Your goal is to extract structured information from the user's input that matches the form described below. When extracting information please make sure it matches the type information exactly. Do not add any attributes that do not appear in the schema shown below.

```TypeScript

 { // Information on the clinical trial characteristics from the abstract
 conditions: string // The condition or disease being treated in the clinical trial
 drug_or_intervention: string // The drug or intervention used in the clinical trial
}
```


Please output the extracted information in JSON format. Do not output anything except for the extracted information. Do not add any clarifying information. Do not add any fields that are not in the schema. If the text contains attributes that do not appear in the schema, please ignore them. All output must be in JSON format and follow the schema specified above. Wrap the JSON in <json> tags.



Input:Liraglutide treatment is associated with a low frequency and magnitude of antibody formation with no apparent impact on glycemic response or increased frequency of adverse events: results from the Liraglutide Effect and Action in Diabetes (LEAD) trials.  Therapeutic proteins/peptides can produce immunogenic responses that may increase the risk of adverse events or reduce efficacy. The objectives were to measure and characterize antibody formation to liraglutide, a glucagon-like peptide-1 receptor agonist, to investigate the impact on glycemic control and safety, and to compare it with exenatide, an agent in the same class. Antibody data were collected during six Liraglutide Effect and Action in Diabetes (LEAD) trials (26-104 wk duration). Samples for determination of antibody formation were collected at LEAD trial sites and analyzed at central laboratories. Antibodies were measured in LEAD trial participants with type 2 diabetes. Interventions included once-daily liraglutide (1.2 or 1.8 mg) or twice-daily exenatide (10 μg). The main outcome measures included the proportion of patients positive for anti-liraglutide or anti-exenatide antibodies, a glucagon-like peptide-1 cross-reacting effect, and an in vitro liraglutide- or exenatide-neutralizing effect. Change in glycosylated hemoglobin A(1c) (HbA(1c)) by antibody status and magnitude [negative, positive (high or low level)]. After 26 wk, 32 of 369 (8.7%) and 49 of 587 (8.3%) patients had low-level antibodies to liraglutide 1.2 and 1.8 mg, respectively [mean 3.3% antibody-bound radioactivity out of total radioactivity (%B/T), range 1.6-10.7%B/T], which did not attenuate glycemic efficacy (HbA(1c) reductions 1.1-1.3% in antibody-positive vs. 1.2% in antibody-negative patients). In LEAD-6, 113 of 185 extension patients (61%) had anti-exenatide antibodies at wk 26 (range 2.4-60.2%B/T). High levels of anti-exenatide antibodies were correlated with significantly smaller HbA(1c) reductions (P = 0.0022). After switching from exenatide to liraglutide, anti-exenatide antibodies did not compromise a further glycemic response to liraglutide (additional 0.4% HbA(1c) reduction). Liraglutide was less immunogenic than exenatide; the frequency and levels of anti-liraglutide antibodies were low and did not impact glycemic efficacy or safety. Output:

conditions: Diabetes|Diabetes Mellitus, Type 2
interventions: Drug: liraglutide|Drug: placebo|Drug: liraglutide|Drug: liraglutide|Drug: glimepiride|Drug: metformin|Drug: placebo