Month: October 2022

Peng, Zhiyang; Guan, Qing; Luo, Jianfei; Deng, Wenhong; Liu, Jiasheng; Yan, Ruicheng; Wang, Weixing published the artcile< Sophoridine exerts tumor-suppressive activities via promoting ESRRG-mediated β-catenin degradation in gastric cancer>, Name: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one, the main research area is sophoridine tumor suppressive activity ESRRG catenin degradation gastric cancer; ESRRG; Gastric cancer; Sophoridine; β-Catenin.

As a natural alkaloid product isolated from Sophora alopecuroides. L, Sophoridine reshapes gastric cancer immune microenvironment via inhibiting chemotaxis and M2 polarization of tumor-associated macrophages (TAMs). However, the exact effects and underlying mechanism of Sophoridine on gastric cancer cells remains poorly known. The potential anti-tumor effects of Sophoridine on gastric cancer cell lines, including AGS and SGC7901 cells, were detected by CCK-8, EDU and colony forming assay, immunofluorescence, transwell assay, and flow cytometry. Mol. mechanisms of Sophoridine were investigated by siRNA transfection, nuclear/cytoplasmic extraction and western blot. The synergistic effects of Sophoridine with cisplatin on gastric cancer cells were further investigated in in vitro functional studies. Sophoridine exhibited potent tumor-suppressive activities in gastric cancer cells, including inhibition of proliferation, colony formulation, migration and invasion, as well as induction of apoptosis. In addition, we further showed that Sophoridine induced G2/M cell cycle arrest via inhibiting double-stranded DNA breaks repair and enhanced the efficacy of cisplatin in gastric cancer cells. Mol. studies further revealed that Sophoridine promoted β-catenin degradation by enhancing Estrogen-related receptor gamma (ESRRG) expression, but not depended on ubiquitination-proteasome pathway, either TRIM33-mediated (GSK3β-independent) or altered GSK3β activity, and thus exerted potent tumor-suppressive activities. Sophoridine depends on targeting ESRRG/β-catenin pathway to exert tumor-suppressive activities in gastric cancer cells and enhances the anti-tumor effect of cisplatin. Our study provided the promising preclin. anti-tumor evidence for the potential application of Sophoridine against gastric cancer.

BMC Cancer published new progress about Animal gene, Bcl-2 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Name: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Soliman, Ghada A.; Shukla, Surendra K.; Etekpo, Asserewou; Gunda, Venugopal; Steenson, Sharalyn M.; Gautam, Nagsen; Alnouti, Yazen; Singh, Pankaj K. published the artcile< The synergistic effect of an ATP-competitive inhibitor of mTOR and metformin on pancreatic tumor growth>, Application of C24H15F3N4O, the main research area is pancreatic tumor mTOR metformin.

We investigated the impact of inhibition of mTORC1/mTORC2 and synergism with metformin on pancreatic tumor growth and metabolomics. Cell lines derived from pancreatic tumors of the KPC (KrasG12D/+; p53R172H/+; Pdx1-Cre) transgenic mice model were implanted into the pancreas of C57BL/6 albino mice (n = 10/group). Two weeks later, the mice were injected i.p. with daily doses of 1) Torin 2 (mTORC1/mTORC2 inhibitor) at a high concentration (TH), 2) Torin 2 at a low concentration (TL), 3) metformin at a low concentration (ML), 4) a combination of Torin 2 and metformin at low concentrations (TLML), or 5) DMSO vehicle (control) for 12 d. Tissues and blood samples were collected for targeted xenometabolomics anal., drug concentration, and cell signaling. Metabolomic anal. of the control and treated plasma samples showed differential metabolite profiles. Phenylalanine was significantly elevated in the TLML group compared with the control (+426%, P = 0.0004), whereas uracil was significantly lower (-38%, P = 0.009). The combination treatment reduced tumor growth in the orthotopic mouse model. TLML significantly decreased tumor weights (0.66 ± 0.08 g; 52%) compared with the control (1.28 ± 0.19 g; 100%) (P < 0.002). The combination of mTOR dual inhibition by Torin 2 and metformin is associated with an altered metabolomic profile and a significant reduction in pancreatic tumor burden compared with single-agent therapy, and it is better tolerated. Current Developments in Nutrition published new progress about Pancreatic neoplasm. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Application of C24H15F3N4O.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Heinzen, Dennis; Dive, Iris; Lorenz, Nadja I.; Luger, Anna-Luisa; Steinbach, Joachim P.; Ronellenfitsch, Michael W. published the artcile< Second generation mTOR inhibitors as a double-edged sword in malignant glioma treatment>, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is mTOR inhibitor malignant glioma antitumor; glioblastoma; hypoxia; mTOR; mTOR inhibition; starvation; tumor microenvironment.

