The Claim

Cyclocreatine is transported into HEK293 cells and human blood-brain barrier model cells primarily through the creatine transporter SLC6A8, as evidenced by saturable uptake kinetics and reduced influx upon inhibition or knockdown of SLC6A8, indicating that cyclocreatine may act as a substrate for creatine transporter-mediated transport in cellular models relevant to brain delivery.

Source: Cyclocreatine Transport by SLC6A8, the Creatine Transporter, in HEK293 Cells, a Human Blood-Brain Barrier Model Cell, and CCDSs Patient-Derived Fibroblasts

What the research says

Roughly balanced

Support and challenge are close. The picture may shift as more studies come in.

Supports
4score
Challenges
0score

These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.

How it works
1 study reviewed
In plain English

Cyclocreatine gets into brain-like cells in a lab mainly using a special doorway called the creatine transporter — when scientists block or remove this doorway, less cyclocreatine gets in, suggesting it relies on that path.

See the scientific wording

Cyclocreatine is transported into HEK293 cells and human blood-brain barrier model cells predominantly via the creatine transporter (SLC6A8), as demonstrated by saturable uptake kinetics and inhibition or knockdown of SLC6A8 reducing its influx, suggesting it may serve as a substrate for CRT-mediated transport in cellular models relevant to brain delivery.

What the research says

1 study

  1. Study: Cyclocreatine Transport by SLC6A8, the Creatine Transporter, in HEK293 Cells, a Human Blood-Brain Barrier Model Cell, and CCDSs Patient-Derived Fibroblasts

    The study shows that cyclocreatine gets into brain-relevant cells using the same gateway as creatine, and when that gateway is blocked or broken, less cyclocreatine gets in—just like the claim says.

Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies

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