What they found

RADA16/EAK16 scaffolds support neuronal attachment, extensive neurite outgrowth (PC12, hippocampal, cerebellar, DRG neurons), and functional synapse formation comparable to Matrigel. First in vivo biocompatibility data: intramuscular injection in Fisher 344 rats (1 mg/ml, 20 μl) showed no inflammation, necrosis, motor impairment, or tissue abnormalities at 9 days to 5 weeks. Injection site was visually undetectable. No immune responses detected (rabbit/goat antibody assay). Scaffold pore size 50–200 nm, >99% water, macroscopic filament diameter 10–20 nm (consistent with Zhang 1993).

How this applies to h09

Biocompatibility data is directly relevant to the ototopical delivery route. The five stabilization mechanisms listed (H-bonds, ionic bonds, hydrophobic interactions, overlap, salt coordination) confirm that assembly depends on all four RADA units — truncation or charge disruption anywhere is likely to impair gelation, which is relevant to the 118 aa tail question. The “no immune response” data supports the scaffold as a safe delivery vehicle.

Key numbers

  • Scaffold filament diameter (EM): 10–20 nm (bundle; consistent with Zhang 1993)
  • Scaffold pore size: 50–200 nm
  • In vivo biocompatibility: no inflammatory response, 9 days–5 weeks, rat IM injection
  • Peptide assembly concentration: 1–10 mg/ml
  • Cell types supporting growth: PC12, hippocampal, cerebellar granule, DRG, sympathetic neurons

Connections