���沙莫瑞林历史与监管定位 — Hands-On Walkthrough

By Editorial Desk · published 2026-06-19 · last reviewed 2026-07-07 · Info

GHRH analog is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.

Updated 2026-07-07. Numbers and descriptions here follow the published literature rather than marketing material.

特沙莫瑞林历史与监管定位

在临床研究之外，特沙莫瑞林常被讨论为生长激素分泌促进剂，但这一说法需要限定。它并不等同于生长激素本身，也不属于普通减重药物。部分研究关注其减少腹部脂肪和改善脂质谱的潜力，另一些研究则关注胰岛素抵抗和 IGF-1 升高等信号。这些效应的临床意义仍在评估中，尚未形成统一结论。

特沙莫瑞林是一种合成肽，其序列与人生长激素释放激素的 44 个氨基酸形式相关。它在 N 端带有反式-3-己烯酰基修饰，这一改动可减缓二肽基肽酶 IV 的降解。该化合物属于生长激素释放激素受体激动剂，可刺激垂体释放生长激素。研究文献通常将其归入合成肽类药物，而非小分子化合物。

Background and Clinical Profile

Clinical study of tesamorelin has centered on adults with HIV-associated lipodystrophy, a condition in which abdominal fat accumulates while peripheral fat is lost. In controlled trials, treated participants showed reductions in visceral adipose tissue measured by imaging, alongside modest shifts in some lipid values. Effects on subcutaneous fat were smaller and less consistent across studies. Whether these changes translate into fewer cardiovascular events remains an open question, because the trials were not designed or powered to answer it.

Tesamorelin is a synthetic peptide that acts as an analog of growth hormone-releasing hormone, a natural hypothalamic signal. Its sequence corresponds to the forty-four amino acid form of the human hormone, with a small acyl group attached near the amino terminus. That modification slows enzymatic breakdown and extends the time the peptide remains active in circulation. The compound was developed as a pharmacological way to raise endogenous growth hormone output rather than supplying the hormone directly.

Tesamorelin at a glance

Biological Role and Origin

Interest in this peptide developed because native GHRH has a short circulating lifetime. The N-terminal modification slows cleavage by dipeptidyl peptidase IV, an enzyme that removes the first two residues of many peptides and terminates their activity. Slower degradation means a longer window of receptor stimulation per administration. This design logic parallels other modified peptide hormones, where a small chemical change at a vulnerable site yields a more durable molecule without altering the core mechanism of action.

The peptide is synthesized chemically rather than extracted from biological sources. Solid-phase synthesis builds the chain from the C-terminus toward the N-terminus, after which the hexenoyl group is attached. Purity is typically assessed by high-performance liquid chromatography, and identity is confirmed by mass spectrometry. Regulatory review of the finished product focuses on these analytical controls, since small deviations in sequence or modification can change biological activity. Questions about long-term effects on the pituitary axis remain areas of continued investigation.

Tesamorelin is a synthetic peptide that belongs to the growth hormone-releasing hormone (GHRH) family. Its sequence corresponds to the fully active 44-amino-acid form of human GHRH, with a single structural modification: the addition of a trans-3-hexenoyl group at the N-terminus. That modification is not found in the naturally occurring hormone and was introduced deliberately during development to improve stability against enzymatic degradation. The compound is therefore best described as a stabilized analogue rather than a naturally occurring peptide.

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Identity and Development Background

Several related peptides act on the same receptor, including sermorelin, a shorter GHRH fragment, and modified analogs such as CJC-1295 and modified GRF(1-29) that are common in research settings rather than approved products. Tesamorelin differs from growth hormone itself in that it acts upstream, prompting the pituitary to release the hormone through physiological signaling rather than supplying it directly. Terminology in the literature distinguishes GHRH analogs, growth hormone secretagogues, and recombinant growth hormone, although popular discussion often blurs these categories together. Precise naming matters when comparing study results.

