Tag: 300-400

Key role of soluble epoxide hydrolase in the neurodevelopmental disorders of offspring after maternal immune activation was written by Ma, Min;Ren, Qian;Yang, Jun;Zhang, Kai;Xiong, Zhongwei;Ishima, Tamaki;Pu, Yaoyu;Hwang, Sung Hee;Toyoshima, Manabu;Iwayama, Yoshimi;Hisano, Yasuko;Yoshikawa, Takeo;Hammock, Bruce D.;Hashimoto, Kenji. And the article was included in Proceedings of the National Academy of Sciences of the United States of America in 2019.Electric Literature of C16H20F3N3O3 The following contents are mentioned in the article:

Maternal infection during pregnancy increases risk of neurodevelopmental disorders such as schizophrenia and autism spectrum disorder (ASD) in offspring. In rodents, maternal immune activation (MIA) yields offspring with schizophrenia- and ASD-like behavioral abnormalities. Soluble epoxide hydrolase (sEH) plays a key role in inflammation associated with neurodevelopmental disorders. Here we found higher levels of sEH in the prefrontal cortex (PFC) of juvenile offspring after MIA. Oxylipin anal. showed decreased levels of epoxy fatty acids in the PFC of juvenile offspring after MIA, supporting increased activity of sEH in the PFC of juvenile offspring. Furthermore, expression of sEH (or EPHX2) mRNA in induced pluripotent stem cell-derived neurospheres from schizophrenia patients with the 22q11.2 deletion was higher than that of healthy controls. Moreover, the expression of EPHX2 mRNA in postmortem brain samples (Brodmann area 9 and 40) from ASD patients was higher than that of controls. Treatment with 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea (TPPU), a potent sEH inhibitor, in juvenile offspring from prenatal day (P) 28 to P56 could prevent cognitive deficits and loss of parvalbumin (PV) immunoreactivity in the medial PFC of adult offspring after MIA. In addition, dosing of TPPU to pregnant mothers from E5 to P21 could prevent cognitive deficits, and social interaction deficits and PV immunoreactivity in the medial prefrontal cortex of juvenile offspring after MIA. These findings suggest that increased activity of sEH in the PFC plays a key role in the etiol. of neurodevelopmental disorders in offspring after MIA. Therefore, sEH represents a promising prophylactic or therapeutic target for neurodevelopmental disorders in offspring after MIA. This study involved multiple reactions and reactants, such as 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7Electric Literature of C16H20F3N3O3).

1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7) belongs to piperidine derivatives. The piperidine ring can be found not only in more than half of the currently known structures of alkaloids, but also in many natural or synthetic compounds with interesting biological activities. Piperidine derivatives are being utilized in different ways as anticancer, antiviral, antimalarial, antimicrobial, antifungal, antihypertension, analgesic, anti-inflammatory, anti-Alzheimer, antipsychotic and/or anticoagulant agents.Electric Literature of C16H20F3N3O3

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Inhibition of soluble epoxide hydrolase alleviates insulin resistance and hypertension via downregulation of SGLT2 in the mouse kidney was written by Luo, Jinlan;Hu, Shuiqing;Fu, Menglu;Luo, Liman;Li, Yuanyuan;Li, Wenhua;Cai, Yueting;Dong, Ruolan;Yang, Yan;Tu, Ling;Xu, Xizhen. And the article was included in Journal of Biological Chemistry in 2021.Formula: C16H20F3N3O3 The following contents are mentioned in the article:

