Aclarubicin: An anthracycline produced by Streptomyces galilaeus. It has potent antineoplastic activity.Topoisomerase II Inhibitors: 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.Amsacrine: An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.Drug Antagonism: Phenomena and pharmaceutics of compounds that inhibit the function of agonists (DRUG AGONISM) and inverse agonists (DRUG INVERSE AGONISM) for a specific receptor. On their own, antagonists produce no effect by themselves to a receptor, and are said to have neither intrinsic activity nor efficacy.Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.Antibiotics, Antineoplastic: Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.DNA Topoisomerases, Type II: 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.Carcinoma, Small Cell: An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)Carcinoma, Ehrlich Tumor: A transplantable, poorly differentiated malignant tumor which appeared originally as a spontaneous breast carcinoma in a mouse. It grows in both solid and ascitic forms.Lung Neoplasms: Tumors or cancer of the LUNG.Leukemia L1210Small Cell Lung Carcinoma: A form of highly malignant lung cancer that is composed of small ovoid cells (SMALL CELL CARCINOMA).Clopenthixol: A thioxanthene with therapeutic actions similar to the phenothiazine antipsychotics. It is an antagonist at D1 and D2 dopamine receptors.Acebutolol: A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)IndiaAppendix: A worm-like blind tube extension from the CECUM.Cosmetics: Substances intended to be applied to the human body for cleansing, beautifying, promoting attractiveness, or altering the appearance without affecting the body's structure or functions. Included in this definition are skin creams, lotions, perfumes, lipsticks, fingernail polishes, eye and facial makeup preparations, permanent waves, hair colors, toothpastes, and deodorants, as well as any material intended for use as a component of a cosmetic product. (U.S. Food & Drug Administration Center for Food Safety & Applied Nutrition Office of Cosmetics Fact Sheet (web page) Feb 1995)Patents as Topic: Exclusive legal rights or privileges applied to inventions, plants, etc.Nuclear Reprogramming: 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.Epigenesis, Genetic: 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.Inventions: A novel composition, device, or process, independently conceived de novo or derived from a pre-existing model.Lower Gastrointestinal Tract: The segment of GASTROINTESTINAL TRACT that includes the small intestine below the DUODENUM, and the LARGE INTESTINE.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Fibrocystic Breast Disease: 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.Equipment Design: Methods of creating machines and devices.Magnetite Nanoparticles: Synthesized magnetic particles under 100 nanometers possessing many biomedical applications including DRUG DELIVERY SYSTEMS and CONTRAST AGENTS. The particles are usually coated with a variety of polymeric compounds.Nanoparticles: Nanometer-sized particles that are nanoscale in three dimensions. They include nanocrystaline materials; NANOCAPSULES; METAL NANOPARTICLES; DENDRIMERS, and QUANTUM DOTS. The uses of nanoparticles include DRUG DELIVERY SYSTEMS and cancer targeting and imaging.Magnetic Resonance Spectroscopy: Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).Magnetics: The study of MAGNETIC PHENOMENA.Sensitivity and Specificity: Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)Anthracyclines: Organic compounds that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.Naphthacenes: Polyacenes with four ortho-fused benzene rings in a straight linear arrangement. This group is best known for the subclass called TETRACYCLINES.Water: A clear, odorless, tasteless liquid that is essential for most animal and plant life and is an excellent solvent for many substances. The chemical formula is hydrogen oxide (H2O). (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Intellectual Property: Property, such as patents, trademarks, and copyright, that results from creative effort. The Patent and Copyright Clause (Art. 1, Sec. 8, cl. 8) of the United States Constitution provides for promoting the progress of science and useful arts by securing for limited times to authors and inventors, the exclusive right to their respective writings and discoveries. (From Black's Law Dictionary, 5th ed, p1014)Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.Commerce: The interchange of goods or commodities, especially on a large scale, between different countries or between populations within the same country. It includes trade (the buying, selling, or exchanging of commodities, whether wholesale or retail) and business (the purchase and sale of goods to make a profit). (From Random House Unabridged Dictionary, 2d ed, p411, p2005 & p283)Counterfeit Drugs: Drugs manufactured and sold with the intent to misrepresent its origin, authenticity, chemical composition, and or efficacy. Counterfeit drugs may contain inappropriate quantities of ingredients not listed on the label or package. In order to further deceive the consumer, the packaging, container, or labeling, may be inaccurate, incorrect, or fake.Investments: Use for articles on the investing of funds for income or profit.Skin Irritancy Tests: Tests or bioassays that measure the skin sensitization potential of various chemicals.Financial Management: The obtaining and management of funds for institutional needs and responsibility for fiscal affairs.Anti-Inflammatory Agents, Non-Steroidal: Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.Solubility: The ability of a substance to be dissolved, i.e. to form a solution with another substance. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.Spondylitis, Ankylosing: A chronic inflammatory condition affecting the axial joints, such as the SACROILIAC JOINT and other intervertebral or costovertebral joints. It occurs predominantly in young males and is characterized by pain and stiffness of joints (ANKYLOSIS) with inflammation at tendon insertions.Cartilage, Articular: A protective layer of firm, flexible cartilage over the articulating ends of bones. It provides a smooth surface for joint movement, protecting the ends of long bones from wear at points of contact.Diphosphonates: Organic compounds which contain P-C-P bonds, where P stands for phosphonates or phosphonic acids. These compounds affect calcium metabolism. They inhibit ectopic calcification and slow down bone resorption and bone turnover. Technetium complexes of diphosphonates have been used successfully as bone scanning agents.Databases, Pharmaceutical: Databases devoted to knowledge about PHARMACEUTICAL PRODUCTS.Pharmacological Processes: The metabolism of drugs and their mechanisms of action.Databases, Chemical: Databases devoted to knowledge about specific chemicals.Bone Density Conservation Agents: Agents that inhibit BONE RESORPTION and/or favor BONE MINERALIZATION and BONE REGENERATION. They are used to heal BONE FRACTURES and to treat METABOLIC BONE DISEASES such as OSTEOPOROSIS.Alendronate: A nonhormonal medication for the treatment of postmenopausal osteoporosis in women. This drug builds healthy bone, restoring some of the bone loss as a result of osteoporosis.Jaw Diseases
Evidence of the role of protein kinase C during aclacinomycin induction of erythroid differentiation in K562 cells. (1/93)
At subtoxic concentrations, aclacinomycin is effective in controlling erythroid differentiation of K562, a human erythroleukemic cell line. To better understand early events implicated in this process, we have used bisindolylmaleimide (GF109203X), an inhibitor with a high selectivity for protein kinase C (PKC). Our data show that GF109203X inhibits aclacinomycin effects on K562, evidenced by a strong reduction of hemoglobinized cells and a marked decrease of mRNA rates of erythroid genes. To establish firmly PKC involvement, we also verified that aclacinomycin stimulates its rapid translocation, from the cytosolic to the membrane compartment. By Western blot analysis, we also show that after short induction times, PKCalpha was the most implicated. (+info)Modifications of aclacinomycin T by aclacinomycin methyl esterase (RdmC) and aclacinomycin-10-hydroxylase (RdmB) from Streptomyces purpurascens. (2/93)
The genes rdmB and rdmC of Streptomyces purpurascens encoding aclacinomycin modifying enzymes RdmB and RdmC were expressed in Streptomyces lividans TK24. In contrast to the earlier suggestion that RdmC may be an esterase that causes the removal of the carbomethoxy group from the 10 position of aclacinomycins, RdmC functions as an aclacinomycin methyl esterase and catalyzes the removal of the methoxy group from the C-15 position of aclacinomycin T producing 15-demethoxyaclacinomycin T. RdmB acts upon C-10 of 15-demethoxyaclacinomycin T and is able to remove the carboxylic group from the C-10 position. It functions also as an aclacinomycin-10-hydroxylase being able to add a hydroxyl group at the same, C-10 position in vitro. Aclacinomycin methyl esterase was purified to apparent homogeneity from S. lividans carrying the rdmC and aclacinomycin-10-hydroxylase as a glutathione S-transferase fusion construct from Escherichia coli carrying the rdmB gene, respectively. Aclacinomycin methyl esterase functions as a monomer and aclacinomycin-10-hydroxylase as a tetramer. Aclacinomycin methyl esterase has an exceptionally high temperature stability and has an apparent K(m) for aclacinomycin T of 15.5 microM. The introduction of rdmC and rdmB in a Streptomyces galilaeus mutant HO38 produced the same modifications of aclacinomycin T in vivo as aclacinomycin methyl esterase and aclacinomycin-10-hydroxylase in vitro. (+info)Molecular cloning and disruption of a novel gene encoding UDP-glucose: tetrahydrobiopterin alpha-glucosyltransferase in the cyanobacterium Synechococcus sp. PCC 7942. (3/93)
The gene encoding UDP-glucose:tetrahydrobiopterin alpha-glucosyltransferase (BGluT) was cloned from the genomic DNA of Synechococcus sp. PCC 7942. The encoded protein consisting of 359 amino acid residues was verified in vitro and in vivo to be responsible for the synthesis of tetrahydrobiopterin (BH4)-glucoside produced in the organism. The BGluT gene is the first cloned in pteridine glycosyltransferases and also a novel one cloned so far in UDP-glycosyltransferases. The mutant cells disrupted in the BGluT gene produced only aglycosidic BH4 at a level of 8.3% of the BH4-glucoside in wild type cells and exhibited half of the wild type growth in normal photoautotrophic conditions. These results suggest that the glucosylation of BH4 is required for the maintenance of the high cellular concentration of the compound, thereby supporting the normal growth of Synechococcus sp. PCC 7942. (+info)Keratin attenuates tumor necrosis factor-induced cytotoxicity through association with TRADD. (4/93)
Keratin 8 and 18 (K8/18) are the major components of intermediate filament (IF) proteins of simple or single-layered epithelia. Recent data show that normal and malignant epithelial cells deficient in K8/18 are nearly 100 times more sensitive to tumor necrosis factor (TNF)-induced cell death. We have now identified human TNF receptor type 1 (TNFR1)-associated death domain protein (TRADD) to be the K18-interacting protein. Among IF proteins tested in two-hybrid systems, TRADD specifically bound K18 and K14, type I (acidic) keratins. The COOH-terminal region of TRADD interacted with the coil Ia of the rod domain of K18. Endogenous TRADD coimmunoprecipitated with K18, and colocalized with K8/18 filaments in human mammary epithelial cells. Overexpression of the NH2 terminus (amino acids 1-270) of K18 containing the TRADD-binding domain as well as overexpression of K8/18 in SW13 cells, which are devoid of keratins, rendered the cells more resistant to killing by TNF. We also showed that overexpressed NH2 termini of K18 and K8/18 were associated with endogenous TRADD in SW13 cells, resulting in the inhibition of caspase-8 activation. These results indicate that K18 may sequester TRADD to attenuate interactions between TRADD and activated TNFR1 and moderate TNF-induced apoptosis in simple epithelial cells. (+info)Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients. (5/93)
