Category: 380843-75-4

On December 31, 2020, G. Lindstroem, H. Jonathan; Friedman, Ran published an article.Reference of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile The title of the article was The effects of combination treatments on drug resistance in chronic myeloid leukaemia: an evaluation of the tyrosine kinase inhibitors axitinib and asciminib. And the article contained the following:

Abstract: Background: Chronic myeloid leukemia is in principle a treatable malignancy but drug resistance is lowering survival. Recent drug discoveries have opened up new options for drug combinations, which is a concept used in other areas for preventing drug resistance. Two of these are (I) Axitinib, which inhibits the T315I mutation of BCR-ABL1, a main source of drug resistance, and (II) Asciminib, which has been developed as an allosteric BCR-ABL1 inhibitor, targeting an entirely different binding site, and as such does not compete for binding with other drugs. These drugs offer new treatment options. Methods: We measured the proliferation of KCL-22 cells exposed to imatinib-dasatinib, imatinib-asciminib and dasatinib-asciminib combinations and calculated combination index graphs for each case. Moreover, using the median-effect equation we calculated how much axitinib can reduce the growth advantage of T315I mutant clones in combination with available drugs. In addition, we calculated how much the total drug burden could be reduced by combinations using asciminib and other drugs, and evaluated which mutations such combinations might be sensitive to. Results: Asciminib had synergistic interactions with imatinib or dasatinib in KCL-22 cells at high degrees of inhibition. Interestingly, some antagonism between asciminib and the other drugs was present at lower degrees on inhibition. Simulations revealed that asciminib may allow for dose reductions, and its complementary resistance profile could reduce the risk of mutation based resistance. Axitinib, however, had only a minor effect on T315I growth advantage. Conclusions: Given how asciminib combinations were synergistic in vitro, our modeling suggests that drug combinations involving asciminib should allow for lower total drug doses, and may result in a reduced spectrum of observed resistance mutations. On the other hand, a combination involving axitinib was not shown to be useful in countering drug resistance. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Reference of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

The Article related to axitinib asciminib antitumor tyrosine kinase inhibitor chronic myeloid leukemia, allosteric inhibitor, drug combination, targeted therapy, Pharmacology: Effects Of Neoplasm Inhibitors and Cytotoxic Agents and other aspects.Reference of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

Mulas, Olga; Caocci, Giovanni; Mola, Brunella; La Nasa, Giorgio published an article in 2021, the title of the article was Arterial hypertension and tyrosine kinase inhibitors in chronic myeloid leukemia: a systematic review and meta-analysis.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile And the article contains the following content:

Off-target effects in chronic myeloid leukemia (CML) patients treated with tyrosine kinase inhibitors (TKIs) are associated with cardiovascular toxicity. Hypertension represents an important cardiovascular complication and, if not appropriately managed, can contribute to developing thrombotic events. Third-generation TKI ponatinib is associated with hypertension development, and its use is more restricted than in the past. Few data are reported for second-generation TKI, nilotinib, dasatinib, and bosutinib. The aim of this article was to evaluate with a systematic review and meta-anal. the real incidence of hypertension in CML patients treated with second- or third-generation TKI. The PubMed database, Web of Science, Scopus, and ClinicalTrials.gov were systematically searched for studies published between Jan. 1, 2000, and Jan. 30, 2021; the following terms were entered in the database queries: Cardiovascular, Chronic Myeloid Leukemia, CML, Tyrosine kinases inhibitor, TKI, and Hypertension. The study was carried out according to the Preferred Reporting Items for Systematic and Meta-Analyses (PRISMA) statement. A pooled anal. of hypertension incidence was 10% for all new-generation TKI, with an even higher prevalence with ponatinib (17%). The comparison with the first-generation imatinib confirmed that nilotinib was associated with a significantly increased risk of hypertension (RR 2; 95% CI; 1.39-2.88, I2 = 0%, z = 3.73, p = 0.0002). The greatest risk was found with ponatinib (RR 9.21; 95% CI; 2.86-29.66, z = 3.72, p = 0.0002). Hypertension is a common cardiovascular complication in CML patients treated with second- or third-generation TKI. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

