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ANA-12 prevented activation of the receptor by BDNF with a high potency. ANA-12 showed direct and selective binding to TrkB and inhibited processes downstream of TrkB without altering TrkA and TrkC functions. Saturation binding studies with TrkBECD-Fc showed that ANA-12 binds TrkBECD-Fc with a Kd of 12 μM . The selective TrkB (tropomyosin-receptor-kinase) antagonist ANA-12 reduced OIH when given one or seven days after cessation of morphine.