If you have been reading about thymalfasin and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-03-28. Numbers and descriptions here follow the published literature rather than marketing material.
Thymosin alpha-1 is a 28-residue peptide first isolated from thymus tissue in the 1970s. It corresponds to the N-terminal portion of thymosin beta-4, from which it is cleaved in vivo. The peptide carries an acetyl group at its N-terminus, a modification that affects its charge and stability. Synthetic material produced by solid-phase peptide synthesis is chemically identical to the natural fragment and is the form used in research and clinical studies.
Laboratory work indicates that the peptide acts on cells of both the innate and adaptive immune systems. Reported effects include signalling through Toll-like receptors on dendritic cells, enhanced T-cell maturation, and increased natural killer cell activity. These actions are described largely from cell-culture and animal experiments, and the precise receptor-level events remain incompletely defined. Studies in humans have generally measured immune markers rather than a single defined molecular target. The resulting picture remains partly descriptive.
Thymosin alpha-1 is a synthetic peptide of 28 amino acid residues that corresponds to a naturally occurring fragment first isolated from thymus tissue. Its chain is acetylated at the amino terminus, a modification that shields the peptide from rapid cleavage by aminopeptidases. The molecule carries a net negative charge at physiological pH and dissolves freely in water. Researchers classify it as an immune-modulating agent rather than a classical hormone, because it acts on several cell types of both the innate and the adaptive immune system.
The peptide was identified during work in the 1970s on thymosin fraction 5, a partially purified extract of calf thymus. Investigators separated that mixture and characterized individual components, one of which they named thymosin alpha-1. The same compound later received the international nonproprietary name thymalfasin. Commercial material is produced by solid-phase peptide synthesis rather than by extraction, so synthetic and natural forms share an identical sequence. Naming conventions vary across the literature, and readers should distinguish the alpha-1 peptide from other thymosins that have unrelated sequences and functions.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Peptide | 28 amino acid residues |
| Molecular weight | Approximately 3108 Da | Depends on acetylation state |
| N-terminal modification | Acetylated | Affects charge and stability |
| Natural source | Fragment of thymosin beta-4 | Cleaved in vivo |
| Sequence length | 28 residues | Synthetic form matches natural |
Thymosin alpha-1 is a synthetic 28-amino-acid peptide whose sequence was first identified in extracts of bovine thymus tissue during the 1970s. The chain carries an acetyl group on its N-terminal serine. Its acidic residue content is high, which produces strong water solubility and an isoelectric point well below neutrality. Material supplied for laboratory and clinical use is manufactured by solid-phase peptide synthesis rather than purified from animal tissue. Different salt forms, such as the acetate, alter the counter-ion content without changing the peptide backbone.
Whether the free 28-residue peptide circulates in human tissue remains debated. The best-documented human source is prothymosin alpha, a larger acidic protein that carries the sequence at its N-terminus. Reports of measurable peptide levels in serum and lymphoid tissue exist, yet some of that signal may come from cross-reacting fragments or from the parent protein. Most reviews therefore treat prothymosin alpha as the established human molecule and describe independent circulation of the small peptide as an unresolved question.
Clinical research has examined the peptide in chronic hepatitis B and C, as a vaccine adjuvant, and in sepsis and oncology settings. Findings across trials are mixed; some report changes in selected immune markers, while others find no clear clinical benefit. Many studies are small and define outcomes differently, which limits comparison. Regulatory approval is confined to a few countries, and the compound is not an approved drug in the United States or most of Europe.
Overall evidence quality varies considerably. A large share of published reports come from single centers, rely on surrogate immunological markers, or lack adequate control groups. Systematic reviews have highlighted this heterogeneity as a barrier to pooling results. Open questions include which patients, if any, might benefit, what treatment duration is appropriate, and whether any effect is independent of standard care. The peptide is often described as an immune modulator rather than a therapy for one disease, which complicates confirmatory trial design.
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The weakening of the fibrous cap of atheromatous plaques by apoptosis of smooth muscle cells has also been linked to granzyme B. More recently, a key role for extracellular granzyme B has been forwarded for a number of autoimmune (e.g. arthritis, autoimmune blistering, scleroderma, lupus)(Reviewed in ) and/or age-related chronic inflammatory disorders (Photoaging, aneurysm, atherosclerosis, COPD, macular degeneration, etc.)(Reviewed in ). In many of these conditions, proof-of-concept has been demonstrated through the use of experimental models, genetic approaches and/or pharmacologic approaches.
