Bendistin Actavis is used to treat or relieve symptoms of the following diseases: Refractory Hodgkin Lymphoma, Chronic Lymphocytic Leukaemia (CLL), Recurrent multiple myeloma, Refractory indolent B cell non-hodgkin lymphoma, Refractory Mantle Cell Lymphoma, Waldenström's Macroglobulinemia (WM), Follicular Non-Hodgkin's Lymphoma Refractory,
Bendamustine may also be used for purposes not listed in this medication guide.
Bendistin Actavis is a drug made in Malta. You need a doctor's prescription to buy it. But its analogues can be bought online anywhere in the world without going to a specialist.
Bendamustine is a complete analogue of Bendistin Actavis. It has the same composition, dosage and methods of use. Also Bendamustine has a lower cost compared to Bendistin Actavis.
To buy Bendistin Actavis, click on the "buy now" button and then in our online store select the medicine and the desired dosage. Follow the instructions below.
Free delivery is valid for purchases from $200. We deliver medicines around the world and provide the best prices.
You can also use a coupon giving a 5% discount.
Severe adverse reactions reported in the study included headache, tiredness; or nausea, vomiting, diarrhea, constipation; pain, swelling, redness, skin changes, or signs of infection where the medicine was injected; fever, chills, or itching during or shortly after the injection; fever, cough, mouth sores, trouble breathing; severe ongoing nausea, vomiting, or diarrhea;
Tell your doctor if you have ever had:
Using bendamustine may increase your risk of developing certain types of cancer. Ask your doctor about this risk.
CloZAPine: Myelosuppressive Agents may enhance the adverse/toxic effect of CloZAPine. Specifically, the risk for neutropenia may be increased. Monitor therapy
Dipyrone: May enhance the adverse/toxic effect of Myelosuppressive Agents. Specifically, the risk for agranulocytosis and pancytopenia may be increased Avoid combination
BCG (Intravesical): Myelosuppressive Agents may diminish the therapeutic effect of BCG (Intravesical). Avoid combination
Due to the short half-life of bendamustine, the standard dosage regimen (2 consecutive days in 21- or 28-day cycles) and the extensive metabolism of bendamustine, the probability of its accumulation in patients with liver failure is unlikely. In particular, bendamustine is primarily metabolized by hydrolysis through the mechanism of extrahepatic pathways (and with limited hepatic metabolism). One study, however, showed a longer average half-life and slower clearance of bendamustine in patients with moderate to severe hepatic impairment. However, bendamustine has been used safely and effectively in patients with bilirubin levels> 20 mg%.
Current status and future directions
As bendamustine became available worldwide, the indications for its use have expanded significantly. Now it is a standard agent for the treatment of CLL, indolent and aggressive B-NHL and T-NHL, ChL, as well as MM. With the accumulation of experience with the use of bendamustine, the understanding of the possible ways of safe administration of the drug is being improved. We are on the verge of a revolutionary period in the treatment prescription drugs CLL and lymphomas. It has been shown to be more effective than rituximab for new anti-CD20 monoclonal antibodies, such as obinutuzumab (at least for CLL patients combined with chlorambucil). Of significant interest are new agents that affect the “targets” within the cell, including Syk Worm Ban tyrosine kinase), BTK (Bruton tyrosine kinases), and PI3K (phosphatidylinostol 3-kinase). Impressive data on the efficacy of a BTK inhibitor (ibrutinib) were obtained in patients with a recurring / refractory form of CLL, especially in an unfavorable subgroup of patients with CLL 17p deletion. A PI3K delta inhibitor (idelalizib) has also been recently approved for the treatment of small lymphocytic lymphomas, follicular NHL and (in combination with rituximab) recurrent CLL. Additionally, active oral preparations include a Bcl-2 venetoclax inhibitor, immunomodulators, proteasome inhibitors and mTOR, as well as kinase inhibitors (SYK, BTK and PI3K). However, at present, these new groups of drugs demonstrate the achievement of only partial responses to therapy when used as monotherapy and therefore require almost constant use. Bendamustine is currently used as the basis for choosing a chemotherapy regimen, including in combination with new targeted drugs.
We hope that these recommendations Actavis contribute to the expansion of the safe and effective administration of this drug, especially in combination with new agents, which will become a solid foundation for the best patient treatment results.
Application. Recommendations Consensus panels of the dose regimen and dose reduction during bendamustine therapy.
Indolent non-Hodgkin L: as a first-line drug, bendamustine should not be used as a monotherapy option. It is considered justified in patients previously treated with dexamethasone (8 mg, intravenously in combination with 5-HT3 antagonists) or hydrocortisone (50-100 mg). Generally recommend withdrawal before dose reduction. Use dose reduction as a first step in patients with transient manifestations of non-hematologic toxicity.
Aggressive non-Hodgkin L: BR can be used in those patients who cannot use the R-CHOP or CHOP-like regimen. Criteria include follicular lymphoma, class 3b. No recommendation for Burkitt's lymphoma or lymphoblastic lymphoma.
T-cell L: the effectiveness of bendamustine as a first-line drug is not clear.
