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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.

Mechanism of action

Abiraterone acetate is converted to abiraterone, an androgen biosynthesis inhibitor. Abiraterone selectively inhibits the enzyme CYP17, which is expressed in testicular, adrenal, and prostate tumor tissue and is required for androgen biosynthesis.

Androgen-sensitive prostate cancers respond to androgen level-lowering treatment. Androgen deprivation therapies, such as treatment with LHRH analogs or orchiectomy, lower androgen production in the testes but do not affect androgen production in the adrenal glands or tumor.

Treatment with abiraterone lowers serum testosterone levels to undetectable levels (using commercially available tests) when given together with LHRH analogues or when an orchiectomy is performed.

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.

Mechanism of action 

Immunostimulant

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.

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.

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.

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’.

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.