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Articles de revues sur le sujet « MKC »

Auteur : Grafiati
Publié le 4 juin 2021
Mis à jour le 7 février 2022

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Rusdiaman, Rusdiaman, et Sisilia Teresia Dewi. « UJI EFEKTIVITAS INFUSA DAUN SAWO (Manilkara zapota L.) TERHADAP PERTUMBUHAN Salmonella thypiUJI EFEKTIVITAS INFUSA DAUN SAWO (Manilkara zapota L.) TERHADAP PERTUMBUHAN Salmonella thypi ». Media Farmasi 15, no 1 (24 mai 2019) : 7. http://dx.doi.org/10.32382/mf.v15i1.859.

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Uji Efektivitas Infus Daun Sawo (Manilkara zapota L.) Terhadap Pertumbuhan Salmonella thypi. Telah dilakukan penelitian tentang Uji Efektivitas Infus Daun Sawo (Manilkara zapota L.) Terhadap Pertumbuhan Salmonella thypi yang bertujuan untuk menentukan nilai MIC (Minimum Inhibitory Concentration) dan MKC (Minimum Killing Concentration) dari infus Daun Sawo terhadap Salmonella thypi. Ekstraksi dilakukan dengan menggunakan metode infus untuk menyari zat aktif dan dibuat dengan konsentrasi 5%, 10%, 15%, 20%, 25%, 30%, 35%, 40%, 45% dan 50%b/v. Penentuan MIC dilakukan dengan metode dilusi cair setelah 1×24 jam diinkubasi sedangkan penentuan MKC dilakukan setelah inkubasi selama 2×24 jam. Hasil penelitian menunjukkan bahwa nilai MIC dari infus Daun Sawo terhadap Salmonella thypi adalah konsentrasi 30% dan nilai MKC dari infus Daun Sawo terhadap Salmonella thypi adalah konsentrasi 50%. Kata kunci : Daun Sawo, Salmonella thypi, Dilusi Cair, MIC dan MKC
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Ratnah, Siti, et Alfrida Monica Salasa. « EFEKTIFITAS EKSTRAK BIJI BUAH KELENGKENG (Euphoria longan Stend) TERHADAP PERTUMBUHAN Staphylococcus aureus dan Propionibacterium acne ». Media Farmasi 16, no 1 (11 mai 2020) : 105. http://dx.doi.org/10.32382/mf.v16i1.1411.

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Biji Buah Kelengkeng merupakan limbah, tetapi mengandung senyawa fitokimia yang dapat dimanfaatkan baik sebagai antibakteri.. Tujuan penelitian ini adalah untuk menentukan konsentrasi Minimum Inhibitory Concentration (MIC) dan Minimum Killing Concentration (MKC) dari ekstrak biji buah kelengkeng terhadap pertumbuhan Staphylococcus aureus dan Propionibacterium acne. Bahan uji dibuat simplisia kering, diekstraksi dengan etanol 96 % dengan metode sokhletasi, diuji nilai MIC dan MKC dengan metode dilusi cair. Hasil yang diperoleh menunjukkan bahwa Minimum Inhibitory Concentration ekstrak biji buah kelengkeng terhadap pertumbuhan Staphylococcus aureus dan Propionibacterium acne adalah 2 %b/v dan Minimum Killing Concentration untuk kedua bakteri tersebut adalah 3 %b/v.Kata Kunci : Ekstraksi, MIC, MKC, Staphylococcus aureus dan Propionibacterium acne
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&NA;. « MKC 242 ». Drugs in R & ; D 2, no 1 (février 1999) : 53–54. http://dx.doi.org/10.2165/00126839-199902010-00016.

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Furman, P. A., et C. Moxham. « MKC-442 ». Drugs of the Future 23, no 7 (1998) : 718. http://dx.doi.org/10.1358/dof.1998.023.07.466749.

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Revel, L., X. Rabasseda et J. Castañer. « MKC-733 ». Drugs of the Future 24, no 9 (1999) : 966. http://dx.doi.org/10.1358/dof.1999.024.09.489134.

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Dulsat, C., R. Castañer et J. Bolós. « MKC-1 ». Drugs of the Future 34, no 4 (2009) : 270. http://dx.doi.org/10.1358/dof.2009.034.04.1365146.

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Tracy, M., J. Prous et J. Castañer. « MKC-242 ». Drugs of the Future 22, no 3 (1997) : 225. http://dx.doi.org/10.1358/dof.1997.022.03.400249.

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Salasa, Alfrida Monica, St Ratnah et Ismail Ibrahim. « PENENTUAN NILAI MIC (MINIMUM INHIBITORY CONCENTRATION) DAN MKC (MINIMUM KILLING CONCENTRATION) EKSTRAK DAUN KECOMBRANG (Etlingera elatior) TERHADAP Candida albicans PENYEBAB KEPUTIHAN ». Media Farmasi 15, no 1 (24 mai 2019) : 30. http://dx.doi.org/10.32382/mf.v15i1.781.

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Tanaman Kecombrang memiliki kandungan kimia seperti alkaloid, flavonoid, polifenol,steroid, saponin, dan minyak atsiri. Kandungan senyawa fitokimia pada tanaman diketahui mempunyai peranan yang sangat penting bagi kesehatan termasuk fungsinya dalam pencegahan terhadap penyakit. Tujuan dari penelitian ini adalah untuk menentukan nilai MIC (Minimum Inhibitory Concentration) dan MKC (Minimum Killing Concentration) dari Ekstrak Daun Kecombrang (Etlingera elatior) terhadap pertumbuhan Candida albicans dengan metode dilusi cair. Penelitian ini merupakan eksperimen murni menggunakan ekstrak daun kecombrang lalu ditentukan nilai MIC dan MKC dengan menggunakan metode dilusi cair. Konsentrasi yang digunakan adalah 1,25 %; 2,5%; 3,75%; 5%; 6,25%; 7,5%; 8,75%; 10%; 12,5%; 15%; 17,5%; 20%; 22,5%; 25% b/v. Hasil penelitian menunjukkan bahwa nilai MIC (Minimum Inhibitory Concentration) ekstrak Daun Kecombrang terdapat pada konsentrasi 6,25% b/v dan nilai MKC (Minimum Killing Concentration) terdapat pada konsentrasi 8,75% b/v. Hal ini menunjukkan bahwa ekstrak Daun Kecombrang (Etlingera elatior) efektif untuk menghambat dan membunuh jamur Candida albicans.
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Denny, Trisha A., Xiaoru Chen, Cassandra L. Waters, Patricia A. Burke, Graham C. Fletcher, John Xu, Carolyn F. Sidor, Mark D. Minden, Theresa M. LaVallee et Mark R. Bray. « MKC-1 Is a Novel Agent That Induces Cell Cycle Arrest and Disrupts Multiple Survival Pathways in Hematologic Cancers. » Blood 108, no 11 (16 novembre 2006) : 4390. http://dx.doi.org/10.1182/blood.v108.11.4390.4390.