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Sources: en.wikipedia.org
About 10–25% of gynecomastia cases are estimated to result from the use of medications or exogenous chemicals. Drugs can increase estrogen activity or increase the estrogen to androgen ratio through various mechanisms, such as binding to estrogen receptors, promoting estrogen synthesis, providing precursors that can be aromatized into estrogen, causing damage to the testes, inhibiting testosterone synthesis, inhibiting the action of androgens, or displacing estrogen from SHBG. Drugs with good evidence for association with gynecomastia include cimetidine, ketoconazole, gonadotropin-releasing hormone analogues, human growth hormone, human chorionic gonadotropin, 5α-reductase inhibitors such as finasteride and dutasteride, certain estrogens used for prostate cancer, and antiandrogens such as bicalutamide, flutamide, and spironolactone. Drugs with fair evidence for association with gynecomastia include calcium channel blockers such as verapamil, amlodipine, and nifedipine; risperidone, olanzapine, anabolic steroids, alcohol, opioids, efavirenz, alkylating agents, and omeprazole. Certain components of personal skin care products such as lavender or tea tree oil have been reported to cause prepubertal gynecomastia due to its estrogenic and anti-androgenic effects. Certain dietary supplements such as dong quai and Tribulus terrestris have also been associated with gynecomastia.
CREST syndrome, also known as the limited cutaneous form of systemic sclerosis (lcSSc), is a multisystem connective tissue disorder. The acronym "CREST" refers to the five main features: calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. CREST syndrome is associated with detectable antibodies against centromeres (a component of the cell nucleus), and usually spares the kidneys (a feature more common in the related condition systemic scleroderma). If the lungs are involved, it is usually in the form of pulmonary arterial hypertension.
Specifically, the FDA found a lack of efficacy for stanozolol as "an adjunct to promote body tissue-building processes and to reverse tissue-depleting processes in such conditions as malignant diseases and chronic nonmalignant diseases; debility in elderly patients, and other emaciating diseases; gastrointestinal disorders resulting in alterations of normal metabolism; use during pre-operative and postoperative periods in undernourished patients and poor-risk surgical cases due to traumatism; use in infants, children, and adolescents who do not reach an adequate weight; supportive treatment to help restore or maintain a favorable metabolic balance, as in postsurgical, postinfectious, and convalescent patients; of value in pre- operative patients who have lost tissue from a disease process or who have associated symptoms, such as anorexia; retention and utilization of calcium; surgical applications; gastrointestinal disease, malnourished adults, and chronic illness; pediatric nutritional problems; prostatic carcinoma; and endocrine deficiencies." The FDA gave Sterling six months to stop marketing stanozolol for the indications for which there was no evidence for efficacy, and one year to submit further data for the two indications for which it found probable efficacy. In August and September 1970, Sterling submitted more data; the data was not sufficient but the FDA allowed the drug to continue to be marketed, since there was an unmet need for drugs for osteoporosis and pituitary dwarfism, but Sterling was required to submit more data.
Sources: en.wikipedia.org
In most of the syntheses described here, it is necessary to attach and remove the starting reagent to/from a solid support. This can lead to the generation of a hydroxyl group, which can potentially affect the biological activity of a target compound. Ellman uses solid phase supports in a multi-step synthesis scheme to obtain 192 individual 1,4-benzodiazepine derivatives, which are well-known therapeutic agents. To eliminate the possibility of potential hydroxyl group interference, a novel method using silyl-aryl chemistry is used to link the molecules to the solid support which cleaves from the support and leaves no trace of the linker.
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== Interactions == Heat shock protein 47 has been shown to interact with collagens I, II, III, IV and V. It is involved in the secretion of collagen as well as the processing, assembly, and folding of collagen proteins. Hsp 47 binds specifically to procollagen and collagen only. The protein recognizes the triple helix of procollagen, two HSP47 proteins will bind to the leading and trailing strands of procollagen.
=== Plants === Putrescine is widely found in plant tissues, often being the most common polyamine present within the organism. Its role in development is well documented, but recent studies have suggested that putrescine also plays a role in stress responses in plants, both to biotic and abiotic stressors. The absence of putrescine in plants is associated with an increase in both parasite and fungal population in plants. Putrescine serves an important role in a multitude of ways, which include: a cation substitute, an osmolyte, or a transport protein. It also serves as an important regulator in a variety of surface proteins, both on the cell surface and on organelles, such as the mitochondria and chloroplasts. A recorded increase of ATP production has been found in mitochondria and ATP synthesis by chloroplasts with an increase in mitochondrial and chloroplastic putrescine, but putrescine has also been shown to function as a developmental inhibitor in some plants, which can be seen as dwarfism and late flowering in Arabidopsis plants.
Sources: en.wikipedia.org
It corresponds to the first 28 amino acids of thymosin beta-4, a larger protein found in many tissues. The fragment is acetylated at its N-terminus and is produced synthetically for research and pharmaceutical use. Synthetic and natural forms share the same sequence.
It is usually described as an immunomodulatory peptide rather than a classical hormone. It does not travel to a single distant organ in the manner of an endocrine hormone. Classification varies across sources, and some texts group it with thymic peptides generally.
The broad outline involves immune cell activation, but the specific molecular steps remain under investigation. Different studies report effects on dendritic cells, T cells, and natural killer cells. No single receptor has been confirmed as the sole mediator.
It is a 28-residue synthetic peptide studied as an immune-modulating agent and approved as a drug in some countries. The sequence matches a naturally occurring fragment isolated from thymus tissue. It is not a hormone in the endocrine sense.