Glioblastomas (GBs) frequently display activation of the epidermal growth factor receptor (EGFR) and mammalian target of rapamycin (mTOR). mTOR exists as part of two multiprotein complexes, mTOR complex 1 (mTORC1) and 2 (mTORC2). In GBs, mTORC1 inhibitors such as rapamycin have performed poorly in clin. trials, and in vitro protect GB cells from nutrient and oxygen deprivation. Next generation ATP-competitive mTOR inhibitors with affinity for both mTOR complexes have been developed, but data exploring their effects on GB metabolism are scarce. In this study, we compared the ATP-competitive mTORC1/2 inhibitors torin2, INK-128 and NVP-Bez235 to the allostericmTORC1 inhibitor rapamycin under conditions that mimic the glioma microenvironment. In addition to inhibiting mTORC2 signaling, INK-128 and NVP-Bez235 more effectively blocked mTORC1 signaling and prompted a stronger cell growth inhibition, partly by inducing cell cycle arrest. However, under hypoxic and nutrient-poor conditions mTORC1/2 inhibitors displayed even stronger cytoprotective effects than rapamycin by reducing oxygen and glucose consumption. Thus, therapies that arrest proliferation and inhibit anabolic metabolism must be expected to improve energy homeostasis of tumor cells. These results mandate caution when treating physiol. or therapeutically induced hypoxic GBs with mTOR inhibitors.

International Journal of Molecular Sciences published new progress about Antitumor agents. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Safety of 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Krishnan, Karthik; Ziniel, Peter; Li, Hao; Huang, Xiuli; Hupalo, Daniel; Gombakomba, Nita; Guerrero, Sandra Mendoza; Dotrang, Thoai; Lu, Xiao; Caridha, Diana; Sternberg, Anna R.; Hughes, Emma; Sun, Wei; Bargieri, Daniel Y.; Roepe, Paul D.; Sciotti, Richard J.; Wilkerson, Matthew D.; Dalgard, Clifton L.; Tawa, Gregory J.; Wang, Amy Q.; Xu, Xin; Zheng, Wei; Sanderson, Philip E.; Huang, Wenwei; Williamson, Kim C. published the artcile< Torin 2 Derivative, NCATS-SM3710, Has Potent Multistage Antimalarial Activity through Inhibition of P. falciparum Phosphatidylinositol 4-Kinase (Pf PI4KIIIβ)>, Recommanded Product: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one, the main research area is plasmodium malaria drug discovery transmission blocking PI4K drug resistance.

Drug resistance is a constant threat to malaria control efforts making it important to maintain a good pipeline of new drug candidates. Of particular need are compounds that also block transmission by targeting sexual stage parasites. Mature sexual stages are relatively resistant to all currently used antimalarials except the 8-aminoquinolines that are not commonly used due to potential side effects. Here, we synthesized a new Torin 2 derivative, NCATS-SM3710(I) with increased aqueous solubility and specificity for Plasmodium and demonstrate potent in vivo activity against all P. berghei life cycle stages. NCATS-SM3710 also has low nanomolar EC50s against in vitro cultured asexual P. falciparum parasites (0.38 ± 0.04 nM) and late stage gametocytes (5.77 ± 1 nM). Two independent NCATS-SM3710/Torin 2 resistant P. falciparum parasite lines produced by growth in sublethal Torin 2 concentrations both had genetic changes in PF3D7_0509800, annotated as a phosphatidylinositol 4 kinase (Pf PI4KIIIβ). One line had a point mutation in the putative active site (V1357G), and the other line had a duplication of a locus containing Pf PI4KIIIβ. Both lines were also resistant to other Pf PI4K inhibitors. In addition NCATS-SM3710 inhibited purified Pf PI4KIIIβ with an IC50 of 2.0 ± 0.30 nM. Together the results demonstrate that Pf PI4KIIIβ is the target of Torin 2 and NCATS-SM3710 and provide new options for potent multistage drug development.

ACS Pharmacology & Translational Science published new progress about Drug mechanism of action. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Recommanded Product: 9-(6-Aminopyridin-3-yl)-1-(3-(trifluoromethyl)phenyl)benzo[h][1,6]naphthyridin-2(1H)-one.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Liu, Yanlin; Duan, Xiaoli; Zhao, Xiaodi; Ding, Wenlong; Wang, Yaowei; Xiong, Yan published the artcile< Diverse nitrogen signals activate convergent ROP2-TOR signaling in Arabidopsis>, SDS of cas: 1223001-51-1, the main research area is diverse nitrogen signal ROP2TOR Arabidopsis; ROP2; TOR; amino acids; cell proliferation; inorganic nitrogen; leaf primordium.

