Selank + Adamax is a two-peptide liquid catalog product. One component, Selank, is a tuftsin-derived anxiolytic with a Russian research and clinical record [1]. The other, Adamax, is a designer Semax/P021 hybrid with no peer-reviewed pharmacology of its own [2]. So the evidence behind the two halves is very uneven, and the combination has never been studied. This monograph covers the composition, what each component's literature shows, the naming confusion around Adamax, and where the evidence stops.
Composition
The catalog listing is "Selank / Adamax Blend Spray – 5/5mg | 10ml". The product is a pre-mixed liquid in a 10 ml spray container. The label figures are reported here only as the catalog states them. The components are:
- Selank, a synthetic heptapeptide derived from tuftsin (Thr-Lys-Pro-Arg-Pro-Gly-Pro), developed by Russian researchers [1][4].
- Adamax, a single synthetic peptide, Ac-MEHFPGPAG-NH₂ (about 1032.23 daltons). It combines the Semax MEHFPGP core with a P021-derived adamantyl-glycine C-terminus [2].
This product should not be confused with the Selank + Semax blend. Some vendors have sold Selank + Semax under the name "Adamax," which is chemically incorrect: Adamax is one defined molecule, not a two-peptide mix [2][4]. A community source reports that a ~984 Da compound (Ac-MEHFPGPAG-OH, with no adamantyl group) also circulates under the name "Adamax" and argues that it is a different molecule from the ~1032 Da structure [11]. Which "Adamax" is in a given product can only be settled by mass spectrometry.
What each component contributes
Selank. The literature describes GABA-system effects, BDNF modulation, effects on enkephalin metabolism, and immunomodulatory activity carried over from tuftsin. No single mechanism is established as primary [1]. In IMR-32 neuroblastoma cells, Selank alone did not change mRNA levels of 84 GABAergic-system genes. Given with GABA, it nearly abolished GABA-induced expression changes. The authors read this as partial support for an effect on how GABA interacts with GABA-A receptors [5]. In rats, Selank changed BDNF expression in the hippocampus [6]. In a rat model of alcohol withdrawal, Selank eliminated withdrawal-associated anxiety-like behaviour and mechanical allodynia without changing ethanol consumption [7]. Selank is used clinically in Russia, but it is not approved by the FDA or EMA, and Western-standard large trials are essentially absent [1]. A 2026 review lists Selank among neuroactive peptides for which clinical trials are currently lacking [12].
Adamax. No receptor, pathway, behavioural or clinical study of Adamax itself is indexed in PubMed. A PubMed search for "adamax peptide" (October 2026) returned one unrelated machine-learning paper. Any Adamax pharmacology is therefore inferred from its parent compounds [2]:
- From the Semax core: in rats, Semax increased hippocampal BDNF protein and TrkB phosphorylation and improved conditioned-avoidance learning [8][3].
- From the P021 modification: P021 is a CNTF-derived peptidergic compound. It crossed the blood–brain barrier and reduced tau in aged rats [9]. Started in early development in 3xTg-AD mice, it prevented cognitive impairment and raised pCREB and BDNF [10].
Whether the hybrid behaves like Semax, like P021, like both or like neither has not been demonstrated, and it has no approved indication anywhere [2].
Combination evidence — the honest boundary
A PubMed search for "selank adamax" (October 2026) returned zero records. No study of any kind has tested Selank and Adamax together, in humans, animals or cells. Adamax also has no direct literature on its own [2].
That leaves this product one evidence tier below the Selank + Semax blend. For Selank + Semax, both components have their own Russian clinical literature and the open question is only the combination [4]. For Selank + Adamax, one component's effects are entirely inferred [2]. The "complementary anxiolytic + neurotrophic" framing sometimes used for this product draws on Selank data [1][5][6] and on Semax/P021 parent data [8][9][10]. It is not drawn from anything measured with Adamax or with the blend.
Research context
Researchers may meet this product as a variant of the Selank + Semax stack. It is not equivalent to that stack. A design that needs a characterised reference compound should use Selank, Semax or P021 directly [2][4]. Any research use of this product is testing an uncharacterised mixture that contains an uncharacterised molecule.
Storage and handling
This is a liquid product, not a lyophilized vial. No published stability data exist for Selank and Adamax together in solution, and vendor-stated storage terms should be treated as unverified. A cloudy or discoloured liquid is a reason to question the batch.
Quality and COA considerations
A meaningful COA must give separate mass-spectrometry identity for both peptides: Selank at about 751 daltons [4], and Adamax at about 1032.23 daltons [2]. It must also show that the Adamax present is the adamantylated ~1032 Da molecule and not the ~984 Da non-adamantylated analog or plain Semax at about 813 daltons [11][2]. Per-component HPLC purity and content should be reported against the label, along with microbial and endotoxin testing appropriate to a liquid product. Selank/Semax mislabelling and "Adamax" identity confusion are reported quality problems in this market [2][4][11].
Key references
- [1] VialTalk monograph — Selank — https://vialtalk.com/forum/peptide-research-library/selank-research-monograph-anxiolytic-heptapeptide
- [2] VialTalk monograph — Adamax — https://vialtalk.com/forum/peptide-research-library/adamax-research-monograph-semax-p021-hybrid-designer-peptide
- [3] VialTalk monograph — Semax — https://vialtalk.com/forum/peptide-research-library/semax-research-monograph-nootropic-neurotrophic
- [4] VialTalk monograph — Selank + Semax — https://vialtalk.com/forum/peptide-research-library/selank-semax-research-monograph-russian-nootropic-stack
- [5] GABA, Selank, and Olanzapine in IMR-32 cells (2017) — https://pubmed.ncbi.nlm.nih.gov/28293190/
- [6] Inozemtseva et al. 2008 — Selank and hippocampal BDNF in rats — https://pubmed.ncbi.nlm.nih.gov/18841804/
- [7] Selank in a rat alcohol-withdrawal model (2014) — https://pubmed.ncbi.nlm.nih.gov/24913576/
- [8] Dolotov et al. 2006 — Semax regulates BDNF and trkB in rat hippocampus — https://pubmed.ncbi.nlm.nih.gov/16996037/
- [9] Khatoon et al. 2015 — P021 and tau in aged rats — https://pubmed.ncbi.nlm.nih.gov/26401692/
- [10] Wei et al. 2021 — P021 in 3xTg-AD mice — https://pubmed.ncbi.nlm.nih.gov/34057082/
- [11] VialTalk forum — 984 Da vs 1032 Da "Adamax" — https://vialtalk.com/forum/general-peptide-discussion/984-da-vs-1032-da-adamax-why-these-are-not-the-same-compound
- [12] Rahman et al. 2026 — Therapeutic peptides in orthopaedics (review) — https://pubmed.ncbi.nlm.nih.gov/41490200/
Research-use note: This is an educational summary of the published research on Selank and on the parent compounds of Adamax. Adamax has no peer-reviewed pharmacology of its own, the Selank + Adamax combination has not been evaluated in any published study, and neither component is FDA- or EMA-approved. Nothing here is medical advice or a usage recommendation.