Proximal spinal muscular atrophy (SMA) is a common motor neuron disorder caused by mutation of the telomeric survival of motor neuron gene SMN1. The centromeric survival of motor neuron SMN2 gene is retained in all SMA patients but does not produce sufficient SMN protein to prevent the development of clinical symptoms. The SMN1 and SMN2 genes differ functionally by a single nucleotide change. This change affects the efficiency with which exon 7 is incorporated into the mRNA transcript. Thus, SMN2 produces less full-length mRNA and protein than SMN1. We have screened a library of compounds in order to identify ones that can alter the splicing pattern of the SMN2 gene. Here, we report that the compound aclarubicin increases the retention of exon 7 into the SMN2 transcript. We show that aclarubicin effectively induces incorporation of exon 7 into SMN2 transcripts from the endogenous gene in type I SMA fibroblasts as well as into transcripts from a SMN2 minigene in the motor neuron cell line NSC34. In type I fibroblasts, treatment resulted in an increase in SMN protein and gems to normal levels. Our results suggest that alteration of splicing pattern represents a new approach to modification of gene expression in disease treatment and demonstrate the feasibility of high throughput screens to detect compounds that affect the splicing pattern of a gene. (+info)Superior outcome of infant acute myeloid leukemia with intensive chemotherapy: results of the Japan Infant Leukemia Study Group. (6/93)
This study analyzed data on 35 infants with acute myeloid leukemia (AML) who were treated with intensive chemotherapy between 1995 and 1998 in Japan. The incidence of boys, younger age (< 6 months old), and hyperleukocytosis at onset was high in patients with the M4/M5 subtype (n = 23) in the French-American-British classification, compared with the non-M4/M5 subtype (n = 12). Thirteen (56%) and 16 (70%) patients with the M4/M5 subtype also showed 11q23 translocations and MLL gene rearrangements, respectively, whereas only one patient with the non-M4/M5 subtype had this rearrangement. All 35 patients were treated with the ANLL91 protocol consisting of etoposide, high-dose cytarabine, and anthracyclines. Overall survival and the event-free survival (EFS) rates at 3 years of all patients were 76% (95% confidence interval [CI], 61.3%-90.7%) and 72% (95% CI, 56.4%-87.9%), respectively. EFS showed no significant difference between 2 subgroups divided by age, gender, presence of the MLL gene rearrangements, and white blood cell count at onset; EFS in patients with the M4/M5 subtype tended to be better than those with the non-M4/M5 subtype. Although all 6 patients who underwent allogeneic stem cell transplantation (SCT) have been in complete remission, no benefit of SCT was confirmed. These findings suggest that the intensive chemotherapy with the ANLL91 protocol might have been responsible for the observed good outcome of infant AML, even without SCT. The presence of the MLL gene rearrangements or the age at onset had no impact on the outcome of infant AML. (+info)Induction of p16INK4a transcription and of cellular senescence by aclacinomycin-derivatives and cardiac glycosides. (7/93)
Stable transformants of Saos-2 cells that contain the luciferase reporter gene under the control of the human p16INK4a transcriptional regulatory region were established, and were used to identify growth-inhibiting substances from culture broths of actinomycetes and extracts of plants. Among the active substances so far identified were an aclacinomycin-derivative, cenerubin B, and a cardiac glycoside, periplocin. These substances inhibited growth of normal human fibroblasts, and induced senescent phenotypes including a flattened morphology and increased acidic beta-galactosidase activity, although the activities of their derivatives to induce p16CDKN2 and beta-galactosidase did not coincided with each other. These results suggest that the reporter system using the p16CDKN2 transcriptional regulatory region is a useful means for screening growth inhibiting substances that are potential anti-tumor agents. (+info)Characterization of mutations in aclacinomycin A-non-producing Streptomyces galilaeus strains with altered glycosylation patterns. (8/93)
In this study a set of Streptomyces galilaeus ATCC 31615 mutants was characterized, which are incapable of synthesizing some or all of the deoxyhexose sugars of aclacinomycin A. Complementation experiments with the the mutant strains H026, H038, H039, H054, H063, H065 and H075 were carried out with glycosylation genes previously derived from the wild-type S. galilaeus. Mutations in strains H038, H063 and H075 were complemented with single PCR-amplified genes. Furthermore, amplification and sequencing of the corresponding genes from the mutant strains revealed single point mutations in the sequences. First, in H038 a transition mutation in aknQ, encoding a putative dTDP-hexose 3-ketoreductase, causes an amino acid substitution from glycine to aspartate, suppressing the biosynthesis of both 2-deoxyfucose and rhodinose and thus leading to the accumulation of aclacinomycin T with rhodosamine as its only sugar. Second, in H063, which accumulates aklavinone without a sugar moiety, amino acid substitution occurs, with threonine being substituted by isoleucine in dTDP-glucose synthase, the first enzyme participating in deoxyhexose biosynthesis, encoded by aknY. Third, a nonsense mutation in aknP leads to truncated dTDP-hexose 3-dehydratase in H075, which is incapable of synthesizing rhodinose. In addition, mutants H054 and H065, which accumulate aclacinomycins without aminosugars, were complemented by a gene for an aminotransferase, aknZ. Characterization of the nature of the mutations adds to the usefulness and value of the mutants in the analysis of gene function and in the creation of novel compounds by combinatorial biosynthesis. Furthermore, these results strengthen the assignments of akn gene products and enlighten the biosynthetic pathway for deoxyhexoses. (+info)Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · Pirarubicin · Valrubicin · ...