The evolutionarily conserved target-of-rapamycin (TOR) kinase coordinates cellular and organismal growth in all eukaryotes. Amino acids (AAs) are key upstream signals for mammalian TOR activation, but how nitrogen-related nutrients regulate TOR signaling in plants is poorly understood. Here, we discovered that, independent of nitrogen assimilation, nitrate and ammonium function as primary nitrogen signals to activate TOR in the Arabidopsis leaf primordium. We further identified that a total of 15 proteinogenic AAs are also able to activate TOR, and the first AAs generated from plant specific nitrogen assimilation (glutamine), sulfur assimilation (cysteine), and glycolate cycle (glycine), exhibit the highest potency. Interestingly, nitrate, ammonium, and glutamine all activate the small GTPase Rho-related protein from plants 2 (ROP2), and constitutively active ROP2 restores TOR activation under nitrogen-starvation conditions. Our findings suggest that specific evolutionary adaptations of the nitrogen-TOR signaling pathway occurred in plant lineages, and ROP2 can integrate diverse nitrogen and hormone signals for plant TOR activation.

Developmental Cell published new progress about Amino acids Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, SDS of cas: 1223001-51-1.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Hussain, Azhar R.; Al-Romaizan, Maha; Ahmed, Maqbool; Thangavel, Saravanan; Al-Dayel, Fouad; Beg, Shaham; Uddin, Shahab; Siraj, Abdul K.; Al-Kuraya, Khawla S. published the artcile< Dual targeting of mTOR activity with Torin2 potentiates anticancer effects of cisplatin in epithelial ovarian cancer>, Electric Literature of 1223001-51-1, the main research area is Torin2 cisplatin antitumor mTOR signaling epithelial ovarian cancer.

Mammalian target of rapamycin (mTOR) and phosphatidylinositol 3-kinase (PI3K) are two key components of PI3K/Akt/mTOR signaling pathway. Dysregulation of these pathways have been found in many cancers, including epithelial ovarian cancer (EOC), however, the role of mTOR has not been fully elucidated in Middle Eastern EOC. Therefore, we investigated the activation of mTOR complexes (mTORC1 and mTORC2) in a cohort of 156 EOC from Saudi Arabia by immunohistochem. in a tissue microarray format. mTORC1 and mTORC2 were found to be activated in 55 of 146 (37.7%) and 63 of 140 (45%) of EOC samples, resp. mTORC1 was significantly associated with mTORC2 (p < 0.0001) activation and both mTOR complexes were significantly associated with p-AKT (p = 0.0205 and 0.0298) and p-P70S6 (p < 0.0001 and 0.0035), resp. Interestingly, mTOR activation incurred a poor progression-free survival (PFS) (p = 0.0188) in EOC. Next, the in vitro effect of inactivation of mTOR complexes was evaluated using a second-generation mTOR inhibitor, Torin2, on a panel of EOC cell lines. Torin2 treatment decreased cell viability and induced apoptosis in a dose-dependent manner via inactivation of mTORC1 and mTORC2 and their downstream targets in EOC cell lines. Furthermore, treatment of EOC cells with a subtoxic dose of Torin2 potentiated a cisplatin-induced apoptotic response in EOC cell lines. Finally, we studied the in vivo effect of a combination of Torin2 and cisplatin and found that this combination synergistically inhibited tumor growth in nude mice. These studies highlight the importance of targeting the mTOR survival pathway and suggest that cotreatment with cisplatin and Torin2 may be beneficial for the management of EOC. Molecular Medicine (Manhasset, NY, United States) published new progress about Antitumor agents. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Electric Literature of 1223001-51-1.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Zhang, Zhengyi; Xie, Ziye; Lv, Shujing; Shi, Yulian; Zhai, Chuanjia; Li, Xuejiao; Qiao, Bin; Gao, Xiaoyan published the artcile< Integrated metabolomics and network pharmacology study on the mechanism of Kangfuxiaoyan suppository for treating chronic pelvic inflammatory disease>, Name: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one, the main research area is pelvic inflammatory disease Kangfuxiaoyan suppository metabolomic UPLCQTOFMS pharmacokinetic antiinflammatory; UPLC-Q-TOF/MS; chronic pelvic inflammatory disease; kangfuxiaoyan suppository; metabolomics; network pharmacology.