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Abstract MKC-1 is a novel, orally active cell cycle inhibitor with in vitro and in vivo activity against a wide range of human solid tumor cell lines, including multi-drug resistant cell lines. MKC-1 has been tested in over 270 patients to date and is currently in Phase II clinical trials. The strong pre-clinical activity of MKC-1 towards solid tumor lines and signs of efficacy in the initial clinical evaluation with lack of neuropathy and cardiotoxicity suggests that MKC-1 may also be of clinical benefit in the treatment of hematopoietic cancers. The antiproliferative activity of MKC-1 was examined against a panel of hematopoietic cell lines including HL-60, U937, MV4;11, THP-1, Jurkat, and OCI-AML 1–5. MKC-1 showed potent and dose-dependent activity towards these cell lines, with IC50 values in the range of 20 – 400 nM. MKC-1 also inhibited in vitro growth of primary cells derived from AML and CML patients. Additionally, MKC-1 showed enhanced activity with Ara-C in combination studies in vitro when added either simultaneously or sequentially using the cell line OCI-AML 4. Binding studies have shown that MKC-1 binds to the colchicine binding site of tubulin and to members of the importin beta family of proteins. Consistent with these results, cell cycle arrest in the G2/M phase of the cell cycle followed by apoptosis was observed in cell lines and patient samples treated with MKC-1. Immunofluorescence analysis of cells treated with MKC-1 revealed that the drug induced a disruption of the microtubule network and the formation of aberrant mitotic spindles. Furthermore, MKC-1 was also shown to induce a dose-dependent reduction in the levels of both phospho-Akt and phospho-p70S6K kinases through Western blot analysis of treated THP-1 cells. In conclusion, our results indicate MKC-1 arrests the cell cycle and disrupts multiple survival pathways to induce apoptosis in hematopoietic cell lines and patient samples. These results suggest that MKC-1 may have clinical potential in the treatment of leukemia either alone or in combination with other agents. Phase I trials in hematological cancers are currently being explored.
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Löser, Christoph, Rainer Rompel, Matthias Möhrle, Hans-Martin Häfner, Christian Kunte, Jessica Hassel, Ulrich Hohenleutner et al. « Mikroskopisch kontrollierte Chirurgie (MKC) ». JDDG : Journal der Deutschen Dermatologischen Gesellschaft 8, no 11 (22 octobre 2010) : 920–25. http://dx.doi.org/10.1111/j.1610-0387.2010.07314_supp.x.

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Mimura, Naoya, Mariateresa Fulciniti, Gullu Gorgun, Yu-Tzu Tai, Diana D. Cirstea, Loredana Santo, Yiguo Hu et al. « Blockade of XBP1 Splicing by Inhibition of IRE1α Is a Promising Therapeutic Option in Multiple Myeloma ». Blood 118, no 21 (18 novembre 2011) : 133. http://dx.doi.org/10.1182/blood.v118.21.133.133.

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Abstract Abstract 133 Multiple myeloma (MM) cells are characterized by high protein synthesis resulting in chronic endoplasmic reticulum (ER) stress, which is adaptively managed by the unfolded protein response (UPR). Therefore blockade of UPR could provide a novel therapeutic option in MM. Upon UPR, inositol-requiring enzyme 1α (IRE1α) is activated by auto-phosphorylation, resulting in activation of its endoribonuclease domain to cleave XBP1 mRNA from XBP1 unspliced form (XBP1u: inactive) to generate the XBP1 spliced form (XBP1s: active). XBP1s protein in turn regulates genes responsible for protein folding and degradation, playing a pro-survival signaling role in the UPR. In this study, we specifically examined whether IRE1α-XBP1 pathway is a potential therapeutic target in MM. We first examined the biologic significance of IRE1α by knockdown using lentiviral shRNA and observed significant growth inhibition in IRE1α knockdown cells. We next examined the impact of inhibition of XBP1 splicing using a novel small molecule IRE1α endoribonuclease domain inhibitor MKC-3946 (MannKind, Valencia CA). MKC-3946 blocked not only the basal level, but also inducible (by tunicamycin) XBP1s, evidenced by RT-PCR analysis in RPMI8226 cells, without affecting phosphorylation of IRE1α. Importantly, MKC-3946 also inhibited XBP1s in primary tumor cells from MM patients. We also confirmed functional inhibition of XBP1s, with target genes including SEC61A1, p58IPK, and ERdj4 downregulated by MKC-3946 treatment. Importantly, MKC-3946 triggered growth inhibition in MM cell lines, without toxicity in normal mononuclear cells. Furthermore, it significantly enhanced cytotoxicity induced by bortezomib or 17-AAG in RPMI8226 and INA6 cells, as well as primary tumor cells from MM patients. Both bortezomib and 17-AAG induced ER stress with XBP1s, which was markedly blocked by MKC-3946. Moreover, apoptosis induced by bortezomib or 17-AAG was enhanced by MKC-3946, associated with increased CHOP mRNA and protein, a proapoptotic factor triggered by ER stress. We next demonstrated that XBP1s was induced by bortezomib in INA6 cells co-cultured with bone marrow (BM) stromal cells, which was inhibited by MKC-3946, associated with enhanced cytotoxicity induced by the combination. Finally, MKC-3946 inhibited XBP1s in a model of in vivo ER stress induced by tunicamycin. To evaluate the anti-MM effect of MKC-3946, we used the subcutaneous RPMI8226 xenograft model in mice. MKC-3946 significantly reduced MM tumor growth in the treatment versus control group, associated with prolonged overall survival. We also confirmed that MKC-3946 treatment significantly inhibited XBP1s in excised tumors, assessed by RT-PCR. In order to examine the activity of MKC-3946 on MM cell growth in the context of the human BM microenvironment in vivo, we used the SCID-hu model, in which INA6 cells are directly injected into a human bone chip implanted subcutaneously in SCID-mice. MKC-3946 treatment significantly inhibited tumor growth compared with vehicle control. Moreover, XBP1s in excised tumor cells was inhibited, evidenced by RT-PCR. In conclusion, these data demonstrate that blockade of XBP1s by MKC-3946 triggers MM cell growth inhibition in vivo and prolongs host survival. Taken together, our results demonstrate that blockade of XBP1 splicing by inhibition of IRE1α endoribonuclease domain is a potential novel therapeutic option in MM. Disclosures: Tam: MannKind Corporation: Employment, Equity Ownership. Zeng:MannKind Corporation: Employment, Equity Ownership. Patterson:MannKind Corporation: Employment, Equity Ownership. Richardson:Bristol Myers Squibb: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees; Johnson & Johnson: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Millennium: Membership on an entity's Board of Directors or advisory committees. Munshi:Millennium: Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees. Anderson:Millennium: Membership on an entity's Board of Directors or advisory committees; Onyx: Membership on an entity's Board of Directors or advisory committees; MannKind: Membership on an entity's Board of Directors or advisory committees.
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Seki, M., Y. Sadakata, S. Yuasa et M. Baba. « Isolation and Characterization of Human Immunodeficiency Virus Type-1 Mutants Resistant to the Non-Nucleotide Reverse Transcriptase Inhibitor MKC-442 ». Antiviral Chemistry and Chemotherapy 6, no 2 (avril 1995) : 73–79. http://dx.doi.org/10.1177/095632029500600201.

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MKC-442, 6-benzy 1-1-ethoxymethyl-5-isopropyIuraciI (l-EBU), is a potent and selective non-nucleoside inhibitor of human immunodeficiency virus type-1 (HIV-1) reverse transcriptase (RT). Nevirapine, another non-nucleoside RT inhibitor (NNRTI), is associated with rapid emergence of drug-resistant variants during in vitro passages of HIV-1. The emergence of resistant viruses to MKC-442 or nevirapine was examined in vitro. MT-4 cells infected with a clinical isolate (HE) of HIV-1 were cultivated in medium containing excess concentrations of these drugs, and the drug susceptibilities of the breakthrough viruses recovered from the medium were measured. Although nevirapine lost its antiviral activity after six passages, a delay in the emergence of fully resistant viruses was observed for MKC-442. Two resistant clones for each drug were isolated and nucleotide sequences within the RT region were analysed. An amino acid substitution at position 181 (Tyr to Cys) was found, with additional substitutions at positions 103 (Lys to Arg) and 108 (Val to lle) in the MKC-442-resistant viruses. These clones showed various susceptibilities to MKC-442, and cross-resistance to other NNRTIs but not to AZT. These results suggest that the major binding site of MKC-442 on the HIV-1 RT is the tyrosine residue common to these NNRTIs, and that drug resistance to NNRTIs is dependent on both the quality and the quantity of mutations within the HIV-1 RT gene.
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Dusane, Menakshi Bhat, et Bimba N. Joshi. « Islet protective and insulin secretion property of Murraya koenigii and Ocimum tenuflorum in streptozotocin-induced diabetic mice ». Canadian Journal of Physiology and Pharmacology 90, no 3 (mars 2012) : 371–78. http://dx.doi.org/10.1139/y11-133.

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The present study investigates the antidiabetogenic effects of Murraya koenigii (L.) Spr. and Ocimum tenuflorum L. on streptozotocin-induced diabetic Swiss mice. Treatment with extracts of M. koenigii (chloroform; MKC) and O. tenuflorum (aqueous; OTA) resulted in proper glucose utilization with an increase in liver glucose-6-phosphate dehydrogenase enzyme activity, and normal glycogenesis in hepatic and muscle tissues. Pancreatic and intestinal glucosidase inhibitory activity observed with MKC and OTA treatment indicated beneficial effects in reducing postprandial hyperglycemia with concomitant improvement in glucose metabolism. The glucosidase inhibition was prolonged, even after discontinuation of MKC and OTA treatment. Normalization of plasma insulin and C-peptide levels was observed in diabetic mice, indicating endogenous insulin secretion after treatment. The histochemical and immunohistochemical analysis of pancreatic islets suggests the role of MKC and OTA in pancreatic β-cell protection and the functional pancreatic islets that produce insulin. The study demonstrates the significance of MKC and OTA in glucosidase inhibition and islet protection in the murine diabetic model. These findings suggest the potential of the extracts in adjuvant therapy for the treatment of diabetes and the possible development of potential neutraceuticals.
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Mimura, Naoya, Mariateresa Fulciniti, Gullu Gorgun, Yu-Tzu Tai, Diana Cirstea, Loredana Santo, Yiguo Hu et al. « Blockade of XBP1 splicing by inhibition of IRE1α is a promising therapeutic option in multiple myeloma ». Blood 119, no 24 (14 juin 2012) : 5772–81. http://dx.doi.org/10.1182/blood-2011-07-366633.

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Abstract Multiple myeloma (MM) cells are characterized by high protein synthesis resulting in chronic endoplasmic reticulum (ER) stress, which is adaptively managed by the unfolded protein response. Inositol-requiring enzyme 1α (IRE1α) is activated to splice X-box binding protein 1 (XBP1) mRNA, thereby increasing XBP1s protein, which in turn regulates genes responsible for protein folding and degradation during the unfolded protein response. In this study, we examined whether IRE1α-XBP1 pathway is a potential therapeutic target in MM using a small-molecule IRE1α endoribonuclease domain inhibitor MKC-3946. MKC-3946 triggered modest growth inhibition in MM cell lines, without toxicity in normal mononuclear cells. Importantly, it significantly enhanced cytotoxicity induced by bortezomib or 17-AAG, even in the presence of bone marrow stromal cells or exogenous IL-6. Both bortezomib and 17-AAG induced ER stress, evidenced by induction of XBP1s, which was blocked by MKC-3946. Apoptosis induced by these agents was enhanced by MKC-3946, associated with increased CHOP. Finally, MKC-3946 inhibited XBP1 splicing in a model of ER stress in vivo, associated with significant growth inhibition of MM cells. Taken together, our results demonstrate that blockade of XBP1 splicing by inhibition of IRE1α endoribonuclease domain is a potential therapeutic option in MM.
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Vieri, Margherita, Christian Preisinger, Mirle Schemionek, Azam Salimi, John B. Patterson, Afshin Samali, Tim H. Brümmendorf, Iris Appelmann et Behzad Kharabi Masouleh. « Synergistic Dual Inhibition of BCR-ABL1 and the Unfolded Protein Response Causes p38 MAPK-Mediated Cell Death and Sensitizes BCR-ABL1+ Acute Lymphoblastic Leukemia to Dexamethasone ». Blood 132, Supplement 1 (29 novembre 2018) : 4674. http://dx.doi.org/10.1182/blood-2018-99-110967.

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Abstract Introduction The IRE1-XBP1 branch of Unfolded Protein Response (UPR) was previously shown to be pivotal for the survival of BCR-ABL1+ Acute Lymphoblastic Leukemia (ALL) cells. In this study, we identified a link between the IRE1 and BCR-ABL1 pathways which we harnessed for the pre-clinical application of a novel IRE1 inhibitor, MKC-8866, in combination with Nilotinib. The underlying mechanism was investigated by analysis of the phosphoproteome of BCR-ABL1+ ALL cell lines SUP-B15 and TOM-1. Upon dual treatment, the main force driving the cells toward death was ascribed to the activation of p38 MAPK. Additionally, the set of proteins affected under dual therapy suggested a possible regulation of glucorticoid receptor (GR) signaling that could modify the response to dexamethasone. Methods and Results SUP-B15 and TOM-1 cell lines were treated with vehicle, MKC-8866 (MKC, 30 µM) and nilotinib (NL, 0.5 µM) as single agents or in combination. Viability assays were performed in order to verify the synergistic effect of the treatment administered, evaluated using the Bliss formula. The combination of NL with MKC showed a striking synergism in both SUP-B15 and TOM-1 (Bliss calculation. Assumed additive effects: SUP-B15 24.2±20.6%, TOM-1 40.9±18.4% versus experimental values: SUP-B15 68.7±12.7%, TOM-1 78.8±4.9%). To validate the effect on a genetic level, pre-B cell derived from conditional Xbp1+/fl mice were transduced with BCR-ABL1and with either inducible cre or empty vector. The ALL-like cells were then treated with NL 0.5 µM and/or 4-hydroxytamoxifen (4OHT) 1µM to induce deletion. In agreement with the synergistic effect observed with the human cell lines, NL was shown to be significantly more effective in the presence of heterozygous deletion of Xbp1 (viable cells after 24 hours. NL: 65.2±0.3%, 4OHT + NL: 6.87±1.2%). To unravel the basis of this synergism, we performed a phosphoproteomic analysis of the two human cell lines treated for 16 hours with vehicle, MKC, NL and dual treatment, respectively. For this analysis, SUP-B15 and TOM-1 were lysed in 8M urea and digested using LysC/trypsin. The obtained peptides were labeled using the dimethyl isotope labeling method. Phosphopeptides were enriched using TiO2 beads and analyzed by nanoLC-MS/MS (Orbitrap Elite). The raw data were analyzed using MaxQuant and the Andromeda search engine against the human Uniprot database. The resulting information was further interpreted using the Perseus software package as well as the String and PhosphoPath apps in Cytoscape. The analysis of the regulated phosphorylated proteins highlighted a p38 MAPK differential regulation, with MKC alone or in combination causing its activation, and, in contrast, NL causing inhibition. Western Blot analyses investigating the activation of p38 MAPK showed increased phosphorylation of its main downstream target, heat shock protein beta-1 (HSPB1), in the presence of MKC alone or together with NL. Pharmacological inhibition of p38 MAPK activity by adding p38 MAPK inhibitor BIRB-796 (BIRB, 10µM) was able to rescue the cells from the concerted action induced by MKC and NL. Furthermore, the phosphoproteome pattern observed in the cells upon dual treatment suggested a regulation of crucial GR interactors. Therefore, we tested whether the studied combination would render the cells more responsive to the GR agonist dexamethasone (DEXA, 10 mg/L), cornerstone in ALL therapy. The viability assay revealed a striking enhancement of its cytotoxic effect. However, most of the effect was conveyed by the action of DEXA together with NL, with MKC adding only a small and non-significant accessory effect (percentages of viable cells compared to DMSO values after 24 hours treatment. SUP-B15: DEXA 83.9±4.2%; MKC + DEXA 81.6±5.1%; NL + DEXA 66.7±7.1% and MKC + NL + DEXA 59.8±7.3%. TOM-1: DEXA 78.2±8.4%; MKC + DEXA 74.1±5.1%; NL + DEXA 45.3±10.1% and MKC + NL + DEXA 45.2±8.1%). Conclusion By studying the phosphoproteome in BCR-ABL1+ ALL, we identified a possible underlying mechanism explaining the success of the combined action of NL and MKC-8866. The p38 MAPK axis was found responsible for the observed cytotoxic effect, elucidating important aspects of BCR-ABL1+ ALL biology. Overall, the successful treatment regime with NL and MKC in vitro, and its positive interaction with DEXA, provide a promising basis for further pre-clinical evaluation. Disclosures Patterson: Fosun Orinove PharmaTech, Inc.: Employment. Samali:Cell Stress Discoveries Ltd.: Other: co-founder, director and share holder . Brümmendorf:Pfizer: Consultancy, Research Funding; Janssen: Consultancy; Merck: Consultancy; Novartis: Consultancy, Research Funding; Takeda: Consultancy. Appelmann:Novartis: Research Funding. Kharabi Masouleh:Janssen Research & Development: Employment.
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Hanna, N. H., D. Estes, J. Arnott, S. Marcotte, A. Hannah, C. F. Sidor, H. West, G. Clamon et T. Hoang. « Phase I/II study of MKC-1 and pemetrexed (PEM) as second-line therapy in patients (pts) with advanced non-small cell lung cancer (NSCLC) ». Journal of Clinical Oncology 27, no 15_suppl (20 mai 2009) : e19005-e19005. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e19005.

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e19005 Background: MKC-1 is a novel oral cell cycle inhibitor with preclinical activity against NSCLC cell lines including multi-drug resistant lines, and single agent activity in NSCLC pts. Binding targets of MKC-1 include microtubules, members of the importin-β family and AKT-mTOR. This phase 1/2 study evaluated MKC-1 in combination with PEM as second-line therapy in pts with advanced NSCLC. Methods: Eligible pts had NSCLC previously treated with one regimen for metastatic disease or disease progression within one year following adjuvant and neoadjuvant therapy. Phase 1 dose escalation used 3+3 design. Phase 2 pts were treated with MKC-1 at 75 mg/m2 given p.o. BID for 14 days along with PEM at 500 mg/m2 given i.v. on day 1 of each 21 day cycle. Following 4 cycles of combined treatment, single agent MKC-1 was continued as maintenance therapy. An interim analysis after 17 pts in phase 2 would allow accrual to continue provided one response was confirmed. Results: 27 pts were enrolled (8 in phase 1 and 19 in phase 2). Median age/PS for phase 2 is 64/1 and 89% had adenocarcinoma. Total # of treatment cycles to date for phase 2 pts is 95, with a median of 4 cycles. Of the 19 phase 2 pts, 18 were evaluable for tumor response. The best response was confirmed PR, noted in 3 pts. 5 additional pts (4 confirmed) had minor responses (>10% but <30% shrinkage). One additional pt continues on study with stable disease for >18 months. In phase 2 (n=19), all grade toxicities were anorexia (59%), fatigue (63%), nausea (58%), and dyspnea (48%). Grade 3/4 toxicities included fatigue (26%); neutropenia (22%); dyspnea, anorexia, AST and ALT elevation (11% each); nausea and constipation (5% each). 7 pts had at least one dose reduction of both PEM and MKC-1 and 3 additional pts had only MKC-1 reduced. Median PFS was 86 days with two pts continuing on study (treated for 530+ days and 140+ days, respectively). Conclusions: The phase 2 dose of MKC-1 (75 mg/m2 BID) and PEM (500 mg/m2) has been defined. The combination is well tolerated with 17% of patients achieving a confirmed PR thus far. A decision to proceed with additional accrual in this single arm study versus initiating a randomized phase 2 study of this combination is pending. [Table: see text]
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Elser, C., H. Hirte, L. Kaizer, H. Mackay, S. Bindra, L. Tinker, K. MacAlpine, L. Wang, C. Sidor et A. Oza. « Phase II study of MKC-1 in patients with metastatic or resistant epithelial ovarian cancer or advanced endometrial cancer ». Journal of Clinical Oncology 27, no 15_suppl (20 mai 2009) : 5577. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.5577.

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5577 Background: MKC-1 is a novel oral cell cycle inhibitor with preclinical activity in xenograft models of human ovarian and endometrial cancers. MKC-1 also reduces pAKT, an attractive target in endometrial cancer due to frequent PTEN mutations. Methods: The objective of this phase II study is to assess the efficacy of MKC-1 in 2 patient (pt) populations: metastatic or recurrent platinum-resistant ovarian cancer (EOC) and advanced endometrial cancer (EC). Three prior lines of treatment were allowed in both groups. A two arm, parallel group multicenter 2-stage design was used. The primary endpoint was tumor response by RECIST or CA-125. MKC-1 125 mg/m2 was administered orally twice daily for 14 days in 28-day cycles. Results: Accrual to stage one is complete with 21 pts in each arm. 19 pts with EOC (median age 56 yrs, range 31–71) and 9 patients with EC (median 63 range 50–74) were available for efficacy. A total of 66 cycles (EOC/EC: 39/27cycles) median 2 per patient (range 1–8) were delivered. 11/4 pts had prior adjuvant CT, 14/10 had prior systemic CT for advanced disease, and 2/6 received prior radiation. In pts with EOC, 7 pts have stable disease (SD), 12 progressive disease (PD), 2 remain on study. Median time to progression is 1.8 months. In pts with EC 4 pts had SD, 5 PD, 6 remain on study. Toxicity data are available in 28 pts (17/11). Most common adverse events (AE) possibly related to MKC-1 were fatigue, nausea, elevated ALT or AST, urine discoloration, anemia, anorexia, elevated AP and gastrointestinal disorder in 55%, 39%, 36%, 24%, 23%, 21%, 21%, and 21 % of cycles respectively. The only possibly related grade 3+ AEs were neutropenia, leucopenia and hyponatremia in 9 %, 3 %, and 2% of cycles. Conclusions: MKC-1 was well tolerated in both patient populations. Single agent MKC-1 has insufficient activity in platinum resistant EOC to warrant further investigation. Updated clinical data for both patient groups will be presented at the meeting. [Table: see text]
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Löser, Christoph R., Rainer Rompel, Matthias Möhrle, Hans-Martin Häfner, Christian Kunte, Jessica Hassel, Ulrich Hohenleutner et al. « S1-Leitlinie : Mikroskopisch kontrollierte Chirurgie (MKC) ». JDDG : Journal der Deutschen Dermatologischen Gesellschaft 13, no 9 (27 août 2015) : 942–51. http://dx.doi.org/10.1111/ddg.140_12665.

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Rante Pakadang, Sesilia, Maria Hilaria, Sisilia Teresia Rosmala Dewi, Santi Sinala et Jumain Jumain J. « MIC and MKC Analysis of Herbal Medicine in Indonesia Against Mycobacterium tuberculosis ». Pharmacognosy Journal 13, no 5 (8 septembre 2021) : 1058–64. http://dx.doi.org/10.5530/pj.2021.13.137.

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Sylvester, L., L. Laufman, K. Jabboury, M. Saleh, K. Tkaczuk, F. Volterra, J. Arnott, A. Hannah, C. Sidor et K. Miller. « Phase 2 study of MKC-1 in patients (pts) with metastatic breast cancer (MBC) who have failed prior therapy with an anthracycline (A) and taxane (T) ». Journal of Clinical Oncology 25, no 18_suppl (20 juin 2007) : 11508. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.11508.

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11508 Background: MKC-1 (previously Ro 31–7453) is a novel cell cycle inhibitor with significant in vitro and in vivo activity against a wide range of tumor cell lines, including multi-drug resistant cell lines. Proteins identified as binding targets of MKC-1 include microtubules (colchicine binding site) and members of the importin-β family (proteins that play a critical role in nuclear transport and spindle formation). Objective responses (ORs) were observed in heavily pre-treated breast and NSCLC pts (Trigo Perez ASCO’03 A62; Kurup ASCO’03 A2725) treated at a dose of 95 mg/m2 BID given 14 days every 4 weeks with little toxicity. Salazar et al (2004 CCR 10:4374) recommended a higher oral dose (125 mg/m2 BID) on this schedule for further studies. This phase 2 trial is exploring the higher dose to maximize potential anticancer activity. Methods: Pts with MBC who had failed prior A and T and met eligibility criteria received MKC-1 at 125mg/m2 BID x 14d every 4 weeks. Pts with known treated and stable CNS metastases could enroll. Primary objective: OR by RECIST. Should 2 or more of the first 23 evaluable pts have an OR, enrollment will continue to 53 pts. Dose escalation/reductions are required based on toxicity (primarily neutropenia). Results: To date, a total of 20 pts have been enrolled (4 active in Cycles 1–5+). All female; median age/KPS of 60/90. 19% / 13% had received A / T in the neo/adjuvant setting; others had received A / T for metastatic disease. To date, a total of 48 cycles (median 2, range 1–8) were administered; of pts proceeding into Cycle 2, 40% and 20% had the dose increased or reduced, respectively. Severe drug-related toxicity (n=17) was observed in 3 pts (18%): ↑AST/ALT in 2 pts and parathesias in 1 pt. Drug related toxicity: nausea (47%), ↑ALT, diarrhea (both 24%), anemia, ↑AST, cough, fatigue, neutropenia and vomiting (all 18%). Two pts discontinued due to toxicity. One pt had complete resolution of measurable disease (1st observed after Cycle 4, confirmed after Cycle 6 with withdrawal for a new lesion at Cycle 8). An additional 2 pts had stable disease for 5 cycles (1 pt remains active). Conclusions: MKC-1 is well tolerated at the initial recommended dose for this schedule. Activity is observed in pts previously treated with A/T for MBC. No significant financial relationships to disclose.
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Schneider, B. P., M. Karwal, L. Laufman, L. Sylvester, M. A. Taylor, C. Sidor, A. Hannah, J. Arnott et K. D. Miller. « A phase II study of oral MKC-1 for metastatic breast cancer (MBC) ». Journal of Clinical Oncology 26, no 15_suppl (20 mai 2008) : 1046. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.1046.

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TERADA, Nobuhisa, Akiyoshi KONNO, Takayuki YAMAKOSHI, Kouichi Nakano, Nanako HAMANO, Masaya HASEGAWA, Gen HOUKI et al. « Clinical Pharmacological Study of Mizolastine (MKC-431). » Practica Oto-Rhino-Laryngologica 91, no 7 (1998) : 741–54. http://dx.doi.org/10.5631/jibirin.91.741.

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Tanaka, H., RT Walker, AL Hopkins, J. Ren, EY Jones, K. Fujimoto, M. Hayashi et al. « Allosteric Inhibitors against HIV-1 Reverse Transcriptase : Design and Synthesis of MKC-442 Analogues Having an Ω-Functionalized Acyclic Structure ». Antiviral Chemistry and Chemotherapy 9, no 4 (août 1998) : 41–48. http://dx.doi.org/10.1177/095632029800900404.

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Based on X-ray crystallographic analysis of MKC-442/human immunodeficiency virus type 1 reverse transcriptase (HIV-1 RT) complex, analogues in which the N1-substituent is replaced with ω-functionalized alkyl groups were designed to improve the affinity for the enzyme. Synthesis of these compounds was carried out starting from MKC-442 by a sequence of reactions (N3-protection, removal of N1-ethoxymethyl group, alkylation, and N3-deprotection). The compounds were evaluated for anti-HIV activity. Structure–activity relationships are discussed in terms of the possible interaction with the enzyme.
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Wamberg, Michael, Erik B. Pedersen et Claus Nielsen. « Synthesis of Furoannelated Analogues of Emivirine (MKC-442) ». Archiv der Pharmazie 337, no 3 (mars 2004) : 148–51. http://dx.doi.org/10.1002/ardp.200300815.

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Gulati, Khushboo, et Krishna Mohan Poluri. « Deciphering the in vitro homo and hetero oligomerization characteristics of CXCL1/CXCL2 chemokines ». RSC Advances 6, no 34 (2016) : 28213–18. http://dx.doi.org/10.1039/c6ra01884j.

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Mimura, Naoya, Teru Hideshima, Gullu Gorgun, Diana Cirstea, Loredana Santo, Yiguo Hu, Claire Fabre et al. « Targeting IRE1α-XBP1 Pathway Is a Novel Therapeutic Strategy In Multiple Myeloma ». Blood 116, no 21 (19 novembre 2010) : 4074. http://dx.doi.org/10.1182/blood.v116.21.4074.4074.

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Abstract Abstract 4074 Aberrant protein folding results in the accumulation of misfolded/unfolded proteins in the endoplasmic reticulum (ER), which in turn triggers ER stress followed by unfolded protein response (UPR), an adaptive response against ER stress. Since multiple myeloma (MM) cells have high protein synthesis, they are sensitive to ER stress and require strict ER quality control for cell survival. Upon UPR, IRE1α is activated by auto-phosphorylation resulting in activation of its endoribonuclease domain to splice XBP1 mRNA from XBP1 unspliced form (XBP1u: inactive) to XBP1 spliced form (XBP1s: active). Since XBP1 is a transcription factor regulating genes which are responsible for protein folding and ER associated degradation (ERAD), IRE1α-XBP1 pathway acts as a pro-survival signaling pathway under the UPR condition. In this study, we examined whether IRE1α-XBP1 pathway is a potential novel therapeutic option in MM. We first examined IRE1α expression and confirmed its expression in all MM cell lines. In contrast, XBP1s was not detected by RT-PCR in most cell lines except in for RPMI8226 cells. To assess biologic significance of IRE1α in MM cell, we knock-downed its expression using shRNA and found that downregulation of IRE1α inhibited MM cell growth, indicating that IRE1α has a crucial role in MM cell survival. We next examined the impact of inhibition of XBP1 splicing by a small molecule IRE1α endoribonuclease inhibitor MKC-3946 (Mannkind, Valencia CA) in MM cells in vitro. As expected, MKC-3946 significantly inhibited tunicamycin-induced XBP1s without affecting phosphorylation of IRE1α. MKC-3946 induced only modest cytotoxicity in MM cell lines without toxicity in normal mononuclear cells from healthy donors; however, it significantly enhanced cytotoxicity in combination with bortezomib or 17-AAG. Both bortezomib and 17-AAG induced ER stress evidenced by induction of XBP1s; conversely, MKC-3946 blocked XBP1s triggered by these agents. Furthermore, apoptosis induced by these agents was enhanced with MKC-3946 associated with increased CHOP, which is a known pro-apoptotic protein induced in uncompensated ER stress condition. Importantly, MKC-3946 enhanced the cytotoxicity of bortezomib or 17-AAG in INA6 cells, even in the presence of increased IL-6 or bone marrow stromal cells. Finally, MKC-3946 was active inhibiting XBP1 splicing in a model of ER stress and significantly inhibited growth of RPMI8226 plasmacytoma in a xenograft murine model when used in combination with a low dose of bortezomib. Taken together, our results demonstrate that inhibition of XBP1 splicing by blockade of IRE1α is a promising therapeutic option in MM. Disclosures: Blumenthal: Mannkind Corporation: Employment, Equity Ownership. Tam:Mannkind Corporation: Employment, Equity Ownership. Kertesz:Mannkind Corporation: Employment, Equity Ownership. Zeng:Mannkind Corporation: Employment, Equity Ownership. Patterson:Mannkind Corporation: Employment, Equity Ownership. Munshi:Celgene: Membership on an entity's Board of Directors or advisory committees; Millennium: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees. Richardson:Celgene: Membership on an entity's Board of Directors or advisory committees; Millennium: Membership on an entity's Board of Directors or advisory committees; Johnson & Johnson: Membership on an entity's Board of Directors or advisory committees. Anderson:Celgene: Membership on an entity's Board of Directors or advisory committees; Millennium: Membership on an entity's Board of Directors or advisory committees; Novartis: Membership on an entity's Board of Directors or advisory committees.
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Takashina, Ken, Tomoko Bessho, Reiko Mori, Kunji Kawai, Junichi Eguchi et Ken-Ichi Saito. « MKC-231, a choline uptake enhancer : (3) mode of action of MKC-231 in the enhancement of high-affinity choline uptake ». Journal of Neural Transmission 115, no 7 (7 mai 2008) : 1037–46. http://dx.doi.org/10.1007/s00702-008-0049-0.

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Pakadang, Sesilia Rante, Santi Sinala, Alfrida Monica Salasa, St Ratnah, Sisilia Teresia Rosmala Dewi et Maria Hilaria. « Potential of Miana Leaf Extract as Expectorant (Profile Place of Growing, Antioxidant, Sputum Contaminants, Antibacterial, MIC, MKC Expectorant) ». Majalah Obat Tradisional 25, no 2 (31 août 2020) : 94. http://dx.doi.org/10.22146/mot.52500.

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Research has been conducted on the treatment of phlegm cough with miana leaf extract in vitro (effective dose of miana leaf extract as an expectorant and antibacterial agent causing cough with phlegm). The study aims to compare the antioxidant activity of miana leaves from 3 locations where it grows, determine the types of contaminant bacteria in the sputum of cough sufferers, determine the minimum value of inhibitor concentration (MIC) and MKC of miana leaves against the test bacteria causing cough with phlegm, determine the effective dose of miana leaves that can used as a reference for coughing up phlegm and proving the potential of miana leaves as a sputum thinner. Miana leaf extraction is done by the juicer method. Antioxidant activity testing uses the DPPH method. Determination of test bacteria is done by isolating and identifying contaminant bacteria in the sputum sample of cough with phlegm. Testing the effectiveness of miana leaves against test bacteria is determined by the liquid dilution method. Expectorant activity testing was determined by measuring the viscosity of mucus viscosity of cow intestine treated with miana leaf extract. The results found that antioxidant activity was influenced by the location where miana leaves grew with an antioxidant potential of IC72 0.072 mg/ml - 0.76 mg/ml. Contaminant bacteria from sputum samples of cough patients are Streptococcus pneumonia, Klebsiella pneumonia, Staphylococcus aureus, Staphylococcus epidermidis and Enterobacter agglomerans. MIC values for contaminant bacteria are 0.1% - 0.75% and MKC values are found between 0.25% - 1.75%. miana leaf extract has the potential as a sputum thinner at a concentration of 0.01% - 0.1%. The recommended dose of miana leaf extract as a cough with phlegm is 1.75% w/v.
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López-Fandiño, Rosina, Mercedes Ramos, Estrella Fernández-García et Agustin Olano. « Proteolytic activity of two commercial proteinases from Aspergillus oryzae and Bacillus subtilis on ovine and bovine caseins ». Journal of Dairy Research 58, no 4 (novembre 1991) : 461–67. http://dx.doi.org/10.1017/s0022029900030065.

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SummaryElectrophoretic analysis of the action of two commercial enzymes, Neutrase 0·5 and MKC Fungal Protease, on whole casein and αs-, β- and κ-caseins from cows' and ewes' milk showed that Neutrase 0·5 chiefly degraded β-casein, giving rise to peptides soluble at pH 4·6 detectable by PAGE. In contrast, although MKC Fungal Protease caused intense hydrolysis of bovine β-casein, in ovine casein it resulted in more active degradation of αs- than β-casein. The latter enzyme did not produce peptides soluble at pH 4·6 detectable by PAGE. Both enzymes degraded κ-casein, yielding a breakdown product that exhibited an electrophoretic mobility similar to that of the breakdown product produced by the action of commercial rennet.
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Hassan, Anisa Mukhtar, Erdal Karapınar et Hamed H. Alsulami. « Ulam-Hyers Stability for MKC Mappings via Fixed Point Theory ». Journal of Function Spaces 2016 (2016) : 1–11. http://dx.doi.org/10.1155/2016/9623597.

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We consider some extension of MKC mappings in the framework of complete dislocated metric spaces. Besides the theoretical results, we also consider some illustrative examples. Further, we state and prove that our main results improved the related results in the frame of generalized Ulam-Hyers stability theory.
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Baba, Masanori, Hlromichi Tanaka, Tadashi Miyasaka, Satoshi Yuasa, Masaru Ubasawa, Richard Walker et Erik De Clercq. « Hept Derivatives : 6-Benzyl-1-ethoxymethyl-5-isopropyluracil (MKC-442) ». Nucleosides, Nucleotides and Nucleic Acids 14, no 3 (1 mai 1995) : 575–83. http://dx.doi.org/10.1080/15257779508012431.

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Vladimirova, Liubov Yu, Oleg Ivanovich Kit, Irina L. Popova et Natalya A. Abramova. « Tyrosine-kinase inhibitors (TKI) in metastatic kidney cancer (mKC) treatment. » Journal of Clinical Oncology 32, no 15_suppl (20 mai 2014) : e15546-e15546. http://dx.doi.org/10.1200/jco.2014.32.15_suppl.e15546.

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Utami, Putri Widya, Isnandar Isnandar, Rahmi Syaflida et Indra Basar Siregar. « Pengaruh ekstrak daun kemangi (Ocimum basilicum L) terhadap Staphylococcus aureus di rongga mulutEffect of basil leaf extract (Ocimum basilicum L.) on oral Staphylococcus aureus ». Jurnal Kedokteran Gigi Universitas Padjadjaran 33, no 1 (30 avril 2021) : 38. http://dx.doi.org/10.24198/jkg.v33i1.29968.

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Pendahuluan: Staphylococcus aureus merupakan mikroorganisme dalam rongga mulut yang bersifat patogen. Di Indonesia, penyakit infeksi masih menjadi masalah umum terutama pada rongga mulut, untuk itu dikembangkan obat antibakteri yang berasal dari tumbuhan salah satunya daun kemangi. Tujuan penelitian untuk menganalisis efektivitas penggunaan ekstrak daun kemangi (Ocimum basilicum L) terhadap jumlah Staphylococcus aureus rongga mulut. Metode: Penelitian ini menggunakan true eksperiment laboratoris, dimana pengujian efektivitas antibakteri dengan metode pengenceran seri. Sampel yang digunakan strain murni Staphylococcus aureus dan isolat klinik Staphylococcus aureus. Konsentrasi ekstrak yang digunakan 50%, 25%, 12,5%, 6,25% dan dilakukan pengulangan sebanyak 4 kali. Data penelitian diolah menggunakan SPSS yaitu uji Kruskal-Wallis dan uji Mann-Whitney.Hasil: Konsentrasi 50% merupakan kadar bunuh minimum (KBM) untuk strain murni bakteri Staphylococcus aureus, dan kadar hambat minimum (KHM) untuk isolat klinik Staphylococcus aureus. Konsentrasi 25% hanya didapati kadar hambat minimum (KHM) untuk strain murni Staphylococcus aureus. Simpulan: Terdapat pengaruh penggunaan ekstrak daun kemangi (Ocimum basilicum L) terhadap penurunan jumlah Staphylococcus aureus rongga mulut.Kata kunci : Daun kemangi, Staphylococcus aureus, pengenceran seri, KHM, KBM. ABSTRACTIntroduction: Staphylococcus aureus is a pathogenic microorganism in the oral cavity. In Indonesia, infectious diseases are still a common problem, especially in the oral cavity. Therefore, a natural antibacterial remedy has been developed, one of which is basil leaves. The study aimed to analyse the effectiveness of using basil leaf extract (Ocimum basilicum L) against the number of oral Staphylococcus aureus. Methods: This study used a true laboratory experiment, where the antibacterial effectiveness was tested by using the series dilution method. The samples used were pure strains of Staphylococcus aureus and clinical isolates of Staphylococcus aureus. The extract concentration used was 50%, 25%, 12.5%, 6.25% and was repeated 4 times. The research data were processed using SPSS, namely the Kruskal-Wallis test and the Mann-Whitney test. Results: The concentration of 50% is the minimum kill rate (MKC) for pure strains of Staphylococcus aureus and the minimum inhibitory level (MIC) for clinical isolates of Staphylococcus aureus. At 25% concentration, only the minimum inhibitory level (MIC) was found for pure strains of Staphylococcus aureus. Conclusion: There is an effect of using basil leaf extract (Ocimum basilicum L) on reducing the number of oral Staphylococcus aureus.Keywords: Basil leaf, Staphylococcus aureus, serial dilution, MIC, MKC.
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Appelmann, Iris, Azam Salimi, Michael Huber, Mirle Schemionek, Margherita Vieri, Tim H. Brümmendorf, John B. Patterson et Behzad Kharabi Masouleh. « Interplay between PI3K/mTOR Signaling and IRE1a-XBP1 Promotes Survival of Pre-B NRASG12D all Cells Providing a Therapeutic Vulnerability for the "Undruggable" Driver RAS ». Blood 136, Supplement 1 (5 novembre 2020) : 47–48. http://dx.doi.org/10.1182/blood-2020-140299.