Mantle cell L: dose reduction of bendamustine is necessary when combined with potentially myelosuppressive agents (e.g., ibrutinib, bortezomib, lenalidomide).show M: bendamustine should be dosed for two days (days 1 + 2, 1 + 8 or 1 + 4) for a 28-day cycle. Bendamustine will be considered first-line therapy in patients who do not need transplantation.
Note: a dose of less than 60 mg / m 2 is considered lower than therapeutic and preferably discontinued .
You can find out more about the Bendamustin-Vista Medical Institute http://vista-mediclub.com/preparaty-vista/1650-bendamustinvista-bendamustinvista.
Information about the appearance in pharmacies in Ukraine and the price can be reached at http://medbrowse.com.ua/bendamustin-vista-cena/ukraina
a Lombardi Comprehensive Cancer Center, Georgetown University Hospital, Washington, DC, USA
b Schwarzwald-Baar Clinic, University of Freiburg, Villingen-Schwenningen, Germany
c University Hospital, University of Basse-Normandie, Caen, France
d Medical Clinic, University Hospital of Munich, Munich, Germany
e University of Wisconsin School of Medicine and Public Health, Madison, WI, USA
f Center for Hematology, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden
g Department of Hematology, Tokai Central Hospital, Gifu, Japan
h Department of Oncology and Hematology, Krankenhaus Nordwest, Frankfurt, Germany
i Klinikum Schwabing, Academic Teaching Hospital of University of Munich, Munich, Germany
j Institute of Hematology, University of Bologna, Bologna, Italy
CONTACT Professor Bruce D. Cheson; Email: ude.nwotegroeg@4cdb, Georgetown University Hospital, Lombardi Comprehensive Cancer Center, 3800 Reservoir Road, NW, Washington, DC, USA
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Antitumor agent with bifunctional alkylating activity. The mechanism of action is mainly associated with the formation of cross-linking of single-stranded and double-stranded DNA molecules due to alkylation. As a result, the matrix function of DNA and its synthesis are disrupted. There is also evidence that bendamustine has additional antimetabolic properties (effect of purine analogue).
The antineoplastic effect of bendamustine has been confirmed in numerous in vitro studies on various tumor cell lines (breast cancer, non-small cell and small cell lung cancer, ovarian cancer and various types of leukemia, as well as colon cancer, melanoma, renal cell carcinoma, and malignant neoplasms of the prostate and brain brain) and in vivo - on various experimental models of tumors (melanoma, breast cancer, sarcoma, lymphoma, leukemia and small cell lung cancer). The absence or presence of only a small degree of cross-resistance in human tumor cell lines with different resistance mechanisms has been shown.
This is partially explained by the interaction with DNA, which, compared with other alkylating agents, lasts longer (for example, only partial cross-resistance was detected with other alkylating agents, such as cyclophosphamide, carmustine or cisplatin). In addition, in clinical studies it was found that there is no complete cross-resistance between bendamustine and anthracyclines or alkylates.
After a single 30-minute iv infusion of bendamustine at a dose of 120 mg / m 2 body surface T1/2 in the beta phase is 28.3 min. Vd with a 30-minute iv infusion is 19.3 l, with subsequent systematic administration and achievement of an equilibrium concentration of Vd is from 15.8 to 20.5 liters. In the systemic circulation, bendamustine actively binds to plasma proteins (> 95%), mainly albumin. The ability of bendamustine to bind to plasma proteins is not impaired at low concentrations of albumin in blood plasma, in patients over the age of 70 years and in advanced stages of tumors.
Bendamustine is metabolized mainly in the liver, mainly by hydrolysis with the formation of monohydroxy and dihydroxybendamustine. In the formation of gamma-hydroxybendamustine (M3) and N-desmethylbendamustine (M4) in the liver, the isoenzyme CYP1A2 of cytochrome P450 is involved. In vitro, bendamustine does not inhibit CYP1A4, CYP2C9 / open this link, CYP2D6, CYP2E1 and CYP3A4.
The average value of the total clearance after a 30-minute iv infusion of the drug to 12 subjects at a dose of 120 mg / m 2 of the body surface was 639.4 ml / min. About 20% of the administered dose of the drug was excreted by the kidneys for 24 hours.
The amount of unchanged bendamustine and its metabolites excreted with the kidneys is arranged in decreasing order as follows: monohydroxybendamustine> bendamustine> dihydroxybendamustine> oxidized metabolite> N-desmethylbendamustine.
Mostly polar metabolites are excreted with bile.
With 30-70% tumor of the liver and slightly reduced liver function (serum bilirubin 10 ml / min, including those on dialysis, did not differ significantly from those in patients with normal renal function in relation to Cmax, Tmax, AUC, T1/2 β, Vd and deductions.
In persons over 18 and under 84 years of age, the pharmacokinetic parameters did not differ significantly.
Chronic lymphocytic leukemia (the effectiveness of the use in first-line therapy compared to other chemotherapy drugs except chlorambucil has not been established).
Indolent non-Hodgkin lymphomas in monotherapy in patients who experienced progression on the background or within 6 months after the end of therapy with rituximab and in combination therapy as a first-line therapy.