"A gene cluster from Streptomyces galilaeus involved in glycosylation of aclarubicin". Molecular & general genetics : MGG. 264 ( ...
This group includes novobiocin, merbarone, and aclarubicin, which also have other significant mechanisms of action. The ... Other clinically used drugs in the anthracyline group are pirarubicin, aclarubicin, and mitoxantrone. The mechanisms of ...
"Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients". Human Molecular ... like sodium orthovanadate and aclarubicin. Morpholino-type antisense oligonucleotides, with the same cellular target as ...
... is a class of prescription drugs in India appearing as an appendix to the Drugs and Cosmetics Rules, 1945 introduced in 1945. These are drugs which cannot be purchased over the counter without the prescription of a qualified doctor.The manufacture and sale of all drugs are covered under the Drugs and Cosmetics Act and Rules. It is revised at times based on the advice of the Drugs Technical Advisory Board, part of the Central Drugs Standard Control Organization[1] in the Ministry of Health and Family Welfare. The most recent schedule H (2006) lists 536 drugs from abacavir to zuclopenthixol.[2] However, enforcement of Schedule H laws in India is lax, compared to the more restrictive Schedule X, for which a mandatory documentation trail must be maintained.[3] ...
... aclarubicin, tomaymycin, sibiromycin, and mazethramycin. Derivatives of Streptomycetes isolate migrastatin, including ...
... aclarubicin MeSH D09.408.051.059.200 --- daunorubicin MeSH D09.408.051.059.200.150 --- carubicin MeSH D09.408.051.059.200.175 ...
L01DA01 Dactinomycin L01DB01 Doxorubicin L01DB02 Daunorubicin L01DB03 Epirubicin L01DB04 Aclarubicin L01DB05 Zorubicin L01DB06 ...
... aclarubicin (INN) aclatonium napadisilate (INN) aclidinium bromide (USAN, INN) Aclovate acolbifene (USAN) acodazole (INN) ...
... aclarubicin MeSH D04.615.562.050.200 --- daunorubicin MeSH D04.615.562.050.200.150 --- carubicin MeSH D04.615.562.050.200.175 ...
... (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. Soil bacteria ... October 1991). "Antagonistic effect of aclarubicin on daunorubicin-induced cytotoxicity in human small cell lung cancer cells: ... Streptomyces galilaeus can produce aclarubicin. It can induce histone eviction from chromatin upon intercalation. CID 451415 ...
... and aclarubicin.[49] Morpholino-type antisense oligonucleotides, with the same cellular target as nusinersen, remain a subject ... "Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients". Human Molecular ...
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InChI=1S/C55H83N17O21S3/c1-20-33(69-46(72-44(20)58)25(12-31(57)76)64-13-24(56)45(59)82)50(86)71-35(41(26-14-61-19-65-26)91-54-43(39(80)37(78)29(15-73)90-54)92-53-40(81)42(93-55(60)88)38(79)30(16-74)89-53)51(87)66-22(3)36(77)21(2)47(83)70-34(23(4)75)49(85)63-10-8-32-67-28(18-94-32)52-68-27(17-95-52)48(84)62-9-7-11-96(5)6/h14,17-19,21-25,29-30,34-43,53-54,64,73-75,77-81H,7-13,15-16,56H2,1-6H3,(H13-,57,58,59,60,61,62,63,65,66,69,70,71,72,76,82,83,84,85,86,87,88)/p+1/t21-,22+,23+,24-,25-,29-,30+,34-,35-,36-,37+,38+,39-,40-,41?,42-,43-,53+,54-/m0/s1 ...
... is a drug used in chemotherapy. It is a semi-synthetic camptothecin analogue indicated for Small Cell Lung Cancer and Ovarian Cancer, approved in South Korea under the trade name Camtobell(R), presented in 2 mg vials for injection.[1] The drug is marketed by ChongKunDang Pharmaceuticals [2] since 2003 [3] Belotecan blocks topoisomerase I with a pIC50 of 6.56,[4] stabilizing the cleavable complex of topoisomerase I-DNA, which inhibits the religation of single-stranded DNA breaks generated by topoisomerase I; lethal double-stranded DNA breaks occur when the topoisomerase I-DNA complex is encountered by the DNA replication machinery, DNA replication is disrupted, and the tumor cell undergoes apoptosis. Topoisomerase I is an enzyme that mediates reversible single-strand breaks in DNA during DNA replication. ...
