Mass · Stability · Evidence
Adamax vs Semax vs P21
Adamax, Semax and P21 are often grouped together, but they are different molecules with very different amounts of published evidence. This page compares what each is, how its stability is designed, and where direct evidence stops.
Short answer: Semax (≈813.9 g/mol) has the most published research. P21 has limited animal data and is a different, CNTF-derived peptide. Adamax 984 Da and 1032 Da are supplier-specified Semax-family constructs with no verified independent studies, so any stability or potency advantage remains a hypothesis.
Side-by-side comparison
| Property | Adamax 984 Da | Adamax 1032 Da | Semax | P21 (P021) |
|---|---|---|---|---|
| Family | Semax family (ACTH(4-10) analog) | Semax family (ACTH(4-10) analog) | ACTH(4-7) fragment with a Pro-Gly-Pro tail | CNTF-derived peptide (not Semax family) |
| Sequence | Ac-MEHFPGPAG-OH (supplier specification) | Ac-MEHFPGP-Adamantylglycine-NH₂ (supplier specification) | Met-Glu-His-Phe-Pro-Gly-Pro | Short acetylated CNTF fragment with adamantylglycine (published P021 design) |
| Molecular mass | ≈984.1 Da average (C₄₄H₆₁N₁₁O₁₃S) | ≈1032.2 Da average (C₅₀H₆₉N₁₁O₁₁S) | ≈813.9 g/mol | Not listed in our catalog; confirm against lot documents |
| Stability design | N-terminal acetylation and an Ala-Gly extension. No adamantane group. No published stability data for this construct. | N-terminal acetylation plus a C-terminal adamantylglycine amide. Greater stability is a design hypothesis, not a measured result for this construct. | The Pro-Gly-Pro tail was added to the ACTH(4-7) fragment to slow breakdown by peptidases. No acetylation or amidation. | Adamantylglycine was used by P021 researchers to investigate stability and brain exposure. This is the origin of the adamantane idea later applied to Adamax. |
| Direct evidence | No independent peer-reviewed study of this construct was verified. | No independent peer-reviewed study of this construct was verified. | The most studied of the three. Rodent studies report BDNF and TrkB changes; most published work comes from a small number of research groups. | Animal studies only, mainly mouse models of Alzheimer's-like pathology. No human trials. |
| Evidence level | None verified | None verified | Moderate | Limited |
Adamax sequences and formulas are supplier specifications that require matching lot documentation. Purity does not by itself establish identity or vial quantity.
Key questions
Are Adamax, Semax and P21 the same compound?
No. Semax is a seven-residue ACTH fragment analog. Adamax 984 Da and 1032 Da are two different supplier-specified Semax-family constructs. P21 (P021) is derived from ciliary neurotrophic factor (CNTF) and is not part of the Semax family.
Why do the molecular masses differ?
Each mass reflects a complete, different molecule. Semax is about 813.9 g/mol. Adamax 984 Da adds acetylation and an Ala-Gly extension. Adamax 1032 Da carries a C-terminal adamantylglycine amide. The roughly 48 Da gap between the two Adamax labels is the difference between whole molecules, not the mass of one added group.
Which one is the most stable?
No study has measured all three side by side. Semax's Pro-Gly-Pro tail is a documented design for resisting peptidase breakdown. Adamantylglycine was studied for stability in P021. Whether it makes Adamax 1032 Da more stable is an untested hypothesis.
How much evidence exists for each?
Semax has the largest body of published animal research. P021 has a smaller set of mouse and rat studies. No independent peer-reviewed study directly characterizing either Adamax construct was verified. Findings for Semax or P021 cannot be transferred to Adamax.
Can mass alone tell these products apart?
Mass spectrometry can separate molecules of clearly different mass, such as 984 and 1032 Da. It supports an identity claim only when matched to a written target construct and a lot record. Purity and vial quantity are separate questions.
References
- Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006. doi:10.1016/j.brainres.2006.07.080
- Baazaoui N, Iqbal K. Prevention of dendritic and synaptic deficits and cognitive impairment with a neurotrophic compound. Alzheimers Res Ther. 2017. doi:10.1186/s13195-017-0273-5
Neither reference studies Adamax. See also the Semax family article and the Adamax FAQ.
Research Use Only. All compounds compared here are sold strictly for in-vitro laboratory research. Not for human consumption, therapeutic use, veterinary use, or any in-vivo application. This page compares published research and specifications only and provides no dosing or administration guidance.