Tesamorelin is a synthetic peptide of 44 amino acids that reproduces the sequence of human growth hormone-releasing hormone (GHRH) and carries a trans-3-hexenoyl group on its N-terminal tyrosine. That small fatty-acid modification blocks cleavage by dipeptidyl peptidase-4, the enzyme that rapidly degrades native GHRH in plasma. The result is a molecule with a longer circulating half-life than the natural hormone while retaining the same receptor target. It is supplied as a lyophilized powder for reconstitution and belongs to the broader class of GHRH analogs studied for effects on pituitary growth hormone secretion.

Tesamorelin Identity And Structure

Several compounds share the GHRH framework, including sermorelin, the shorter 1-29 fragment, and other analogs built on the full 1-44 chain. Naming follows a common convention: a stem that identifies the peptide plus a suffix marking analog status. Reports may describe tesamorelin by its sequence fragment, as a GHRH(1-44) analog, or by its amino-terminal modification. Indexing the compound therefore requires searching all of these forms, since some older literature predates the current international nonproprietary name.

Tesamorelin is a synthetic peptide built from 44 amino acids and classified with the growth hormone–releasing hormone family. Its sequence corresponds to the human GHRH(1-44) backbone, carrying one structural change at the amino terminus. That change is a trans-3-hexenoyl group placed where the natural peptide would have an unmodified end. The modification is the feature that separates the compound from the endogenous hormone in name, in stability, and in how it is handled in the laboratory.

Background and Clinical Development

Clinical interest in tesamorelin arose from the need to address visceral adiposity in people living with HIV. Antiretroviral therapy improved survival but was associated in some patients with central fat accumulation, altered lipid profiles, and metabolic complications. This condition, often called HIV-associated lipodystrophy, involves excess visceral adipose tissue that is difficult to manage through diet and exercise alone. Investigators evaluated tesamorelin because GHRH analogs can stimulate growth hormone secretion and influence fat distribution without direct liposuction or invasive procedures.

A Phase 3 program led to regulatory approval in the United States in 2010 for reduction of excess visceral abdominal fat in adults with HIV and lipodystrophy. Subsequent studies examined effects on liver fat, muscle area, and metabolic markers, with mixed findings for some endpoints. Long-term cardiovascular outcomes and effects on mortality remain uncertain because most trials were relatively short and focused on imaging-based fat measurements. Use in populations without HIV has been studied experimentally but is not part of the approved indication.

Tesamorelin is a synthetic analog of growth hormone-releasing hormone, a peptide hormone produced by the hypothalamus. The molecule retains the 44-amino-acid sequence of human GHRH and carries a trans-3-hexenoyl modification at its N-terminus. This modification increases resistance to enzymatic degradation and extends the peptide's functional stability relative to native GHRH. The compound is supplied as a lyophilized powder for reconstitution and subcutaneous administration in clinical settings. Its development code was TH9507, and it belongs to the GHRH analog class. It is not a growth hormone product; instead, it acts upstream to stimulate endogenous growth hormone release.

Reference notes

=== Biology === The dragon's blood tree usually produces its flowers around March, though flowering does vary with location. The flowers tend to grow at the end of the branches. The plants have inflorescences and bear small clusters of fragrant, white, or green flowers. The fruits take five months to completely mature. The fruits are described as a fleshy berry, which changes from green to black as it gradually ripens. The fleshy berry fruit ends up being an orange-red color that contains one to three seeds. The berries are usually eaten and dispersed by birds and other animals. The tree's umbrella-shaped crown is adapted to arid conditions and is influenced by atmospheric moisture. Its leaves are scleromorphic, helping to prevent excessive water loss. The dragon's blood tree's distinctive umbrella shape is made possible by its unusual growth pattern. Unlike most monocots, Dracaena cinnabari undergoes secondary growth⁠—a rare ability that allows its trunk to thicken over time. While its stem develops growth ring-like zones, these do not reliably indicate age since they form from irregular vascular bundle patterns rather than seasonal growth cycles. This growth mechanism differs significantly from dicot trees. Instead of forming continuous growth rings, D. cinnabari produces scattered vascular strands in its secondary tissue. This unique structure provides the necessary support for its broad crown while being efficient in its harsh, resource-limited environment.

