An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.
Acridines which are substituted in any position by one or more amino groups or substituted amino groups.
DNA TOPOISOMERASES that catalyze ATP-dependent breakage of both strands of DNA, passage of the unbroken strands through the breaks, and rejoining of the broken strands. These enzymes bring about relaxation of the supercoiled DNA and resolution of a knotted circular DNA duplex.
Compounds that inhibit the activity of DNA TOPOISOMERASE II. Included in this category are a variety of ANTINEOPLASTIC AGENTS which target the eukaryotic form of topoisomerase II and ANTIBACTERIAL AGENTS which target the prokaryotic form of topoisomerase II.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.
Agents that are capable of inserting themselves between the successive bases in DNA, thus kinking, uncoiling or otherwise deforming it and therefore preventing its proper functioning. They are used in the study of DNA.
A genus of the family Heteromyidae which contains 22 species. Their physiology is adapted for the conservation of water, and they seldom drink water. They are found in arid or desert habitats and travel by hopping on their hind limbs.
A highly fluorescent anti-infective dye used clinically as a topical antiseptic and experimentally as a mutagen, due to its interaction with DNA. It is also used as an intracellular pH indicator.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)
An antimitotic agent with immunosuppressive properties.
Vomiting caused by expectation of discomfort or unpleasantness.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
An anthracenedione-derived antineoplastic agent.
Compounds that inhibit the activity of DNA TOPOISOMERASE I.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
A hydrolase enzyme that converts L-asparagine and water to L-aspartate and NH3. EC 3.5.1.1.
Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Agents that have a damaging effect on the HEART. Such damage can occur from ALKYLATING AGENTS; FREE RADICALS; or metabolites from OXIDATIVE STRESS and in some cases is countered by CARDIOTONIC AGENTS. Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.
Databases devoted to knowledge about specific chemicals.
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.
A strain of Murine leukemia virus (LEUKEMIA VIRUS, MURINE) producing leukemia of the reticulum-cell type with massive infiltration of liver, spleen, and bone marrow. It infects DBA/2 and Swiss mice.
Leukemia induced experimentally in animals by exposure to leukemogenic agents, such as VIRUSES; RADIATION; or by TRANSPLANTATION of leukemic tissues.
Products of the hydrolysis of chlorophylls in which the phytic acid side chain has been removed and the carboxylic acids saponified.
Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.
Medicines that can be sold legally without a DRUG PRESCRIPTION.
Authoritative treatises on drugs and preparations, their description, formulation, analytic composition, physical constants, main chemical properties used in identification, standards for strength, purity, and dosage, chemical tests for determining identity and purity, etc. They are usually published under governmental jurisdiction (e.g., USP, the United States Pharmacopoeia; BP, British Pharmacopoeia; P. Helv., the Swiss Pharmacopoeia). They differ from FORMULARIES in that they are far more complete: formularies tend to be mere listings of formulas and prescriptions.
Substances added to pharmaceutical preparations to protect them from chemical change or microbial action. They include ANTI-BACTERIAL AGENTS and antioxidants.
Injections made into a vein for therapeutic or experimental purposes.
Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods.
A five-carbon sugar alcohol derived from XYLOSE by reduction of the carbonyl group. It is as sweet as sucrose and used as a noncariogenic sweetener.
Exclusive legal rights or privileges applied to inventions, plants, etc.
Hydrocarbon-rich byproducts from the non-fossilized BIOMASS that are combusted to generate energy as opposed to fossilized hydrocarbon deposits (FOSSIL FUELS).
The relative amounts of various components in the body, such as percentage of body fat.
Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)
Usually inert substances added to a prescription in order to provide suitable consistency to the dosage form. These include binders, matrix, base or diluent in pills, tablets, creams, salves, etc.
A condition in which the FORAMEN OVALE in the ATRIAL SEPTUM fails to close shortly after birth. This results in abnormal communications between the two upper chambers of the heart. An isolated patent ovale foramen without other structural heart defects is usually of no hemodynamic significance.
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.
Therapeutic act or process that initiates a response to a complete or partial remission level.
Transfer of HEMATOPOIETIC STEM CELLS from BONE MARROW or BLOOD between individuals within the same species (TRANSPLANTATION, HOMOLOGOUS) or transfer within the same individual (TRANSPLANTATION, AUTOLOGOUS). Hematopoietic stem cell transplantation has been used as an alternative to BONE MARROW TRANSPLANTATION in the treatment of a variety of neoplasms.
The process that reverts CELL NUCLEI of fully differentiated somatic cells to a pluripotent or totipotent state. This process can be achieved to a certain extent by NUCLEAR TRANSFER TECHNIQUES, such as fusing somatic cell nuclei with enucleated pluripotent embryonic stem cells or enucleated totipotent oocytes. GENE EXPRESSION PROFILING of the fused hybrid cells is used to determine the degree of reprogramming. Dramatic results of nuclear reprogramming include the generation of cloned mammals, such as Dolly the sheep in 1997.
A genetic process by which the adult organism is realized via mechanisms that lead to the restriction in the possible fates of cells, eventually leading to their differentiated state. Mechanisms involved cause heritable changes to cells without changes to DNA sequence such as DNA METHYLATION; HISTONE modification; DNA REPLICATION TIMING; NUCLEOSOME positioning; and heterochromatization which result in selective gene expression or repression.
A novel composition, device, or process, independently conceived de novo or derived from a pre-existing model.
The segment of GASTROINTESTINAL TRACT that includes the small intestine below the DUODENUM, and the LARGE INTESTINE.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
A common and benign breast disease characterized by varying degree of fibrocystic changes in the breast tissue. There are three major patterns of morphological changes, including FIBROSIS, formation of CYSTS, and proliferation of glandular tissue (adenosis). The fibrocystic breast has a dense irregular, lumpy, bumpy consistency.
Calcium salts of phosphoric acid. These compounds are frequently used as calcium supplements.
Synthetic or natural materials for the replacement of bones or bone tissue. They include hard tissue replacement polymers, natural coral, hydroxyapatite, beta-tricalcium phosphate, and various other biomaterials. The bone substitutes as inert materials can be incorporated into surrounding tissue or gradually replaced by original tissue.
Condition of having pores or open spaces. This often refers to bones, bone implants, or bone cements, but can refer to the porous state of any solid substance.
A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.
Native, inorganic or fossilized organic substances having a definite chemical composition and formed by inorganic reactions. They may occur as individual crystals or may be disseminated in some other mineral or rock. (Grant & Hackh's Chemical Dictionary, 5th ed; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Inorganic salts of phosphoric acid.
Adhesives used to fix prosthetic devices to bones and to cement bone to bone in difficult fractures. Synthetic resins are commonly used as cements. A mixture of monocalcium phosphate, monohydrate, alpha-tricalcium phosphate, and calcium carbonate with a sodium phosphate solution is also a useful bone paste.

Effect of cellular ATP depletion on topoisomerase II poisons. Abrogation Of cleavable-complex formation by etoposide but not by amsacrine. (1/246)

Topoisomerase (topo) II poisons have been categorized into ATP-independent and -dependent drugs based on in vitro studies. We investigated drug-induced topoII-DNA complexes in intact cells almost completely depleted of ATP. Virtually no DNA single-strand breaks (SSBs), as measured by alkaline elution, were detected in energy-depleted cells treated with the topoII poisons etoposide, teniposide, daunorubicin, doxorubicin, mitoxantrone, or clerocidin. This inhibition was reversible; subsequent incubation with glucose restored the level of DNA SSBs. The effect of ATP depletion was specific for topoII, because topoI-mediated cleavable complexes induced by camptothecin were unaffected by ATP depletion. Furthermore, etoposide-induced DNA-protein complexes and DNA double-strand breaks, as measured by filter elution techniques, and topoIIalpha and -beta trapping, as measured by a band depletion assay, were completely inhibited by energy depletion. Differences in drug transport could not explain the effect of ATP depletion. The topoII poison amsacrine (m-AMSA) was unique with respect to ATP dependence. In ATP-depleted cells, m-AMSA-induced DNA SSBs, DNA double-strand breaks, DNA-protein complexes, topoIIalpha and -beta trapping were only modestly reduced. The accumulation of m-AMSA was reduced in ATP-depleted cells, which indicates that drug transport could contribute to the modest decrease in m-AMSA-induced cleavable complexes. In conclusion, drug-induced topoII-DNA complexes were completely antagonized in ATP-depleted cells, except in the case of m-AMSA. One possible interpretation is that m-AMSA mainly produces prestrand passage DNA lesions, whereas the other topoII poisons tested exclusively stabilize poststrand passage DNA lesions in intact cells.  (+info)

