Valfix Drug Interactions

100 mg: The likelihood of metabolic interactions is low due to limited metabolism and plasma protein-binding and almost complete renal elimination of unchanged drug.
Lamivudine is predominantly eliminated by active organic cationic secretion. The possibility of interactions with other drugs administered concurrently should be considered, particularly when their main route of elimination is active renal sceretion via the organic cationic transport system eg. trimethoprim. Other drugs (eg. ranitidine, cimetidine) are eliminated only in part by this mechanism and were shown not to interact with lamivudine.
Drugs shown to be predominantly excreted either via the active organic anionic pathway or by glomerular filtration are unlikely to yield clinically significant interactions with lamivudine.
Lamivudine has no pharmacokinetic interaction with α-interferon when the 2 drugs are concurrently administered. There were no observed clinically significant adverse interactions in patients taking this product with commonly used immunosuppressant drugs (eg. cyclosporine A). However, formal interaction studies have not been performed.
Lamivudine may inhibit the intracellular phosphorylation of zalcitabine when the 2 medicinal products are used concurrently. This product is therefore not recommended to be used in combination with zalcitabine.
Emtricitabine: Due to similarities, lamivudine should not be administered concomitantly with other cytidine analogues, such as emtricitabine. Moreover, lamivudine should not be taken with any other medicinal products containing lamivudine.
150 mg: The likelihood of metabolic interactions is low due to limited metabolism and plasma protein-binding and almost complete renal clearance.
Administration of trimethoprim/sulfamethoxazole 160 mg/800 mg results in an increase in lamivudine exposure, because of the trimethoprim component; the sulfamethoxazole component did not interact. However, unless the patient has renal impairment, no dosage adjustment of lamivudine is necessary. Lamivudine has no effect on the pharmacokinetics of trimethoprim or sulfamethoxazole. When concomitant administration is warranted, patients should be monitored clinically. Co-administration of lamivudine with high doses of co-trimoxazole for the treatment of Pneumocystis carinii pneumonia (PCP) and toxoplasmosis should be avoided.
The possibility of interactions with other medicinal products administered concurrently should be considered, particularly when the main route of elimination is active renal secretion via the organic cationic transport system e.g. trimethoprim. Other medicinal products (e.g. ranitidine, cimetidine) are eliminated only in part by this mechanism and were shown not to interact with lamivudine. The nucleoside analogues (e.g. didanosine and zidovudine) are not eliminated by this mechanism and are unlikely to interact with lamivudine.
A modest increase in C_max was observed for zidovudine when administered with lamivudine, however overall exposure (AUC) is not significantly altered. Zidovudine has no effect on the pharmacokinetics of lamivudine.
Due to similarities, lamivudine should not be administered concomitantly with other cytidine analogues, such as emtricitabine. Moreover, lamivudine should not be taken with any other medicinal products containing lamivudine.
In vitro lamivudine inhibits the intracellular phosphorylation of cladribine leading to a potential risk of cladribine loss of efficacy in case of combination in the clinical setting. Some clinical findings also support a possible interaction between lamivudine and cladribine. Therefore, the concomitant use of lamivudine with cladribine is not recommended.
Lamivudine metabolism does not involve CYP3A, making interactions with medicinal products metabolised by this system (e.g. PIs) unlikely.