Strict breeding and farm management to reduce Salmonella prevalence in hens. Washing and sterilizing eggs at GP Centers (Grading and Packing facilities), often using hypochlorous acid solutions, before packaging. A best-before date system based on the assumption of raw consumption. Most producers set this date at about two weeks from packing, after which eggs are still considered safe if cooked thoroughly. A cold chain distribution system maintaining low temperatures from farm to retailer. Despite these measures, the risk is not zero. Salmonella can contaminate eggs externally via feces or internally if the hen itself is infected. Consumers are advised not to use cracked eggs for raw consumption.

== Benefits == One of the main advantages of this method of preparing frozen food is that the freezing process takes only a few minutes. The exact time depends on the type of IQF freezer and the product. The short freezing prevents formation of large ice crystals in the product's cells, which destroys the membrane structures at the molecular level. This makes the product keep its shape, colour, smell and taste after defrost, to a far greater extent. Another advantage of IQF technology is its ability to separate units of the products during freezing, which produces a higher quality product compared to block freezing. This is important for food sustainability, as the consumer can defrost and use the exact quantity needed. A growing demand in IQF products is registered at global level due to the higher quality of these products and to the benefit of having separately frozen pieces. IQF is also a common pre-treatment for freeze-drying food because both processes preserve the size, taste and cell structure of the food better than methods such as traditional block freezing or air drying.

Type 1 accounts for 5 to 10% of diabetes cases and is the most common type of diabetes diagnosed in patients under 20 years; however, the older term "juvenile-onset diabetes" is no longer used as onset in adulthood is possible. The disease is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to severe insulin deficiency, and can be further classified as immune-mediated or idiopathic (without known cause). The majority of cases are immune-mediated, in which a T cell-mediated autoimmune attack causes loss of beta cells and thus insulin deficiency. Patients often have irregular and unpredictable blood sugar levels due to very low insulin and an impaired counter-response to hypoglycemia. Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans. The genes that are responsible for diabetes are still being researched, but scientists have narrowed them down by investigating the gene mutations related to the capability of the body's β-cells to produce insulin. Genes related to environmental responses (metabolism, pregnancy symptoms, autoimmune disorder development, etc.) also contribute to a person's amount of genetic risk for diabetes.

=== Insomnia === An extended-release pharmaceutical formulation of melatonin is approved under the brand name Circadin for the treatment of insomnia in certain settings, such as in people aged 55 years of age or older. It is approved in the European Union, Israel, Australia, and countries in Asia and elsewhere in the world, but not in the United States (where it reached phase III clinical trials but was not approved). The medication has been licensed since 2007. The 2023, European Insomnia Guideline recommended use of prolonged-release melatonin for treatment of insomnia in people age 55 year of age or older for up to three months. It recommended against fast-release or over-the-counter melatonin for treatment of insomnia. These recommendations were based on several meta-analyses published in 2022 and 2023. The American Academy of Sleep Medicine's 2017 clinical practice guidelines recommended against the use of melatonin in the treatment of insomnia due to poor effectiveness and very low quality of evidence.

Sources: en.wikipedia.org

Reference notes

=== Phase 3 === Clomipramine/sildenafil (CDFR-0812) – combination of clomipramine (tricyclic antidepressant (TCA), serotonin–norepinephrine reuptake inhibitor (SNRI), other actions) and sildenafil (phosphodiesterase PDE5 inhibitor) – premature ejaculation [5] Gepirone (Ariza; BMY-13805-1; BMY-13805; Exxua; Gepirone ER; MJ-13805; Org-33062; TGFK07AD; Travivo; Variza) – serotonin 5-HT1A receptor agonist, other actions – decreased libido [6] Nitroglycerin gel (Eroxon; glyceryl trinitrate topical gel; MED-2001; MED-2003; MED-2004; MED-2005; MED-3000; MED2002) – guanylate cyclase stimulant, nitric oxide donor, nitric oxide stimulant – erectile dysfunction [7] Prasterone vaginal (dehydroepiandrosterone; DHEA; Intrarosa; Vaginorm) – androgen (androgen receptor agonist), other actions – decreased libido [8] Sacubitril/valsartan (AHU-377/valsartan; Enrest; Enresuto; Entresto; Entresto Sprinkle; LCZ-696; LCZ-696A; Neparvis; valsartan/AHU-377; valsartan/sacubitril) – combination of sacubitril (neprilysin inhibitor) and valsartan (angiotensin II receptor type 1 (AT1) antagonist) – erectile dysfunction [9]

== Awards and distinctions == Turner was awarded an Honorary Fellowship of the New Zealand College of Public Health Medicine in 2021, and is a Fellow of the Royal New Zealand College of General Practitioners (RNZCGP). In 2020, Turner was a finalist for the Green Cross Health award for outstanding contribution to health at the inaugural New Zealand Primary Healthcare Awards. Turner was the principal investigator leading the Vaccine Effectiveness arm for The Southern Hemisphere Influenza and Vaccine Effectiveness Research and Surveillance (SHIVERS) project (2012–2016) designed to measure the effectiveness of vaccination for influenza and other respiratory infectious diseases. In 2019, in recognition of their major contribution to influenza research, the SHIVERS team, including Turner, received the New Zealand Association of Scientists' Shorland Medal.

In 1995, the largest sperm bank in New York State was ordered to close (and no longer operate semen banks and blood banks), over the objections of its owner the Daxor Corporation and its president, CEO, and majority shareholder Joseph Feldschuh, by New York State Supreme Court Justice Harold Tompkins. The Justice found that Daxor had repeatedly endangered the public health over several years. A 1993 inspection had documented 517 violations by the sperm bank, including its failure to screen sperm donors properly for sexually transmitted diseases. Rather, the inspection showed that Daxor had, in fact, made available semen from men who had tested positive for hepatitis, chlamydia, and gonorrhea. Daxor employees told government investigators that Feldschuh had instructed them to make false entries on business records and to lie to investigators. Feldschuh claimed New York State Health Department officials were conspiring to shut down his business, sued them three times, appealed three times, and lost each of the six times. The Daxor sperm bank was sued for negligence by customers. In one case, a White mother sued the sperm bank because though her White terminally ill husband's sperm had been stored at the sperm bank, when she asked for the sperm and used it to artificially inseminate her, she ended up giving birth to a Black baby. In 2007 another mother settled her own claims against Daxor for $250,000, which she said was a fraction of the estimated $7 million in care that will be needed for both of her children.