Kangfuxiaoyan suppository (KFXYS) is a commonly used traditional Chinese medicine (TCM) preparation for the treatment of chronic pelvic inflammatory disease (CPID) clin., and its safety and effectiveness have been well verified. However, the potential mechanism remains unclear. The integrated strategy of metabolomics and network pharmacol. was employed in the study to reveal the potential mechanism of KFXYS in the treatment of CPID. Our research consists of five steps. First, the effect of KFXYS in reversing uterine inflammation indexes was verified. Second, based on the comprehensive characterization of 123 chem. ingredients of KFXYS, the ingredients of KFXYS absorbed into blood were identified by UPLC-Q-TOF/MS, then ADME research was carried out on the main ingredients. Third, the differential metabolites with significant correlation to inflammatory indexes were discovered by metabolomics and correlation anal. Fourth, the potential targets and pathways of KFXYS in treating CPID were predicted by network pharmacol. based on the ingredients which had good ADME behavior. Fifth, the proteins in common pathways of metabolomics and network pharmacol. were used to screen the key targets from the potential targets of network pharmacol., and the potential mechanism of KFXYS in treating CPID was clarified. As a result, KFXYS significantly reversed the uterine inflammation indexes, including IL-1 and IL-6. The ingredients absorbed into blood including matrine, sophocarpine, aloin, esculetin-O-glucuronide, 7,4″”-dihydroxyisoflavone-O-glucuronide, and 4″”-methoxyisoflavone-7-O-glucuronide had good ADME behavior in vivo. Among the differential metabolites, Leukotriene A4, 5- Hydroxyindoleacetic acid, Ornithine, Arginine, and PC (20:1 (11Z)/20:4 (8Z,11Z,14Z,17Z)) were significant correlation to inflammation indexes. The integration anal. of metabolomics and network pharmacol. shows that KFXYS may regulate the key targets including ARG1, NOS2, NOS3, etc. We speculate that ingredients of KFXYS, such as matrine, sophocarpine, aloin etc. act on the key proteins including ARG1, NOS2, and NOS3, to exert anti-inflammatory effect.

Frontiers in Pharmacology published new progress about Alkaloids Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Name: (41S,7aR,13aR,13bR)-Dodecahydro-1H-dipyrido[2,1-f:3′,2′,1′-ij][1,6]naphthyridin-10(41H)-one.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Huo, Zhixia; Chen, Lei published the artcile< Base-deactivated and alkaline-resistant chromatographic stationary phase based on functionalized polymethylsilsesquioxane microspheres>, Formula: C15H24N2O, the main research area is base deactivated chromatog stationary phase functionalized polymethylsilsesquioxane microsphere; basic compounds; co-condensation; functionalization; polymethylsilsesquioxane; silanol activity.

Vinyl, chloropropyl, and mercaptopropyl functionalized particles were prepared by a two-step acidic/alk. catalyzed co-hydrolysis/condensation of methyltrimethoxysilane with a different silane precursor that carries chem. reactive functional group including vinyl, chloropropyl, and mercaptopropyl, resp. The morphol., pore structure, and functional groups of the synthesized packings were studied by SEM, nitrogen adsorption-desorption measurements, and solid-state 13C 29Si NMR spectroscopy, resp. The particles show ordered sphere, narrow particle size distribution, and mesoporous structure. The carbon contents of the microspheres are in the range of 17-19%, comparable to those of octadecyl-bonded silica packings. The three-kind of microspheres were directly used as packing materials for high-performance liquid chromatog. without size classification. The chromatog. performance of the columns was evaluated and compared with a com. available C18 phase. The results revealed that these columns possess typical reversed-phase chromatog. properties with increased hydrophobicity than polymethylsilsesquioxane and sym. peaks for basic compounds They were applied to the simultaneous separation of combination bendazol hydrochlorothiazide capsules containing polar and basic drugs with peaks identified by tandem with mass spectrometry. In general, a novel method is provided for the synthesis of different methyltrimethoxysilane-derived microspheres for high-performance liquid chromatog., which are advantageous for separating basic compounds

Journal of Separation Science published new progress about Chromatographic stationary phases (base-deactivated and alk.-resistant). 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Formula: C15H24N2O.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Song, Limei; Xu, Guoyun; Li, Tingting; Zhou, Huina; Lin, Qinlu; Chen, Jia; Wang, Long; Wu, Dousheng; Li, Xiaoxu; Wang, Lifeng; Zhu, Sirui; Yu, Feng published the artcile< The RALF1-FERONIA complex interacts with and activates TOR signaling in response to low nutrients>, COA of Formula: C24H15F3N4O, the main research area is TOR signaling RALF1 FERONIA complex; FERONIA; TOR; amino acid response; energy metabolism; nitrogen response.