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Background Activating RAS mutations drive around 30% of pre-B cell acute lymphoblastic leukemias (pre-B ALL) and are particularly common in relapsed ALL with a consecutively poor outcome. Recently published data demonstrated the critical role of the unfolded protein response (UPR) network, namely its IRE1α-XBP1 axis, for the survival of pre-B ALL cells: High expression of XBP1 confers a poor prognosis in pre B-ALL. However, the mechanism of XBP1 activation has not yet been elucidated in RAS mutated pre-B ALL. In this study, we aimed at identifying the molecular mechanism underlying pro-survival IRE1α-XBP1 signaling in RAS mutated pre-B ALL. Methods For a TET-ON inducible NRASG12D model in conditional Xbp1 knockout mice, we used interleukin 7 (IL-7)-dependent murine Mx1-Cre;Xbp1fl/fl pre-B cells transduced with a TET-ON inducible NRASG12D. We performed in vitro cell cycle and apoptosis assays with propidium iodide (PI) and annexin-V/PI. Furthermore, Western Blot and RT-qPCR were applied to analyze target gene expression. In a second approach, we focused on the signaling events following the blockade of RAS downstream targets using the MEK inhibitor PD0325901 and the dual PI3K/mTOR inhibitor BEZ235. We then assessed the efficacy of small molecule inhibition of IRE1α by MKC-8866 on XBP1 inactivation in RAS-mutated pre-B ALL cells either as a single treatment and in combination with the above mentioned drugs. Results We found the expression of Xbp1 significantly increased at the mRNA level with induction of NRASG12D. To determine the significance of Xbp1 in NRASG12D-driven pre-B ALL, we genetically deleted the IRE1α target Xbp1 using Cre-mediated deletion of Xbp1fl/fl in our mouse model of pre-B ALL. Genetic loss of Xbp1 significantly induced apoptosis (2.0-fold, p&lt;0.0001) and caused cell cycle arrest (induction of G0/1, 1.7-fold, p=0.0003) along with an increase in the expression of CDK inhibitors, p21CIP1 and p27KIP1 at the protein level. Genetic ablation of Xbp1 abrogated IL-7 receptor (IL-7R) signaling by reducing the phosphorylation levels of STAT5-Y694 and JAK1-Y1022/Y1023. In an additional approach, we revealed that IL-7-deprived pre-B ALL cells reduce the mRNA expression of Xbp1s, indicating that Xbp1 acts as a downstream linchpin of the IL-7 receptor signaling pathway. Both IL-7-deprivation and genetic loss of Xbp1 increased the phosphorylation levels of ERK1/2-T202/Y204, AKT-S473 and the protein levels of NRASG12D and MAPK negative regulator DUSP6. Pharmacological inhibition of XBP1 activation using MKC-8866 resulted in similar effects on the expression of RAS downstream targets. We therefore tested MKC-8866 in combination with MEK inhibition by PD0325901 as a potential therapeutic strategy against pre-B ALL, which proved non-efficient. As a second option with therapeutic implications, we focused on the PI3K pathway which acts downstream of both the IL-7R and RAS signaling pathways. Strikingly, we observed that genetic ablation of Xbp1 (viable cells after 72 h, BEZ: 71.9 ± 9.0 vs BEZ+ Mx1-Cre;Xbp1fl/f: 10.0 ± 4.9) or pharmacological inhibition of its production with MKC-8866 (viable cells after five days, BEZ: 58.0 ± 6.8 vs BEZ+ MKC-8866: 13.3 ± 7.4) sensitizes pre-B ALL to dual inhibition of PI3K/mTOR with BEZ235. By applying the Bliss formula, we were able to show that BEZ235 in combination with MKC-8866 synergistically reduces the viability of RAS-mutated pre-B ALL cells. Gene expression analysis indicated that BEZ235 in combination with MKC-8866 fully blocked IL-7R signaling and caused an aberrant activation of Ras-Erk signaling. Targeting PI3K/mTOR signaling along with XBP1 inactivation increased expression of NRASG12D and its target DUSP6. In addition, we showed that combined therapy increased expression levels of p19Arf in RAS-mutated pre-B ALL, implicating cell senescence mediated by activated RAS signaling. Conclusion Our work strongly supports the hypothesis that XBP1 induces its positive effects on progression of pre-B ALL cells through the IL-7R signaling pathway. IL-7R signaling through its downstream effector XBP1 counteracts the RAS signaling pathway to promote leukemogenesis in pre-B ALL cells. Active XBP1 prevents the cytotoxic effects of BEZ235 in pre-B ALL cells, and hence targeting XBP1 in combination with dual PI3K/mTOR inhibition by BEZ235 appears as a promising targeted strategy against the "undruggable" driver RAS in NRASG12D-mutated pre-B ALL. Disclosures Brümmendorf: Janssen: Consultancy; Merck: Consultancy; Novartis: Consultancy, Other: travel, accommodation, expenses, Research Funding; Takeda: Consultancy; Pfizer: Consultancy, Honoraria, Other: Travel, Accommodation, Expenses, Research Funding.
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Azim, Mohammad Anwar Ul, Takashi Kozaka, Izumi Uno, Daisuke Miwa, Yoji Kitamura, Kazuma Ogawa et Kahuhiro Shiba. « Syntheses and In-vitro Evaluation of Tetrahydroaminoacridine (THA) Based Analogues as High Affinity Choline Transporter (HAChT) Imaging Probe ». Bangladesh Journal of Nuclear Medicine 17, no 2 (14 juin 2016) : 97–102. http://dx.doi.org/10.3329/bjnm.v17i2.28192.

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Introduction: In cholinergic neurons, high affinity choline uptake (HACU) by the high affinity choline transporter (HAChT) is a rate-limiting and regulatory step for the synthesis of Acetylcholine (Ach).Thus, HAChT appear to be a relatively specific presynaptic marker for cholinergic neurons in Alzheimer’s disease.Objectives: The principle objective of the study is to check the affinity of tetrahydroaminoacridine (THA) derivatives for HAChT. Another objective of the research work is to clarify whether the hemicholinium-3 (ChT inhibitor) and HACU enhancer molecules share the same binding sites or not.Materials and Methods: The inhibition activities of tacrine, the 2,3-dimethylfuran derivative of tacrine (DMTA) and their corresponding 2-oxo-1-pyrrolidineacetyl derivatives, namely PTAA and MKC-231 were measured by displacement of a typical HAChT antagonist [3H]HC-3 in rat cerebral membrane. The percentage of inhibition against the binding of [3H]HC-3 to HAChT were calculated using GraphPad Prism v4 software.Results: Hemicholinium-3 showed affinity for HAChT (IC50 = 20 nM) in the in vitro binding assay. A very insignificant inhibition activity (IC50 = 1000 nM) of Tacrine was revealed. The newly synthesized tacrine derivatives, DMTA and PTAA did not show any affinity for HAChT. Although MKC-231 was reported to enhance cholinergic activity at synaptic terminals, it did not show any affinity for the HAChT in [3H]HC-3 binding assay.Conclusion: In vitro [3H]HC-3 binding assay revealed no affinity of MKC-231, tacrine and its corresponding2-oxo-1-pyrrolidineacetate derivative towards HAChT. So, it is worthy to develop radiolabeled HC-3 derivatives with high affinity for HAChT, which can diffuse the BBB, to enable the in vivo investigation of HACU system.Bangladesh J. Nuclear Med. 17(2): 97-102, July 2014
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YOKOTA, SHIN'ICHI. « Pharmacodynamics and pharmacokinetics of hypoglycemic drug MKC-542 in old people. » Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 30, no 1 (1999) : 269–70. http://dx.doi.org/10.3999/jscpt.30.269.