===== MeSH D08.811.913.696 – phosphotransferases (EC 2.7) ===== MeSH D08.811.913.696.175 – diphosphotransferases MeSH D08.811.913.696.175.300 – gtp pyrophosphokinase MeSH D08.811.913.696.175.650 – ribose-phosphate pyrophosphokinase MeSH D08.811.913.696.175.825 – thiamin pyrophosphokinase MeSH D08.811.913.696.310 – myosin type iii MeSH D08.811.913.696.445 – nucleotidyltransferases MeSH D08.811.913.696.445.035 – n-acylneuraminate cytidylyltransferase MeSH D08.811.913.696.445.184 – choline-phosphate cytidylyltransferase MeSH D08.811.913.696.445.308 – dna nucleotidyltransferases MeSH D08.811.913.696.445.308.300 – dna-directed dna polymerase MeSH D08.811.913.696.445.308.300.112 – dna polymerase beta MeSH D08.811.913.696.445.308.300.225 – dna polymerase i MeSH D08.811.913.696.445.308.300.230 – dna polymerase ii MeSH D08.811.913.696.445.308.300.235 – dna polymerase iii MeSH D08.811.913.696.445.308.300.750 – RNA-directed dna polymerase MeSH D08.811.913.696.445.308.300.750.375 – hiv-1 reverse transcriptase MeSH D08.811.913.696.445.308.300.750.750 – telomerase MeSH D08.811.913.696.445.308.300.875 – taq polymerase MeSH D08.811.913.696.445.308.325 – dna nucleotidylexotransferase MeSH D08.811.913.696.445.400 – glucose-1-phosphate adenylyltransferase MeSH D08.811.913.696.445.600 – nicotinamide-nucleotide adenylyltransferase MeSH D08.811.913.696.445.625 – 2',5'-oligoadenylate synthetase MeSH D08.811.913.696.445.650 – polynucleotide adenylyltransferase MeSH D08.811.913.696.445.692 – rec a recombinases MeSH D08.811.913.696.445.735 – rna nucleotidyltransferases MeSH D08.811.913.696.445.735.265 – dna, catalytic MeSH D08.811.913.696.445.735.270 – dna-directed rna polymerases MeSH D08.811.913.696.445.735.270.375 – dna primase MeSH D08.811.913.696.445.735.270.750 – rna polymerase i MeSH D08.811.913.696.445.735.270.762 – rna polymerase ii MeSH D08.811.913.696.445.735.270.775 – rna polymerase iii MeSH D08.811.913.696.445.735.270.887 – rna polymerase sigma 54 MeSH D08.811.913.696.445.735.532 – polyribonucleotide nucleotidyltransferase MeSH D08.811.913.696.445.735.630 – q beta replicase MeSH D08.811.913.696.445.735.720 – rna helicases MeSH D08.811.913.696.445.735.720.500 – eukaryotic initiation factor-4a MeSH D08.811.913.696.445.735.780 – rna replicase MeSH D08.811.913.696.445.735.917 – rna, ribosomal, self-splicing MeSH D08.811.913.696.445.800 – sulfate adenylyltransferase MeSH D08.811.913.696.445.825 – transposases MeSH D08.811.913.696.445.825.500 – hiv integrase MeSH D08.811.913.696.445.837 – transposon resolvases MeSH D08.811.913.696.445.850 – UDP-glucose—hexose-1-phosphate uridylyltransferase MeSH D08.811.913.696.445.875 – UTP—glucose-1-phosphate uridylyltransferase MeSH D08.811.913.696.445.900 – UTP—hexose-1-phosphate uridylyltransferase MeSH D08.811.913.696.445.950 – vdj recombinases MeSH D08.811.913.696.620 – phosphotransferases (alcohol group acceptor) MeSH D08.811.913.696.620.010 – adenosine kinase MeSH D08.811.913.696.620.155 – choline kinase MeSH D08.811.913.696.620.175 – deoxycytidine kinase MeSH D08.811.913.696.620.200 – diacylglycerol kinase MeSH D08.811.913.696.620.225 – fructokinases MeSH D08.811.913.696.620.225.850 – phosphofructokinases MeSH D08.811.913.696.620.225.850.500 – phosphofructokinase-1 MeSH D08.811.913.696.620.225.850.500.249 – phosphofructokinase-1, liver type MeSH D08.811.913.696.620.225.850.500.500 – phosphofructokinase-1, muscle type MeSH D08.811.913.696.620.225.850.500.750 – phosphofructokinase-1, type c MeSH D08.811.913.696.620.225.850.750 – phosphofructokinase-2 MeSH D08.811.913.696.620.240 – galactokinase MeSH D08.811.913.696.620.250 – glucokinase MeSH D08.811.913.696.620.275 – glycerol kinase MeSH D08.811.913.696.620.300 – hexokinase MeSH D08.811.913.696.620.475 – kanamycin kinase MeSH D08.811.913.696.620.525 – 1-phosphatidylinositol 3-kinase MeSH D08.811.913.696.620.550 – 1-phosphatidylinositol 4-kinase MeSH D08.811.913.696.620.650 – phosphoenolpyruvate sugar phosphotransferase system MeSH D08.811.913.696.620.680 – polynucleotide 5'-hydroxyl-kinase MeSH D08.811.913.696.620.682 – protein kinases MeSH D08.811.913.696.620.682.650 – phosphorylase kinase MeSH D08.811.913.696.620.682.700 – protein-serine-threonine kinases MeSH D08.811.913.696.620.682.700.062 – activin receptors MeSH D08.811.913.696.620.682.700.062.500 – activin receptors, type i MeSH D08.811.913.696.620.682.700.062.750 – activin receptors, type ii MeSH D08.811.913.696.620.682.700.109 – bone morphogenetic protein receptors MeSH D08.811.913.696.620.682.700.109.500 – bone morphogenetic protein receptors, type i MeSH D08.811.913.696.620.682.700.109.750 – bone morphogenetic protein receptors, type ii MeSH D08.811.913.696.620.682.700.125 – ca(2+)-calmodulin dependent protein kinase MeSH D08.811.913.696.620.682.700.125.500 – myosin-light-chain kinase MeSH D08.811.913.696.620.682.700.140 – casein kinases MeSH D08.811.913.696.620.682.700.140.300 – casein kinase i MeSH D08.811.913.696.620.682.700.140.300.100 – casein kinase ialpha MeSH D08.811.913.696.620.682.700.140.300.200 – casein kinase idelta MeSH D08.811.913.696.620.682.700.140.300.300 – casein kinase iepsilon MeSH D08.811.913.696.620.682.700.140.600 – casein kinase ii MeSH D08.811.913.696.620.682.700.150 – cyclic nucleotide-regulated protein kinases MeSH D08.811.913.696.620.682.700.150.125 – cyclic amp-dependent protein kinases MeSH D08.811.913.696.620.682.700.150.125.500 – beta-adrenergic-receptor kinase MeSH D08.811.913.696.620.682.700.150.150 – cyclic gmp-dependent protein kinases MeSH D08.811.913.696.620.682.700.150.575 – protamine kinase MeSH D08.811.913.696.620.682.700.200 – cyclin-dependent kinases MeSH D08.811.913.696.620.682.700.200.067 – cdc2-cdc28 kinases MeSH D08.811.913.696.620.682.700.200.067.249 – cdc2 protein kinase MeSH D08.811.913.696.620.682.700.200.067.500 – cdc28 protein kinase, s cerevisiae MeSH D08.811.913.696.620.682.700.200.067.875 – cyclin-dependent kinase 5 MeSH D08.811.913.696.620.682.700.200.067.900 – cyclin-dependent kinase 9 MeSH D08.811.913.696.620.682.700.200.323 – cyclin-dependent kinase 2 MeSH D08.811.913.696.620.682.700.200.451 – cyclin-dependent kinase 4 MeSH D08.811.913.696.620.682.700.200.515 – cyclin-dependent kinase 6 MeSH D08.811.913.696.620.682.700.200.580 – maturation-promoting factor MeSH D08.811.913.696.620.682.700.200.580.500 – cdc2 protein kinase MeSH D08.811.913.696.620.682.700.250 – dna-activated protein kinase MeSH D08.811.913.696.620.682.700.300 – eif-2 kinase MeSH D08.811.913.696.620.682.700.429 – glycogen synthase kinases MeSH D08.811.913.696.620.682.700.429.500 – glycogen synthase kinase 3 MeSH D08.811.913.696.620.682.700.494 – i-kappa B kinase MeSH D08.811.913.696.620.682.700.559 – map kinase kinase kinases MeSH D08.811.913.696.620.682.700.559.100 – map kinase kinase kinase 1 MeSH D08.811.913.696.620.682.700.559.200 – map kinase kinase kinase 2 MeSH D08.811.913.696.620.682.700.559.300 – map kinase kinase kinase 3 MeSH D08.811.913.696.620.682.700.559.400 – map kinase kinase kinase 4 MeSH D08.811.913.696.620.682.700.559.500 – map kinase kinase kinase 5 MeSH D08.811.913.696.620.682.700.559.800 – proto-oncogene proteins c-mos MeSH