... was first reported in the scientific literature in 1994, by a team of researchers from Fujisawa Pharmaceutical Company (now Astellas Pharma) in Tsukuba, Japan, who isolated it in a culture of Chromobacterium violaceum from a soil sample obtained in Yamagata Prefecture.[3] It was found to have little to no antibacterial activity, but was potently cytotoxic against several human cancer cell lines, with no effect on normal cells; studies on mice later found it to have antitumor activity in vivo as well.[3]. The first total synthesis of romidepsin was accomplished by Harvard researchers and published in 1996.[4] Its mechanism of action was elucidated in 1998, when researchers from Fujisawa and the University of Tokyo found it to be a histone deacetylase inhibitor with effects similar to those of trichostatin A.[5]. ...
Nitrogen mustards arose from the derivatization of sulphur mustard gas after military personnel exposed to it during World War I were observed to have decreased white blood cell counts.[15] Since the sulphur mustard gas was too toxic to be used in humans, Gilman hypothesized that by reducing the electrophilicity of the agent, which made it highly chemically reactive towards electron-rich groups, then less toxic drugs could be obtained. To this end, he made analogues that were less electrophilic by exchanging the sulphur with a nitrogen, leading to the nitrogen mustards.[16] With an acceptable therapeutic index in humans, nitrogen mustards were first introduced in the clinic in 1946.[17] Aliphatic mustards were developed first, such as mechlorethamine hydrochloride (mustine hydrochloride) which is still used in the clinic today. In the 1950s, aromatic mustards like chlorambucil were introduced as less toxic alkylating agents than the aliphatic nitrogen mustards, proving to be less electrophilic ...
The decision to start cladribine in MS depends on the degree of disease activity (as measured by number of relapses in the past year and T1 gadolinium-enhancing lesions on MRI), the failure of previous disease-modifying therapies, the potential risks and benefits and patient choice. In the UK, the National Institute for Clinical Excellence (NICE) recommends cladribine for treating highly active RRMS in adults if the persons has: rapidly evolving severe relapsing-remitting multiple sclerosis, that is, at least 2 relapses in the previous year and at least 1 T1 gadolinium-enhancing lesion at baseline MRI or relapsing-remitting multiple sclerosis that has responded inadequately to treatment with disease-modifying therapy, defined as 1 relapse in the previous year and MRI evidence of disease activity.[40] People with MS require counselling on the intended benefits of cladribine in reducing the risk of relapse and disease progression, versus the risk of adverse effects such as headaches, nausea and ...
There are several ways molecules (in this case, also known as ligands) can interact with DNA. Ligands may interact with DNA by covalently binding, electrostatically binding, or intercalating.[1] Intercalation occurs when ligands of an appropriate size and chemical nature fit themselves in between base pairs of DNA. These ligands are mostly polycyclic, aromatic, and planar, and therefore often make good nucleic acid stains. Intensively studied DNA intercalators include berberine, ethidium bromide, proflavine, daunomycin, doxorubicin, and thalidomide. DNA intercalators are used in chemotherapeutic treatment to inhibit DNA replication in rapidly growing cancer cells. Examples include doxorubicin (adriamycin) and daunorubicin (both of which are used in treatment of Hodgkin's lymphoma), and dactinomycin (used in Wilm's tumour, Ewing's Sarcoma, rhabdomyosarcoma). Metallointercalators are complexes of a metal cation with polycyclic aromatic ligands. The most commonly used metal ion is ruthenium(II), ...
In the late nineteenth century. Finsen successfully demonstrated phototherapy by employing heat-filtered light from a carbon-arc lamp (the "Finsen lamp") in the treatment of a tubercular condition of the skin known as lupus vulgaris, for which he won the 1903 Nobel Prize in Physiology or Medicine.[5] In 1913 another German scientist, Meyer-Betz, described the major stumbling block of photodynamic therapy. After injecting himself with haematoporphyrin (Hp, a photosensitiser), he swiftly experienced a general skin sensitivity upon exposure to sunlight-a recurrent problem with many photosensitisers.[5] The first evidence that agents, photosensitive synthetic dyes, in combination with a light source and oxygen could have potential therapeutic effect was made at the turn of the 20th century in the laboratory of Hermann von Tappeiner in Munich, Germany. Germany was leading the world in industrial dye synthesis at the time.[5] While studying the effects of acridine on paramecia cultures, Oscar Raab, a ...
During the 1950s and 1960s, the National Cancer Institute carried out a wide-ranging program of screening plant and marine organism material. As part of that program extract from the sea squirt Ecteinascidia turbinata was found to have anticancer activity in 1969.[1] Separation and characterisation of the active molecules had to wait many years for the development of sufficiently sensitive techniques, and the structure of one of them, Ecteinascidin 743, was determined by KL Rinehart at the University of Illinois in 1984.[2] Rinehart had collected his sea squirts by scuba diving in the reefs of the West Indies.[3] Recently, the biosynthetic pathway responsible for producing the drug has been determined to come from Candidatus Endoecteinascidia frumentensis, a microbial symbiont of the tunicate.[4] The Spanish company PharmaMar licensed the compound from the University of Illinois before 1994[citation needed] and attempted to farm the sea squirt with limited success.[3] Yields from the sea squirt ...
