The following research states that Cocaine misuse keeps on being a genuine medical issue around the world. Regardless of exceptional exploration, there is still no FDA-affirmed drug to treat cocaine use problem (CUD). In this report, we investigated the possible utility of beta-caryophyllene (BCP), a FDA-affirmed food added substance for the treatment of CUD. We found that BCP, when managed intraperitoneally or intragastrically, portion conditionally constricted cocaine self-organization, cocaine-adapted spot inclination, and cocaine-prepared restoration of medication looking for rodents. Interestingly, BCP neglected to change food self-organization or cocaine-prompted hyperactivity. It likewise neglected to keep up self-organization in a medication replacement test, proposing that BCP has no maltreatment potential. BCP was recently answered to be a particular CB2 receptor agonist. Out of the blue, pharmacological bar or hereditary cancellation of CB1, CB2, or GPR55 receptors in quality knockout mice neglected to change BCP’s activity against cocaine self-organization, proposing the contribution of non-CB1, non-CB2, and non-GPR55 receptor components. Besides, pharmacological bar of μ narcotic receptor or Toll-like receptors complex neglected to modify, while barricade of peroxisome proliferator-enacted receptors (PPARα, PPARγ) turned around BCP-actuated decrease in cocaine self-organization, recommending the inclusion of PPARα and PPARγ in BCP’s activity. At last, we utilized electrical and optogenetic intracranial self-incitement (eICSS, oICSS) ideal models to consider the hidden neural substrate systems. We found that BCP is more successful in lessening cocaine-improved oICSS than eICSS, the previous driven by optical initiation of midbrain dopamine neurons in DAT-cre mice. These discoveries demonstrate that BCP might be helpful for the treatment of CUD, likely by incitement of PPARα and PPARγ in the mesolimbic framework.