International Journal of Cancer Therapeutics

Synthesis of 4-amino-N-(4-((3-nitroacridin-9-yl)amino) phenyl)butane-1-sulfonamide (Acridine): A Novel Tyrosine Kinase Inhibitor Targeting Oncogenic Pathways

Suryakiran Navath — 2024-04-24

This manuscript outlines the efficient synthesis of Acridine, a novel tyrosine kinase inhibitor designed to target oncogenic pathways. The synthesis involves a strategic combination of nitration, amination, condensation, and reduction steps to afford the final compound. Acridine exhibits a unique structure, incorporating a 3-nitroacridin-9-yl moiety, positioning it as a promising candidate for further investigation in cancer therapy.

The abstract provides a concise overview of the synthesis of Acridine, a novel tyrosine kinase inhibitor designed to target oncogenic pathways. The strategic synthesis involves nitration, amination, condensation, and reduction steps, yielding a compound with a 3-nitroacridin-9-yl moiety. Acridine emerges as a promising candidate for cancer therapy, exhibiting unique structural features poised for inhibition of tyrosine kinase pathways.

The synthesis of Acridine commenced with the nitration of a carefully selected acridine derivative, introducing a crucial nitro functionality. Subsequent amination and condensation reactions facilitated the incorporation of an amino group, forming the core structure of Acridine through condensation with phenylbutane-sulfonamide. The reduction of the nitro group resulted in the final product, Acridine, characterized by ^1H NMR, ^13C NMR, mass spectrometry, and HPLC.

Acridine's unique structure, featuring a 3-nitroacridin-9-yl moiety, positions it as a promising tyrosine kinase inhibitor for targeted cancer therapy. The abstract concludes by highlighting the potential of Acridine in inhibiting oncogenic pathways, paving the way for further studies to explore its biological activity, selectivity, and therapeutic applications in cancer treatment.

Imatinib “Miracle Medicine” for the Treatment of Ph+ Chronic Myeloid Leukemia (CML)

Suryakiran Navath — 2024-01-10

Chronic Myeloid Leukemia (CML) is a hematological malignancy characterized by the abnormal proliferation of myeloid cells. The presence of the Philadelphia chromosome (Ph+) is a hallmark of CML, leading to the activation of the BCR-ABL1 fusion gene. Imatinib, a tyrosine kinase inhibitor, has emerged as a groundbreaking treatment for Ph+ CML, revolutionizing the landscape of leukemia therapy.

Chronic Myeloid Leukemia (CML) characterized by the Philadelphia chromosome (Ph+) poses a significant therapeutic challenge. Imatinib, a tyrosine kinase inhibitor, has gained acclaim as a transformative treatment, earning the moniker of a "miracle medicine."Literature analysis of clinical trials, studies, and reviews was conducted to compile evidence supporting the miraculous efficacy of imatinib.

Imatinib, by selectively inhibiting the BCR-ABL1 fusion protein, disrupts the aberrant signaling cascade, leading to impressive hematological and cytogenetic responses. Clinical trials have demonstrated its ability to induce complete molecular remission and significantly enhance overall survival.

Imatinib stands as a beacon of hope for patients with Ph+ CML, representing a paradigm shift in leukemia treatment. Ongoing research aims to refine therapeutic strategies, ensuring sustained success in managing this challenging hematological malignancy.

Synthesis and structural evaluation of (5-(6-(Furan-2-ylmethylamino)-9H-purin-9-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl Dihydrogen Phosphate as a Redox Drug Discovery Targeting Human Skin Cancer

Suryakiran Navath — 2024-06-08

The aim of this study was to synthesize and characterize (5-(6-(Furan-2-ylmethylamino)-9H-purin-9-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl Dihydrogen Phosphate as a potential redox drug targeting human skin cancer. The compound was synthesized through a series of chemical reactions and characterized using various spectroscopic and analytical techniques. Preliminary in vitro studies were conducted to assess its potential as a therapeutic agent against human skin cancer cells.

This manuscript outlines the synthesis of a novel compound, (5-(6-(Furan-2-ylmethylamino)-9H-purin-9-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl Dihydrogen Phosphate, strategically designed and synthesized as a potential redox drug for targeting human skin cancer. The synthetic pathway involved a series of meticulously optimized steps utilizing key reagents such as Furan-2-ylmethylamine, 9H-purine, and tetrahydrofuran.

The synthesized compound underwent comprehensive characterization through NMR spectroscopy, mass spectrometry, and elemental analysis, affirming its structural integrity and purity. Beyond synthesis, the compound's efficacy in modulating redox pathways relevant to human skin cancer was explored through in vitro assays, revealing promising redox-modulating properties.

This study positions the synthesized compound as a potential lead in redox drug discovery for human skin cancer treatment. The observed modulation of redox pathways signifies its potential utility in addressing the oxidative stress associated with skin cancer. Future investigations will delve into further optimization of the compound's structure and comprehensive preclinical studies, aiming to contribute to the development of effective therapeutic interventions for human skin cancer.

Advances in the Treatment of Ph+ Chronic Myeloid Leukemia: A Comprehensive Study

Suryakiran Navath — 2024-03-12

Chronic Myeloid Leukemia (CML) is a myeloproliferative disorder characterized by the presence of the Philadelphia chromosome (Ph+), resulting from a reciprocal translocation between chromosomes 9 and 22. The discovery of tyrosine kinase inhibitors (TKIs) has revolutionized the treatment landscape for Ph+ CML. This review article provides an in-depth analysis of the recent advancements in the treatment of Ph+ CML, focusing on the efficacy, safety, and emerging therapeutic strategies.

The introduction outlines the historical progression from conventional therapies to the advent of tyrosine kinase inhibitors (TKIs), marking a pivotal shift in CML management. The abstract delves into the first-line treatment strategies, with a focus on imatinib, dasatinib, and nilotinib, highlighting their individual efficacies and safety profiles.

A significant portion is dedicated to the exploration of second and third-generation TKIs, elucidating their distinct mechanisms of action, resistance patterns, and comparative effectiveness. Insights into the evolution of treatment strategies in response to emerging resistance and intolerance are provided, emphasizing the importance of mutation analysis in guiding therapeutic decisions.

The abstract underscores the transformative impact of targeted therapy on Ph+ CML outcomes. It emphasizes the need for ongoing research to address challenges, optimize treatment sequencing, and explore novel agents that hold the promise of further improving the prognosis and quality of life for patients with Ph+ CML.

Cancer versus anticancer factors: A review of these factors, health impacts, and awareness

Uttam Chowdhury — 2024-02-15

Cancer is a disease that is caused when cells begin to divide without stopping and spreading into surrounding tissues by any changes or damage to DNA. Most cancer disease cases are due to environmental risk factors, and many of these factors are controllable lifestyle choices.

Free radicals are risk factors that cause cancer, but antioxidants are anti-risk factors that work as anticancer and protect our health from diseases like cancer. It would be very important to know how these risk and anti-risk factors work, and how we could maintain and protect our health.

Free radicals (FRs) have an unpaired electron in their outer orbit that make them very unstable because they want to keep pair of electrons in their outer orbit, and their reactivity is very strong for that missing electron to become stable. Due to that, FRs attack healthy/normal cells for electrons that they can find to become stable. Free radicals could take electrons from DNA molecules, proteins, fats, carbohydrates, and other molecules, damaging and turning them into new free radicals. In this process, free radical chain reactions damage the entire cell, then their neighbors, and so on. Having too many free radicals in the body increases the likelihood of damage to healthy cells. This resulting damage is called oxidative damage