The epoxyeicosatrienoic acid (EET) exerts beneficial effects on insulin resistance and/or hypertension. EETs could be readily converted to less biol. active diols by soluble epoxide hydrolase (sEH). However, whether sEH inhibition can ameliorate the comorbidities of insulin resistance and hypertension and the underlying mechanisms of this relationship are unclear. In this study, C57BL/6 mice were rendered hypertensive and insulin resistant through a high-fat and high-salt (HF-HS) diet. The sEH inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), was used to treat mice (1 mg/kg/day) for 8 wk, followed by anal. of metabolic parameters. The expression of sEH and the sodium-glucose cotransporter 2 (SGLT2) was markedly upregulated in the kidneys of mice fed an HF-HS diet. We found that TPPU administration increased kidney EET levels, improved insulin resistance, and reduced hypertension. Furthermore, TPPU treatment prevented upregulation of SGLT2 and the associated increased urine volume and the excretion of urine glucose and urine sodium. Importantly, TPPU alleviated renal inflammation. In vitro, human renal proximal tubule epithelial cells (HK-2 cells) were used to further investigate the underlying mechanism. We observed that 14,15-EET or sEH knockdown or inhibition prevented the upregulation of SGLT2 upon treatment with palmitic acid or NaCl by inhibiting the inhibitory kappa B kinase α/β/NF-κB signaling pathway. In conclusion, sEH inhibition by TPPU alleviated insulin resistance and hypertension induced by an HF-HS diet in mice. The increased urine excretion of glucose and sodium was mediated by decreased renal SGLT2 expression because of inactivation of the inhibitory kappa B kinase α/β/NF-κB-induced inflammatory response. This study involved multiple reactions and reactants, such as 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7Formula: C16H20F3N3O3).

1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7) belongs to piperidine derivatives. The piperidine structural motif is present in numerous natural alkaloids. These include piperine, which gives black pepper its spicy taste. Industrially, piperidine is produced by the hydrogenation of pyridine, usually over a molybdenum disulfide catalyst. Pyridine can also be reduced to piperidine via a modified Birch reduction using sodium in ethanol.Formula: C16H20F3N3O3

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Soluble epoxide hydrolase inhibitor trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea prevents hyperalgesia through regulating NLRC4 inflammasome-related pro-inflammatory and anti-inflammatory signaling pathways in the lipopolysaccharide-induced pain mouse model was written by Cagli, Ali;Senol, Sefika Pinar;Temiz-Resitoglu, Meryem;Guden, Demet Sinem;Sari, Ayse Nihal;Sahan-Firat, Seyhan;Tunctan, Bahar. And the article was included in Drug Development Research in 2021.Recommanded Product: 1222780-33-7 The following contents are mentioned in the article:

Epoxyeicosatrienoic acids (EETs) have anti-inflammatory effects and soluble epoxide hydrolase (sEH) inhibition might be a useful therapeutic approach to manage inflammatory disorders. The purpose of the study was to investigate whether nucleotide-binding and oligomerization domain-like receptor (NLR) C4 inflammasome-related pro-inflammatory and anti-inflammatory signaling pathways in the central nervous system (CNS) participates in the effect of trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl)urea (TPPU), a potent sEH inhibitor, to prevent hyperalgesia in the LPS-induced pain mouse model. The latency of pain within 30 s was measured by the hot plate test in male mice injected with saline, lipopolysaccharide (LPS) (10 mg/kg), and/or TPPU (0.3, 0.5, or 1 mg/kg) after 6 h. Hyperalgesia induced by LPS was associated with decreased 14,15-dihydroxyeicosatrienoic acid and interleukin (IL)-1β levels and enhanced expression of NLRC4, apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC), caspase-1 p20, IL-1β, and caspase-11 p20 in the brains and spinal cords of the animals. Besides the increased expression of NADP oxidase (NOX) subunits (gp91^phox and p47^phox) and nitrotyrosine, a decrease in NLRC3, inducible nitric oxide synthase (iNOS), and neuronal NOS (nNOS) expression was also observed in the tissues of LPS-treated mice. TPPU at 0.5 mg/kg dose prevented the changes induced by LPS. Likely, decreased activity of pro-inflammatory NLRC4/ASC/pro-caspase-1 and caspase-11 inflammasomes and NOX in addition to enhanced levels of anti-inflammatory EETs and expression of NLRC3, iNOS, and nNOS in the CNS of mice participates in the protective effect of TPPU against LPS-induced hyperalgesia. This study involved multiple reactions and reactants, such as 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7Recommanded Product: 1222780-33-7).

