Disease relevance of Rubidazon

• Myelofibrosis associated with rubidazone [1].
• Two patients with hairy cell leukemia treated with the anthracycline antibiotic rubidazone are presented [2].
• However, if life-threatening granulocytopenia and thrombocytopenia occur secondary to bone marrow replacement by leukemic cells, and improvement does not occur using alternative methods of therapy, consideration could be given to chemotherapy with rubidazone [2].
• Clinical toxicity and the stability of rubidazone were studied in nine patients with advanced solid tumors [3].
• Moderate leukopenia was the dose-limiting toxicity in four of six patients treated at 150 mg sq/m. Assay of rubidazone in plasma samples obtained after administration of rubidazone showed that the drug was stable for at least 7 hr [3].

High impact information on Rubidazon

• Kinetic response to cultured human lymphoid cells to rubidazone [4].
• Thus rubidazone induced a G2-block, the magnitude and duration of which were dependent on concentration and incubation time [4].
• This age-dependent kinetic response may account for the smaller G2-accumulation in asynchronous cultures and the closer correlation of the magnitude of this kinetic effect with concentration and duration of rubidazone treatment [4].
• The effectiveness of rubidazone in hairy cell leukemia (leukemic reticuloendotheliosis) [2].
• A randomized trial of amsacrine and rubidazone in 39 patients with acute promyelocytic leukemia [5].

Chemical compound and disease context of Rubidazon

• Transport and binding of daunorubicin, adriamycin, and rubidazone in Ehrlich ascites tumour cells [6].
• Combination of rubidazone and cytosine arabinoside in the treatment of first relapse in acute myelocytic leukemia [7].
• Randomized phase II trial of rubidazone and adriamycin in women with advanced breast cancer [8].
• Resistance to a new daunorubicin derivative, rubidazone, was developed in a strain of Ehrlich ascites tumor in vivo by treatment with the drug during 11 weekly passages of the tumor [9].
• Cardiac toxicity of adriamycin-DNA complex and rubidazone: evaluation by electrocardiogram and endomyocardial biopsy [10].

Biological context of Rubidazon

• Interesting structure-activity relationships were observed in a series of rubidazone derivatives substituted at the benzhydrazone part of the molecule [11].
• The results indicate that in vivo, doxorubicin, daunorubicin, rubidazone and aclacinomycin A cause a rapid release of histamine from rat mast cells and an increase in vascular permeability in rat sin [12].

Anatomical context of Rubidazon

• The anthraquinones, doxorubicin, mitoxantrone, daunorubicin and rubidazone are shown to be potent stimulators of Ca2+ release from skeletal muscle sarcoplasmic reticulum (SR) vesicles and to trigger transient contractions in chemically skinned psoas muscle fibers [13].
• The total drug level is significantly lower after rubidazone administration in kidney, heart, gastrointestinal tract, spleen, and urine, and the biliary excretion of rubidazone is more important than that of daunorubicin [14].
• Clinical trial of rubidazone in advanced squamous cell carcinoma of the lung and adenocarcinoma of the large intestine [15].

Associations of Rubidazon with other chemical compounds

• Substituent effects were essentially absent among the rubidazone analogues in in vivo and in vitro test systems which measure cytotoxic characteristics; however, the rubidazone analogues varied substantially in their cardiotoxic effects and this variation was closely correlated with the electronic character of the phenyl substituent [16].
• Combination chemotherapy with an anthracycline, Adriamycin or rubidazone, cytosine arabinoside, vincristine and prednisone resulted in a complete remission rate of 62% in 325 consecutive unselected adults with acute leukemia [17].
• Cells of the mouse L strain and the Chinese hamster CHO line were treated with 33258 Hoechst, rubidazone, and a combination of these [18].
• Induction therapy with vincristine, cytoxan, and prednisone (VCP) gave the same complete remission rate after one course as more aggressive induction with vincristine, rubidazone, araC, and prednisone (VRAP) due to increased toxic death in the aggressive arm [19].

Gene context of Rubidazon

• Chronic treatment with these anthracyclines also resulted in significantly less cardiomyopathy, especially in the case of N-L-leucyl-daunorubicin and rubidazone [20].

Analytical, diagnostic and therapeutic context of Rubidazon

• Determination of rubidazone and its metabolites in human plasma and urine by reversed-phase ion-pair high-performance liquid chromatography [21].

References