Adamax 1032 Da (5mg)

What is Adamax 1032 Da?

Adamax 1032 Da is a supplier-specified Semax-family research construct. Its listed structure is Ac-Met-Glu-His-Phe-Pro-Gly-Pro-Adamantylglycine-NH₂. The 1032 Da label describes molecular identity; this catalog item contains 5mg per vial.

Listed vial contents: 5mg. These are supplied quantities, not administration doses. Current pricing and availability are shown in the strength selector.

Which identity should I verify?

For this product, verify Ac-MEHFPGP-Adamantylglycine-NH₂, formula C₅₀H₆₉N₁₁O₁₁S and an average molecular mass near 1032.2 Da. The roughly 48 Da difference from the 984 label is the net difference between complete specified molecules, not the mass of a simply added adamantane group. Purity alone does not establish identity or 5mg vial quantity.

What mechanisms are being studied?

The specified molecule combines an N-acetylated Semax-family core with a C-terminal adamantylglycine amide. Adamantane is a cage-shaped hydrocarbon group. P021 researchers used an adamantylglycine modification to investigate stability and brain exposure in a different, CNTF-derived peptide. That design rationale has not been demonstrated for Adamax 1032 Da.

What are the research questions?

• LC-MS identity assignment for the specified 1032.2 Da construct
• Comparisons with the distinct 984 Da non-adamantane construct
• Testing whether the terminal modification changes measured stability or model-specific responses

What does the published work describe?

Semax studies provide background for the parent peptide family. P021 mouse studies provide background for an adamantylglycine design rationale in a different peptide. Neither literature set tests Adamax 1032 Da. No independent peer-reviewed study directly characterizing or comparing the two Adamax constructs was verified for this page.

Experimental models in the cited papers

• Rat hippocampus; parent Semax only
• 3×Tg-AD mouse model; P021 only

What could future research explore?

A defined pharmacokinetic and analytical comparison could test whether the specified terminal modification changes stability, exposure or duration relative to confirmed Semax-family comparators. Those proposed properties should not be treated as established before direct compound-specific data exist.

These are research directions, not established applications of the product sold here.

What are the limits of this evidence?

Claims that Adamax is stronger, longer acting, more brain-penetrant or clinically beneficial are not supported by direct evidence for this construct. Semax and P021 findings cannot be transferred to Adamax 1032 Da. The listed structure and formula are supplier specifications and require matching batch confirmation.

Study references

1. 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
2. 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

How should I check lot documentation?

Match the product, strength and lot to an original analysis document. Literature describes experimental findings; it does not verify the contents of this inventory. Generated sample reports illustrate the reporting flow and are not evidence of testing, purity or accreditation.