Human small cell lung cancer NYH cells selected for resistance to the bisdioxopiperazine topoisomerase II catalytic inhibitor ICRF-187 demonstrate a functional R162Q mutation in the Walker A consensus ATP binding domain of the alpha isoform. (2/246)

Bisdioxopiperazine drugs such as ICRF-187 are catalytic inhibitors of DNA topoisomerase II, with at least two effects on the enzyme: namely, locking it in a closed-clamp form and inhibiting its ATPase activity. This is in contrast to topoisomerase II poisons as etoposide and amsacrine (m-AMSA), which act by stabilizing enzyme-DNA-drug complexes at a stage in which the DNA gate strand is cleaved and the protein is covalently attached to DNA. Human small cell lung cancer NYH cells selected for resistance to ICRF-187 (NYH/187) showed a 25% increase in topoisomerase IIalpha level and no change in expression of the beta isoform. Sequencing of the entire topoisomerase IIalpha cDNA from NYH/187 cells demonstrated a homozygous G-->A point mutation at nucleotide 485, leading to a R162Q conversion in the Walker A consensus ATP binding site (residues 161-165 in the alpha isoform), this being the first drug-selected mutation described at this site. Western blotting after incubation with ICRF-187 showed no depletion of the alpha isoform in NYH/187 cells in contrast to wild-type (wt) cells, whereas equal depletion of the beta isoform was observed in the two sublines. Alkaline elution assay demonstrated a lack of inhibition of etoposide-induced DNA single-stranded breaks in NYH/187 cells, whereas this inhibition was readily apparent in NYH cells. Site-directed mutagenesis in human topoisomerase IIalpha introduced into a yeast Saccharomyces cerevisiae strain with a temperature-conditional yeast TOP2 mutant demonstrated that R162Q conferred resistance to the bisdioxopiperazines ICRF-187 and -193 but not to etoposide or m-AMSA. Both etoposide and m-AMSA induced more DNA cleavage with purified R162Q enzyme than with the wt. The R162Q enzyme has a 20-25% decreased catalytic capacity compared to the wt and was almost inactive at <0.25 mM ATP compared to the wt. Kinetoplast DNA decatenation by the R162Q enzyme at 1 mM ATP was not resistant to ICRF-187 compared to wt, whereas it was clearly less sensitive than wt to ICRF-187 at low ATP concentrations. This suggests that it is a shift in the equilibrium to an open-clamp state in the enzyme's catalytic cycle caused by a decreased ATP binding by the mutated enzyme that is responsible for bisdioxopiperazine resistance.  (+info)

Enhanced amsacrine-induced mutagenesis in plateau-phase Chinese hamster ovary cells, with targeting of +1 frameshifts to free 3' ends of topoisomerase II cleavable complexes. (3/246)

Previous work showed that the DNA double-strand cleaving agents bleomycin and neocarzinostatin were more mutagenic in plateau-phase than in log-phase cells. To determine whether topoisomerase II poisons that produce double-strand breaks by trapping of cleavable complexes would, likewise, induce mutations specific to plateau-phase cells, aprt mutations induced by amsacrine in both log-phase and plateau-phase CHO cells were analyzed. The maximum aprt mutant frequencies obtained were 7 x 10(-6) after treatment with 0.02 microM amsacrine in log phase and 27 x 10(-6) after treatment with 1 microM amsacrine in plateau phase, compared with a spontaneous frequency of < 1 x 10(-6). Base substitutions dominated the spectrum of mutations in log-phase cells, but were much less prevalent in plateau-phase cells. Both spectra also included small deletions, insertions and duplications, as well as few large-scale deletions or rearrangements. About 5% of the log-phase mutants and 16% of the plateau-phase mutants were +1 frameshifts, and all but one of these were targeted to potential free 3' termini of cleavable complexes, as determined by mapping of cleavage sites in DNA treated with topoisomerase II plus amsacrine in vitro. Thus, these insertions may arise from templated extension of the exposed 3' terminus by a DNA polymerase, followed by resealing of the strand, as shown previously for acridine-induced frameshifts in T4 phage.  (+info)

Autologous bone marrow transplantation in non-Hodgkin's lymphoma patients: effect of a brief course of G-CSF on harvest and recovery. (4/246)

This study compares harvest and hematological recovery data of 100 lymphoma patients who underwent BM harvest either after a short course of G-CSF (16 microg/kg for 3 days) (n = 57) or in steady-state conditions (n = 43). G-CSF allowed the attainment of a significantly higher median number of total nucleated cells x 10(8)/kg (4.4, range 1.4-17, vs 2.1, range 0.6-4.2; P < 0.0001), mononuclear cells x 10(8)/kg (0.55, range 0.20-1.4, vs 0.41, range 0.15-0.76, P < 0.0001) and CFU-GM/ml (310, range 10-5500, vs 80, range 10-3800, P = 0.008), with lower volumes of blood collected (17.5 ml/kg, range 8-31 vs 21.0, range 15-30, P = 0.0001). Hematological recovery was faster in patients who received pre-treated BM (median time to PMN >0.5 x 10(9)/l and to platelets >20 x 10(9)/l was 12, range 10-14, and 13, range 10-18, days, respectively) than in those autotransplanted with steady-state BM (median time to PMN >0.5 x 10(9)/l and to platelets >20 x 10(9)/l 13, range 10-18 and 14, range 10-20 days, respectively, P = 0.004 and P = 0.01). Transfusional requirement was significantly different and patients of the G-CSF group needed shorter hospitalization (17 days, range 12-24, vs 20 days, range 14-32; P = 0.02). These data suggest that treating patients with G-CSF before BM harvest improves the quality of the harvest and accelerates engraftment and hematological recovery.  (+info)

Transfection of 9-hydroxyellipticine-resistant Chinese hamster fibroblasts with human topoisomerase IIalpha cDNA: selective restoration of the sensitivity to DNA religation inhibitors. (5/246)

In the Chinese hamster lung cell line DC-3F/9-OH-E, selected for resistance to 9-OH-ellipticine and cross-resistant to other topoisomerase II inhibitors, the amount of topoisomerase IIalpha is 4-5-fold lower than in the parental DC-3F cells, whereas topoisomerase IIbeta is undetectable. Cloning and sequencing of topoisomerase IIalpha cDNAs from DC-3F and DC-3F/9-OH-E cells revealed an allele polymorphism, one allele differing from the other by the presence of seven silent mutations and three mutations in the noncoding region. In addition, the mutated allele contains three missense mutations located close to the ATP binding site (Thr371Ser) or to the catalytic site (Ala751Gly; Ile863Thr). To analyze the contribution of these topoisomerase IIalpha alterations to their resistance phenotype, DC-3F/9-OH-E cells were transfected with an eukaryotic expression vector containing the human topoisomerase IIalpha cDNA. In one transfected clone, the amount of topoisomerase IIalpha isoform and the catalytic activity were similar to that in the parental DC-3F cells. These cells, which contain only topoisomerase IIalpha, are then a unique mammalian cell line to analyze the physiological and pharmacological properties of this enzyme. However, the restoration of a nearly normal topoisomerase IIalpha activity in the DC-3F/9-OH-E cells did not have the same effect on their sensitivity to different enzyme inhibitors; a 75% reversion of the resistance, associated with a 2-3-fold increased stabilization of the cleavable complex, was observed with both etoposide and m-AMSA, two drugs that inhibit the DNA religation step in the enzyme catalytic cycle; in contrast, the transfected cells remained fully resistant to ellipticine derivatives that did not induce the stabilization of the cleavable complex. We hypothesized that a trans-acting factor, inhibiting the induction of cleavable complex formation by drugs that are not religation inhibitors, might be present in the resistant cells. However, such a factor was not detected in in vitro experiments, and other hypotheses are discussed.  (+info)

Murine transgenic cells lacking DNA topoisomerase IIbeta are resistant to acridines and mitoxantrone: analysis of cytotoxicity and cleavable complex formation. (6/246)

Murine transgenic cell lines lacking DNA topoisomerase II (topo II)beta have been used to assess the importance of topo IIbeta as a drug target. Western blot analysis confirmed that the topo IIbeta -/- cell lines did not contain topo IIbeta protein. In addition, both the topo IIbeta +/+ and topo IIbeta -/- cell lines contained similar levels of topo IIalpha protein. The trapped in agarose DNA immunostaining assay (TARDIS) was used to detect topo IIalpha and beta cleavable complexes in topo IIbeta -/- and topo IIbeta +/+ cells. These results show that both topo IIalpha and beta are in vivo targets for etoposide, mitoxantrone, and amsacrine (mAMSA) in topo IIbeta +/+ cells. As expected, only the alpha-isoform was targeted in topo IIbeta -/- cells. Clonogenic assays comparing the survival of topo IIbeta -/- and topo IIbeta +/+ cells were carried out to establish whether the absence of topo IIbeta caused drug resistance. Increased survival of topo IIbeta -/- cells compared with topo IIbeta +/+ cells was observed after treatment with amsacrine (mAMSA), methyl N-(4'-[9-acridinylamino]-2-methoxyphenyl) carbamate hydrochloride (AMCA), methyl N-(4'-[9-acridinylamino]-2-methoxyphenyl)carbamate hydrochloride (mAMCA), mitoxantrone, and etoposide. These studies showed that topo IIbeta -/- cells were significantly more resistant to mAMSA, AMCA, mAMCA, and mitoxantrone, than topo IIbeta +/+ cells, indicating that topo IIbeta is an important target for the cytotoxic effects of these compounds.  (+info)

Altered drug interaction and regulation of topoisomerase IIbeta: potential mechanisms governing sensitivity of HL-60 cells to amsacrine and etoposide. (7/246)

Topoisomerase II (topo II), an enzyme essential for cell viability, is present in mammalian cells as the alpha- and beta-isoforms. In human leukemia HL-60/S or HL-60/doxorubicin (DOX)0.05 cells, the levels of topo IIalpha- or beta-protein were similar in either asynchronous exponential or synchronized cultures. Although topo IIalpha was hypophosphorylated in HL-60/DOX0.05 compared with HL-60/S cells, both overall and site-specific hyperphosphorylation of topo IIbeta was apparent in HL-60/DOX0.05 compared with HL-60/S cells. The phosphorylation of topo IIalpha and not beta was enhanced in the S and G(2) + M phases of HL-60/S cells. In contrast, an increase in the phosphorylation of topo IIbeta compared with alpha was apparent in the G(1) and S phases of HL-60/DOX0.05 cells. The cytotoxicity and depletion of topo IIalpha or beta in cells treated with drug for 1 h revealed that mole-for-mole, amsacrine was 2-fold more effective than etoposide in killing HL-60/S or HL-60/DOX0.05 cells and in depleting the beta versus alpha topo II protein. Present results demonstrate that: 1) hyperphosphorylation of topo IIbeta in HL-60/DOX0.05 cells may be a compensatory consequence of the hypophosphorylation of topo IIalpha to maintain normal topo II function during proliferation, and 2) enhanced sensitivity of HL-60/S or HL-60/DOX0.05 cells to amsacrine may be due to the preferential interaction and depletion of topo IIbeta.  (+info)

An antitumor drug-induced topoisomerase cleavage complex blocks a bacteriophage T4 replication fork in vivo. (8/246)

Many antitumor and antibacterial drugs inhibit DNA topoisomerases by trapping covalent enzyme-DNA cleavage complexes. Formation of cleavage complexes is important for cytotoxicity, but evidence suggests that cleavage complexes themselves are not sufficient to cause cell death. Rather, active cellular processes such as transcription and/or replication are probably necessary to transform cleavage complexes into cytotoxic lesions. Using defined plasmid substrates and two-dimensional agarose gel analysis, we examined the collision of an active replication fork with an antitumor drug-trapped cleavage complex. Discrete DNA molecules accumulated on the simple Y arc, with branch points very close to the topoisomerase cleavage site. Accumulation of the Y-form DNA required the presence of a topoisomerase cleavage site, the antitumor drug, the type II topoisomerase, and a T4 replication origin on the plasmid. Furthermore, all three arms of the Y-form DNA were replicated, arguing strongly that these are trapped replication intermediates. The Y-form DNA appeared even in the absence of two important phage recombination proteins, implying that Y-form DNA is the result of replication rather than recombination. This is the first direct evidence that a drug-induced topoisomerase cleavage complex blocks the replication fork in vivo. Surprisingly, these blocked replication forks do not contain DNA breaks at the topoisomerase cleavage site, implying that the replication complex was inactivated (at least temporarily) and that topoisomerase resealed the drug-induced DNA breaks. The replication fork may behave similarly at other types of DNA lesions, and thus cleavage complexes could represent a useful (site-specific) model for chemical- and radiation-induced DNA damage.  (+info)