1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7) belongs to piperidine derivatives. Piperidine has a role as a reagent, a protic solvent, a base, a catalyst, a plant metabolite, a human metabolite and a non-polar solvent. Some chemotherapeutic agents have piperidine moiety within their structure, foremost among them, vinblastine and raloxifene.Recommanded Product: 1222780-33-7

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Suppression of inflammation and fibrosis using soluble epoxide hydrolase inhibitors enhances cardiac stem cell-based therapy was written by Sirish, Padmini;Thai, Phung N.;Lee, Jeong Han;Yang, Jun;Zhang, Xiao-Dong;Ren, Lu;Li, Ning;Timofeyev, Valeriy;Lee, Kin Sing Stephen;Nader, Carol E.;Rowland, Douglas J.;Yechikov, Sergey;Ganaga, Svetlana;Young, Nilas;Lieu, Deborah K.;Yamoah, Ebenezer N.;Hammock, Bruce D.;Chiamvimonvat, Nipavan. And the article was included in Stem Cells Translational Medicine in 2020.Recommanded Product: 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea The following contents are mentioned in the article:

Stem cell replacement offers a great potential for cardiac regenerative therapy. However, one of the critical barriers to stem cell therapy is a significant loss of transplanted stem cells from ischemia and inflammation in the host environment. Here, we tested the hypothesis that inhibition of the soluble epoxide hydrolase (sEH) enzyme using sEH inhibitors (sEHIs) to decrease inflammation and fibrosis in the host myocardium may increase the survival of the transplanted human induced pluripotent stem cell derived-cardiomyocytes (hiPSC-CMs) in a murine postmyocardial infarction model. A specific sEHI (1-trifluoromethoxyphenyl-3-(1-propionylpiperidine-4-yl)urea [TPPU]) and CRISPR/Cas9 gene editing were used to test the hypothesis. TPPU results in a significant increase in the retention of transplanted cells compared with cell treatment alone. The increase in the retention of hiPSC-CMs translates into an improvement in the fractional shortening and a decrease in adverse remodeling. Mechanistically, we demonstrate a significant decrease in oxidative stress and apoptosis not only in transplanted hiPSC-CMs but also in the host environment. CRISPR/Cas9-mediated gene silencing of the sEH enzyme reduces cleaved caspase-3 in hiPSC-CMs challenged with angiotensin II, suggesting that knockdown of the sEH enzyme protects the hiPSC-CMs from undergoing apoptosis. Our findings demonstrate that suppression of inflammation and fibrosis using an sEHI represents a promising adjuvant to cardiac stem cell-based therapy. Very little is known regarding the role of this class of compounds in stem cell-based therapy. There is consequently an enormous opportunity to uncover a potentially powerful class of compounds, which may be used effectively in the clin. setting. This study involved multiple reactions and reactants, such as 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7Recommanded Product: 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea).

1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7) belongs to piperidine derivatives. Piperidine and its derivatives have become increasingly popular in many synthetic schemes. Fluorinated piperidines are also the subject of continued interest in medicinal chemistry, for example in the synthesis of selective dipeptidyl peptidase II (DPP II) inhibitors. Piperidine derivatives are also used in solid-phase peptide synthesis (SPPS) and many degradation reactions.Recommanded Product: 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Gene deficiency and pharmacological inhibition of soluble epoxide hydrolase confers resilience to repeated social defeat stress was written by Ren, Qian;Ma, Min;Ishima, Tamaki;Morisseau, Christophe;Yang, Jun;Wagner, Karen M.;Zhang, Ji-chun;Yang, Chun;Yao, Wei;Dong, Chao;Han, Mei;Hammock, Bruce D.;Hashimoto, Kenji. And the article was included in Proceedings of the National Academy of Sciences of the United States of America in 2016.HPLC of Formula: 1222780-33-7 The following contents are mentioned in the article:

Depression is a severe and chronic psychiatric disease, affecting 350 million subjects worldwide. Although multiple antidepressants have been used in the treatment of depressive symptoms, their beneficial effects are limited. The soluble epoxide hydrolase (sEH) plays a key role in the inflammation that is involved in depression. Thus, the authors examined here the role of sEH in depression. In both inflammation and social defeat stress models of depression, a potent sEH inhibitor, TPPU, displayed rapid antidepressant effects. Expression of sEH protein in the brain from chronically stressed (susceptible) mice was higher than of control mice. Furthermore, expression of sEH protein in postmortem brain samples of patients with psychiatric diseases, including depression, bipolar disorder, and schizophrenia, was higher than controls. This finding suggests that increased sEH levels might be involved in the pathogenesis of certain psychiatric diseases. In support of this hypothesis, pretreatment with TPPU prevented the onset of depression-like behaviors after inflammation or repeated social defeat stress. Moreover, sEH KO mice did not show depression-like behavior after repeated social defeat stress, suggesting stress resilience. The sEH KO mice showed increased brain-derived neurotrophic factor (BDNF) and phosphorylation of its receptor TrkB in the prefrontal cortex, hippocampus, but not nucleus accumbens, suggesting that increased BDNF-TrkB signaling in the prefrontal cortex and hippocampus confer stress resilience. All of these findings suggest that sEH plays a key role in the pathophysiol. of depression, and that epoxy fatty acids, their mimics, as well as sEH inhibitors could be potential therapeutic or prophylactic drugs for depression. This study involved multiple reactions and reactants, such as 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7HPLC of Formula: 1222780-33-7).

1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7) belongs to piperidine derivatives. Piperidine has a role as a reagent, a protic solvent, a base, a catalyst, a plant metabolite, a human metabolite and a non-polar solvent. Piperidine derivatives bearing a masked aldehyde function in the ε-position are easily transformed into quinolizidine compounds through intramolecular reductive amination.HPLC of Formula: 1222780-33-7

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Structure-Activity Relationships of Cyclic Peptide-Based Chemokine Receptor CXCR4 Antagonists: Disclosing the Importance of Side-Chain and Backbone Functionalities was written by Ueda, Satoshi;Oishi, Shinya;Wang, Zi-xuan;Araki, Takanobu;Tamamura, Hirokazu;Cluzeau, Jerome;Ohno, Hiroaki;Kusano, Shuichi;Nakashima, Hideki;Trent, John O.;Peiper, Stephen C.;Fujii, Nobutaka. And the article was included in Journal of Medicinal Chemistry in 2007.HPLC of Formula: 86069-86-5 The following contents are mentioned in the article:

Previously, we have identified a highly potent CXCR4 antagonist 2 [cyclo(-D-Tyr¹-Arg²-Arg³-Nal⁴-Gly⁵-)] and its Arg² epimer 3 [cyclo(-D-Tyr¹–D-Arg²-Arg³-Nal⁴-Gly⁵-)] by the screening of cyclic pentapeptide libraries that were designed based on the structure-activity relationship studies on 14-residue peptidic CXCR4 antagonist 1. In the present study, a new series of analogs of 2 and 3 were synthesized to evaluate the influences of peptide side-chain and backbone modification on bioactivities. Based on the Ala-scanning study, in which each residue in 2 and 3 was replaced with Ala having the identical chirality, substitution of Arg³ and Nal⁴ [Nal = L-3-(2-naphthyl)alanine] with Ala (compounds 6, 7, 10, 11) led to significant loss of the potency, indicating these amino acids are more important contributors to the bioactivity. For the cyclic peptide backbone, several modifications including D/L-Ala or cyclic amino acids substitution at the Gly⁵ position and sequential N-methylation on amide nitrogens were conducted. Among the analogs, compounds 13 [cyclo(-D-Tyr¹-Arg²-Arg³-Nal⁴–D-Ala⁵-)] and 32 [cyclo(-D-Tyr¹–D-MeArg²-Arg³-Nal⁴-Gly⁵-)] were close in potency to the most potent lead 2. NMR and conformational anal. indicated that both of these analogs favor the same backbone conformation as 2, whereas similar anal. of less potent analogs indicates that an altered backbone conformation is favored. The conformational anal. showed that steric repulsion by a 1,3-allylic strain-like effect across the planar peptide bond might contribute to the conformational preferences of cyclic pentapeptides. This study involved multiple reactions and reactants, such as (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5HPLC of Formula: 86069-86-5).