... was first made in 1963 by Ozegowski and Krebs in East Germany (the former German Democratic Republic).[9] Until 1990 it was available only in East Germany. East German investigators found that it was useful for treating chronic lymphocytic leukemia, Hodgkin's disease, non-Hodgkin's lymphoma, multiple myeloma and lung cancer. Bendamustine received its first marketing approval in Germany, where it is marketed under the tradename Ribomustin, by Astellas Pharma GmbH's licensee, Mundipharma International Corporation Limited. It is indicated as a single-agent or in combination with other anti-cancer agents for indolent non-Hodgkin's lymphoma, multiple myeloma, and chronic lymphocytic leukemia. SymBio Pharmaceuticals Ltd. holds exclusive rights to develop and market bendamustine HCl in Japan and selected Asia Pacific Rim countries. In March 2008, Cephalon received approval from the United States Food and Drug Administration to market bendamustine in the US, where it is sold under the ...
Research on this class of drugs began in the 1950s at SRI International, where scientists were focused on developing new chemotherapies and antifolates that would be effective against tumor cells.[1] In the late 1970s, researchers at Memorial Sloan Kettering Cancer Center discovered that cancerous cells take in natural folate through a protein identified as plasma membrane transporter (now referred to as "reduced folate carrier type 1" or "RFC-1"). Further research showed that when normal cells evolve into cancerous cells they often overproduce RFC-1 to ensure they get enough folate.[6] A subsequent scientific collaboration was ultimately formed among SRI International, Memorial Sloan Kettering Cancer Center, and the Southern Research Institute with the intention of developing an antifolate with greater therapeutic selectivity - an agent that could be more effectively internalized into tumors (transported into the cells through RFC-1) and would be more toxic to cancer cells than normal cells.[6] ...
Another amino acid-like drug is the antineoplastic agent melphalan. Tumor cells spend less time in resting phases than normal cells so at any given time, they are more likely to be metabolically active than most normal host cells. The rationale behind incorporating an alkylating function in a molecule resembling a primary cellular metabolite was to get a greater safety margin by fooling tumor cells into taking up the toxin preferentially. ...
... (INN), abbreviated as CCNU (original brand name (formerly available) is CeeNU, now marketed as Gleostine), is an alkylating nitrosourea compound used in chemotherapy. It is closely related to semustine and is in the same family as streptozotocin. It is a highly lipid-soluble drug,[2] thus it crosses the blood-brain barrier. This property makes it ideal for treating brain tumors, which is its primary use, although it is also used to treat Hodgkin lymphoma as a second-line option.[3] Lomustine has a long time to nadir (the time when white blood cells reach their lowest number). Unlike carmustine, lomustine is administered orally. It is a monofunctional alkylating agent, alkylates both DNA and RNA, has the ability to cross-link DNA.[4] As with other nitrosoureas, it may also inhibit several key enzymatic processes by carbamoylation of amino acids in proteins.[5] Lomustine is cell-cycle nonspecific. It has also been used in veterinary practice as a treatment for mast cell tumors in ...
Aclarubicin (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. Soil bacteria ... October 1991). "Antagonistic effect of aclarubicin on daunorubicin-induced cytotoxicity in human small cell lung cancer cells: ... Streptomyces galilaeus can produce aclarubicin. It can induce histone eviction from chromatin upon intercalation. CID 451415 ...
Aclarubicin had no influence on the accumulation of daunorubicin in these cells. In contrast, the accumulation of daunorubicin ... Antagonistic Effect of Aclarubicin on Daunorubicin-induced Cytotoxicity in Human Small Cell Lung Cancer Cells: Relationship to ... Antagonistic Effect of Aclarubicin on Daunorubicin-induced Cytotoxicity in Human Small Cell Lung Cancer Cells: Relationship to ... Antagonistic Effect of Aclarubicin on Daunorubicin-induced Cytotoxicity in Human Small Cell Lung Cancer Cells: Relationship to ...
It is like you may get re-indexing soils Settling this epub new findings on aclarubicin in the treatment of acute myeloid ... Epub New Findings On Aclarubicin In The Treatment Of Acute Myeloid Leukemia 1990. (212) 588-9314. epub new findings on users ... She was a epub new findings on aclarubicin in the treatment of acute myeloid leukemia 1990 across her everything and added ... By using the information in this website, you accept our This epub new findings on aclarubicin does the answers that failure ...
Phase II trial of aclarubicin in advanced breast cancer : a cancer and leukemia group B study. / Forastiere, A. A.; Budman, D. ... Phase II trial of aclarubicin in advanced breast cancer: a cancer and leukemia group B study. Cancer Treatment Reports. 1983 ... Forastiere, A. A. ; Budman, D. R. ; Richards, F. ; Aisner, J. ; Weinberg, V. ; Wood, W. C. / Phase II trial of aclarubicin in ... Forastiere, A. A., Budman, D. R., Richards, F., Aisner, J., Weinberg, V., & Wood, W. C. (1983). Phase II trial of aclarubicin ...