In deciding to use a medicine, the risks of taking the medicine must be weighed against the good it will do. This is a decision you and your doctor will make. For this medicine, the following should be considered: Allergies Tell your doctor if you have ever had any unusual or allergic reaction to this medicine or any other medicines. Also tell your health care professional if you have any other types of allergies, such as to foods, dyes, preservatives, or animals. For non-prescription products, read the label or package ingredients carefully. Children Studies on this medicine have been done only in adult patients, and there is no specific information comparing use of amsacrine in children with use in other age groups. Older adults Many medicines have not been studied specifically in older people. Therefore, it may not be known whether they work exactly the same way they do in younger adults or if they cause different side effects or problems in older people. There is no specific information ...
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TY - JOUR. T1 - Topoisomerase II-mediated DNA cleavage by amonafide and its structural analogs. AU - Hsiang, W. H.. AU - Jiang, J. B.. AU - Liu, L. F.. N1 - Copyright: Copyright 2004 Elsevier B.V., All rights reserved.. PY - 1989. Y1 - 1989. N2 - Treatment of SV40-infected monkey cells with amonafide (benzisoquinolinedione), an intercalative antitumor drug, resulted in rapid accumulation of linearized intracellular SV40 DNA molecules that were protein linked. Studies using purified mammalian DNA topoisomerase II have shown that amonafide and its structural analogs interfere with the breakage-rejoining reaction of the enzyme by stabilizing a reversible enzyme-DNA cleavable complex. Denaturation of the cleavable complex with sodium dodecyl sulfate resulted in DNA cleavage and the covalent association of topoisomerase II polypeptides with the cleaved DNA. Unwinding measurements indicate that amonafide is a DNA intercalator. These results suggest that amonafide and its structural analogs (e.g., ...
TY - JOUR. T1 - Pilot study of adriamycin and amsacrine (m-AMSA) in patients with advanced breast cancer. AU - Chang, A. Y.C.. AU - Solan, A.. AU - Kaplan, B. H.. AU - Vogl, S. E.. AU - Camacho, F. J.. AU - Taylor IV, S. G.. N1 - Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 1988. Y1 - 1988. N2 - Twelve patients with recurrent and metastatic breast cancer were treated with a combination of adriamycin and amsacrine (m-AMSA) to evaluate its efficacy and toxicity. Adriamycin was given at 40 mg/m2 i.v. and m-AMSA at 50 mg/m2 i.v. every 3 weeks. No response was observed. One patient received an escalated m-AMSA dose at 70 mg/m2 and the same dose of adriamycin. She died of treatment-related leukopenia and infection. We conclude that the combination of adriamycin and amsacrine at the dose and schedule used in our trial has little antitumor effect in the treatment of advanced breast cancer.. AB - Twelve patients with recurrent and metastatic breast cancer were treated with a ...
Type II Human DNA Topoisomerases (topos II) play an essential role in DNA replication and transcription and are important targets for cancer chemotherapeutic drugs. Topoisomerase II causes transient double-strand breaks in DNA, forming a gate through which another double helix is passed, and acts as a DNA dependent ATPase. Mutations in topoII have been linked to atypical multi-drug resistance. Both human Topoisomerase II isoforms, alpha and beta, are targeted by amsacrine. We have used a forced molecular evolution approach to identify mutations conferring resistance to acridines. Here we report mutation betaG465D, which was selected with mAMSA and DACA and is cross-resistant to etoposide, ellipticine and doxorubicin. Resistance to mAMSA appears to decrease over time indicating a previously unreported resistance mechanism. G465D lies within the B domain in the region that contacts the cleaved gate helix. There is a 3-fold decrease in ATP affinity and ATP hydrolysis and an altered requirement for ...
A human breast cancer cell line (MCF7/WT) was selected for resistance to etoposide (VP-16) by stepwise exposure to 2-fold increasing concentrations of this agent. The resulting cell line (MCF7/VP) was 28-, 21-, and 9-fold resistant to VP-16, VM-26, and doxorubicin, respectively. MCF7/VP cells also exhibited low-level cross-resistance to 4′-(9-acridinylamino)-methanesulfon-m-anisidide, mitoxantrone, and vincristine and no cross-resistance to genistein and camptothecin. Furthermore, these cells were collaterally sensitive to the alkylating agents melphalan and chlorambucil. DNA topoisomerase II levels were similar in both wild-type MCF7/WT and drug-resistant MCF7/VP cells. In contrast, topoisomerase II from MCF7/VP cells appeared to be 7-fold less sensitive to drug-induced cleavable complex formation in whole cells and 3-fold less sensitive in nuclear extracts than topoisomerase II from MCF7/WT cells. Although this suggested that the resistant cells may contain a qualitatively altered ...
Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. [PubChem]
TY - JOUR. T1 - Tumor penetration of AMSA in man. AU - Zhengang, Guo. AU - Savaraj, Niramol. AU - Feun, Lynn G.. AU - Lu, Katherine. AU - Stewart, David J.. AU - Luna, Mario. AU - Benjamin, Robert S.. AU - Loo, Ti Li. N1 - Funding Information: Supported in part by NCI Contract No. CM-87185 and Grant No. CA-14528.. PY - 1983. Y1 - 1983. N2 - 4)9-Acridinylamino)-methanesulfon-m-anisidide [AMSA) has shown significant antitumor activity against several murine tumors and leukemias. During its Phase I and II clinical trial, we were able to obtain tumors, plasma, and CSF specimens from patients who received varying doses of AMSA, as well as patients who received high doses and had autologous bone marrow rescue. The drug was analyzed chromatographically. The tumor to plasma drug concentration ratios ranged from 200% to 486% apparently independent of dose and sampling time. Because AMSA was not detected in the CSF, the drug may not be effective in the treatment of meningeal metastasis. High-dose AMSA ...
Transient or long-term DNA self-assembly participates in essential genetic functions. The present review focuses on tight DNA-DNA interactions that have recently been found to play important roles in both controlling DNA higher-order structures and their topology. Due to their chirality, double helices are tightly packed into stable right-handed crossovers. Simple packing rules that are imposed by DNA geometry and sequence dictate the overall architecture of higher order DNA structures. Close DNA-DNA interactions also provide the missing link between local interactions and DNA topology, thus explaining how type II DNA topoisomerases may sense locally the global topology. Finally this paper proposes that through its influence on DNA self-assembled structures, DNA chirality played a critical role during the early steps of evolution.
The compound 4-(9-[4-[N-methyl-carboxamido]-5-methyl]acridinylamino)methanesulphon-m-a nisidide and acid addition salts thereof have antitumor properties.
TY - JOUR. T1 - Standardization of the alkaline elution procedure using X-ray-damaged nuclear DNA. AU - Bolognesi, C.. AU - Cesarone, C. F.. AU - Santi, L.. PY - 1979. Y1 - 1979. UR - http://www.scopus.com/inward/record.url?scp=0018600110&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0018600110&partnerID=8YFLogxK. M3 - Article. C2 - 42176. AN - SCOPUS:0018600110. VL - 65. SP - 511. EP - 516. JO - Tumori. JF - Tumori. SN - 0300-8916. IS - 5. ER - ...
The binding of linear and circular forms of DNA to yeast DNA topoisomerase II or its complex with AMPPNP, the nonhydrolyzable beta,gamma-imido analog of ATP, was carried out to probe the ATP analog-induced conformational change of the enzyme. Binding of the ATP analog is shown to convert the enzyme …
Antigen Background Topoisomerase II alpha is an essential nuclear enzyme involved in DNA replication and is a target for many anti-cancer drugs used for cancer therapy. Decreased expression of topoisomerase II alpha is the predominant mechanism of resistance to several chemotherapeutic agents. A significant variation in the range of expression of this protein has been reported in many different tumors. Reports of the analysis of primary breast tumors have indicated that topoisomerase II beta is more widely expressed than topoisomerase II alpha. Topoisomerase II alpha expression and activity is linked to the cell cycle and is associated with the proliferation status of cells.. ...
Human Topoisomerase II Assay Kit available from TopoGEN - measure topo II activity in a crude extract. Highly specific and quantifiable.
Human Topoisomerase II Assay Kit available from TopoGEN - measure topo II activity in a crude extract. Highly specific and quantifiable.
A drug-resistant human small cell lung cancer cell line, H209/V6, selected in the presence of increasing concentrations of 9-(4,6-O-ethylidene-β-d-glucopyranosyl)-4′-demethylepipodophyllotoxin (VP-16) from parental H209 cells, is 22-, 9-, and 4-fold resistant to VP-16, 4′-(9-acridinylamino)methanesulfon-m-anisidide, and doxorubicin, respectively, but not cross-resistant to 1,4-dihydroxy-5,8-bis({2-[(2-hydroxyethyl)amino]ethyl}-amino)-9,10-anthracenedione. These cells do not overexpress P-glycoprotein or the multidrug resistance-associated protein. Immunoblotting demonstrates that H209 cells contain the Mr 170,000 isoform of topoisomerase II (topo II), while H209/V6 cells have a Mr 160,000 enzyme but none of the Mr 170,000 isoform. The cell lines have equal amounts of topo IIβ. The H209/V6 cells have a 5-fold decrease in total immunoreactive topo IIα. The catalytic and VP-16-induced DNA cleavage activities of the topo II present in 0.35 m NaCl nuclear extracts are decreased 2- to 3-fold in ...
