An anthracycline produced by Streptomyces galilaeus. It has potent antineoplastic activity.
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.
An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.
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.
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
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.
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)
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.

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)

Aclarubicin is an anthracycline antibiotic used in cancer chemotherapy. It works by interfering with the DNA in cancer cells, preventing them from dividing and growing. Aclarubicin is often used to treat acute leukemias, lymphomas, and solid tumors.

Like other anthracyclines, aclarubicin can cause significant side effects, including damage to the heart muscle, suppression of bone marrow function, and hair loss. It may also cause nausea, vomiting, and mouth sores. Aclarubicin is usually given by injection into a vein.

It's important to note that the use of aclarubicin should be under the supervision of a healthcare professional, as its administration requires careful monitoring due to potential toxicities.

Topoisomerase II inhibitors are a class of anticancer drugs that work by interfering with the enzyme topoisomerase II, which is essential for DNA replication and transcription. These inhibitors bind to the enzyme-DNA complex, preventing the relaxation of supercoiled DNA and causing DNA strand breaks. This results in the accumulation of double-stranded DNA breaks, which can lead to apoptosis (programmed cell death) in rapidly dividing cells, such as cancer cells. Examples of topoisomerase II inhibitors include etoposide, doxorubicin, and mitoxantrone.

Amsacrine is a chemotherapeutic agent, which means it is a medication used to treat cancer. It is classified as an antineoplastic drug, and more specifically, as an intercalating agent and a topoisomerase II inhibitor. Amsacrine works by intercalating, or inserting itself, into the DNA of cancer cells, which prevents the DNA from replicating and ultimately leads to the death of the cancer cell. It is primarily used in the treatment of acute myeloid leukemia (AML) and other hematologic malignancies.

The chemical name for Amsacrine is 5-[3-amino-1-(3-aminopropyl)-2-hydroxybut-1-yloxy]-8-chloro-1,4-naphthoquinone. It has a molecular formula of C16H17ClNO5 and a molecular weight of 359.8 g/mol.

Amsacrine is typically administered intravenously, and its use is usually reserved for patients who have not responded to other forms of chemotherapy. It may be used in combination with other anticancer drugs as part of a treatment regimen. As with any chemotherapeutic agent, Amsacrine can have significant side effects, including nausea, vomiting, and hair loss. It can also cause damage to the heart and other organs, so it is important for patients to be closely monitored during treatment.

It's worth noting that while Amsacrine can be an effective treatment for some types of cancer, it is not a cure-all, and its use must be carefully considered in the context of each individual patient's medical history and current health status.

Drug antagonism is a type of interaction between two or more drugs, where one drug (known as the antagonist) reduces or blocks the effects of another drug (known as the agonist). This can occur through various mechanisms, such as binding to the same receptor site as the agonist and preventing it from activating the receptor, or by increasing the metabolism or excretion of the agonist.

Drug antagonism is often used in medical treatment to counteract the negative effects of certain drugs. For example, naloxone is an opioid antagonist that can be used to reverse the respiratory depression caused by opioid overdose. Similarly, flumazenil is a benzodiazepine antagonist that can be used to reverse the sedative effects of benzodiazepines in cases of overdose or adverse reactions.

However, drug antagonism can also lead to unintended consequences, such as when one medication reduces the effectiveness of another medication that a patient is taking for a different condition. Therefore, it is important for healthcare providers to be aware of potential drug interactions and to carefully monitor their patients' responses to medications.

Daunorubicin is an anthracycline antibiotic used in the treatment of various types of cancer, including leukemia, Hodgkin's lymphoma, and breast cancer. It works by intercalating with DNA and inhibiting topoisomerase II, which results in DNA damage and ultimately cell death.

The drug is administered intravenously and may cause side effects such as nausea, vomiting, hair loss, mouth sores, and damage to the heart muscle (cardiotoxicity) with long-term use. Regular monitoring of cardiac function is recommended during treatment with daunorubicin.

It's important to note that this medication should only be used under the supervision of a qualified healthcare professional, as it can have serious and potentially life-threatening consequences if not used correctly.

Antibiotics are a type of medication used to treat infections caused by bacteria. They work by either killing the bacteria or inhibiting their growth.

Antineoplastics, also known as chemotherapeutic agents, are a class of drugs used to treat cancer. These medications target and destroy rapidly dividing cells, such as cancer cells, although they can also affect other quickly dividing cells in the body, such as those in the hair follicles or digestive tract, which can lead to side effects.

Antibiotics and antineoplastics are two different classes of drugs with distinct mechanisms of action and uses. It is important to use them appropriately and under the guidance of a healthcare professional.

DNA topoisomerases are enzymes that regulate the topological state of DNA during various cellular processes such as replication, transcription, and repair. They do this by introducing temporary breaks in the DNA strands and allowing the strands to rotate around each other, thereby relieving torsional stress and supercoiling. Topoisomerases are classified into two types: type I and type II.

Type II topoisomerases are further divided into two subtypes: type IIA and type IIB. These enzymes function by forming a covalent bond with the DNA strands, cleaving them, and then passing another segment of DNA through the break before resealing the original strands. This process allows for the removal of both positive and negative supercoils from DNA as well as the separation of interlinked circular DNA molecules (catenanes) or knotted DNA structures.

Type II topoisomerases are essential for cell viability, and their dysfunction has been linked to various human diseases, including cancer and neurodegenerative disorders. They have also emerged as important targets for the development of anticancer drugs that inhibit their activity and induce DNA damage leading to cell death. Examples of type II topoisomerase inhibitors include etoposide, doxorubicin, and mitoxantrone.

Carcinoma, small cell is a type of lung cancer that typically starts in the bronchi (the airways that lead to the lungs). It is called "small cell" because the cancer cells are small and appear round or oval in shape. This type of lung cancer is also sometimes referred to as "oat cell carcinoma" due to the distinctive appearance of the cells, which can resemble oats when viewed under a microscope.

Small cell carcinoma is a particularly aggressive form of lung cancer that tends to spread quickly to other parts of the body. It is strongly associated with smoking and is less common than non-small cell lung cancer (NSCLC), which accounts for about 85% of all lung cancers.

Like other types of lung cancer, small cell carcinoma may not cause any symptoms in its early stages. However, as the tumor grows and spreads, it can cause a variety of symptoms, including coughing, chest pain, shortness of breath, hoarseness, and weight loss. Treatment for small cell carcinoma typically involves a combination of chemotherapy, radiation therapy, and sometimes surgery.

I'm sorry for any confusion, but "Carcinoma, Ehrlich Tumor" is not a recognized medical term or a valid medical definition. The term "Ehrlich tumor" is sometimes used to refer to a type of transplantable tumor that was first developed by the German physician Paul Ehrlich in the early 20th century for cancer research purposes. However, it's important to note that this type of tumor is not a naturally occurring cancer and is typically used only in laboratory experiments.

Carcinoma, on the other hand, is a medical term that refers to a type of cancer that starts in cells that line the inner or outer surfaces of organs. Carcinomas can develop in various parts of the body, including the lungs, breasts, colon, and skin.

If you have any specific questions about cancer or a particular medical condition, I would be happy to try to help answer them for you.