(S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5) belongs to piperidine derivatives. Piperidine is a saturated organic heteromonocyclic parent, an azacycloalkane, a secondary amine and a member of piperidines. Industrially, piperidine is produced by the hydrogenation of pyridine, usually over a molybdenum disulfide catalyst. Pyridine can also be reduced to piperidine via a modified Birch reduction using sodium in ethanol.HPLC of Formula: 86069-86-5

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Structure-Activity Relationships of Cyclic Peptide-Based Chemokine Receptor CXCR4 Antagonists: Disclosing the Importance of Side-Chain and Backbone Functionalities was written by Ueda, Satoshi;Oishi, Shinya;Wang, Zi-xuan;Araki, Takanobu;Tamamura, Hirokazu;Cluzeau, Jerome;Ohno, Hiroaki;Kusano, Shuichi;Nakashima, Hideki;Trent, John O.;Peiper, Stephen C.;Fujii, Nobutaka. And the article was included in Journal of Medicinal Chemistry in 2007.Formula: C21H21NO4 The following contents are mentioned in the article:

Previously, we have identified a highly potent CXCR4 antagonist 2 [cyclo(-D-Tyr¹-Arg²-Arg³-Nal⁴-Gly⁵-)] and its Arg² epimer 3 [cyclo(-D-Tyr¹–D-Arg²-Arg³-Nal⁴-Gly⁵-)] by the screening of cyclic pentapeptide libraries that were designed based on the structure-activity relationship studies on 14-residue peptidic CXCR4 antagonist 1. In the present study, a new series of analogs of 2 and 3 were synthesized to evaluate the influences of peptide side-chain and backbone modification on bioactivities. Based on the Ala-scanning study, in which each residue in 2 and 3 was replaced with Ala having the identical chirality, substitution of Arg³ and Nal⁴ [Nal = L-3-(2-naphthyl)alanine] with Ala (compounds 6, 7, 10, 11) led to significant loss of the potency, indicating these amino acids are more important contributors to the bioactivity. For the cyclic peptide backbone, several modifications including D/L-Ala or cyclic amino acids substitution at the Gly⁵ position and sequential N-methylation on amide nitrogens were conducted. Among the analogs, compounds 13 [cyclo(-D-Tyr¹-Arg²-Arg³-Nal⁴–D-Ala⁵-)] and 32 [cyclo(-D-Tyr¹–D-MeArg²-Arg³-Nal⁴-Gly⁵-)] were close in potency to the most potent lead 2. NMR and conformational anal. indicated that both of these analogs favor the same backbone conformation as 2, whereas similar anal. of less potent analogs indicates that an altered backbone conformation is favored. The conformational anal. showed that steric repulsion by a 1,3-allylic strain-like effect across the planar peptide bond might contribute to the conformational preferences of cyclic pentapeptides. This study involved multiple reactions and reactants, such as (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5Formula: C21H21NO4).

(S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5) belongs to piperidine derivatives. The piperidine moiety constitutes an important building block for the synthesis of a variety of bioactive natural products, alkaloids and other drugs. Some chemotherapeutic agents have piperidine moiety within their structure, foremost among them, vinblastine and raloxifene.Formula: C21H21NO4

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Novel urea-linked cinchona-calixarene hybrid-type receptors for efficient chromatographic enantiomer separation of carbamate-protected cyclic amino acids was written by Krawinkler, Karl Heinz;Maier, Norbert M.;Sajovic, Elisabeth;Lindner, Wolfgang. And the article was included in Journal of Chromatography A in 2004.Safety of (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid The following contents are mentioned in the article:

Two novel diastereomeric cinchona-calixarene hybrid-type receptors (SOs) were synthesized by inter-linking 9-amino(9-deoxy)-quinine (AQN)/9-amino(9-deoxy)-epiquinine (eAQN) and a calix[4]arene scaffold via an urea functional unit. Silica-supported chiral stationary phases (CSPs) derived from these SOs revealed, for N-protected amino acids, complementary chiral recognition profiles in terms of elution order and substrate specificity. The AQN-derived CSP showed narrow-scoped enantioselectivity for open-chained amino acids bearing π-acidic aromatic protecting groups, preferentially binding the (S)-enantiomers. In contrast, the eAQN congener exhibited broad chiral recognition capacity for open-chained as well as cyclic amino acids, and preferential binding of the (R)-enantiomers. Exceedingly strong retention due to nonenantioselective hydrophobic analyte-calixarene interactions observed with hydro-organic mobile phases could be largely suppressed with organic mobile phases containing small amounts of acetic acid as acidic modifier. With the eAQN-calixarene hybrid-type CSP particularly high levels of enantioselectivity could be achieved for tert-butoxycarbonyl (Boc)-, benzyloxycarbonyl (Z)- and fluorenylmethoxycarbonyl (Fmoc)-protected cyclic amino acids using chloroform as mobile phase, e.g. an enantioselectivty factor α > 5.0 for Boc-proline. Increasing amounts of acetic acid compromised enantioselectivity, indicating the crucial contributions of hydrogen bonding to chiral recognition. Comparison of the performance characteristics of the urea-linked eAQN-calixarene hybrid-type CSP with those of structurally closely related mutants provided evidence for the active involvement of the urea and calixarene units in the chiral recognition process. The urea linker motif was shown to contribute to analyte binding via multiple hydrogen bonding interactions, while the calixarene module is believed to support stereodiscrimination by enhancing the shape complementarity of the SO binding site. This study involved multiple reactions and reactants, such as (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5Safety of (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid).

(S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5) belongs to piperidine derivatives.Piperidine is a key saturated heterocyclic scaffold found in several of the top-selling small molecule pharmaceuticals and natural alkaloids, with a diverse range of biological activities. Industrially, piperidine is produced by the hydrogenation of pyridine, usually over a molybdenum disulfide catalyst. Pyridine can also be reduced to piperidine via a modified Birch reduction using sodium in ethanol.Safety of (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Novel urea-linked cinchona-calixarene hybrid-type receptors for efficient chromatographic enantiomer separation of carbamate-protected cyclic amino acids was written by Krawinkler, Karl Heinz;Maier, Norbert M.;Sajovic, Elisabeth;Lindner, Wolfgang. And the article was included in Journal of Chromatography A in 2004.COA of Formula: C21H21NO4 The following contents are mentioned in the article:

Two novel diastereomeric cinchona-calixarene hybrid-type receptors (SOs) were synthesized by inter-linking 9-amino(9-deoxy)-quinine (AQN)/9-amino(9-deoxy)-epiquinine (eAQN) and a calix[4]arene scaffold via an urea functional unit. Silica-supported chiral stationary phases (CSPs) derived from these SOs revealed, for N-protected amino acids, complementary chiral recognition profiles in terms of elution order and substrate specificity. The AQN-derived CSP showed narrow-scoped enantioselectivity for open-chained amino acids bearing π-acidic aromatic protecting groups, preferentially binding the (S)-enantiomers. In contrast, the eAQN congener exhibited broad chiral recognition capacity for open-chained as well as cyclic amino acids, and preferential binding of the (R)-enantiomers. Exceedingly strong retention due to nonenantioselective hydrophobic analyte-calixarene interactions observed with hydro-organic mobile phases could be largely suppressed with organic mobile phases containing small amounts of acetic acid as acidic modifier. With the eAQN-calixarene hybrid-type CSP particularly high levels of enantioselectivity could be achieved for tert-butoxycarbonyl (Boc)-, benzyloxycarbonyl (Z)- and fluorenylmethoxycarbonyl (Fmoc)-protected cyclic amino acids using chloroform as mobile phase, e.g. an enantioselectivty factor α > 5.0 for Boc-proline. Increasing amounts of acetic acid compromised enantioselectivity, indicating the crucial contributions of hydrogen bonding to chiral recognition. Comparison of the performance characteristics of the urea-linked eAQN-calixarene hybrid-type CSP with those of structurally closely related mutants provided evidence for the active involvement of the urea and calixarene units in the chiral recognition process. The urea linker motif was shown to contribute to analyte binding via multiple hydrogen bonding interactions, while the calixarene module is believed to support stereodiscrimination by enhancing the shape complementarity of the SO binding site. This study involved multiple reactions and reactants, such as (S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5COA of Formula: C21H21NO4).

