Which peptides are studied in relation to the mTOR pathway?

The mTOR pathway is a central node in cell-growth signalling, and a range of peptides and peptide-adjacent compounds have been studied in relation to it. The most directly peptide-focused entry in the available evidence is LL-37, the human cathelicidin peptide, investigated in osteosarcoma models via the PTEN/AKT/mTOR axis [1]. Beyond LL-37, the literature captured here includes small-molecule and biological agents whose proposed mechanisms intersect with mTOR — fingolimod (FTY720) in kidney transplantation [4], anlotinib in glioma [6], alpha ketoglutarate in colorectal surgery [3] — alongside non-peptide research models such as bovine embryos [7] and Yanbian yellow cattle [2].

LL-37 is the human cathelicidin peptide, a host-defence peptide of the cathelicidin family. The evidence block for this page does not supply its sequence, molecular formula or molecular weight, so those identifiers are not stated here. The pathway family at the centre of the peptide work described below is the PTEN/AKT/mTOR signalling axis [1].

Research Studies

LL-37 and SQLE-mediated cholesterol synthesis in osteosarcoma cells

In vitro work used osteosarcoma cell lines alongside normal human bone marrow mesenchymal stem cells (hBMSCs) to assess viability, clonogenic survival, migration, invasion, cell-cycle distribution, cell death and cholesterol metabolism. The study reported that LL-37 inhibits osteosarcoma progression by suppressing SQLE-mediated cholesterol synthesis via the PTEN/AKT/mTOR pathway [1]. Transcriptomic profiling and siRNA approaches were part of the method set [1]. These findings are in vitro and should be read as such.

Fingolimod and RhoA/mTOR signalling in kidney transplant recipients

Fingolimod (brand name Gilenya, candidate name FTY720) is being tested in a randomized, double-blind, placebo-controlled trial in de novo kidney transplant patients. The stated hypothesis is that abrogating the fibrogenic effects of both the RhoA and mTOR pathways with fingolimod will reduce structural damage in transplanted kidneys and possible subsequent transplant failure [4]. The endpoint of interest is expansion of the interstitial compartment, described as a precursor of interstitial fibrosis and graft loss [4].

Anlotinib and c-MET/AKT/mTOR signalling in glioma cells

Anlotinib was investigated in human glioma cells for direct antitumour effects, with the study examining whether those effects were associated with hepatocyte growth factor receptor (c-MET)/protein kinase B (AKT)/mTOR signalling and with altered autophagy-associated protein expression [6]. Glioma is described as difficult to treat because malignant cells show rapid proliferation, diffuse invasion and frequent recurrence [6]. This is a cell-based study.

Alpha ketoglutarate and inflammatory response in colorectal surgery

The RISIS-CR trial proposes to identify inflammatory responsiveness of patients before colorectal cancer surgery and to administer prophylactic anti-inflammatory treatment targeted only to those with an excessive pro-inflammatory response. Alpha ketoglutarate (AKG), described as a geroprotector supplement, is the agent named in the proposal [3]. The rationale given is that geroprotectors reduce inflammation and may reduce postoperative systemic inflammatory response and complications after colorectal cancer surgery [3]. This is a registered trial proposal, not a completed efficacy finding.

mTOR pathway activation and trophectoderm differentiation in bovine embryos

In mice, the mTOR pathway influences the Hippo pathway, leading to expression of trophectoderm (TE)-related genes. The bovine study examined whether these mechanisms are fully characterized in bovine embryos, and reported that pharmacological mTOR pathway activation does not enhance trophectoderm differentiation in bovine embryos [7]. This is an embryo-model finding and does not translate directly to other species or systems.

lncRNA DANCR and the miR-19a-3p/PTEN/AKT/mTOR pathway in BMSC osteogenic differentiation

A study of long non-coding RNA DANCR examined its role in osteogenic differentiation of bone marrow mesenchymal stem cells and the underlying mechanisms, with BMSCs intervened using sh-DANCR [5]. The work is framed around the miR-19a-3p/PTEN/AKT/mTOR pathway and the context of osteoporosis [5]. This is a reference-only entry supporting the broader picture of PTEN/AKT/mTOR involvement in bone biology.

Mitochondria-enriched BMSC exosomes and PI3K/Akt/mTOR in Parkinson's disease models

Mitochondrial dysfunction and neuroinflammation are described as drivers of dopaminergic neuron loss in Parkinson's disease. BMSC-derived small extracellular vesicles are reported as neuroprotective but limited in repairing mitochondrial deficits, prompting engineering of mitochondrial-enriched sEVs (Exo-Mito) [8]. The reported pathways include PINK1/parkin and PI3K/Akt/mTOR [8]. This is a reference-only entry and is not built around a peptide.

Intramuscular fat deposition and upstream mTOR signalling in Yanbian yellow cattle

Sixty 24-month-old Yanbian yellow cattle (n = 30 per group) were categorized into high-IMF and low-IMF groups. Integrated transcriptomics and non-targeted metabolomics (n = 8 per group) associated intramuscular fat deposition with a dual-layered regulatory framework: an upstream signalling layer comprising PPAR, PI3K-Akt and mTOR pathways, and a downstream metabolic execution layer [2]. This is an animal-production study, not a peptide study.

Across the entries above, the recurring pattern is that mTOR appears as one arm of a larger signalling axis — PTEN/AKT/mTOR, PI3K/Akt/mTOR, c-MET/AKT/mTOR — rather than as an isolated target. Where the evidence is animal-only or in vitro, that is stated in the relevant section. No human dose, clinical recommendation or outcome promise is made anywhere on this page.

If you are reading this for personal health reasons

The materials described here are sold for laboratory research use only, and we do not provide dosing or medical guidance. Anyone considering a compound for themselves should speak to a licensed clinician. Nothing on this page should be read as a treatment recommendation.

Sources

• [1] LL-37 inhibits osteosarcoma progression by suppressing SQLE-mediated cholesterol synthesis via the PTEN/AKT/mTOR pathway — https://europepmc.org/article/PMC/PMC13321046
• [2] Integrated transcriptomics and metabolomics reveal the molecular mechanisms of intramuscular fat deposition in Yanbian yellow cattle — https://pubmed.ncbi.nlm.nih.gov/42025074/
• [3] Reducing Inflammatory Syndrome in Surgery - Colorectal (RISIS-CR) Trial — https://clinicaltrials.gov/study/NCT06646809
• [4] Fingolimod for the Abrogation of Interstitial Fibrosis and Tubular Atrophy Following Kidney Transplantation — https://clinicaltrials.gov/study/NCT05285878
• [5] Regulatory role of lncRNA DANCR in osteogenic differentiation of bone marrow mesenchymal stem cells through targeting the miR-19a-3p/PTEN/AKT/mTOR pathway — https://pubmed.ncbi.nlm.nih.gov/42686955/
• [6] Anlotinib inhibits glioma cell proliferation, migration, and invasion by suppressing c-MET/AKT/mTOR signaling and altering autophagy-associated protein expression — https://pubmed.ncbi.nlm.nih.gov/42687323/
• [7] Pharmacological mTOR pathway activation does not enhance trophectoderm differentiation in bovine embryos — https://pubmed.ncbi.nlm.nih.gov/42641359/
• [8] Mitochondria-enriched BMSC exosomes restore microglia-neuron cross-talk in Parkinson's disease via PINK1/parkin and PI3K/Akt/mTOR pathways — https://pubmed.ncbi.nlm.nih.gov/42556769/