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The EU is committed to promoting human rights through its development policy. This article argues that its expansive human rights framework has led to EU‐internal and outside‐in politicization of LGBTI rights in Uganda. It views contestation as a mechanism of politicization and suggests two paths through which contestation occurs; based on the normative core or on the application of human rights conditionality. We establish these paths through a case study of politicization of LGBTI rights promotion in the Uganda–EU partnership. While member states' policies are more affected by political pressure from domestic constituents, EU institutions aim to depoliticize the issue and prioritizes diplomatic channels. Conversely, conditionality operates as a driver for contestation in beneficiary states. Whereas postcolonial studies interpret claims of universal rights as neo‐colonial intervention, our findings highlight a more nuanced applicatory contestation by rights activists. These actors insert themselves as change agents aiming to reshape the policies of international norm promoters.

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Cocaine metabolism has been studied previously with respect to the formation of predominant hydrolytic or hepatotoxic metabolites via oxidative pathways. In the present study, cocaine and eight of its metabolites (norcocaine, ecgonine methyl ester, benzoylecgonine, benzoylnorecgonine, 3-hydroxy-benzoylecgonine, cocaethylene, norcocaethylene, and ecgonine ethyl ester) were incubated with microsomes from rat liver, kidney, lung, and brain. Qualitative analysis of the metabolites produced was performed using solid phase extraction (SPE), trimethylsilylation, and GC/MS. It was found that the metabolites with a free carboxylic group (e.g., benzoylecgonine) were not further oxidized by microsomal enzymes and their presence in urine or blood may therefore be due to hydrolysis of the respective alkylated entities. Although microsomes from all organs exhibited oxidative metabolism, significant differences were noted. Kidney microsomes produced essentially the same results as liver, but aryl hydroxylated metabolites were not found in incubations with lung and brain microsomes. N-Hydroxy-norcocaine was found only in traces with brain microsomes. It appears that cocaine is converted to N-hydroxy-norcocaine (which is the precursor of toxic metabolites) not only in the liver but also in other organs of rat. This might be relevant in the development of lung toxicity observed in smokers of cocaine ("crack").