medac’s complete range of products
Here you can find an overview of all the preparations offered by medac, alphabetically arranged from A to Z. For further information about the medicament in question, please just click on the entry.
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50 mg/ml, concentrate for solution for injection (10 ml)
50 mg/ml, concentrate for solution for injection (20 ml)
50 mg/ml, concentrate for solution for injection (100 ml)
50 mg/ml, concentrate for solution for injection (200 ml)
Mechanism of action
5-fluorouracil in itself is a non-antineoplastic synthetic fluorinated pyrimidine derivate. After metabolism, cell division is inhibited by the active metabolites 5-fluorouridine triphosphate (FUTP) and 5-fluorodeoxyuridine monophosphate (FdUMP).
Known mechanism of action
- Blockade of DNA synthesis (inhibition of thymidylate synthase by FdUMP)
- Inhibition of RNA synthesis (faulty structuring of RNA by incorporation of FUTP)
- DNA strand breaks following incorporation of 5‑fluorodeoxyuridine triphosphate (phosphorylated FdUMP) in DNA
The inhibitory effects are particularly evident in cells that grow rapidly and thus absorb 5‑fluorouracil to a greater extent.
1 vial with 5 ml solution for infusion
1 vial with 25 ml solution for infusion
1 vial with 100 ml solution for infusion
Mechanism of action
Adrimedac® 2 mg/ml solution for infusion has a cytotoxic effect, inhibiting DNA and RNA synthesis through several mechanisms: intercalation between DNA bases, inhibition of various enzymes such as topoisomerase II, helicase and DNA and RNA polymerases and formation of free oxygen radicals.
with solvent and instillation set
with solvent and instillation set
Mechanism of action
Immunostimulant
25 mg
100 mg
Mechanism of action
Bendamustin medac is an alkylating substance containing the active substance bendamustine hydrochloride. The alkalising effect of bendamustine hydrochloride is essentially based on the cross-linking of DNA single and double strands, which impairs the synthesis and repair of DNA.
Particularities:
Bendamustine induces more rapid and frequent DNA double strand breaks compared to melphalan and cyclophosphamide.
Moreover, the repair of bendamustine-induced DNA strand breaks has been shown to be more difficult and slower compared to cyclophosphamide and carmustine.
Another advantage is that bendamustine does not show any cross-resistance with other alkylating agents.
package contains 30 or 90 film-coated tablets
01712501
package contains 30 or 90 film-coated tablets
01712524
1 vial contains 15,000 I.U. lyophilised bleomycin sulphate (1 x 1)
1 vial contains 30,000 I.U. lyophilised bleomycin sulphate (1 x 1)
Mechanism of action
Bleomycin has a cytostatic effect because of its specific binding to DNA, where it causes strand breaks.
After administration, bleomycin forms an active complex with copper (Cu2+) and thus passes through the cell membrane into the cell interior. When the copper splits off in the cell plasma, bleomycin binds to DNA in the nucleus. Activated by free oxygen radicals, it induces strand breaks in the DNA. The greatest susceptibility is shown in cells in the G2 and M phases of the cell cycle.
60 film-coated tablets
120 film-coated tablets
Mechanism of action
Capecitabine is an orally administered precursor (prodrug) of 5‑fluorouracil (5-FU) and is activated in a three-step process in the liver and tumour tissue.
1. After rapid absorption in the gastrointestinal tract, capecitabine in the liver is first metabolised by hepatic carboxylesterase to 5’-deoxy-5-fluorocytidine (5’-DFCR).
2. 5’-DFCR is then converted to 5’-deoxy-5-fluorouridine (5’-DFUR) by cytidine deaminase, principally located in the liver and tumour tissues.
3. The final catalytic activation occurs by thymidine phosphorylase, which is expressed in the tumour tissue in greater quantity. This transforms the 5’-DFUR into 5‑FU, resulting in cytostatic action affecting the tumour tissue in particular.
contains 150 mg carboplatin (1 x 1)
contains 450 mg carboplatin (1 x 1)
contains 600 mg carboplatin (1 x 1)
Mechanism of action
Carboplatin has biochemical properties similar to those of cisplatin, thus producing predominantly interstrand and intrastrand DNA crosslinks. Carboplatin exhibited comparable activity to cisplatin against a wide range of tumours regardless of implant site. Alkaline elution techniques and DNA binding studies have demonstrated the qualitatively similar modes of action of carboplatin and cisplatin. Like cisplatin, carboplatin induces changes in the superhelical structure of the DNA, consistent with a ‘DNA-shortening effect’.
1 vial with 100 mg powder
1 ampoule with 3 ml of solvent
1 capsule contains 40 mg lomustine
Mechanism of action
After oral administration, lomustine breaks down spontaneously, first into a chlorethyl diazonium ion and then into a chlorethyl carbonium ion. Its cytostatic effect is the result of the alkylation of the O6 of guanine by the chlorethyl carbonium ion. Bifunctional alkylation leads to DNA crosslinking and induces apoptosis.