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Frommedchem Express, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/frommedchem+express/Irinotecan/pm38508144-279-12-14
Average 94 stars, based on 26 article reviews

frommedchem express - by Bioz Stars, 2026-09

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Article Title: Quercetin Rejuvenates Sensitization of Colistin-Resistant Escherichia coli and Klebsiella Pneumoniae Clinical Isolates to Colistin.
Article Snippet: Quercetin was purchased fromMedChem Express (MCE) Co., Ltd. (New Jersey, United States), and all antibiotics used in this study, including colistin, aztreonam, ceftazidime, cefepime, imipenem, ciprofloxacin, levofloxacin, gentamicin, tobramycin, and amikacin were purchased from Wenzhou Kangtai Biological Technology Co., Ltd. (Zhejiang, China).

Article Title: Histone lysine demethylase 4 family proteins maintain the transcriptional program and adrenergic cellular state of MYCN-amplified neuroblastoma
Article Snippet: Compound resource and QC6352 synthesis Vincristine (HY-N0488) and Irinotecan (HY-16562A) were purchased fromMedChem Express (MCE).

Article Title: Biosynthesis and antimicrobial activities of Tinospora cordifolia zinc nanoparticles
Article Snippet: Nanoparticles are important features that reflect the size, morphology, and other properties.. The current study focuses on the biosynthesis of zinc nanomaterials utilizing Tinospora cordifolia stem extract.. Green synthesis of zinc nanoparticles (ZnNPs) can terminate chemical pathogens that may have adverse consequences, hence manufacturing nanoparticles is more accordant with an environmentally sustainable strategy.

Article Title: Binding and functional pharmacological characteristics of gepant-type antagonists in rat brain and mesenteric arteries.
Article Snippet: Article history: Received 23 November 2016 Received in revised form 13 January 2017 Accepted 5 February 2017 Available online xxxx Aim: The neuropeptide calcitonin gene-related peptide (CGRP) is found in afferent sensory nerve fibers innervating the resistance arteries and plays a pivotal role in a number of neurovascular diseases such as migraine and subarachnoid bleedings.. The present study investigates the binding and antagonistic characteristics of small non-peptide CGRP receptor antagonists (i.e. gepants) in isolated rat brain and mesenteric resistance arteries.. Methods: The antagonistic behavior of gepants was investigated in isolated rat mesenteric arteries using a wire myograph setup while binding of gepants to CGRP receptors was investigated in rat brain membranes using a radioligand competitive binding assay.

Article Title: Histone lysine demethylase 4 family proteins maintain the transcriptional program and adrenergic cellular state of MYCN-amplified neuroblastoma.
Article Snippet: Compound resource and QC6352 synthesis Vincristine (HY-N0488) and Irinotecan (HY-16562A) were purchased fromMedChem Express (MCE).

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Figure 4. A and B, Representative snapshot from the MDs trajectory of the com- plex of c-MET and merestinib. Meres- tinib is shown in yellow, interacting amino acids in cyan and the F1200 or I1200 aa residue in green. A, As merestinib binds to WT MET, three phenyl rings from the F1134/F1200/ ﬂuorophenyl tail of merestinib form an aromatic cluster, stabilizing the inter- action. Bottom panel shows protein– ligand interaction histograms for 100 nanoseconds MD simulation of WT MET with merestinib. Red denotes hydrogen bond interactions and blue denotes hydrophobic interac- tions. B, The F1200I mutation destroys the aromatic cluster, weakening the merestinib–MET interaction. Bottom pane shows protein–ligand interaction histograms for 100 nanoseconds MD simulation of MET F1200I mutant with merestinib. Red denotes hydrogen bond interactions and blue denotes hydrophobic interactions. The pro- tein–ligand interaction at I1200 is fully abolished. C and D, Representative snapshot from the MDs trajectory of the complex of MET and capmatinib. Capmatinib is shown in yellow, inter- acting amino acids in cyan and the F1200 or I1200 aa residue in green. C, As capmatinib binds to the WT MET, p–p stacking with Y1230 in the activa- tion loop forms, stabilizing the inter- action. Bottom panel shows protein– ligand interaction histograms for 100 nanoseconds MD simulation of WT MET with capmatinib. Red denotes hydrogen bond interactions and blue denotes hydrophobic interactions. D, Capmatinib keeps an effective p–p stacking interaction with Y1230 in MET F1200I mutant c-Met mutant. Bottom panel shows protein–ligand interaction histograms for 100 nano- seconds MD simulation of MET F1200I with capmatinib. Capmatinib exhibits an efﬁcient binding interac- tion with the mutant. Red denotes hydrogen bond interactions and blue denotes hydrophobic interactions.

