Mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that regulates fundamental cellular processes including growth control, autophagy and metabolism. mTOR constitutes the catalytic subunit of two signalling complexes: mTOR complex 1 (mTORC1) and 2 (mTORC2). Manipulating mTORC1 signalling in animal models has shown that this pathway has key roles in neurogenesis, and mTORC1 hyperactivation during neurodevelopment causes a group of disorders known as mTORopathies. mTORopathies typically involve brain malformations and neurological manifestations like epilepsy. One example is tuberous sclerosis complex (TSC), which is caused by loss-of-function mutations in mTORC1 negative regulators TSC1 or TSC2. The molecular mechanisms by which mTORC1 regulates neurodevelopment and leads to mTORopathies when dysregulated remain poorly understood, in part because the targets of mTORC1 during neurodevelopment have not been systematically characterised. To identify novel neurodevelopmental mTORC1 substrates, we used an unbiased Tandem Mass Tag and quantitative mass spectrometry approach on embryonic brain tissue from mice with a conditional knockout of Tsc1 in the brain using Nestin-Cre. An analysis pipeline then identified 25 high-confidence, novel mTORC1 targets in the developing brain. These targets have various molecular functions, and at least 7 of them have roles in neurodevelopmental disorders with previously unknown connection to the mTORC1 pathway and TSC. To validate these findings in humans, we also performed quantitative phosphoproteomic analysis of surgical tuber and SEGA tissue from TSC patients. Our characterisation of novel mTORC1 targets during neurodevelopment reveals new mechanisms and identifies potential therapeutic targets for mTORopathy patients.