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Piras, Giovanna, Kouji Nakade, Satoshi Yuasa et Masanori Baba. « Three-drug combination of MKC-442, lamivudine and zidovudine in vitro ». AIDS 11, no 4 (mars 1997) : 469–75. http://dx.doi.org/10.1097/00002030-199704000-00010.

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Al-Salami, Hani, Grant Butt, Ian Tucker, Paul J. Fawcett, Svetlana Golo-Corbin-Kon, Ivan Mikov et Momir Mikov. « Gliclazide reduces MKC intestinal transport in healthy but not diabetic rats ». European Journal of Drug Metabolism and Pharmacokinetics 34, no 1 (mars 2009) : 43–50. http://dx.doi.org/10.1007/bf03191383.

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V. G., Meenu Krishnan, Greeshma Murukan, Aswathy J. M., Bosco Lawarence et Murugan K. « MICROBICIDAL POTENTIALITY OF PURIFIED ANTHOCYANIN FROM IN VITRO CULTURE OF CLERODENDRON INFORTUNATUM L. AGAINST SELECTED PATHOGENS ». International Journal of Pharmacy and Pharmaceutical Sciences 10, no 6 (1 juin 2018) : 68. http://dx.doi.org/10.22159/ijpps.2018v10i6.18649.

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Objective: Clerodendron infortunatum L. is a widely used medicinal herb over centuries for curing many skin-borne disorders. The present study was designed to validate the tribal knowledge by evaluating antimicrobial potential of purified anthocyanin extracted from in vitro cell suspension culture.Methods: The explants were inoculated on murashige and skoog (MS) medium mixed with various combinations of 2, 4-D a+BAP for callus induction. Green compact callus was initiated within 30 d from the explants on MS medium fortified with benzylaminopurine (BAP) (2.0 mg/l)+2, 4-D (0.5 mg/l). Subsequently, anthocyanin was triggered from the compact callus by subculturing in the medium containing 2, 4-D and Kinetin. Cell suspension culture was also developed. Anthocyanin production was enhanced by elicitation using salicylic acid and others. Three chromatographic methods such as solid phase extraction by Sepharose C18 column, Oasis-MCX and Amberlite XAD 7+Sephadex LH 120 sorbents were used to purify the in vitro synthesized anthocyanin from the cell cultures. HPLC and molar absorptivity assay were carried to check the purity. Antimicrobial analysis was also carried using standard protocols to check minimum inhibitory concentration (MIC) and minimum killing concentration (MKC).Results: The mean purity values obtained by high-performance thin layer chromatography (HPLC) were 90.9%±1.9, 80.60%±2.3 for Oasis MCX, Amberlite XAD-7+Sephadex LH-20 column respectively. However, the purity by molar absorptivity was found to be less. HPLC chromatogram revealed 12 fractions of anthocyanin. Inhibition zone diameter, MIC and MKC values obtained for the purified anthocyanin revealed its antimicrobial potentiality but at different levels among the selected bacteria and fungi. C. albicans, S. aureus, P. aerugenosa showed significant values followed by MRSA, E. coli and A. flavus. The results are comparable with the synthetic antibiotics. However, E. faecalis was more resistance. Mode of action was confirmed from the results of intracellular potassium leakage and bacterial membrane integrity analysis.Conclusion: Thus, the study confirms the efficacy of anthocyanin as natural antimicrobial and suggests the possibility of employing it as drugs for the treatment of infectious diseases caused by the pathogens.
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KUMAGAI, Yuji, Shinichi YOKOTA, Shinano ISAWA, Tomoe WATANABE, Mika SAWADA, Mitsukuni MURASAKI, Keiko NAKAI et Ayako KANNAMI. « Pharmacokinetics of Mizolastine (MKC-431), a Novel Antiallergic Drug, in the Elderly. » Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 29, no 4 (1998) : 699–705. http://dx.doi.org/10.3999/jscpt.29.699.

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Terada, Kaori, Takeharu Yokota, Yutaka Tamura et Akinori Akaike. « Protective effect of MKC-231 on glutamate cytotoxicity in cultured cortical neurons. » Japanese Journal of Pharmacology 64 (1994) : 202. http://dx.doi.org/10.1016/s0021-5198(19)50442-5.

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El-Brollosy, Nasser R., Erik B. Pedersen et Claus Nielsen. « Synthesis of Novel MKC-442 Analogues with Potent Activities against HIV-1 ». Archiv der Pharmazie 336, no 45 (juillet 2003) : 236–41. http://dx.doi.org/10.1002/ardp.200300742.

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BABA, M., H. TANAKA, T. MIYASAKA, S. YUASA, M. UBASAWA, R. T. WALKER et E. DE CLERCQ. « ChemInform Abstract : HEPT Derivatives : 6-Benzyl-1-ethoxymethyl-5-isopropyluracil (MKC-442). » ChemInform 26, no 40 (17 août 2010) : no. http://dx.doi.org/10.1002/chin.199540256.

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Tchernev, Georgi, Stanislav Philipov, Anastasiya Atanasova Chokoeva, Uwe Wollina, Torello Lotti, Ilia Lozev, Irina Yungareva et Georgi Konstantinov Maximov. « A Patient with Multiple Keratinocytic Cancers (MKC) : Uncommon Presentation in a Bulgarian Patient ». Open Access Macedonian Journal of Medical Sciences 6, no 1 (13 janvier 2018) : 120–22. http://dx.doi.org/10.3889/oamjms.2018.010.

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Keratinocyte skin cancers, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), are the most common cancer occurring in people with fair skin, worldwide. Despite all known triggers, several suggested contributors are still investigated. We will focus our attention on the personal history of previous cancers and radiation exposure as occupational risk factors, as in the presented case. We report a patient, with multiple BCCs, and subsequent occurrence of a SCC on photo-exposed area of the face, as we want to emphasize the importance of strict following up of these patients, regarding the risk for developing new tumors in short periods of time, no matter if the triggering exposure factor is known from the history, or not. Although keratinocytes tumours are associated with the low mortality rate, we focus the attention on the fact, that the history of non-melanoma skin cancer is associated with increased mortality.
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Vargas-Nadal, Guillem, Mónica Muñoz-Úbeda, Patricia Álamo, Montserrat Mitjans, Virtudes Céspedes, Mariana Köber, Elisabet González-Mira et al. « MKC-Quatsomes : a stable nanovesicle platform for bio-imaging and drug-delivery applications ». Nanomedicine : Nanotechnology, Biology and Medicine 24 (février 2020) : 102136. http://dx.doi.org/10.1016/j.nano.2019.102136.

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COLEMAN, N., J. WRIGHT, M. PARKER et R. SPILLER. « MKC-733, a selective 5-HT3 receptor agonist, stimulates fasting human antral motility ». Gastroenterology 120, no 5 (avril 2001) : A460—A461. http://dx.doi.org/10.1016/s0016-5085(01)82282-4.

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Takeuchi, Annie H. « Maximum key-profile correlation (MKC) as a measure of tonal structure in music ». Perception & ; Psychophysics 56, no 3 (mai 1994) : 335–46. http://dx.doi.org/10.3758/bf03209767.

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Coleman, Nicholas S., Jeff Wright, Margaret Parker et Robin C. Spiller. « MKC-733, a selective 5-HT3 receptor agonist, stimulates fasting human antral motility ». Gastroenterology 120, no 5 (avril 2001) : A460—A461. http://dx.doi.org/10.1016/s0016-5085(08)82282-2.

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Yamazaki, Satoshi, Takashi Yano et Akihiro Tobe. « Species difference in the intrinsic activity of MKC-733 for 5-HT3 receptor. » Japanese Journal of Pharmacology 71 (1996) : 62. http://dx.doi.org/10.1016/s0021-5198(19)36488-1.

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El-Hamid, Abd, A. A. Ismail et Adel M. E. Attia. « Synthesis of Some New Quinazoline Derivatives Analogues to MKC-442 and TNK 561 ». Phosphorus, Sulfur, and Silicon and the Related Elements 178, no 6 (juin 2003) : 1231–40. http://dx.doi.org/10.1080/10426500307910.

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