenase.2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7HPLC of Formula: 106392-48-7) was used in this study.

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole. The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors.“,” In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. HPLC of Formula: 106392-48-7

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Computed Properties of C16H20N2O2On May 31, 1995, Poole, Alastair W.; Watson, Stephen P. published an article in British Journal of Pharmacology. The article was 《Regulation of cytosolic calcium by collagen in single human platelets》. The article mentions the following:

There is controversy in the literature as to whether collagen is able to induced directly a rise in cytosolic calcium concentration ([Ca2+]i) in human platelets. We have addressed this question by observing the cytosolic calcium response of single fura-2-loaded human platelets setting onto a collagen-coated surface using dynamic fluorescence ratio imaging. Following a short lag phase after adherence to collagen fibers, platelets underwent a rapid rise in cytosolic calcium from basal values of 80 ± 13 nM (n = 24) to a peak of 475 ± 42 nM (n = 24) which was sustained for the remaining period of the experiment The tyrphostin protein tyrosine kinase inhibitor, ST271, reduced substantially the proportion of platelets which exhibited a rise in [Ca2+]i on adherence to collagen and transformed the response in remaining cells to one of oscillations. In contrast, and as a control for collagen, laminin-coated surfaces induced adherence of human platelets without elevating intracellular [Ca2+]; the cells however remained responsive to ADP. We conclude that collagen directly induces a rise in cytosolic calcium in single human platelets through a tyrosine kinase-mediated pathway. After reading the article, we found that the author used 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Computed Properties of C16H20N2O2)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole.Computed Properties of C16H20N2O2 The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

《[Tyrosine kinase inhibitor–hematological malignancies].》 was published in Gan to kagaku ryoho. Cancer & chemotherapy in 2001. These research results belong to Ohno, R. Application In Synthesis of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide The article mentions the following:

STI571 selectively inhibits the ABL-tyrosine kinase, the activity of which is activated by the formation of chimeric BCR/ABL. A phase I study in the USA showed STI571 to be remarkably effective in cases of interferon-refractory chronic myeloid leukemia, with almost no adverse effects. STI571 may become the first choice drug prior to stem cell transplantation and interferon treatment. The experimental process involved the reaction of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7Application In Synthesis of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide)

2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide(cas: 106392-48-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole.Application In Synthesis of 2-Cyano-3-(4-hydroxy-3,5-diisopropylphenyl)acrylamide The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well.

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics