Research
Hormonal
DL001 effectively suppresses hyperactive mTORC1 signaling in cells lacking a functional TSC (Tuberous Sclerosis Complex), restoring normal gene expression.
DL001 is shown to be as effective as rapamycin in suppressing the overactive mTORC1 signaling found in Tuberous Sclerosis Complex (TSC) cells. This suggests DL001 could be a safer alternative for treating TSC, as it may avoid the metabolic side effects associated with current rapalog treatments, although this is currently limited to cell culture models.
GoodSupportsHIGH confidence
We find that MEFs lacking Tsc1 have increased expression of a number of genes involved in metabolic pathways... and that the expression of these genes can be repressed to normal levels by treatment with either 100 nM rapamycin or 100 nM DL001.
Why this rating
Strong in vitro data showing gene expression normalization.
Source
A novel rapamycin analog is highly selective for mTORC1 in vivo
Katherine H. Schreiber et al. · Nature Communications · 2019
DOI 10.1038/s41467-019-11174-0
mechanism_onlyCited 197×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- The novel rapamycin analog DL001 selectively inhibits mTORC1 in vivo without disrupting glucose or lipid homeostasis, unlike conventional rapamycin which causes metabolic side effects via mTORC2 inhibition.Good
- DL001 reduces the immunosuppressive effects of mTOR inhibition compared to rapamycin, specifically preserving more T cell and Treg populations.Good
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