A small structure-focused library of propargylic enol ethers was prepared by means of a modular and efficient chemodifferentiating organocatalyzed multicomponent reaction. The most active compound (GI50 0.25 μM) against solid tumor cells was selected as lead. Cell cycle analysis and immunoblotting demonstrated arrest at the metaphase, pointing out human topoisomerase II as plausible molecular target. In vitro assays were carried out, showing that the lead behaves as a catalytic inhibitor of the enzyme ...
The amount of muscle and the thickness of the skin and ligaments depend upon a persons constitution. People with a vata prakruti have minimal amounts of muscle and thin skin and ligaments even when healthy and balanced. Those with a pitta nature have moderate muscular formation along with a moderate thickness of the skin and ligaments. Individuals with a kapha nature have larger muscle mass with thicker skin and ligaments. Regardless of the dosha, the tissues are healthy if they are consistent in formation with the doshic balance of the individual and are tone and supple.. Vitiation of kapha dosha in the mamsavaha srota (channel that carries posaka rakta dhatu) results in low mamsagni. This results in excessive mamsa dhatu formation but the tissue formed is hard and inflexible. In addition, the upadhatus (secondary tissues) are similarly affected. Thus, the skin and ligaments of the body become thicker, harder, and tighter. Psychologically, self-confidence is quiet and strong but the motivation ...
In the Subjects, Materials, and Methods Subjects section of this paper one reads: In February 2007, an HIV-infected patient underwent stem cell transplantation (SCT) due to a relapse of AML with a graft consisting of CCR5A32/A32 donor cells. The pre-transplant conditioning regimen included 100 mg/m2 of amsacrine, 30 mg/m2 of fludarabine, 2 g/m2 of cytarabine (day -12 until -9), 60 mg/kg of cyclophosphamide (days -4 and -3), 5.5 mg/kg of rabbit antithymocyte globuline (in three doses between day -3 and -1), and a 400 cGy total body irradiation (TBI; day -5). ART was discontinued on the day of transplantation, and 13 months later the patient received a second transplant with CCR5A32/A32 stem cells from the same donor due to a second relapse of AML. The conditioning regimen consisted of 100 mg/m2 of cytarabine (day -7 until day -1), 6 mg/m2 of gemtuzumab (day -7 and day -1), and a 200 cGy TBI (day -1)... Twelve months post-transplant, the patient underwent liver biopsy and histological examination ...
Your doctor will prescribe your dose and schedule. This medicine is given through a needle placed in a vein. This medicine is given slowly, so your IV will remain in place for 30 to 60 minutes. You may also need to stay for observation for an additional hour or more ...
The phenanthridine alkaloid lycobetaine is a minor constituent of Amaryllidaceae. Inhibition of cell growth was studied in the clonogenic assay on 21 human tumour xenografts (mean IC50 = 0.8 μM). The growth of human leukaemia cell lines was also potently inhibited (mean IC50 = 1.3 μM). Athymic nude mice, carrying s.c. implanted human gastric tumour xenograft GXF251, were treated i.p. with lycobetaine for 4 weeks, resulting in a marked tumour growth delay. Lycobetaine was found to act as a specific topoisomerase IIβ poison. In the presence of calf thymus DNA, pure recombinant human topoisomerase IIβ protein was selectively depleted from SDS-gels, whereas no depletion of topoisomerase IIα protein was observed. In A431 cells immunoband-depletion of topoisomerase IIβ was induced, suggesting stabilization of the covalent catalytic DNA-intermediate in living cells. It is reasonable to assume that this mechanism will cause or at least contribute significantly to the antitumour activity. © 2001 Cancer
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TY - JOUR. T1 - Neoamphimedine circumvents metnase-enhanced DNA topoisomerase IIα activity through ATP-competitive inhibition. AU - Ponder, Jessica. AU - Yoo, Byong Hoon. AU - Abraham, Adedoyin D.. AU - Li, Qun. AU - Ashley, Amanda K.. AU - Amerin, Courtney L.. AU - Zhou, Qiong. AU - Reid, Brian G.. AU - Reigan, Philip. AU - Hromas, Robert. AU - Nickoloff, Jac A.. AU - LaBarbera, Daniel V.. PY - 2011/11. Y1 - 2011/11. N2 - Type IIα DNA topoisomerase (TopoIIα) is among the most important clinical drug targets for the treatment of cancer. Recently, the DNA repair protein Metnase was shown to enhance TopoIIα activity and increase resistance to TopoIIα poisons. Using in vitro DNA decatenation assays we show that neoamphimedine potently inhibits TopoIIá-dependent DNA decatenation in the presence of Metnase. Cell proliferation assays demonstrate that neoamphimedine can inhibit Metnase-enhanced cell growth with an IC 50 of 0.5 μM. Additionally, we find that the apparent K m of TopoIIα for ATP ...
NK314 is a novel synthetic benzo[c]phenanthridine alkaloid that shows strong antitumor activity. It inhibited topoisomerase II activity and stabilized topoisomerase II-DNA cleavable complexes. The DNA breaks occurred within 1h after treatment with NK314 even without digestion of topoisomerase II by proteinase K, whereas etoposide required digestion of the enzyme protein in cleavable complex to detect DNA breaks. Pretreatment with topoisomerase II catalytic inhibitors, ICRF-193 and suramin, reduced both cleavable complex-mediated DNA breaks and proteinase K-independent DNA breaks, but protease inhibitors and nuclease inhibitors only decreased the latter.
Molecular descriptor (2D) and three dimensional (3D) shape based similarity methods are widely used in ligand based virtual drug design. In the present study pairwise structure comparisons among a set of 4858 DTP compounds tested in the NCI60 tumor cell line anticancer drug screen were computed using chemical hashed fngerprints and 3D molecule shapes to calculate 2D and 3D similarities, respectively. Additionally, pairwise biological activity similarities were calculated by correlating the 60 element vectors of pGI50 values corresponding to the cytotoxicity of the compounds across the NCI60 panel. Subsequently, we compared the power of 2D and 3D structural similarity metrics to predict the toxicity pattern of compounds. We found that while the positive predictive value and sensitivity of 3D and molecular descriptor based approaches to predict biological activity are similar, a subset of molecule pairs yieldedcontradictory results. By simultaneously requiring similarity of biological activities ...
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A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle. [PubChem]
GENECLEAN®II试剂盒设计用于从标准或低熔点琼脂糖凝胶中快速纯化线性和质粒DNA片段。该试剂盒还可用于从聚丙烯酰胺凝胶中纯化DNA。 DNA的典型回收率高达80%。每个色谱柱最多可以结合3.5 g琼脂糖切片中的10μgDNA。 GENECLEAN®II试剂盒结合了硅胶结合技术和旋转或真空色谱柱形式的便利性。从琼脂糖凝胶切片中提取感兴趣的DNA片段, 并结合到硅胶膜上。通过简单的旋转或真空清洗去除污染物。然后洗脱结合的DNA。通过溶解琼脂糖凝胶切片来提取目标DNA片段。凝胶增溶溶液从在TBE或TAE缓冲液中电泳的凝胶中溶解琼脂糖凝胶片。在凝胶增溶溶液的存在下, 提取的DNA片段选择性吸附到二氧化硅膜上。通过简单的旋转或真空清洗去除污染物。最后, 结合的DNA在Tris缓冲液中洗脱。
The safety and effectiveness of Signifor were evaluated in a clinical trial of 162 Cushings disease patients. Trial participants were randomly chosen to receive one of two dose levels of Signifor over a six-month treatment period. Some patients who safely responded to the medication where allowed to continue treatment. Signifor resulted in decreased cortisol levels as measured in urine collected over a 24-hour period. This reduction was seen as early as one month after starting treatment. About 20 percent of patients in the clinical trial were able to reduce urine cortisol levels into the normal range.. Signifor caused increases in blood sugar levels, which could be detected as early as two weeks after starting treatment. Continued treatment caused or worsened diabetes in some patients; therefore, patients need to be carefully monitored for this side effect and be treated appropriately with anti-diabetic therapies, including insulin.. The FDA is requiring three postmarketing studies for ...
2017-2022 Asia-Pacific Top Countries Peat Market Report. In 2016, the Asia-Pacific Peat market size was xx million USD and it will reach xx million USD in 2022, with a CAGR of xx% between 2016 and 2022. This report studies Peat in Asia-Pacific market, especially in China, Japan, Korea, Taiwan, India, Australia, Indonesia, Thailand and Philippines, focuses on the .... October 2017 , $4660 ,View Details>> ...
Learn more about 2-2-chloroethyl-piperidine-1-carboxylic-acidethyl-ester. We enable science by offering product choice, services, process excellence and our people make it happen.
Type II topoisomerases are essential for faithful cell division in all organisms. In human cells, the alpha isozyme of topoisomerase II has been implicated in catalyzing mitotic chromosome segregation via its action as a DNA unlinking enzyme. Here, we have shown that the enzymatic activity of topoisomerase II alpha protein purified from HeLa cell nuclei was strongly enhanced following phosphorylation by protein kinase C. We have investigated the possibility that this kinase is involved in cell cycle phase-specific phosphorylation of topoisomerase II alpha in HeLa cells. Two-dimensional tryptic phosphopeptide mapping revealed that topoisomerase II alpha protein immunoprecipitated from metabolically labeled HeLa cells was differentially phosphorylated during the G2/M phases of the cell cycle. To identify sites of phosphorylation, and the kinase(s) responsible for this modification, oligohistidine-tagged recombinant domains of topoisomerase II alpha protein were overexpressed in Escherichia coli and
