How is gelatide absorbed, distributed, metabolized, and excreted in humans?
Executive summary
Available reporting does not describe a molecule named “gelatide”; instead, literature discusses gelatin (a mixture of peptides from collagen), gelatin-based carriers and gelatin hydrolysates. Human and animal ADME data for gelatin show rapid oral absorption of hydrolyzed gelatin peptides (95% absorbed in mice within 12 hours; 41.9% of digested gelatin absorbed as peptides in one report), and degradation/excretion pathways that involve proteolysis, hepatic handling and renal elimination [1] [2] [3].
1. What you actually asked for — and what sources cover
You asked about absorption, distribution, metabolism and excretion (ADME) for “gelatide.” None of the provided sources mention a compound named “gelatide.” The available documents instead discuss gelatin, gelatin hydrolysates, gelatin carriers and gelatin-based pharmaceutical excipients and plasma substitutes — distinct entities for which experimental ADME data are reported (not found for “gelatide” in these sources) [4] [5] [6].
2. Absorption: gelatin peptides cross the gut quickly in animal models and are seen in plasma
Animal tracer studies show rapid enteral uptake: a 14C-labeled gelatin hydrolysate given to mice produced 95% absorption of the applied dose within 12 hours, and peptides of 2.5–15 kDa were detected after intestinal passage [1]. Human-focused reviews and product monographs note that digested gelatin yields peptides and amino acids that appear in plasma — one analysis reported ~41.9% of digested gelatin absorbed from the intestine in peptide form [2]. Gelatin in oral formulations can alter gastric emptying but is not necessarily rate‑limiting for absorption in humans [7] [8].
3. Distribution: amino-acid–like tissue patterns with notable cartilage accumulation in mice
Where distribution data exist, gelatin-derived radioactivity tracks much like proline and other collagen amino acids, with particular accumulation in cartilage (mouse study) — radioactivity in cartilage more than doubled versus controls [1]. Reviews of gelatin carriers and nanoparticles stress that particle size, crosslinking and surface modifications (e.g., PEGylation) change organ targeting and plasma half-life, implying that engineered gelatin materials will distribute differently than simple hydrolysates [9] [10].
4. Metabolism: proteolytic breakdown, hepatic handling and peptide cleavage dominate
Gelatin is a complex mixture of peptides produced by collagen hydrolysis; metabolic fate is therefore proteolysis to amino acids and smaller peptides. Plasma‑substitute literature and product monographs describe proteolytic degradation (including hepatic processing) and adaptive metabolism that prevents accumulation even in renal insufficiency for some gelatin products [3] [11]. Therapeutic‑protein and macromolecule ADME literature underscores that large peptide/protein materials follow different metabolic paths from small molecules, mainly via proteolysis and subsequent conjugation or catabolic clearance [12].
5. Excretion: renal elimination of small fragments and proteolytic clearance of larger fractions
Sources describe dual pathways: low‑molecular-weight gelatin fragments are filtered by the kidney and excreted in urine; larger gelatin molecules are first degraded proteolytically (including in liver) and their catabolites are then excreted, so net urinary elimination predominates for gelatin-based plasma substitutes [3] [11]. Reviews of gelatin carriers note that modifying gelatin (crosslinking, PEGylation) can prolong plasma half-life and change clearance routes [9] [13].
6. Formulation matters: “gelatin” is not a single pharmacokinetic entity
The ADME profile changes dramatically with form: free digested gelatin peptides (hydrolysates) behave like proteins/amino acids; liquid-filled soft gelatin capsules alter drug absorption kinetics by changing dissolution and Tmax; gelatin nanoparticles and PEGylated carriers change distribution and half-life due to size and surface chemistry [1] [14] [9]. Product‑level data and reviews emphasize that gelatin matrices are engineered to tune release and PK [15] [13].
7. Limitations, gaps and alternative viewpoints in the available reporting
No source in the provided set uses the name “gelatide”; therefore any definitive ADME statements about “gelatide” are unsupported here. Human ADME data for intact gelatin macromolecules are sparse in this collection — much evidence is animal or in vitro, or concerns engineered gelatin carriers rather than a single defined chemical [1] [9] [12]. Some product monographs claim no clinically relevant accumulation even with renal impairment for specific gelatin products, but that reflects particular formulations and cannot be generalized to all gelatin derivatives or hypothetical “gelatide” molecules [3].
8. Bottom line for readers
If you meant a gelatin-derived material, existing studies and product literature show fast absorption of hydrolysates (animal tracer and peptide‑detection data), proteolytic metabolism with hepatic involvement, and predominant urinary excretion of small fragments — while engineered gelatin carriers can markedly alter distribution and clearance [1] [2] [3] [9]. If you meant a distinct molecule called “gelatide,” that name is not found in the provided reporting; no ADME data for “gelatide” are available in these sources (not found in current reporting).