The Article related to arterial hypertension tyrosine kinase inhibitor chronic myeloid leukemia metaanalysis, cardiovascular, chronic myeloid, hypertension, leukemia, tyrosine kinase inhibitor, Pharmacology: Other (All Agents and Effects Not Otherwise Assignable) and other aspects.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

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Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On August 31, 2020, Petzer, Andreas L.; Sperr, Wolfgang R.; Buxhofer-Ausch, Veronika; Sliwa, Thamer; Schmidt, Stefan; Greil, Richard; Woelfler, Albert; Pichler, Petra; Dormann, Clemens; Burgstaller, Sonja; Tinchon, Christoph; Lang, Alois; Goebel, Florian; Uthman, Shanow; Muenchmeier, Niklas; Valent, Peter published an article.COA of Formula: C26H29Cl2N5O3 The title of the article was A multicenter retrospective evaluation of Chronic Myeloid Leukemia (CML) therapy in Austria assessing the impact of early treatment response on patient outcomes in a real-life setting – R-Effect study. And the article contained the following:

Methods: The Retrospective Evaluation of Early response in CML for long-term Treatment outcome (R-Effect), a multicenter, retrospective chart review, documented patients with newly diagnosed CML-CP starting first-line TKI therapy in routine clin. practice. The primary aim was to assess the 5-yr overall survival rate. Results: Of the 211 patients from 12 centers across Austria (Jan. 2004-May 2010), 176 (median age, 56 years) were included in the anal. All patients received first-line therapy with imatinib. Overall, 136 patients (77.3%) achieved ETR (ETR+ group), whereas 40 (22.7%) did not reach ETR (ETR- group). The ETR+ group had higher 5-yr overall survival (92.5% vs. 77.5%, P = 0.018) and progression-free survival (95.6% vs. 87.5%, P = 0.06) rates compared with the ETR- group. As expected, more patients in the ETR- group were switched to another TKI. At the last contact, 120 patients were still on imatinib and 44 had switched to another TKI (25 to nilotinib, 15 to dasatinib, and 4 to bosutinib). Conclusion: The data are in line with randomized trials demonstrating that ETR is associated with improved survival and thus confirmed these results in patients treated in daily clin. routine. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).COA of Formula: C26H29Cl2N5O3

The Article related to chronic myeloid leukemia therapy, chronic myeloiud leukemia, chronic phase, clinical routine, retrospective evaluation, tyrosine kinase inhibitors, Pharmacology: Effects Of Cardiovascular, Hematologic, and Renal Drugs and other aspects.COA of Formula: C26H29Cl2N5O3

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On January 31, 2022, Balboa Ramilo, Amanda; Becirovic-Agic, Mediha; Petri, Marcelo Heron; Mani, Kevin; Wanhainen, Anders; Waagsaeter, Dick published an article.SDS of cas: 380843-75-4 The title of the article was The tyrosine kinase inhibitor Bosutinib does not inhibit angiotensin II-induced abdominal aortic aneurysm: Validation of the importance of PDGFR and c-Kit tyrosine kinases by Imatinib. And the article contained the following:

Validation of the importance of PDGFR and c-Kit tyrosine kinases by imatinib. All experiments were approved by the Animal Experiments Ethical Committee in Uppsala. Mice were divided into four groups. One group of control mice (n =8) was infused with Ringer’s solution In the other three groups, aneurysm was induced by infusion of 1000 ng/kg/min of AngII. AngII-infused animals were treated with vehicle (n = 20), 10 mg/kg of Bosutinib (Bos, Cat.number S1014, Selleckchem, TX, USA) (n = 20) or 100 mg/kg of Bosutinib (n = 10) by oral gavage, for 22 days. Control animals also received vehicle by oral gavage. On the last day of the experiment, an abdominal ultrasound (Vevo 1100 ultrasound, VisualSonics) was performed for measurement of aortic diameter Control animals had an average aortic diameter of 1.2 ± 0.108 mm. Aneurysm was defned as an aortic diameter equal or superior to 1.8 mm (1.5-fold increase relative to control). These results indicate that treatment of AngII-induced mice with Bosutinib, in a similar dose to Imatinib or higher, does not have an effect on AAA development. This confirms that inhibition of the PDGFR and/or c-Kit is necessary for the effect of Imatinib on abdominal aortic aneurysm development. Thus, drugs inhibiting c-Kit and PDGFR should be of more interest to test in the context of abdominal aortic aneurysm. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).SDS of cas: 380843-75-4