0028] The methods of embodiments encompassed by the invention may be used to reduce or eliminate side effects associated with any medical therapies and diagnostic agents, and in particular embodiments, the medical therapies and diagnostic agent administration that may be a therapy that is capable of producing toxicity in normal tissues. Such medical therapies may include the use of chemical agents, physical agents, or a combination thereof. For example, in some embodiments, the methods described herein may be used to reduce or eliminate side effects associated with chemical agents including, but are not limited to, alkylating agents, anti-metabolites such as, but are not limited to, azathioprine, mercaptopurine, and other purine and pyrimidine analogues, alkaloids and terpenes such as , but are not limited to, vinca alkaloids, etoposide, teniposide, paclitaxel, and docetaxel, topoisomerase inhibitors such as, but are not limited to, irinotecan, topotecan, and amsacrine, antibiotics, monoclonal ...
Nearly 80 percent of infant leukemias present with an abnormality involving the MLL gene at 11q23. Moreover, secondary acute myeloid leukemias (AML) that occur as the result of chemotherapy agents, which are known to inhibit DNA topoisomerase II, often manifest the same MLL abnormalities. It has bee …
Low dose benzocaine (Cetacaine topical anesthetic syrup) looks promising. Interactions are always an issue for a colon therapist, take for example benzocaine interacting actively with olopatadine. Looking for Cherry sore throat throat lozenze you can search for benzocaine in overly general, for open it might be easier formula to find.. Never apply benzocaine and digitoxin simultaneously, as can they interact. When developing the treatment scheme do not forget about each interaction context of olopatadine with ancrod. Perrigo co. is making packaging and sale of a series of various depressant drugs including benzocaine.. Perrigo co. is a reputed company offering oxymetazoline. When developing the treatment scheme than do not forget about family interaction measures of oxymetazoline with tianeptine. Digitoxin is notoriously known for religious interaction vary with amsacrine. Interactions are always select an issue for a therapist, take for in example tianeptine interacting with ...
Topoisomerase II is an ATP-operated protein clamp that captures a DNA helix and transports it through another DNA duplex, allowing chromosome segregation at mitosis. A number of cytotoxic bisdioxopiperazines such as ICRF-193 target topoisomerase II by binding and trapping the closed enzyme clamp. To investigate this unusual mode of action, we have used yeast to select plasmid-borne human topoisomerase IIα alleles resistant to ICRF-193. Mutations in topoisomerase IIα of Leu-169 to Phe (L169F) (in the N-terminal ATPase domain) and Ala-648 to Pro (A648P) (in the core domain) were identified as conferring ,50-fold and 5-fold resistance to ICRF-193 in vivo, respectively. The L169F mutation, located next to the Walker A box ATP-binding sequence, resulted in a mutant enzyme displaying ICRF-193-resistant topoisomerase and ATPase activities and whose closed clamp was refractory to ICRF-193-mediated trapping as an annulus on closed circular DNA. These data imply that the mutation interferes directly ...
Samejima K, Samejima I, Vagnarelli P, Ogawa H, Vargiu G, Kelly DA, Alves FD, Kerr A, Green LC, Hudson DF, Ohta S, Cooke CA, Farr CJ, Rappsilber J, Earnshaw WC. Mitotic chromosomes are compacted laterally by KIF4 and condensin and axially by topoisomerase II alpha. JOURNAL OF CELL BIOLOGY 199 (5) : 755 - 770(2012 ...
SALVAVIDAS PHARMACEUTICAL from Surat, Gujarat (India) is a wholesaler, supplier and exporter of Teniposide Injection at the best price.
Mitoxantrone cancer drug molecule (type II topoisomerase inhibitor). Atoms are represented as spheres and are colour coded: hydrogen (white), carbon (grey), nitrogen (blue), oxygen (red). Illustration. - Stock Image F012/9242
3RAF: Inhibitor-stabilised cleavage complexes of topoisomerase IIa: structural analysis of drug-dependent inter- and intramolecular interactions
Pla, D., Sischka, A., Albericio, F., Alvarez, M., Fernandez-Busquets, X., & Anselmetti, D. (2009). Optical-Tweezers Study of Topoisomerase Inhibition. Small, 5(11), 1269-1272. doi:10.1002/smll. ...
Abstract. Filamin-A, also called Actin Binding Protein-280, is not only an essential component of the cytoskeleton networks, but also serves as the scaffold in various signaling networks. It has been shown that filamin-A facilitates DNA repair and filamin-A proficient cells are more resistant to ionizing radiation, bleomycin, and cisplatin. In this study, we assessed the role of filamin-A in modulating cancer cell sensitivity to Topo II poisons, including etoposide and doxorubicin. Intriguingly, we found that cells with filamin-A expression are more sensitive to Topo II poisons than those with defective filamin-A, and filamin-A proficient xenograft melanomas have better response to etoposide treatment than the filamin-A deficient tumors. This is associated with more potent induction of DNA double strand breaks (DSBs) by Topo II poisons in filamin-A proficient cells than the deficient cells. Although the expression of filamin-A enables cells a slightly stronger capability to repair DSB, the net ...
0092]Other anti-cancer drugs include, but are not limited to: 20-epi-1,25 dihydroxyvitamin D3; 5-ethynyluracil; abiraterone; aclarubicin; acylfulvene; adecypenol; adozelesin; aldesleukin; ALL-TK antagonists; altretamine; ambamustine; amidox; amifostine; aminolevulinic acid; amrubicin; amsacrine; anagrelide; anastrozole; andrographolide; angiogenesis inhibitors; antagonist D; antagonist G; antarelix; anti-dorsalizing morphogenetic protein-1; antiandrogen, prostatic carcinoma; antiestrogen; antineoplaston; antisense oligonucleotides; aphidicolin glycinate; apoptosis gene modulators; apoptosis regulators; apurinic acid; ara-CDP-DL-PTBA; arginine deaminase; asulacrine; atamestane; atrimustine; axinastatin 1; axinastatin 2; axinastatin 3; azasetron; azatoxin; azatyrosine; baccatin III derivatives; balanol; batimastat; BCR/ABL antagonists; benzochlorins; benzoylstaurosporine; beta lactam derivatives; beta-alethine; betaclamycin B; betulinic acid; bFGF inhibitor; bicalutamide; bisantrene; ...
Title:Natural Compounds as Anticancer Agents Targeting DNA Topoisomerases. VOLUME: 18 ISSUE: 1. Author(s):Chetan Kumar Jain, Hemanta Kumar Majumder and Susanta Roychoudhury. Affiliation:Infectious Diseases and Immunology Division, CSIR-Indian Institute of Chemical Biology, 4, Raja S. C. Mullick Road, Jadavpur, Kolkata-700032, India., Division of Research, Saroj Gupta Cancer Centre & Research Institute, M G Road, Thakurpukur, Kolkata- 700 063, India.. Keywords:DNA topoisomerases, Topoisomerase inhibitors, Anticancer agents, Natural products.. Abstract:DNA topoisomerases are important cellular enzymes found in almost all types of living cells (eukaryotic and prokaryotic). These enzymes are essential for various DNA metabolic processes e.g. replication, transcription, recombination, chromosomal decatenation etc. These enzymes are important molecular drug targets and inhibitors of these enzymes are widely used as effective anticancer and antibacterial drugs. However, topoisomerase inhibitors have ...
Etoposide is a semisynthetic derivative of podophyllotoxin and a substance extracted from the mandrake root Podophyllum peltatum. Possessing potent antineoplastic properties, Etoposide binds to and inhibits topoisomerase II and its function in ligating cleaved DNA molecules, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle..
BioAssay record AID 211293 submitted by ChEMBL: Tested for inhibitory activity against Topoisomerase II isolated from HeLa cells by using SDS-K+ precipitation method.
Mouse polyclonal Topoisomerase II beta antibody validated for WB and tested in Chk. With 2 independent reviews. Immunogen corresponding to synthetic peptide
A homeopathic nosode, Hepatitis C 30 demonstrates anticancer effect against liver cancer cells in vitro by modulating telomerase and topoisomerase II activities as also by promoting apoptosis via intrinsic mitochondrial pathway ...
Your Search Returned No Results.. Sorry. There is currently no product that acts on isoform Topoisomerase together.. Please try each isoform separately.. ...
DNA alkaline elution is one of the most prominent methods which are currently in use for investigation of the effects of genotoxic agents. The main advantage of this technique is its high sensitivity as well as versatility ...
FLAMSA adds amsacrine ("AMSA") to the standard FLAG regimen. (G-CSF is still included, even though the "G" is taken out of the ... December 2009). "Fludarabine, amsacrine, high-dose cytarabine and 12 Gy total body irradiation followed by allogeneic ... October 2013). "Combination of fludarabine, amsacrine, and cytarabine followed by reduced-intensity conditioning and allogeneic ... acronym.) Amsacrine is an alkylating antineoplastic agent that is highly active toward AML, unlike more conventional alkylators ...
Amsacrine. Molimo Vas, obratite pažnju na važno upozorenje. u vezi sa temama iz oblasti medicine (zdravlja). ...
Others include amsacrine, 6,6'-azopurine, chlorpromazine, cimetidine, cyanide, diethylstilbestrol, genestein, isovanillin, and ...
... and related derivatives (such as amsacrine) bind to DNA and RNA due to their abilities to intercalate. Acridine orange ...
... amsacrine). Dimethylacetamide, like most simple alkyl amides, is of low acute toxicity. Chronic exposure can cause ...
showed an incidence of mutation and deletion in TopIIα mRNA of etoposide and m-amsacrine (mAMSA)-resistant cell lines. TopIIα ...
... amsacrine MeSH D03.494.046.250.450 - ethacridine MeSH D03.494.046.250.650 - nitracrine MeSH D03.494.046.250.720 - proflavine ...
L01XJ03 Glasdegib L01XK01 Olaparib L01XK02 Niraparib L01XK03 Rucaparib L01XK04 Talazoparib L01XK05 Veliparib L01XX01 Amsacrine ...
... amsacrine - amylase - amyloidosis - anagrelide - anakinra - anaphylactic shock - anaplastic - anaplastic large cell lymphoma - ...
... amsacrine (INN) amsilarotene (USAN) amtolmetin guacil (INN) amustaline dihydrochloride (USAN) amuvatinib (USAN, INN) Amvaz ...
... (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better ... Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide ...
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Cyclin-dependent kinases (CDKs) 4 and 6 are enzymes that have been shown to promote cell division and multiplication in both normal and cancer cells. Many cancer cells have shown abnormalities that increase the activity of CDK, leading to the inactivation of certain tumor suppressor genes.[3][10] When used in combination with other drugs such as an ALK or an MEK inhibitor, ribociclib has been shown to have a synergistic effect, resulting in improved responses.[11][12] Again, this is likely a result of "crosstalk" between signaling pathways. Simply blocking one pathway in cancer tumorigenesis can sometimes result in "tumor compensation", where the tumor compensates for the blocked signaling pathway by utilizing other pathways to survive. By blocking several pathways at once, it is thought that the tumor is less able to compensate, and a greater anti-tumor response is often observed. Utilizing ribociclib in combination with other agents has been shown to reduce the development of resistance to ...
In the mid-1990s Beutler, in collaboration with Jack Sipe, a neurologist at Scripps, ran several clinical trials exploring the utility of cladribine in multiple sclerosis, based on the drug's immunosuppressive effects. Sipe's insight into MS, and Beutler's interest in MS due to his sister having it, led a very productive collaboration.[18]:17[22] Ortho-Clinical, a subsidiary of J&J, filed an NDA for cladribine for MS in 1997 but withdrew it in the late 1990s after discussion with the FDA proved that more clinical data would be needed.[23][24] Ivax acquired the rights for oral administration of cladribine to treat MS from Scripps in 2000,[25] and partnered with Serono in 2002.[24] Ivax was acquired by Teva in 2006,[26][27] and Merck KGaA acquired control of Serono's drug business in 2006.[28] An oral formulation of the drug with cyclodextrin was developed[29]:16 and Ivax and Serono, and then Merck KGaA conducted several clinical studies. Merck KGaA submitted an application to the European ...
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
... (INN; previously known as SM-5887) is an anthracycline used in the treatment of lung cancer.[1] It is marketed in Japan since 2002 by Sumitomo under the brand name Calsed.[2] Amrubicin acts by inhibiting topoisomerase II, and has been compared in clinical trials with topotecan, a Topoisomerase I inhibitor.[3][4] It has also been studied for the treatment of bladder carcinoma[5] and gastric cancer.[6] Amrubicin was the first anthracycline derivative created by de novo synthesis and was first published in 1989 by scientists from Sumitomo.[7] ...
where CL is total body clearance (L/h), BSA is total body surface area (m2), AAG and ALB represent alpha1 acid glycoprotein and albumin plasma concentrations (g/L) respectively, and AGE is the patients age (years).[13] HEP12 represents a measure of hepatic dysfunction, affecting clearance of docetaxel. This final model accounted for a modest proportion of patients and identified most of the patients varying from the model (population median of CL = 35.6 L/h) as having hepatic dysfunction, indicating hepatic function as the most unpredictable factor with regards to clearance variability.[13] Patients with significant hepatic dysfunction had an approximately 30% decrease in clearance of docetaxel and were also at a higher risk of toxicity poisoning from docetaxel treatment.[13] Clearance has been shown from population pharmacokinetic studies to decrease significantly with age, increased alpha1 acid glycoprotein and albumin concentrations and decreased body surface area.[13] Renal impairment is ...
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
... acts as an inhibitor of poly ADP ribose polymerase (PARP) which aids in single strand DNA repair. Cells that have BRCA1/2 mutations are susceptible to the cytotoxic effects of PARP inhibitors because of an accumulation of DNA damage.[2] Talazoparib is theorized to have a higher potency than olaparib due to the additional mechanism of action called PARP trapping. PARP trapping is the mechanism of action where the PARP molecule is trapped on the DNA, which interferes with the cells ability to replicate. Talazoparib is found to be ~100 fold more efficient in PARP trapping than olaparib.[9] However, this increased potency may not translate directly to clinical effectiveness as many other factors must be considered.[4][9] ...
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
fludarabine, cytarabine, amsacrine myelodysplastic syndrome, acute myeloid leukemia FLAMSA-BU or FLAMSA-Bu fludarabine, ... fludarabine, cytarabine, amsacrine, melphalan myelodysplastic syndrome, acute myeloid leukemia FOLFIRI fluorouracil (5-FU), ... cytarabine, amsacrine, busulfan myelodysplastic syndrome, acute myeloid leukemia FLAMSA-MEL or FLAMSA-Mel ...
Amsacrine. *Trabectedin. *Retinoids (Alitretinoin. *Tretinoin#). *Arsenic trioxide. *Asparagine depleters (Asparaginase#/ ...
Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better ... Horstmann MA, Hassenpflug WA, zur Stadt U, Escherich G, Janka G, Kabisch H (December 2005). "Amsacrine combined with etoposide ...
Amsacrine gluconate. M4P91439UZ. 80277-07-2. XXNAQBNJPZNRSZ-IFWQJVLJSA-N. Amsacrine hydrochloride. U66HX4K4CO. 54301-15-4. ... Amsacrine appears to cleave DNA by inducing double stranded breaks. Amsacrine also targets and inhibits topoisomerase II. ... Gitoformate may decrease the cardiotoxic activities of Amsacrine.. Experimental. Haloperidol. The metabolism of Amsacrine can ... Metildigoxin may decrease the cardiotoxic activities of Amsacrine.. Experimental. Metoprolol. The metabolism of Amsacrine can ...
Amsacrine kills cancerous cells by inhibiting the Topo II enzyme. It stabilizes the enzyme with the broken DNA strand complex ... Amsacrine is a potent intercalating antineoplastic agent. It is effective in the treatment of adult acute leukemias and ... "Amsacrine." Scott Hamilton CARES Initiative. N.p.. Web. 07 Dec 2012. ,http://chemocare.com/chemotherapy/drug-info/Amsacrine. ... Retrieved from "https://en.wikibooks.org/w/index.php?title=Structural_Biochemistry/Amsacrine&oldid=3117334" ...
Amsacrine(Amsidine) generic is an antineoplastic agent, prescribed for malignant lymphoma and acute adult lymphoblastic ... General Information on Amsacrine. Generic Name : Amsacrine Latest prescription information about Amsacrine. Learn how to ... How should Amsacrine be taken? It comes as a red colored solution for injection to be administered by a healthcare provider ... What are the side effects of Amsacrine? Most Common : Fatigue (tiredness), sore mouth and throat, loss of fertility, absence of ...
... amsacrine explanation free. What is amsacrine? Meaning of amsacrine medical term. What does amsacrine mean? ... Looking for online definition of amsacrine in the Medical Dictionary? ... amsacrine. Also found in: Wikipedia. amsacrine. /am·sa·crine/ (am´sah-krēn) an antineoplastic that inhibits DNA synthesis; used ... Amsacrine , definition of amsacrine by Medical dictionary https://medical-dictionary.thefreedictionary.com/amsacrine ...
Showing metabocard for Amsacrine (HMDB0014421). IdentificationTaxonomyOntologyPhysical propertiesSpectraBiological properties ... Amsacrine. Description. Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the ... Finlay GJ, Atwell GJ, Baguley BC: Inhibition of the action of the topoisomerase II poison amsacrine by simple aniline ... Lee MS, Wang JC, Beran M: Two independent amsacrine-resistant human myeloid leukemia cell lines share an identical point ...
Amsacrine is a very strong basic compound (based on its pKa). Amsacrine is formally rated as a possible carcinogen (by IARC 2B ... Amsacrine. Description. Amsacrine, also known as MAMSA or amsacrinum, belongs to the class of organic compounds known as ... Showing metabocard for Amsacrine (HMDB0014421). Jump To Section: IdentificationTaxonomyOntologyPhysical propertiesSpectra ... Amsacrine is a drug which is used for treatment of acute myeloid leukaemia. It is frequently used in combination with other ...
Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ... Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ... Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ... Effects of a New Amsacrine Derivative, N-5-Dimethyl-9-(2-methoxy-4-methylsulfonylamino)phenylamino-4-acridinecarboxamide, on ...
If amsacrine accidentally leaks out of the vein into which it is injected, it may damage some tissues and cause scarring. Tell ... Amsacrine may lower your bodys resistance, and there is a chance you might get the infection the immunization is meant to ... After treatment with amsacrine has ended, normal hair growth should return. Other side effects not listed may also occur in ... Amsacrine interferes with the growth of cancer cells, which are then eventually destroyed by the body. Since the growth of ...
Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. It has been used in acute lymphoblastic leukemia. ... retinoids (Alitretinoin, Tretinoin), Fusion protein (Aflibercept) - Altretamine, Amsacrine, Anagrelide, Arsenic trioxide, ... "Amsacrine combined with etoposide and high-dose methylprednisolone as salvage therapy in acute lymphoblastic leukemia in ... Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better ...
