Life sciences · Journal article
Acs Chemical Biology · October 28, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract Though immune checkpoint blockade (ICB) therapy has been a promising advance in cancer treatment, response rates to ICB are low owing to other mechanisms that cancers employ to evade the immune system. SULT2B1b is an enzyme known to produce cholesterol sulfate (CS), an immunosuppressive metabolite that inhibits T-cell migration. Cancers expressing high levels of SULT2B1b thus generate a tumor microenvironment that excludes T cells, which leads to increased tumor growth and renders ICB therapy ineffective. Here, we identify a novel class of azasteroid SULT2B1b inhibitors with greater potency and selectivity than previously identified compounds. X-ray co-crystal structures indicate that these inhibitors bind in a conformation different from that of native substrates, enabling inhibition without acting as a substrate. Additionally, these new compounds effectively reduce CS levels in tumors in mice and, as such, have potential as cancer therapeutics in combination with ICB therapy.