Journal: Molecular Cancer Therapeutics

Article Title: Combination of Type I and Type II MET Tyrosine Kinase Inhibitors as Therapeutic Approach to Prevent Resistance

doi: 10.1158/1535-7163.mct-21-0344

Figure Lengend Snippet: Figure 4. A and B, Representative snapshot from the MDs trajectory of the com- plex of c-MET and merestinib. Meres- tinib is shown in yellow, interacting amino acids in cyan and the F1200 or I1200 aa residue in green. A, As merestinib binds to WT MET, three phenyl rings from the F1134/F1200/ ﬂuorophenyl tail of merestinib form an aromatic cluster, stabilizing the inter- action. Bottom panel shows protein– ligand interaction histograms for 100 nanoseconds MD simulation of WT MET with merestinib. Red denotes hydrogen bond interactions and blue denotes hydrophobic interac- tions. B, The F1200I mutation destroys the aromatic cluster, weakening the merestinib–MET interaction. Bottom pane shows protein–ligand interaction histograms for 100 nanoseconds MD simulation of MET F1200I mutant with merestinib. Red denotes hydrogen bond interactions and blue denotes hydrophobic interactions. The pro- tein–ligand interaction at I1200 is fully abolished. C and D, Representative snapshot from the MDs trajectory of the complex of MET and capmatinib. Capmatinib is shown in yellow, inter- acting amino acids in cyan and the F1200 or I1200 aa residue in green. C, As capmatinib binds to the WT MET, p–p stacking with Y1230 in the activa- tion loop forms, stabilizing the inter- action. Bottom panel shows protein– ligand interaction histograms for 100 nanoseconds MD simulation of WT MET with capmatinib. Red denotes hydrogen bond interactions and blue denotes hydrophobic interactions. D, Capmatinib keeps an effective p–p stacking interaction with Y1230 in MET F1200I mutant c-Met mutant. Bottom panel shows protein–ligand interaction histograms for 100 nano- seconds MD simulation of MET F1200I with capmatinib. Capmatinib exhibits an efﬁcient binding interac- tion with the mutant. Red denotes hydrogen bond interactions and blue denotes hydrophobic interactions.

Article Snippet: Antibodies against phospho-MET (Tyr1234; sc-101736; RRID: AB_2143892) and HSP90 (sc-7947; RRID:AB_2121235) were purchased from Santa Cruz Biotechnology; total-MET (D1C2; No. 8198; RRID:AB_10858224) and anti-rabbit IgG-HRP (No. 7074; RRID: AB_2099233) from Cell Signaling Technology; savolitinib, crizotinib, cabozantinib, and glesatinib were purchased from Selleckchem; merestinib fromMedChem Express and Selleckchem.

Techniques: Residue, Mutagenesis, Binding Assay

Figure 5. The merestinib/capmatinib combination shows efﬁcacy and tolerability in vivo. A, A box plot of volume of tumors harvested from mice on day 18 of treatment. , # denote signiﬁcance. B, Plot of body weight percent change of treated mice as a function of treatment time. C, The individual contribution of each TPR-MET mutant was determined by ddPCR at the end of the study and expressed as percent tumor volume. Each bar represents an individual treatment subject.

Journal: Molecular Cancer Therapeutics

Article Title: Combination of Type I and Type II MET Tyrosine Kinase Inhibitors as Therapeutic Approach to Prevent Resistance

doi: 10.1158/1535-7163.mct-21-0344

Figure Lengend Snippet: Figure 5. The merestinib/capmatinib combination shows efﬁcacy and tolerability in vivo. A, A box plot of volume of tumors harvested from mice on day 18 of treatment. , # denote signiﬁcance. B, Plot of body weight percent change of treated mice as a function of treatment time. C, The individual contribution of each TPR-MET mutant was determined by ddPCR at the end of the study and expressed as percent tumor volume. Each bar represents an individual treatment subject.

Techniques: In Vivo, Mutagenesis