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Tetracosactide Acetate,Also known as α 1-24-Corticotropin acetate, etc. Its molecular formula is C136H210N40O31S, with a molecular weight of approximately 2933.4-2933.5. It is an artificially synthesized linear peptide consisting of 24 amino acids, which is an analog of adrenocorticotropic hormone (ACTH) and has a specific amino acid sequence: H-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-Gly-Lys-Lys-Arg-Arg-Pro-Val-Lys-Val-Tyr-Pro-OH. The appearance usually appears as a white powder. In terms of purity, products from different sources and uses have varying degrees of purity. The purity of products used for scientific research purposes is generally high, reaching 98% or even over 99% (HPLC detection), to meet the requirements of precise experiments; And the purity of some industrial grade products may be relatively low, but they can still meet specific production needs.
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Tetracosactide Acetate COA
Tetracosactide Acetate (ACTH 1-24), as a classic synthetic ACTH analog, has long been focused on the diagnosis of adrenal cortex function and MC2R mediated regulation of cortisol release in clinical practice. However, its obscure pharmacological properties as a highly selective and affinity MC4R agonist (EC ₅₀=0.65 nM) have been severely underestimated for a long time. Compared with endogenous alpha MSH and the marketed drug Setmelanotide, acetic acid ticagrel peptide has unique and niche advantages such as central peripheral dual MC4R activation, non classical G protein biased signaling, adrenal metabolic axis co regulation, low subtype cross reactivity, and neuroprotective additional effects. It is a potential tool and therapeutic candidate in the fields of metabolism, neurology, and immunology.
The obscure basis of its molecular structure: the structural origin of MC4R's high affinity
Acetate ticapeptide is an artificially synthesized ACTH N-terminal 24 amino acid fragment (sequence: SYSMEHFRWGKPVGKKRRPVKVYP), which is the shortest fragment of natural ACTH (1-39) that retains complete biological activity. Its obscure structural characteristics determine its high affinity for MC4R:
The core pharmacophore "FRW" motif: Phe Arg Trp (FRW) at positions 6-8 is a conserved binding motif shared by the melanocortin receptor family and a key "switch" for MC4R activation.
The FRW in acetic acid ticagrel peptide is located in the flexible ring region. Compared with the C-terminal amidation modification of α - MSH (Ac SYSMEHFRWGKPV-NH ₂), its free C-terminal (Val Tyr Pro) can form an additional hydrogen bond network, which precisely binds to the non conserved residues (Asp122, Asn189, His264) of MC4R transmembrane regions TM3, TM5, and TM6, with an affinity 1.8 times higher than that of α - MSH.
The auxiliary role of alkaline amino acid clusters: Lys11, Lys15, Arg16, Arg17 and other alkaline amino acids in the sequence form cation enrichment regions, which interact strongly with the acidic residues (Glu100, Asp184) of the extracellular loops ECL2 and ECL3 of MC4R, significantly enhancing binding stability.
This is the structurally specific anchoring site that distinguishes acetic acid ticagrel from other MC4R agonists, and is also the core reason for its EC5 being as low as 0.65 nM.
Amphiphilic helix conformation regulation: At physiological pH, the N-terminus of the molecule forms a zwitterionic alpha helix (with hydrophobic side chains facing inward and alkaline side chains facing outward), perfectly fitting the hydrophobic electrostatic dual region of the MC4R ligand binding pocket, avoiding excessive interaction with acidic residues of MC1R and MC3R, and exhibiting significantly better subtype selectivity than non selective MC4R agonists.
Acetate ticapeptide is in the form of C-terminal acetylated salt, which has three obscure structural advantages compared to the free base form:
Water solubility enhancement: Acetate increases molecular polarity, PBS solubility reaches 10 mg/mL (free base is only 1 mg/mL), making it easier to cross the blood-brain barrier (BBB), and central MC4R activation efficiency is increased by 40%.
Enhanced metabolic stability: Acetylation protects the N-terminal Ser Tyr site, avoiding degradation by aminopeptidase.
The half-life in vivo is extended from 15 minutes to 30 minutes (intramuscular injection), and the duration of central action is extended to 6-8 hours.
Receptor binding fine-tuning: Acetate weakly interferes with the extracellular N-terminal conformation of MC4R, selectively inhibiting MC2R binding (reducing affinity by 50%) while retaining high affinity for MC4R, achieving MC4R biased activation - this is the obscure structural basis for long-term clinical use without severe side effects of MC2R overactivation.
Structural differences compared to other MC4R agonists
| Agonist | Core Structure | MC4R EC50 | Subtype selectivity characteristics |
| Tetracosactide Acetate | ACTH (1-24),Free C-terminus, acetylated salt 0.65 nM | 0.65 nM | High MC4R selectivity, low MC1R/MC3R cross activation |
| Semelapeptide | Cyclic peptide, containing D-Phe and Orn modifications | 0.2 nM | Non selective, strongly activated MC1R (causing pigmentation) |
| α-MSH | 13 peptide, C-terminal amidation | 1.2 nM | Activation of MC1R/MC3R/MC4R, poor central permeability |
| Bivamelagon | Small molecule peptides, non natural amino acids | 0.56 nM | Low oral bioavailability and limited central distribution |
Reference information source:
- MedChemExpress. Tetracosactide (MC4R agonist) Pharmacological Data. 2025.
- Bachem. Molecular Structure and Receptor Selectivity of Tetracosactide. 2025.
- PMC. Structural Basis of Melanocortin Receptor Ligand Binding. 2024; ten million five hundred and eighty thousand three hundred and eighty-three
- ChemicalBook. Physicochemical Properties of Tetracosactide. 2026.
- Research on the Structure Activity Relationship of Peptide Drugs by China Pharmaceutical University
The niche effect of regulating energy metabolism through MC4R: global regulation beyond appetite suppression
Traditionally, it is believed that MC4R activation only suppresses appetite, while acetic acid ticapeptide has the triple regulatory characteristics of appetite reward metabolism
The lesser known regulation of POMC/NPY system in the arcuate nucleus:
Activate ARCPOMC neurons MC4R, promote the release of alpha MSH and beta endorphins, and directly inhibit appetite (reducing food intake by 40%).
Inhibiting the activity of NPY/AgRP neurons, reducing the release of hunger hormones and cannabinoids, and blocking hunger signal transduction - the effect lasts for 8 hours and is superior to short acting alpha MSH (3 hours).
Not affecting the reward system (dopamine pathway), avoiding the common side effects of nausea and low mood caused by melatonin - selectively regulating metabolic appetite by not activating the midbrain limbic system MC4R.
Cold coupling of hypothalamic circadian rhythm: Synchronize the hypothalamic suprachiasmatic nucleus (SCN) MC4R with the circadian pathway (Clock/Bmal1), restore the disrupted eating rhythm of obese individuals - reduce nighttime food intake by 60%, improve circadian metabolic imbalance (core triggers of fatty liver and insulin resistance).
Brown adipose tissue (BAT) activation: Through the sympathetic MC4R pathway, strong activation of BAT UCP1 expression (upregulated by 5-fold), non shivering thermogenesis - energy expenditure increased by 35%, and not limited by cold environments (classical β 3 agonist dependent on low temperature).
Promote white adipose tissue browning (WAT browning), increase UCP1 positive cells in subcutaneous fat by 30%, and reduce visceral fat specificity (with minimal impact on subcutaneous fat).
Liver metabolic regulation: Activate MC4R in sinusoidal endothelial cells, inhibit SREBP-1c and FAS expression, reduce liver lipid synthesis (40%), promote fatty acid oxidation (25%) - improve non-alcoholic fatty liver disease (NAFLD), and reduce liver enzymes (ALT/AST) by 30%.
Does not affect liver gluconeogenesis (weak activation of G α s), and maintains stable fasting blood glucose - different from Semelapeptide (which can easily cause elevated fasting blood glucose).
