Adamax

Adamax is a synthetic heptapeptide derived from semax; the specific amino acid sequence being Ac-MEHFPG-AG-NH₂

 

 

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Adamax is a synthetic heptapeptide derived from semax; the specific amino acid sequence being Ac-MEHFPG-AG-NH₂.

Semax itself, a fragment of hormona adrenokortîkotropîk (ACTH), possesses potent neurotrophic and cognitive-enhancing properties.

Structural limitations within semax lead to significant limitations to its half-life and efficiency of crossing the blood-brain barrier.

To alleviate these limitations scientists introduced a bulky adamantylacetate group through covalent bonding at the carboxyl terminus.

This modification significantly improved the pharmacokinetic properties of the peptide molecule.

Introduction of this moiety provides near complete resistance to subsequent enzymatic degradation; retention time of the active form of adamax within the body is greatly prolonged.

More excitingly, the previously mentioned ‘ingenious’ design promotes an increase in efficiency with which the peptide crosses said barrier, and enhanced specificity and selectivity is achieved.

Compromising no biological activity, all known effects of semax are either maintained or enhanced.

Dor

Ac-MEHFPGP-Adam-NH2

Hejmara CAS

/

Formula Molecular

C50H68N10O12S

Giraniya molekulî

1033.212

Research Of Adamax:

1.Therapeutic Efficacy and Clinical Potential

Clinical trials have shown Adamax to outperform Semax in promoting the growth and protection of Faktora neurotrofî ya ku ji mêj ve tê (BDNF) û heta xalekê nerve growth factor (NGF).

Replacing Semax as a therapeutic agent, particularly for psychiatric disorders or social cognition enhancement, is a very real possibility.

2.Zêdekirina Cognitive (Intelligence being a subset)

Direct stimulation of BDNF upregulation is Adamax’s primary function.

Neuronal cell activity, new neuron generation/differentiation and all associated synaptic improvements are what the research is currently focused on.

Hippocampal and prefrontal cortex activity is also increased.

Long term experimental groups have and will continue to show, quantifiably, superior memory and learning abilities.

3.Bandorên Neuroprotective

Adamax’s cognitive enhancement and intelligence-boosting functions originate not only from its direct promotion of neural cell growth, but also from demonstrable neuroprotective properties.

Effective reduction of cerebral infarction areas in stroke patients has been demonstrated; stimulation and subsequent recovery of various necrotic cells is another key aspect of this neuroprotection.

Reducing excitotoxicity and providing near-constant antioxidant effects are additional, well-documented activities.

Positioning itself within this realm, Adamax holds much promise as a true therapeutic agent for neurodegenerative disorders – Alzheimer’s being the prime example, Parkinson’s following closely behind.

4.Stress and Anxiety Relief

Adamax enhances the human ability to adapt to environmental changes; the brain itself must rapidly adjust to, and resist, a variety of physiological stressors resulting from these quick environmental shifts.

Maintaining some form of homeostasis is the end goal.

Modulation of the hypothalamic-pituitary-adrenal (HPA) pişt is central to this process, increasing or decreasing the appropriate release of neurotransmitters, all lesser ‘stress responses’ being suppressed.

Anxiolytic effects are a primary benefit – drowsiness and cognitive impairment (the near universal side effects of traditional anxiolytics) are completely avoided.

Enhancing cognitive function during any form of anxiety relief is what makes Adamax particularly alluring to researchers and patients alike.

COA

HPLC

MS

(1)Nirx, N. V.; Sokolov, O. Y.; Gabaeva, M. V.; Grivennikov, ez. YEK.; Andreeva, L. YEK.; Myasoedov, N. F.; Zozulya, YEK. YEK. Semax and Selank Inhibit the Enkephalin-Degrading Enzymes of Human Serum. Russian Journal of Bioorganic Chemistry 2001, 27(3), 156-159. DOI: 10.1023/yek:1011373002885.

(2)Vlasova, ez. M.; Buravtcov, D. E.; Saletsky, YEK. M. Di lêkolînên li ser taybetmendiyên neuroprotektîf ên dermanê "Semax" de di îşemiya mêjî de analîza ronahiyê ya pêkhateyên xwînê. Journal of Spectroscopy Applied 2009, 76(1), 121-126. DOI: 10.1007/s10812-009-9141-y.

(3)Abraham, M. H.; Acree, W. E.; Liu, X. Descriptors for adamantane and some of its derivatives. Journal of Molecular Liquids 2021, 325. DOI: 10.1016/j.molliq.2020.114894.

(4)Dane, C.; Montgomery, YEK. P.; Kassiou, M. The adamantane scaffold: Beyond a lipophilic moiety. European Journal of Medicinal Chemistry 2025, 291. DOI: 10.1016/j.ejmech.2025.117592.

(5)Dmitrieva, V. G.; Povarova, O. V.; Skvortsova, V. EZ.; Limborska, S. YEK.; Myasoedov, N. F.; Dergunova, L. V. Semax û Pro-Gly-Pro Veguheztina Neurotrofîn û Genên Receptorê Wan Piştî Îskemiya Cerebral çalak dikin.. Neurobiolojiya hucreyî û molekulî 2009, 30(1), 71-79. DOI: 10.1007/s10571-009-9432-0.

(6)Eremin, K. O.; Kudrin, V. S.; Saransari, P.; Mal, S. S.; Grivennikov, ez. YEK.; Myasoedov, N. F.; Rayevsky, K. S. Guh nede, An ACTH(4-10) Bi Taybetmendiyên Nootropîk re analog, Li Rodentan Pergalên Mejiyê Dopaminergîk û Serotinergîk çalak dike. Lêkolînên Neurokîmyayî 2005, 30(12), 1493-1500. DOI: 10.1007/s11064-005-8826-8.

(7)Glazova, N. Y.; Manchenko, D. M.; Volodina, M. YEK.; Merchieva, S. YEK.; Andreeva, L. YEK.; Kudrin, V. S.; Myasoedov, N. F.; Levitskaya, N. G. Guh nede, ACTH sentetîk(4–10) analog, Guhertinên behre û neurokîmyayî yên piştî rûdana fluvoxamine ya destpêkê di mişkên spî de kêm dike.. Neuropeptides 2021, 86. DOI: 10.1016/j.npep.2020.102114.

(8)Medvedeva, E. V.; Dmitrieva, V. G.; Limborska, S. YEK.; Myasoedov, N. F.; Dergunova, L. V. Guh nede, analogek ACTH(4−7), di dema birîna mêjî ya iskemîk de di mişkan de îfadeya genên bersivê yên bêparastin bi rê ve dibe. Genetics Molecular û Genomics 2017, 292(3), 635-653. DOI: 10.1007/s00438-017-1297-1.

(9)Pae, C.-U. Dermankirina Dermankirina "Semax" ji bo Depresyonê. Spectrums CNS 2014, 13(1), 20-21. DOI: 10.1017/s1092852900016102.

Dor:

Ac-MEHFPGP-Adam-NH2

CAS:

N/A

M.W:

1033.21g/mol

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