There has been growing interest in using pharmacological fMRI to identify novel treatments for fear, yet these models are limited with respect to determining process-specific effects on the actual subjective experience of fear which represents the key symptom why patients seek treatment. Combining a selective angiotensin II type 1 receptor (ATR1) antagonist with a fear vigilance fMRI paradigm and neurofunctional decoding in n = 87 individuals we demonstrate that AT1R blockade selectively reduces the neurofunctional reactivity to fear-inducing visual oddballs in terms of attenuating dorsolateral prefrontal activity and amygdala-ventral anterior cingulate (vACC) communication, and further show that the observed effect is due to reduced subjective fear, but not threat or non-specific negative affect, using a decoding analysis. Our findings demonstrate a highly specific role of AT1R in subjective fear experience and demonstrate the feasibility of a precision approach to the affective characterization of novel receptor targets for fear in humans.