... (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 ...
Early leads also included sodium orthovanadate and aclarubicin. Morpholino-type antisense oligonucleotides, with the same ... "Aclarubicin treatment restores SMN levels to cells derived from type I spinal muscular atrophy patients". Human Molecular ...
Anthracyclines (Aclarubicin · Daunorubicin · Doxorubicin · Epirubicin · Idarubicin · Amrubicin · Pirarubicin · Valrubicin · ...
This group includes novobiocin, merbarone, and aclarubicin, which also have other significant mechanisms of action. The ... Other clinically used drugs in the anthracycline group are pirarubicin, aclarubicin, and mitoxantrone. The mechanisms of ...
Dexrazoxane Novobiocin Merbarone Anthrycycline aclarubicin Dexrazoxane also known as ICRF-187 is currently the only clinically ... Common catalytic inhibitors that target TopII are dexrazoxane, novobiocin, merbarone and anthrycycline aclarubicin. ...
Since 2019, Jacques Neefjes is co-financing the production of a promising cancer drug, Aclarubicin, which disappeared from the ...
... aclarubicin MeSH D09.408.051.059.200 - daunorubicin MeSH D09.408.051.059.200.150 - carubicin MeSH D09.408.051.059.200.175 - ...
L01CX01 Trabectedin L01DA01 Dactinomycin L01DB01 Doxorubicin L01DB02 Daunorubicin L01DB03 Epirubicin L01DB04 Aclarubicin ...
... aclarubicin, tomaymycin, sibiromycin, and mazethramycin.[citation needed] Derivatives of Streptomycetes isolate migrastatin, ...
... 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 - ...
Semustine Streptozotocin Temozolomide Thiotepa Treosulfan Triaziquone Triethylenemelamine Trofosfamide Uramustine Aclarubicin ...
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 ...
The mechanism of action of aclarubicin is based on its capacity to insert its trisaccharide chain into the minor DNA groove: ... Aclarubicin is an anthracycline antibiotic produced by Streptomyces galilaeus and also has potent antineoplastic activity. It ... Aclarubicin. L Antineoplastic and immunomodulating agents → L01 Antineoplastic agents → L01D Cytotoxic antibiotics and related ... Aclarubicin is an anthracycline antibiotic produced by Streptomyces galilaeus and also has potent antineoplastic activity. It ...
Aclarubicin 1. View Price - 51. Acrivastine 2. - View Price 52. Activated Charcoal 1. - View Price ...
Aclarubicin / analogs & derivatives* * Aclarubicin / biosynthesis* * Cloning, Molecular * DNA, Bacterial / chemistry * DNA, ...
Aclarubicin HCl. USD. 102.72 €. -. Toku-e. a053-100g. Acrylamide, Grade II, 99.9%. USD. 66.34 €. -. Toku-e. ...
Aclarubicin 4.479395 5.527251 Actinomycin D 6.951308 6.530922 Actinonin 88.53803 103.1408 AG014699 (Rucaparib) 18.73871 ...
In dieser Liste finden sich die Substanzen (Wirkstoffe) mit einer eindeutigen Zurordnung zu einer systemischen ,Therapieart,. Mehrfachangaben im Feld ,Menge_Substanz, sind möglich.. Die Liste ist für die Nutzung als Vorschlagsliste vorgesehen. Eventuell kann dabei auch eine Vorfilterung nach ,Therapieart, vorgesehen werden, um die Fehler bei der Auswahl einer Substanz weiter zu minimieren.. Die Liste beruht auf dem Register- und Literaturstand August 2021 und erhebt keinen Anspruch auf Vollständigkeit. Es muss für die Dokumentationskraft die Möglichkeit erhalten bleiben, eine nicht in der Liste enthaltene Substanz zu erfassen.. In das Tabellenblatt Substanzen wurde zusätzlich Placebo und Studienmedikament aufgenommen als Platzhalter für unbekannte Wirkstoffe, die im Rahmen einer Studie gegeben werden. Die Substanzen G-CSF und Mesna sind eigentlich keine tumorspezifischen Substanzen, als Bestandteil von Therapieprotokollen wurden sie jedoch in die Liste der Substanzen aufgenommen.. ...
aclarubicin; and acridines.. 4. A pharmaceutical composition as claimed in claim 3 wherein said topo II catalytic inhibitor is ... One is the inhibition of the initial binding of topo II to DNA as in the case of chloroquine (3) and aclarubicin (4,5). The ... The catalytic inhibitors act either at stage 1 (chloroquine and aclarubicin) or at stage 5 {ICRF-187).. Figure 3 shows the ... Mapping of DNA topoisomerase II poisons (etoposide, cle-rocidin) and catalytic inhibitors (aclarubicin, ICRF-187) to four ...
Doxorubicin as well as Aclarubicin: Auto shuffling Anthracycline Glycans regarding Increased Anticancer Real estate agents.. * ... No Comments on Doxorubicin as well as Aclarubicin: Auto shuffling Anthracycline Glycans regarding Increased Anticancer Real ...
There is currently no text in this page. You can search for this page title in other pages, or search the related logs, but you do not have permission to create this page. ...
Other clinically used drugs in the anthracycline group are pirarubicin, aclarubicin, and mitoxantrone. The mechanisms of ... This group includes novobiocin, merbarone, and aclarubicin, which also have other significant mechanisms of action. ...
She did not achieve CR by salvage chemotherapy with cytarabine-aclarubicin-G-CSF regimen. Comprehensive genomic analysis of ...
Efficacy and safety of homoharringtonine plus cytarabine and aclarubicin for patients with myelodysplastic syndrome-RAEB ...
Two patients initially received infusions of Aclarubicin for four consecutive days with blood work and other testing prior to ... The first clinical trial utilizing Aclarubicin for treatment of RVCL commenced December 5, 2016 at Washington University School ...
Cytotoxic antibiotics, such as the anthracyclines (Doxorubicin, Idarubicin, Daunorubicin, Epirubicin, Aclarubicin, Mitoxantrone ...
Bookfi is one of the most phenomenal modern Bengali artifacts in the epub New Findings on Aclarubicin in the Treatment of Acute ...
... hypochloremic alkalosis with hypopotassemia and myocardial damage by anticancer drugs such as daunomycin and aclarubicin ...
... aclarubicin, cytosine arabinoside (Ara-C), hydroxyurea and even (8) medicinal plant-derived products and plant growth ...
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  • Soil bacteria Streptomyces galilaeus can produce aclarubicin. (wikipedia.org)
  • Aclarubicin is an anthracycline antibiotic produced by Streptomyces galilaeus and also has potent antineoplastic activity. (rxreasoner.com)
  • Aclarubicin (INN) or aclacinomycin A is an anthracycline drug that is used in the treatment of cancer. (wikipedia.org)
  • The first clinical trial utilizing Aclarubicin for treatment of RVCL commenced December 5, 2016 at Washington University School of Medicine. (wustl.edu)
  • We evaluated the risk status and survival outcomes of 125 elderly acute myeloid leukemia (AML) patients treated with decitabine in combination with low-dose cytarabine, aclarubicin, and G-CSF (D-CAG). (nih.gov)
  • 10. [Combination chemotherapy of ovarian cancer with cisplatinum, aclarubicin and tegafur]. (nih.gov)