Target of rapamycin (TOR) kinase is an evolutionarily conserved major regulator of nutrient metabolism and organismal growth in eukaryotes. In plants, nutrients are remobilized and reallocated between shoots and roots under low-nutrient conditions, and nitrogen and nitrogen-related nutrients (e.g., amino acids) are key upstream signals leading to TOR activation in shoots under low-nutrient conditions. However, how these forms of nitrogen can be sensed to activate TOR in plants is still poorly understood. Here we report that the Arabidopsis receptor kinase FERONIA (FER) interacts with the TOR pathway to regulate nutrient (nitrogen and amino acid) signaling under low-nutrient conditions and exerts similar metabolic effects in response to nitrogen deficiency. We found that FER and its partner, RPM1-induced protein kinase (RIPK), interact with the TOR/RAPTOR complex to pos. modulate TOR signaling activity. During this process, the receptor complex FER/RIPK phosphorylates the TOR complex component RAPTOR1B. The RALF1 peptide, a ligand of the FER/RIPK receptor complex, increases TOR activation in the young leaf by enhancing FER-TOR interactions, leading to promotion of true leaf growth in Arabidopsis under low-nutrient conditions. Furthermore, we showed that specific amino acids (e.g., Gln, Asp, and Gly) promote true leaf growth under nitrogen-deficient conditions via the FER-TOR axis. Collectively, our study reveals a mechanism by which the RALF1-FER pathway activates TOR in the plant adaptive response to low nutrients and suggests that plants prioritize nutritional stress response over RALF1-mediated inhibition of cell growth under low-nutrient conditions.

Molecular Plant published new progress about Alkaloids Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, COA of Formula: C24H15F3N4O.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Jia, Ya-qian; Yuan, Zi-wen; Zhang, Xiao-song; Dong, Jia-qi; Liu, Xue-nan; Peng, Xiao-ting; Yao, Wan-ling; Ji, Peng; Wei, Yan-ming; Hua, Yong-li published the artcile< Total alkaloids of Sophora alopecuroides L. ameliorated murine colitis by regulating bile acid metabolism and gut microbiota>, HPLC of Formula: 6882-68-4, the main research area is Sophora alkaloids ulcerative colitis bile acid metabolism; Bile acid metabolism; Gut microbiota; Total alkaloids of Sophora alopecuroides L.; Ulcerative colitis.

Sophora alopecuroides L. is one of the most commonly used plants in traditional medicine for the management conditions including inflammatory and gastrointestinal disease. However, the therapeutic mechanism of Sophora alopecuroides L.particularly in inflammatory bowel disease (IBD) remains unclear. To evaluate the treatment effects of total alkaloids of Sophora alopecuroides L. in ulcerative colitis (UC) mice model and explore the therapeutic mechanism of KDZ on UC based on bile acid metabolism and gut microbiota. Colitis were induced in BALB/c mice by administering 3.5% dextran sulfate sodium (DSS) in drinking water for 7 days. The mice were then given KDZ (300, 150 and 75 mg/kg) and the pos. drug sulfasalazine (SASP, 450 mg/kg) via oral administration for 7 days. The levels of 23 bile acids in the liver, bile, serum, cecum content and colon were determined through ultra-performance liquid chromatog./tandem mass spectrometry (UPLC-MS/MS). The cecum microbiota was characterized through high-throughput Illumina MiSeq sequencing. KDZ treatment significantly decreased the disease activity index (DAI) scores and ameliorated colonic injury in DSS-treated mice. The expression of IL-1β and TGF-β1 were suppressed, yet, IL-10 was up-regulated by KDZ and SASP treatment compared with those in the model group. Meanwhile, the serum contents of total bile acid and total cholesterol in the DSS group increased significantly compared with those in the control group, but reversed by SASP and KDZ. The relative abundance of Firmicutes increased after KDZ was administration, whereas the abundance of Bacteroidetes decreased. αMCA, βMCA, ωMCA and CA in the SASP and KDZ groups did not differ from those in the control group, whereas these parameters significantly increased in the DSS group. KDZ had a protective effect on DSS-induced colitis by mitigating colonic injury, preventing gut microbiota dysbiosis and regulating bile acid metabolism

Journal of Ethnopharmacology published new progress about Adlercreutzia. 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, HPLC of Formula: 6882-68-4.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem