Background and Purpose: Phthalates are a group of synthetic compounds that are widely used in the manufacturing of polymers and are found in a variety of consumer products. Di-isodecyl phthalate (DIDP) is a high molecular weight phthalate (complex mixture of branched C9-C11 isomers), and a high production volume chemical that is present in range of products. Evaluation of its potential to be an endocrine disruptor (ED) is important to understand its potential hazard. In the present evaluation, a comprehensive literature review was conducted to identify toxicological data from in silico, in vitro and in vivo (e.g., reproductive, developmental, sub-chronic toxicity and cancer) studies related to perturbation of the estrogen, androgen, thyroid, or steroidogenesis (EATS) pathways. Methods: A structured primary literature search was performed for DIDP and DIDP metabolites. Citation mining and reviews of stakeholder toxicology reports describing DIDP in vivo studies were also included in the evaluation. Relevant studies were identified by title and abstract (TiAb) screening. Inclusion/exclusion criteria were defined by a PECO (Population, Exposure, Comparator and Outcome) as follows: P: Human or mammalian species at any life stage; E: DIDP or metabolites; C: Humans exposed to lower levels of DIDP or experimental animal receiving vehicle-only; O: any EATS pathway endpoints for in vivo, in vitro, in silico or epidemiological studies. 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 ED 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 DIDP and its primary and secondary metabolites using Leadscope models. Each line of evidence from these sources of data were independently evaluated and integrated to assess the potential of DIDP to perturb one or more of the EATS pathways. Results: The literature search for DIDP and DIDP metabolites identified 271 articles in PubMed. Following TiAb screening, 18 primary peer-reviewed publications met the inclusion criteria (i.e., PECO statement) and were therefore considered relevant for inclusion in this EATS evaluation. Following deduplication between the published and stakeholder toxicology reports, 30 studies were evaluated in the full text review. Data for a total of 88 ToxCast HT, mapped to EATS endpoints, were also evaluated. Weight of evidence assessments showed exposure to DIDP did not perturb the estrogen or thyroid pathways or estradiol biosynthesis. For the androgen pathway, a lack of endocrine activity was observed for DIDP, including a lack of endocrine activity in the ToxCast HT assays. A lack of data was identified for DIDP metabolites; however, this limitation was mitigated by sufficient in vivo studies of DIDP where rapid and extensive metabolism is observed, and any potential effects would be captured within the study design. DIDP did not produce adverse outcomes stemming from disruption of the androgen pathway in adult male rodents. In utero DIDP exposure did not produce adverse reproductive outcomes or changes in anogenital distance in off-spring. Additionally, consistent changes in testosterone biosynthesis in fetuses were not observed after in utero exposure. Conclusions: Overall, it was concluded that DIDP is not an endocrine disruptor. This conclusion is based on a lack of evidence across EATS pathways with no biologically plausible link that could established between endocrine activity and adverse effects in vivo.