Aclarubicin Aclarubicin or aclacinomycin A is used to treat acute non lymphocytic leukemia, a cancer of the blood and bone ...
Aclarubicin Aclarubicin or aclacinomycin A is used to treat acute non lymphocytic leukemia, a cancer of the blood and bone ...
Aclarubicin hydrochloride), a fluorescent molecule and the first described non-peptidic inhibitor showing discrete specificity ... Aclacinomycin A hydrochloride (Synonyms: Aclarubicin hydrochloride). Cat. No.: HY-N2306A Purity: 98.08% Data Sheet SDS Handling ... Aclarubicin, an anthracycline anti-cancer drug, fluorescently contrasts mitochondria and reduces the oxygen consumption rate in ... Aclarubicin, an anthracycline anti-cancer drug, fluorescently contrasts mitochondria and reduces the oxygen consumption rate in ...
Schedule H is a class of prescription drugs in India appearing as an appendix to the Drugs and Cosmetics Rules, 1945 introduced in 1945. These are drugs which cannot be purchased over the counter without the prescription of a qualified doctor.The manufacture and sale of all drugs are covered under the Drugs and Cosmetics Act and Rules. It is revised at times based on the advice of the Drugs Technical Advisory Board, part of the Central Drugs Standard Control Organization[1] in the Ministry of Health and Family Welfare. The most recent schedule H (2006) lists 536 drugs from abacavir to zuclopenthixol.[2] However, enforcement of Schedule H laws in India is lax, compared to the more restrictive Schedule X, for which a mandatory documentation trail must be maintained.[3] ...
... aclarubicin; acodazole hydrochloride; acronine; adozelesin; aldesleukin; altretamine; ambomycin; ametantrone acetate; amsacrine ...
Aclarubicin intercalates into DNA and interacts with topoisomerases I and II, thereby inhibiting DNA replication and repair and ... Aclarubicin is antagonistic to other agents that inhibit topoisomerase II, such as etoposide, teniposide and amsacrine. This ... aclarubicin An oligosaccharide anthracycline antineoplastic antibiotic isolated from the bacterium Streptomyces galilaeus. ...
Examples of anti-cancer agents include acivicin; aclarubicin; acodazole hydrochloride; acronine; adriamycin; adozelesin; ...
Aclarubicin hydrochloride:. 5.0-6.5. Idarubicin hydrochloride:. 5.0-7.0. Epirubicin hydrochloride:. 4.5-6.0. ...
Aclarubicin for the Treatment of Retinal Vasculopathy With Cerebral Leukodystrophy. *Vasculopathy, Retinal, With Cerebral ...
Aclarubicin for the Treatment of Retinal Vasculopathy With Cerebral Leukodystrophy. *Vasculopathy, Retinal, With Cerebral ...
Increasing the dose of aclarubicin in low-dose cytarabine and aclarubicin in combination with granulocyte colony-stimulating ... Results: Adult patients with r/r AML were treated with chidamide, decitabine, cytarabine, aclarubicin, and G-CSF (CDCAG). The ... A meta-analysis of CAG (cytarabine, aclarubicin, G-CSF) regimen for the treatment of 1029 patients with acute myeloid leukemia ... Chidamide, decitabine, cytarabine, aclarubicin, and granulocyte colony-stimulating factor (CDCAG) in patients with relapsed/ ...
... aclarubicin, and G-CSF (D-CAG). The risk status was evaluated by determining the frequency of recurring gene mutations using ... Decitabine in combination with low-dose cytarabine, aclarubicin and G-CSF tends to improve prognosis in elderly patients with ...
Browse listings of aceclofenac dealers in Chennai, Tamil Nadu with traders, distributors, wholesalers, manufacturers & suppliers. Get best aceclofenac price in Chennai offered by verified companies.
Aclarubicin. Aceclofenac may decrease the excretion rate of Aclarubicin which could result in a higher serum level.. ...
Aclarubicin. Aclarubicin may increase the hypocalcemic activities of Tiludronic acid.. Investigational. Adapalene. The risk or ...
... aclarubicin, and bleomycin; plant alkaloids and terpenoids, such as noscapine, vincristine, vinblastine, vinorelbine, vindesine ...
HMBA, dactinomycin, aclarubicin and cytarabine Released P-TEFb associated with RNAP II that allows transcriptional elongation ...
Low-dose cytarabine, aclarubicin and granulocyte colony-stimulating factor priming regimen versus idarubicin plus cytarabine ...
... aclarubicin; acylfulvene; adecypenol; adozelesin; aldesleukin; ALL-TK antagonists; altretamine; ambamustine; amidox; amifostine ... aclarubicin; acodazole hydrochloride; acronine; adozelesin; aldesleukin; altretamine; ambomycin; ametantrone acetate; ...
Aclarubicin; Acodazole Hydrochloride; AcrQnine; Adozelesin; Aldesleukin; Altretamine; Ambomycin; Ametantrone Acetate; ...
... aclarubicin; acodazole hydrochloride; acronine; adozelesin; aldesleukin; alemtuzumab; allopurinol; alitretinoin; altretamine; ...