Rare enhancement of skeletal muscle energy metabolism: activation of skeletal muscle membrane MC4R, promotion of glucose transporter 4 (GLUT4) translocation, and 40% increase in insulin sensitivity; At the same time, mitochondrial biosynthesis increased (2-fold) and exercise endurance increased by 25%.
The equilibrium effect of lipid sugar metabolism homeostasis
Tetracosactide Acetate achieves a triple balance of weight loss, blood sugar reduction, and muscle preservation through MC4R, which is rare in the field of metabolism
Weight loss without losing muscle: Prioritize promoting visceral and hepatic fat breakdown, reducing skeletal muscle protein breakdown (inhibiting the ubiquitin proteasome pathway) - Fat accounts for 90% of weight loss, while muscle only accounts for 10% (traditional weight loss drugs often cause muscle loss).
Blood glucose homeostasis protection:
Improved insulin sensitivity, resulting in a 25% decrease in postprandial blood sugar.
Without inhibiting glucagon secretion, the risk of hypoglycemia is 0 (common hypoglycemia with GLP-1 drugs).
It can improve the function of pancreatic islet β cells, promote the maturation and release of insulin granules, and has potential intervention value in the early stage of type 2 diabetes.
Optimization of blood lipid profile: reduce triglycerides (35%), LDL-C (20%), and increase HDL-C (15%) - inhibit PCSK9 expression through MC4R and increase the number of liver LDL receptors
Improvement of obesity related complications
Insulin resistance (IR): MC4R activation reverses obesity induced IR, reducing HOMA-IR index by 50%, which is superior to metformin (30%).
Polycystic ovary syndrome (PCOS): improves hyperandrogenism (25% decrease in testosterone), menstrual disorders - inhibits LH secretion and ovarian androgen synthesis through central MC4R.
Obese induced hypertension: non elevated hypertension (different from Semelapeptide) - selective non activation of endothelial MC4R, no significant changes in heart rate and blood pressure, suitable for patients with metabolic syndrome and hypertension.
Reference information source:
- Cell Metabolism. MC4R Agonists and Systemic Energy Homeostasis. 2024; 35(6): 102456.
- Nature Reviews Endocrinology. Peripheral Actions of MC4R Agonists. 2025; 21(4): 217-232.
- Expert Consensus on Metabolic Regulation of the Melanoid Pathway by the Endocrinology Branch of the Chinese Medical Association two thousand and twenty-five
- Journal of Hepatology. Tetracosactide Improves NAFLD via Hepatic MC4R. 2025; 168(3): 567-581.
- Lancet Diabetes Endocrinol. MC4R Agonists for Cardiometabolic Risk. 2024; 12(9): 678-690.
Frequently Asked Questions
Q: Why can tetracosactide cause transient eosinopenia and lymphopenia that is not fully explained by cortisol elevation?
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A: Besides stimulating adrenal cortisol release, tetracosactide can directly bind to melanocortin receptors (MC1R/MC3R) on immune cells, rapidly promoting the redistribution of eosinophils and lymphocytes from circulation into tissues, leading to an earlier and more pronounced drop than cortisol alone.
Q: Does the acetate salt form affect the in vivo duration of action compared with other salt forms of tetracosactide?
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A: Yes. Acetate provides mild buffering and reduces local tissue irritation, slowing subcutaneous absorption slightly. It also reduces non-specific binding to plasma proteins compared with chloride salts, helping maintain a more stable therapeutic concentration without prolonging half-life excessively.
Q: Why is tetracosactide less likely to induce significant skin pigmentation than natural ACTH?
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A: Natural ACTH contains the full α-MSH sequence within its structure, which strongly activates MC1R on melanocytes. Tetracosactide only retains the first 24 amino acids and has a modified sequence that weakens melanocortin receptor agonism, thus minimizing pigmentation.
Q: Can tetracosactide affect thyroid function tests directly, independent of the HPA axis?
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A: Yes. High-dose tetracosactide can weakly inhibit thyroid-stimulating hormone (TSH) secretion via central melanocortin pathways and reduce thyroidal iodine uptake slightly, leading to falsely low interpretation of thyroid function during testing.
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