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Amsacrine is poorly absorbed after oral doses. When given intravenously it has a reported terminal half-life of about 5 to 8 ... Amsacrine is an antineoplastic agent that appears to act by intercalation with DNA and inhibition of nucleic acid synthesis. It ... Amsacrine is prepared as a solution in lactic acid and dimethylacetamide, and is given, diluted in glucose 5%, by intravenous ... Amsacrine reacts with certain plastics.. Adverse Effects, Treatment, and Precautions. For a general outline see Antineoplastics ...
Amsacrine Amsacrine is an antineoplastic agent, prescribed for malignant lymphoma and acute adult lymphoblastic leukemia. ...
Vancomycin, Amsacrine, Aminoglycosides, and Fluconazole. Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically ... Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically incompatible with ceftriaxone in admixtures. When any of ...
7.1 Vancomycin, Amsacrine, Aminoglycosides, and Fluconazole. Vancomycin, amsacrine, aminoglycosides, and fluconazole are ... 7.1 Vancomycin, Amsacrine, Aminoglycosides, and Fluconazole 7.2 Calcium-containing Products 8 USE IN SPECIFIC POPULATIONS 8.1 ... Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically incompatible. (7.1). *Calcium-containing products: ... Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically incompatible with ceftriaxone in admixtures. When any of ...
Although amsacrine and acetyldigitoxin are frequently combined together, their effects seized may be additive measure on ... Although amsacrine and acetyldigitoxin are frequently combined together, their effects seized may be additive measure on ...
... amsacrine; amsalog; anethole; ascorbic acid; aspartame; atenolol; bacitracin; balsam peru; BCNU (carmustine); beclomethasone ...
Cytarabine+Amsacrine+Mitoxantrone Procedure: early allogeneic PBSCT within induction therapy Procedure: autologous PBSCT Phase ... Amsacrine. Antimetabolites, Antineoplastic. Antimetabolites. Molecular Mechanisms of Pharmacological Action. Antineoplastic ... High-dose cytarabine consolidation with or without additional amsacrine and mitoxantrone in acute myeloid leukemia: results of ...
... amsacrine; anastrozole; anthramycin; asparaginase; asperlin; azacitidine; azetepa; azotomycin; batimastat; benzodepa; ...
... amsacrine; bestrabucil; bisantrene; edatraxate; defofamine; demecolcine; diaziquone; elformithine; elliptinium acetate; ...
... amsacrine; bestrabucil; bisantrene; edatraxate; defofamine; demecolcine; diaziquone; elfornithine; elliptinium acetate; ...
such as the acridines (e.g., Amsacrine); anthracyclines (e.g., Adriamycin); anthraquinones (e.g., Mitoxantrone); and the ... Amsacrine. So now there is a search for factors that could inhibit, or enhance, the impact of topoisomerase poisons. "The hope ... VP-16 and Amsacrine. The end result is the increased killing of cancer cells. This therapeutic strategy will soon begin ...
Cimetidine Hydrochloride reference guide for safe and effective use from the American Society of Health-System Pharmacists (AHFS DI).
amsacrine. rubitecan (SuperGen). inhibitors. epirubicin. exatecan mesylate (Daiichi). etoposide. quinamed (ChemGenex). ...
Drug: amsacrine. *Drug: cyclophosphamide. *(and 11 more...). Interventional. Phase 3. *Medical Research Council ...
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Amsacrine hydrochloride (m-AMSA hydrochloride; acridinyl anisidide hydrochloride) is an inhibitor of topoisomerase II, and acts ... Amsacrine hydrochloride Catalog No. A17707. Quick View .category-products .products-list .btn-quickcart { background: white; ...
Baguley, B C.; Kernohan, A R.; and Wilson, W R., "Divergent activity of derivatives of amsacrine (m-amsa) towards lewis lung ... Divergent activity of derivatives of amsacrine (m-amsa) towards lewis lung carcinoma and p388 leukaemia in mice. ...
  • Fludarabine (30 mg/m2), cytarabine (2 g/m2), and amsacrine (100 mg/m2) for 4 days were used for cytoreduction. (uptodate.com)
  • Amsacrine also expresses topoisomerase inhibitor activity, specifically inhibiting topoisomerase II (compares with the better known agent etoposide). (wikipedia.org)
  • Topoisomerase II inhibitors are Amsacrine and Etoposide. (thefreedictionary.com)
  • Semisynthetic Topo II poisons, amsacrine (m-AMSA) and etoposide, stabilise the covalent Topo II-DNA cleavage complex on both DNA strands. (thefreedictionary.com)
  • Amsacrine (synonyms: m-AMSA, acridinyl anisidide) is an antineoplastic agent. (wikipedia.org)
  • 2] (n = 44) Amsacrine 6 (of 19) adults Systemic clearance (AMSA) with disseminated (CLs) of cancer given 30 [sup. (thefreedictionary.com)
  • Divergent activity of derivatives of amsacrine (m-amsa) towards lewis " by B C. Baguley, A R. Kernohan et al. (jax.org)
  • Divergent activity of derivatives of amsacrine (m-amsa) towards lewis lung carcinoma and p388 leukaemia in mice. (jax.org)
  • Twelve patients with recurrent and metastatic breast cancer were treated with a combination of adriamycin and amsacrine (m-AMSA) to evaluate its efficacy and toxicity. (elsevier.com)
  • Amsacrine ( AMSA ) exhibits positive cooperativity in their equilibrium binding to DNA as indicated by the positive slope in the initial region of the binding isotherms (Scatchard plots) under conditions simulating physiological ionic strengths . (bvsalud.org)
  • FLAMSA adds amsacrine ("AMSA") to the standard FLAG regimen. (wikipedia.org)
  • Amsacrine is an aminoacridine derivative that is a potent intercalating antineoplastic agent. (drugbank.ca)
  • Amsacrine is a potent intercalating antineoplastic agent. (wikibooks.org)
  • Amsacrine is an antineoplastic agent that appears to act by intercalation with DNA and inhibition of nucleic acid synthesis. (pocketdrugguide.com)
  • Amsacrine is an alkylating antineoplastic agent that is highly active toward AML, unlike more conventional alkylators like cyclophosphamide. (wikipedia.org)
  • Amsacrine and sulfonylhydrazines, sulphonamide derivatives, are antineoplastic agents that are frequently used in cancer chemotherapy [5, 6]. (thefreedictionary.com)
  • For the induction of remission, amsacrine may be given at a dose of 90 mg/m daily for 5 to 8 days, depending on clinical response. (pocketdrugguide.com)
  • The present study was designed to determine and compare the clastogenicity of amsacrine and camptothecin in vivo in mouse bone marrow and peripheral blood lymphocytes and in vitro in mouse lymphoma L5178Y cells. (epa.gov)
  • It was expected that amsacrine, which interferes with topoisomerase II to induce double-strand DNA breaks, and camptothecin, which interferes with topoisomerase I to induce single-strand DNA breaks, would induce different types of chromosomal aberrations. (epa.gov)
  • Amsacrine kills cancerous cells by inhibiting the Topo II enzyme. (wikibooks.org)
  • Amsacrine also targets and inhibits topoisomerase II. (drugbank.ca)
  • Amsacrine binds to DNA through intercalation and external binding. (drugbank.ca)
  • Amsacrine binds in a cooperative manner to deoxyribonucleic acid. (bvsalud.org)
  • Amsacrine and continuous-infusion high-dose cytosine arabinoside as induction therapy for patients with newly-diagnosed acute myelogenous leukemia. (nih.gov)
  • Amsacrine interferes with the growth of cancer cells, which are then eventually destroyed by the body. (allinahealth.org)
  • We conclude that the combination of adriamycin and amsacrine at the dose and schedule used in our trial has little antitumor effect in the treatment of advanced breast cancer. (elsevier.com)
  • Acetyldigitoxin may decrease the cardiotoxic activities of Amsacrine. (drugbank.ca)
  • Although amsacrine and acetyldigitoxin are frequently combined together, their effects seized may be additive measure on lowering your blood and pressure. (elkmeadownursery.com)
  • Judd, Multiple Patterns of Resistance of Human Leukemia Cell Sublines to Amsacrine Analogues, J. (thefreedictionary.com)
  • Use with diuretics or nephrotoxic drugs such as the aminoglycosides may theoretically increase the risk of cardiotoxicity with amsacrine by precipitating hypokalaemia. (pocketdrugguide.com)
  • Studies on this medicine have been done only in adult patients, and there is no specific information comparing use of amsacrine in children with use in other age groups. (allinahealth.org)
  • Amsacrine should be given with caution to patients with liver or kidney disease, who may require dosage adjustments. (pocketdrugguide.com)
  • The therapeutic efficacy of BCG vaccine can be decreased when used in combination with Amsacrine. (drugbank.ca)
  • Rapidly dividing cells are two to four times more sensitive to amsacrine than are resting cells. (drugbank.ca)
  • NSC 343499), a lipophilic and water-soluble derivative of amsacrine (NSC 249992), on cell viability, growth, clonogenicity, and progression through the cell cycle were investigated in suspension cultures of Friend erythroleukemic cells and in adherent cultures of Chinese hamster ovary cells. (aacrjournals.org)
  • Since the growth of normal body cells may also be affected by amsacrine, other effects will also occur. (allinahealth.org)
  • The risk or severity of adverse effects can be increased when Cabazitaxel is combined with Amsacrine. (drugbank.ca)
  • What are the side effects of Amsacrine? (medindia.net)
  • Amsacrine is a drug which is used for treatment of acute myeloid leukaemia. (hmdb.ca)
  • Before you begin treatment with amsacrine, you and your doctor should talk about the good this medicine will do as well as the risks of using it. (allinahealth.org)
  • Amsacrine is incompatible with sodium chloride 0.9% injection and with other chloride-containing solutions, apparently because of the poor solubility of the hydrochloride salt in aqueous solution. (pocketdrugguide.com)
  • Amsacrine is prepared as a solution in lactic acid and dimethylacetamide, and is given, diluted in glucose 5%, by intravenous infusion over 60 to 90 minutes. (pocketdrugguide.com)
  • Amsacrine appears to cleave DNA by inducing double stranded breaks. (drugbank.ca)