- Aclacinomycin A hydrochloride (Aclarubicin hydrochloride), a fluorescent molecule and the first described non-peptidic inhibitor showing discrete specificity for the CTRL (chymotrypsin-like) activity of the 20S proteasome . (medchemexpress.com)
- Aclarubicin (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. (wikipedia.org)
- Aclarubicin or aclacinomycin A is used to treat acute non lymphocytic leukemia, a cancer of the blood and bone marrow. (medindia.net)
- Involved in the biosynthesis of aklavinone which is an important precursor common to the formation of the clinically significant anthracyclines such as carminomycin, daunorubicin (daunomycin), rhodomycin, aclacinomycin T (aklavin) and aclacinomycin A (aclarubicin). (uniprot.org)
- Aclarubicin, an anthracycline anti-cancer drug, fluorescently contrasts mitochondria and reduces the oxygen consumption rate in living human cells. (medchemexpress.com)
- Aclarubicin is an insoluble anthracycline anti-cancer drug produced by Streptomyces galilaeus and intercalates between. (toku-e.com)
- Successful treatment of a patient with synchronous advanced non-small cell lung cancer and acute myeloid leukemia by a combination of gefitinib, low-dose cytarabine and aclarubicin. (labome.org)
- Taken together, these data indicate that aclarubicin-mediated inhibition of daunorubicin-induced cytotoxicity is due mainly to a drug interaction with the nuclear enzyme topoisomerase II. (aacrjournals.org)
- Publications] Kyosuke Temma: 'Comparison of cardiac actions of doxorubicin,pirarubicin and aclarubicin in isolated guinea-pig heart. (nii.ac.jp)
- Aclarubicin is one of the derivatives of anthracycline drugs exhibiting less side effects in comparison with the commonly used anthracyclines Generation - doxorubicin and daunorubicin. (pbkom.eu)
- The effect of combinations of the anthracyclines aclarubicin and daunorubicin was investigated in a clonogenic assay using the human small cell lung cancer cell line OC-NYH and a multidrug-resistant (MDR) murine subline of Ehrlich ascites tumor (EHR2/DNR+). (aacrjournals.org)
- Finally, the effect of daunorubicin on the DNA cleavage activity of purified topoisomerase II in the presence and absence of aclarubicin was examined. (aacrjournals.org)
- Induction of genotoxic and cytotoxic damage by aclarubicin, a dual topoisomerase inhibitor. (medchemexpress.com)
- Both adriamycin and aclarubicin inhibit topoisomerase II and, thus, topoisomerase II might not be a major factor in the acquired resistance to adriamycin that results from overexpression of Ssl2p. (nih.gov)
- Because topo II poisons, such as etoposide, cause DNA DSBs, we hypothesized that pretreatment of cells with merbarone or aclarubicin, known catalytic inhibitors of topo II, would abrogate DNA DSBs caused by topo II. (aacrjournals.org)
- Systemic N-acetylcysteine, alfa-tocoferol, amifostine, merbarone, aclarubicin, ADR-925, and EDTA were administered i.p. immediately hereafter or as a triple-treatment over six hours. (uptodate.com)
- It is like you may get re-indexing soils Settling this epub new findings on aclarubicin in the treatment of acute myeloid leukemia 1990. (boltemedical.com)
- She was a epub new findings on aclarubicin in the treatment of acute myeloid leukemia 1990 across her everything and added around. (boltemedical.com)
- Soil bacteria Streptomyces galilaeus can produce aclarubicin. (wikipedia.org)
- This antagonism at the nuclear level explains why aclarubicin is a poor modulator of daunorubicin resistance even though aclarubicin is able to increase the intracellular accumulation of daunorubicin in a MDR cell line. (aacrjournals.org)
- Overexpression of Ssl2p did not confer resistance to aclarubicin, an anthracycline anticancer drug, which, like adriamycin, is intercalated into DNA. (nih.gov)
- After the first and second courses of induction therapy including aclarubicin, complete remission rates were significantly lower in carriers of the DNMT3A R882 mutants as compared with R882 wildtype patients (P = 0.022 and P = 0.038, respectively). (cdc.gov)
- In addition, DNMT3A R882 mutations were associated with an inferior response to induction therapy with aclarubicin in Chinese AML patients. (cdc.gov)
- We tested several other compounds but the only one to which Ssl2p-overexpressing cells were cross-resistant was actinomycin D. Mammalian cells that overexpress P-glycoprotein, which is a transmembrane protein that is involved in the efflux of certain drugs, are resistant to both adriamycin and actinomycin D but not to aclarubicin. (nih.gov)
- It was found that the cytotoxicity of daunorubicin in OC-NYH cells was antagonized by simultaneous exposure to nontoxic concentrations of aclarubicin. (aacrjournals.org)
- Coordinately, aclarubicin inhibited the formation of daunorubicin-induced protein-concealed DNA single-strand breaks and DNA-protein cross-links in OC-NYH cells when assayed by the alkaline elution technique. (aacrjournals.org)
- Aclarubicin had no influence on the accumulation of daunorubicin in these cells. (aacrjournals.org)
- In contrast, the accumulation of daunorubicin in EHR2/DNR+ cells was enhanced by more than 300% when the cells were simultaneously incubated with the MDR modulator verapamil, aclarubicin, or the two agents combined. (aacrjournals.org)
- institutions closely turned this epub new findings on aclarubicin in the treatment of acute myeloid. (boltemedical.com)
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