The Article related to abdominal aortic aneurysm pdgfr ckit tyrosine kinase imatinib, aneurysm, inhibitor, rupture, tyrosine kinase, Pharmacology: Effects Of Cardiovascular, Hematologic, and Renal Drugs and other aspects.SDS of cas: 380843-75-4

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Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On February 29, 2020, Shinoda, Kazunobu; Morita, Shinya; Tamaki, Satoshi; Takahashi, Ryohei; Kitaoka, Sotaro; Asanuma, Hiroshi; Yoshida, Tadashi; Okayama, Mikio; Kasahara, Hidenori; Okamoto, Shinichiro; Oya, Mototsugu published an article.Name: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile The title of the article was Successful Treatment of End-stage Renal Disease in a Patient With Chronic Myeloid Leukemia by Kidney Transplantation and Tyrosine Kinase Inhibitors: A Case Report. And the article contained the following:

Consensus regarding kidney transplantation feasibility in patients with chronic myeloid leukemia (CML) well controlled by tyrosine kinase inhibitors has not yet been achieved. Here, we report a patient with CML well controlled by tyrosine kinase inhibitors who developed end-stage renal disease during treatment and underwent kidney transplantation. CML activity has been carefully and successfully controlled for 4 years post-transplant. Very cautious dose adjustment and temporary cessation of nilotinib were required because kidney function fluctuated in reference to the doses of nilotinib. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Name: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

The Article related to tki renal disease chronic myeloid leukemia kidney transplantation human, Pharmacology: Effects Of Cardiovascular, Hematologic, and Renal Drugs and other aspects.Name: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On May 31, 2021, Valencia, Hugo J.; de Aguiar, Mara C. A. M.; Costa, Mariana A.; Mendonca, Diogo C.; Reis, Erik V.; Arias, Nidia E. C.; Drumond, Betania P.; Bonjardim, Claudio A. published an article.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile The title of the article was Evaluation of kinase inhibitors as potential therapeutics for flavivirus infections. And the article contained the following:

The recent introduction of Zika virus (ZIKV), the recurrence of dengue virus (DENV), and the lethality of yellow fever virus (YFV) have had a significant impact on Brazilian society and public health. Here, we targeted two cellular kinases implicated in cell proliferation and cancer that are also important for viral replication: mitogen-activated protein kinase kinase (MEK) and Src. We used two MEK inhibitors – trametinib and selumetinib – and two Src inhibitors – saracatinib and bosutinib – to inhibit ZIKV, DENV, and YFV replication in cell culture. The cytotoxicity of the four inhibitors was determined by the observation of abnormal morphol. and quantification of adherent cells by crystal violet staining. The antiviral activity of these drugs was assessed based on the reduction of plaque-forming units in cell culture as evidence of the inhibition of the replication of the selected flaviviruses. All four inhibitors showed antiviral activity, but among them, trametinib was the safest and most efficacious against all of the viruses, inhibiting the replication of ZIKV and YFV by 1000-fold, and DENV2/3 by nearly 100-fold. This pan-antiviral effect shows that trametinib could be repurposed for the treatment of flaviviral infections. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

The Article related to mek src kinase inhibitor therapeutics flavivirus infection, Pharmacology: Other (All Agents and Effects Not Otherwise Assignable) and other aspects.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On August 31, 2020, Hochhaus, Andreas; Gambacorti-Passerini, Carlo; Abboud, Camille; Gjertsen, Bjoern Tore; Bruemmendorf, Tim H.; Smith, B. Douglas; Ernst, Thomas; Giraldo-Castellano, Pilar; Olsson-Stroemberg, Ulla; Saussele, Susanne; Bardy-Bouxin, Nathalie; Viqueira, Andrea; Leip, Eric; Russell-Smith, T. Alexander; Leone, Jocelyn; Rosti, Gianantonio; Watts, Justin; Giles, Francis J.; on behalf of the BYOND Study Investigators published an article.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile The title of the article was Bosutinib for pretreated patients with chronic phase chronic myeloid leukemia: primary results of the phase 4 BYOND study. And the article contained the following:

Bosutinib is approved for newly diagnosed Philadelphia chromosome-pos. (Ph+) chronic phase (CP) chronic myeloid leukemia (CML) and for Ph+ CP, accelerated (AP), or blast (BP) phase CML after prior treatment with tyrosine kinase inhibitors (TKIs). In the ongoing phase 4 BYOND study (NCT02228382), 163 CML patients resistant/intolerant to prior TKIs (n = 156 Ph+ CP CML, n = 4 Ph+ AP CML, n = 3 Ph-neg./BCR-ABL1+ CML) received bosutinib 500 mg once daily (starting dose). As of ≥1 yr after last enrolled patient (median treatment duration 23.7 mo), 56.4% of Ph+ CP CML patients remained on bosutinib. Primary endpoint of cumulative confirmed major cytogenetic response (MCyR) rate by 1 yr was 75.8% in Ph+ CP CML patients after one or two prior TKIs and 62.2% after three prior TKIs. Cumulative complete cytogenetic response (CCyR) and major mol. response (MMR) rates by 1 yr were 80.6% and 70.5%, resp., in Ph+ CP CML patients overall. No patient progressed to AP/BP on treatment. Across all patients, the most common treatment-emergent adverse events were diarrhea (87.7%), nausea (39.9%), and vomiting (32.5%). The majority of patients had confirmed MCyR by 1 yr and MMR by 1 yr, further supporting bosutinib use for Ph+ CP CML patients resistant/intolerant to prior TKIs. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

The Article related to human bosutinib chronic myeloid leukemia pretreatment, Pharmacology: Effects Of Cardiovascular, Hematologic, and Renal Drugs and other aspects.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

Abbas, Hosna Hasan; Al Mosawy, Karrar Kadim published an article in 2020, the title of the article was Overview of chronic myeloid leukemia patients in the holy city of Karbala.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile And the article contains the following content:

Chronic myeloid leukemia (CML) is a clonal myeloproliferative disorder characterized by presence of Philadelphia chromosome. Over time CML treatment has change dramatically; especially when Tyrosine Kinase Inhibitor (TKI) introduced, which significantly increase survival and improve quality of life for all patients especially when its associated with good drug adherence and sequential response monitoring to TKI. To study the characteristics of CML patient’s in the Holy City of Karbala and the outcome of Tyrosine Kinase Inhibitor in control of their disease. The present descriptive study included 56 patients, conducted in Al Imam Al Hussein Hematol./Oncol. center at the Holy city of Karbala in Iraq from June 2017 – June 2018. Data from patients with CML were collected and critically analyzed for the demog. data, type of treatment they used and their compliance to drug. The median age was 46 years; male-to-female ratio was 1.24:1. 96.4% patients were diagnosed in chronic phase of their disease. Major mol. response achieved in 79% (27/34) of patients on Gleevec. 37.5% patients were switch to Tasigna after Imatinib resistant or intolerance, 52% of them achieved major mol. response. Drug adherence found in 68% (38/56) patients. CML slightly male predominance, diagnosed at age younger than that report in the United States and Europe, response to TKI nearly similar to that report in international study. Drug adherence and sequential monitoring of patients can improve therapeutic effect of TKI therapy. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

The Article related to chronic myeloid leukemia patients holy city karbala, Pharmacology: Effects Of Cardiovascular, Hematologic, and Renal Drugs and other aspects.Recommanded Product: 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On May 31, 2020, Chow, Amanda; McCrea, Liam; Kimball, Elizabeth; Schaub, Julie; Quigley, Harry; Pitha, Ian published an article.Product Details of 380843-75-4 The title of the article was Dasatinib inhibits peripapillary scleral myofibroblast differentiation. And the article contained the following:

Scleral fibroblast activation occurs in glaucomatous and myopic eyes. Here we perform an unbiased screen to identify kinase inhibitors that reduce fibroblast activation to diverse stimuli in vitro and to in vivo intraocular pressure (IOP) elevation. Primary cultures of peripapillary scleral (PPS) fibroblasts from two human donors were screened using a library of 80 kinase inhibitors to identify compounds that inhibit TGFbeta-induced extracellular matrix (ECM) synthesis. Inhibition of myofibroblast differentiation was verified by alpha smooth muscle actin (aSMA) immunoblot and collagen contraction assay. Three kinase inhibitors were verified to reduce TGFbeta-induced aSMA expression and cellular contractility (rottlerin, PP2, tyrphostin 9). The effect of three Src inhibitors, bosutinib, dasatinib, and SU-6656, on myofibroblast differentiation was evaluated, with only dasatinib significantly inhibiting TGFbeta-induced ECM synthesis, aSMA expression, and cellular contractility at nanomolar dosages. Subconjunctival injection of dasatinib reduced IOP-induced scleral fibroblast proliferation compared to control (4.9 ± 11.1 ng/sclera with 0.1 muM vs. 88.7 ± 38.6 ng/sclera in control, P < 0.0001). Dasatinib inhibits scleral myofibroblast differentiation and there is pharmacol. evidence that this inhibition is not solely due to Src-kinase inhibition. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Product Details of 380843-75-4

The Article related to glaucoma peripapillary scleral myofibroblast differentiation dasatinib, fibroblast, fibrosis, glaucoma, kinase inhibitor, peripapillary sclera, scleral remodeling, src kinase and other aspects.Product Details of 380843-75-4

Referemce:
Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics

On September 30, 2021, Kikuya, Megumi; Furuichi, Kenta; Hirao, Takuya; Endo, Satoshi; Toyooka, Naoki; Ito, Kousei; Aoki, Shigeki published an article.Computed Properties of 380843-75-4 The title of the article was Aldo-keto reductase inhibitors increase the anticancer effects of tyrosine kinase inhibitors in chronic myelogenous leukemia. And the article contained the following:

Tyrosine kinase inhibitors (TKIs) are widely utilized in clin. practice to treat carcinomas, but secondary tumor resistance during chronic treatment can be problematic. AKR1B1 and AKR1B10 of the aldo-keto reductase (AKR) superfamily are highly expressed in cancer cells and are believed to be involved in drug resistance. The aim of this study was to understand how TKI treatment of chronic myelogenous leukemia (CML) cells changes their glucose metabolism and if inhibition of AKRs can sensitize CML cells to TKIs. K562 cells were treated with the TKIs imatinib, nilotinib, or bosutinib, and the effects on glucose metabolism, cell death, glutathione levels, and AKR levels were assessed. To assess glucose dependence, cells were cultured in normal and low-glucose media. Pretreatment with AKR inhibitors, including epalrestat, were used to determine AKR-dependence. Treatment with TKIs increased intracellular glucose, AKR1B1/10 levels, glutathione oxidation, and nuclear translocation of nuclear factor erythroid 2-related factor 2, but with minimal cell death. These effects were dependent on intracellular glucose accumulation. Pretreatment with epalrestat, or a selective inhibitor of AKR1B10, exacerbated TKI-induced cell death, suggesting that especially AKR1B10 was involved in protection against TKIs. Thus, by disrupting cell protective mechanisms, AKR inhibitors may render CML more susceptible to TKI treatments. The experimental process involved the reaction of 4-((2,4-Dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methylpiperazin-1-yl)propoxy)quinoline-3-carbonitrile(cas: 380843-75-4).Computed Properties of 380843-75-4

The Article related to anticancer aldoketo reductase tyrosine kinase inhibitor chronic myelogenous leukemia, akr1b1/10, chronic myelogenous leukemia, epalrestat, glucose, tyrosine kinase inhibitor and other aspects.Computed Properties of 380843-75-4

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Piperazine – Wikipedia,
Piperazines – an overview | ScienceDirect Topics