Background and Purpose: Phthalates are synthetic compounds that can be grouped into two types according to the number of carbon atoms in their backbone, short- and long-chain. In utero exposure of rodents to certain low molecular weight phthalate compounds (carbon backbone C3-C6), particularly during the window of susceptibility for male development, can result in a testicular dysgenesis-like syndrome in rats. Di-isononyl phthalate (DINP) is a high molecular weight phthalate (complex mixture of branched chains, predominantly C9 isomers), and a high production volume chemical. Evaluation of the endocrine disrupting potential of DINP was conducted by comprehensive literature review to identify toxicological data from in silico, in vitro and in vivo (e.g., reproductive, developmental, subchronic toxicity and cancer) studies related to the perturbation of the estrogen, androgen, thyroid, or steroidogenesis (EATS) pathways. Methods: A structured primary literature search was performed for DINP and DINP metabolites. Citation mining and reviews of stakeholder toxicology reports describing DINP in vivo studies were also included in the evaluation. For studies identified as relevant, endocrine-related and general toxicity endpoints were reviewed and extracted into the Excel-based tool referenced in the ECHA/EFSA guidance document for the identification of endocrine disruptors. Information from high throughput (HT) assays available from the US Environmental Protection Agency Toxicity Forecaster (ToxCast) program were queried and reviewed for activity in a battery of assays that map to each of the EATS pathways. QSAR predictions were performed for DINP and its primary and secondary metabolites using Leadscope models. Each line of evidence was independently evaluated and integrated to assess the potential of DINP to perturb one or more of the EATS pathways. A mode of action (MoA) assessment was performed to assess the biological plausibility of endocrine pathway disruption resulting in adverse outcomes. Results: A total of 64 primary peer-reviewed publications were identified in the literature search with six stakeholder toxicology reports identified that contain endocrine endpoints relevant to the EATS assessment. Data for a total of 153 ToxCast HT assays, mapped to EATS endpoints were also identified and evaluated. Weight of evidence assessments for each of the EATS pathways showed exposure to DINP did not perturb the estrogen or thyroid pathways. For the androgen pathway, DINP had negative QSAR predictions for AR binding or antagonism and was negative in 24/25 AR binding/agonist or antagonist HT assays. In silico, in vitro and mechanistic (Hershberger) studies showed no evidence to support antiandrogenic effects. Some evidence of reduced fetal testicular testosterone (T) levels was observed with no change in plasma T in adult animals (P0, F1) and no consistent effects on fertility indices. For the steroidogenesis pathway, the evidence showed no activity in aromatase inhibition assays or changes in steroid hormones in the H295R HT assay. Conclusions: Based on this assessment of DINP endocrine activity, exposure did not exhibit perturbations in the estrogen, thyroid, or steroidogenesis pathways. For consideration of perturbation of the androgen pathway, while there was some evidence of changes in fetal testicular T levels resulting from in utero exposure to DINP, other plausible molecular initiating or early key events that could potentially drive anti-androgen apical outcomes were not activated.