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:Preclinical and clinical investigation of a CCR5 antagonist, AZD5672, in patients with rheumatoid arthritis receiving methotrexate.  To investigate both the preclinical effects of blocking the chemokine receptor CCR5 and the clinical effects of this approach on the signs and symptoms of rheumatoid arthritis (RA) in patients with active disease. Preclinical evaluations of AZD5672, a small-molecule antagonist of CCR5, were performed, including studies of ligand binding and chemotaxis. The pharmacokinetics of AZD5672 were assessed in both single- and multiple-dose studies in healthy volunteers. A randomized, placebo-controlled, phase IIb study was conducted in patients with active RA receiving methotrexate. Treatment arms were AZD5672 (20, 50, 100, or 150 mg orally, once daily), matched placebo, or open-label etanercept (50 mg subcutaneously, once weekly). The primary end point was the proportion of patients achieving a 20% improvement response on the American College of Rheumatology improvement criteria (ACR20) at week 12. Secondary end points included the ACR20 over time, as well as 50% (ACR50) and 70% (ACR70) improvement responses, changes in individual components of the ACR improvement criteria, and disease activity measured with the Disease Activity Score based on the 28-joint count. AZD5672 was a highly potent and selective antagonist of CCR5, displaying nonproportional steady-state pharmacokinetics while inhibiting internalization of CCR5 in an ex vivo macrophage inflammatory protein 1β stimulation assay in which AZD5672 was evaluated over the 20-150-mg dose range. In the phase IIb study testing this dose range in patients with RA (n = 371 patients randomized to received treatment), AZD5672 was generally well tolerated, with no unexpected adverse events. There was no statistically significant difference in the proportion of patients achieving an ACR20 response at week 12 between those receiving any dose of AZD5672 and those receiving placebo; etanercept was significantly more efficacious than AZD5672 and placebo. Despite a clear rationale for targeting CCR5, this clinical study showed that AZD5672, administered orally, did not have any clinical benefit, suggesting that CCR5 antagonism alone is unlikely to be a viable therapeutic strategy in RA. Output:
{'conditions': 'Rheumatoid Arthritis', 'interventions': 'Drug: AZD5672|Drug: Etanercept|Drug: Placebo|Drug: AZD5672|Drug: AZD5672|Drug: AZD5672'}