diphenylamine/cáncer

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Metabolically Stable Diphenylamine Derivatives Suppress Androgen Receptor and BET Protein in Prostate Cancer.

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Androgen receptor (AR) is a crucial driver of prostate cancer (PC). AR-relevant resistance remains a major challenge in castration-resistant prostate cancer (CRPC). Bromodomain and extra-terminal domain (BET) family are critical AR coregulators. Here, we developed several diphenylamine derivatives

Flat revertant inducers, styryl diphenylamine derivatives, inhibit growth and metastasis of murine tumor cells in vivo.

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Previously, we reported that a novel styryl diphenylamine derivative, RX-465, reverts the transformed phenotype of human fibrosarcoma HT1080 cells in vitro. To determine whether agents inducing such phenotypic reversion show antitumor and/or antimetastatic effects in vivo, we assessed tumor growth

Discovery and biological evaluation of novel androgen receptor antagonist for castration-resistant prostate cancer.

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Prostate cancer (PC) is the second most common malignancy in men worldwide. Among current therapies, two antiandrogens, Abiraterone Acetate and Enzalutamide (Enza) have become the standard of care for patients with metastatic castration-resistant prostate cancer (mCRPC). Here, we designed and

Structure-function relationship and role of tumor necrosis factor-alpha-converting enzyme in the down-regulation of L-selectin by non-steroidal anti-inflammatory drugs.

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It has been recently described that some non-steroidal anti-inflammatory drugs (NSAIDs) are able to induce the shedding of L-selectin in neutrophils, an adhesion molecule that plays an essential role in the inflammatory response. We have found that, according to this capability, NSAIDs could be

Formation and cytotoxicity of a new disinfection by-product (DBP) phenazine by chloramination of water containing diphenylamine.

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Disinfection by-products (DBPs) in drinking water have caused worldwide concern due to their potential carcinogenic effects. The formation of phenazine from diphenylamine (DPhA) chloramination was studied and its cytotoxicities for two human cancer cells were also investigated. Phenazine was

Delayed Fluorescence, Room Temperature Phosphorescence, and Mechanofluorochromic Naphthalimides: Differential Imaging of Normoxia and Hypoxia Live Cancer Cells

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We study the effect of molecular conformation on the electronic coupling between the donor amines and acceptor 1,8-naphthalimide (NPI) in a series of D-A systems 1-4 (A = NPI; D = phenothiazine, phenoxazine, carbazole, diphenylamine, respectively, for 1, 2, 3, and

Proliferation inhibition of novel diphenylamine derivatives.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely used drugs in the world but some NSAIDs such as diclofenac and tolfenamic acid display levels of cytotoxicity, an effect which has been attributed to the presence of diphenylamine contained in their structures. A novel series of

Orally active anti-proliferation agents: novel diphenylamine derivatives as FGF-R2 autophosphorylation inhibitors.

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(6,7-Disubstituted-quinolin-4-yloxy-phenyl)(4-substituted-phenyl)amine derivatives were synthesized and evaluated by a cellular autophosphorylation assay for FGF-R2 in the human scirrhous gastric carcinoma cell line, OCUM-2MD3. We also performed metabolic stability studies showing that substitutions

[Effects of recombinant human tumor-necrosis factor related to apoptosis inducing ligand protein on apoptosis of human lung adenocarcinoma cell line resistant to cisplatin].

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BACKGROUND Tumor-necrosis factor related to apoptosis inducing ligand protein(TRAIL), like tumor-necrosis factor (TNF) and Fas, is a member of TNF cytokine supper family. Many researches have showed that TNF-α can reverse the resistance to some chemotherapeutic agents in cancer cell lines, and some

Novel diphenylamine 2,4'-dicarboxamide based azoles as potential epidermal growth factor receptor inhibitors: synthesis and biological activity.

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Several hybrid molecules of diphenylamine-2,4'-dicarboxamide with various azolidinones and related heterocyclic rings have been synthesized and explored as epidermal growth factor receptor (EGFR) kinase inhibitors. Most of them displayed promising in vitro tyrosine kinase inhibition as well as

Anticancer effects of synthetic hexahydrobenzo [g]chromen-4-one derivatives on human breast cancer cell lines.

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BACKGROUND Cancer results from a series of molecular changes that alter the normal function of cells. Breast cancer is the second leading cause of cancer death in women. To develop novel anticancer agents, new series of chromen derivatives were synthesized and evaluated for their cytotoxic activity

Leaves of Cassia tora as a novel cancer therapeutic--an in vitro study.

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Cassia tora Linn (Leguminacea) is a medicinal plant traditionally used as laxative, for the treatment of leprosy and various skin disorders. Preliminary phytochemical analysis of leaf showed the presence of polyphenols (3.7 mg gallic acid equivalent per gram dried leaves). The presence of phenolic

Synthesis, quantitative structure-activity relationship and biological evaluation of 1,3,4-oxadiazole derivatives possessing diphenylamine moiety as potential anticancer agents.

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Synthesis of 2,5-disubstituted-1,3,4-oxadiazole (2a-c), 3-substituted aminomethyl-5-substituted-1,3,4-oxadiazole-2(3H)-thione (4a-m) and 2-substituted thio-5-substituted-1,3,4-oxadiazole (5a, b) had been described. All the synthesized derivatives were screened for anticancer activity against HT29

Synthesis and In Vitro Anticancer Evaluation of Novel Chrysin and 7-Aminochrysin Derivatives.

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Chrysin is a naturally occurring flavonoid with mild anticancer activity. In this paper we report the synthesis of new chrysin derivatives alkylated with N-phenylchloroacetamides in position 7. A novel method was developed for the preparation of 7-aminochrysin derivatives via the Smiles

Flow cytometric measurement of mitochondrial mass and function: a novel method for assessing chemoresistance.

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BACKGROUND Chemotherapeutic agents induce apoptosis in cancer cells. Drugs failing to induce apoptosis are likely to have decreased clinical efficacy. We hypothesize that (1) chemotherapeutic agents induce mitochondrial changes and apoptosis through mechanisms associated with reactive oxidant

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