(S)-1-(((9H-Fluoren-9-yl)methoxy)carbonyl)piperidine-2-carboxylic acid (cas: 86069-86-5) belongs to piperidine derivatives. The piperidine moiety constitutes an important building block for the synthesis of a variety of bioactive natural products, alkaloids and other drugs. The piperidine and polyhydroxylated indolizidine derivatives have shown to be promising α-glucosidase inhibitors. The former are analogs of DNJ with an improved α-glucosidase inhibitory profile than that of DNJ. Boisson et al.COA of Formula: C21H21NO4

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem

Inhibition of Soluble Epoxide Hydrolase Attenuates Bosutinib-Induced Blood Pressure Elevation was written by Cui, Zhen;Li, Bochuan;Zhang, Yanhong;He, Jinlong;Shi, Xuelian;Wang, Hui;Zhao, Yinjiao;Yao, Liu;Ai, Ding;Zhang, Xu;Zhu, Yi. And the article was included in Hypertension in 2021.Formula: C16H20F3N3O3 The following contents are mentioned in the article:

Endothelial cells play a critical role in maintaining homeostasis of vascular function, and endothelial activation is involved in the initial step of atherogenesis. Previously, we reported that Abl kinase mediates shear stress-induced endothelial activation. Bosutinib, a dual inhibitor of Src and Abl kinases, exerts an atheroprotective effect; however, recent studies have demonstrated an increase in the incidence of side effects associated with bosutinib, including increased arterial blood pressure (BP). To understand the effects of bosutinib on BP regulation and the mechanistic basis for novel treatment strategies against vascular dysfunction, we generated a line of mice conditionally lacking c-Abl in endothelial cells (endothelial cell-Abl^KO). Knockout mice and their wild-type littermates (Abl^f/f) were orally administered a clin. dose of bosutinib, and their BP was monitored. Bosutinib treatment increased BP in both endothelial cell-Abl^KO and Abl^f/f mice. Furthermore, acetylcholine-evoked endothelium-dependent relaxation of the mesenteric arteries was impaired by bosutinib treatment. RNA sequencing of mesenteric arteries revealed that the CYP (cytochrome P 450)-dependent metabolic pathway was involved in regulating BP after bosutinib treatment. Addnl., bosutinib treatment led to an upregulation of soluble epoxide hydrolase in the arteries and a lower plasma content of eicosanoid metabolites in the CYP pathway in mice. Treatment with 1-Trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea, a soluble epoxide hydrolase inhibitor, reversed the bosutinib-induced changes to the eicosanoid metabolite profile, endothelium-dependent vasorelaxation, and BP. Thus, the present study demonstrates that upregulation of soluble epoxide hydrolase mediates bosutinib-induced elevation of BP, independent of c-Abl. The addition of soluble epoxide hydrolase inhibitor in patients treated with bosutinib may aid in preventing vascular side effects. This study involved multiple reactions and reactants, such as 1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7Formula: C16H20F3N3O3).

1-(1-Propionylpiperidin-4-yl)-3-(4-(trifluoromethoxy)phenyl)urea (cas: 1222780-33-7) belongs to piperidine derivatives. The piperidine moiety constitutes an important building block for the synthesis of a variety of bioactive natural products, alkaloids and other drugs. Fluorinated piperidines are also the subject of continued interest in medicinal chemistry, for example in the synthesis of selective dipeptidyl peptidase II (DPP II) inhibitors. Piperidine derivatives are also used in solid-phase peptide synthesis (SPPS) and many degradation reactions.Formula: C16H20F3N3O3

Referemce:
Piperidine – Wikipedia,
Piperidine | C5H11N – PubChem