D08.811.913.696.620.682.700.559.842 – raf kinases MeSH D08.811.913.696.620.682.700.559.842.249 – oncogene proteins v-raf MeSH D08.811.913.696.620.682.700.559.842.374 – proto-oncogene proteins b-raf MeSH D08.811.913.696.620.682.700.559.842.500 – proto-oncogene proteins c-raf MeSH D08.811.913.696.620.682.700.565 – mitogen-activated protein kinase kinases MeSH D08.811.913.696.620.682.700.565.100 – map kinase kinase 1 MeSH D08.811.913.696.620.682.700.565.200 – map kinase kinase 2 MeSH D08.811.913.696.620.682.700.565.300 – map kinase kinase 3 MeSH D08.811.913.696.620.682.700.565.400 – map kinase kinase 4 MeSH D08.811.913.696.620.682.700.565.500 – map kinase kinase 5 MeSH D08.811.913.696.620.682.700.565.600 – map kinase kinase 6 MeSH D08.811.913.696.620.682.700.565.700 – map kinase kinase 7 MeSH D08.811.913.696.620.682.700.567 – mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.567.342 – extracellular signal-regulated map kinases MeSH D08.811.913.696.620.682.700.567.342.500 – mitogen-activated protein kinase 1 MeSH D08.811.913.696.620.682.700.567.342.750 – mitogen-activated protein kinase 3 MeSH D08.811.913.696.620.682.700.567.342.875 – mitogen-activated protein kinase 6 MeSH D08.811.913.696.620.682.700.567.342.937 – mitogen-activated protein kinase 7 MeSH D08.811.913.696.620.682.700.567.513 – jnk mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.567.513.500 – mitogen-activated protein kinase 8 MeSH D08.811.913.696.620.682.700.567.513.750 – mitogen-activated protein kinase 9 MeSH D08.811.913.696.620.682.700.567.513.800 – mitogen-activated protein kinase 10 MeSH D08.811.913.696.620.682.700.567.878 – p38 mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.586 – oncogene protein v-akt MeSH D08.811.913.696.620.682.700.606 – phytochrome a MeSH D08.811.913.696.620.682.700.646 – proline-directed protein kinases MeSH D08.811.913.696.620.682.700.646.500 – cyclin-dependent kinases MeSH D08.811.913.696.620.682.700.646.500.500 – cdc2-cdc28 kinases MeSH D08.811.913.696.620.682.700.646.500.500.500 – cyclin-dependent kinase 5 MeSH D08.811.913.696.620.682.700.646.500.750 – cyclin-dependent kinase 2 MeSH D08.811.913.696.620.682.700.646.500.875 – cyclin-dependent kinase 4 MeSH D08.811.913.696.620.682.700.646.500.937 – cyclin-dependent kinase 6 MeSH D08.811.913.696.620.682.700.646.625 – glycogen synthase kinase 3 MeSH D08.811.913.696.620.682.700.646.750 – mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.646.750.249 – extracellular signal-regulated map kinases MeSH D08.811.913.696.620.682.700.646.750.249.500 – mitogen-activated protein kinase 1 MeSH D08.811.913.696.620.682.700.646.750.249.750 – mitogen-activated protein kinase 3 MeSH D08.811.913.696.620.682.700.646.750.249.875 – mitogen-activated protein kinase 6 MeSH D08.811.913.696.620.682.700.646.750.249.937 – mitogen-activated protein kinase 7 MeSH D08.811.913.696.620.682.700.646.750.374 – jnk mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.646.750.374.500 – mitogen-activated protein kinase 8 MeSH D08.811.913.696.620.682.700.646.750.374.750 – mitogen-activated protein kinase 9 MeSH D08.811.913.696.620.682.700.646.750.374.800 – mitogen-activated protein kinase 10 MeSH D08.811.913.696.620.682.700.646.750.843 – p38 mitogen-activated protein kinases MeSH D08.811.913.696.620.682.700.725 – protein kinase C MeSH D08.811.913.696.620.682.700.725.100 – protein kinase C-alpha MeSH D08.811.913.696.620.682.700.725.400 – protein kinase C-delta MeSH D08.811.913.696.620.682.700.725.750 – protein kinase C-epsilon MeSH D08.811.913.696.620.682.700.755 – proto-oncogene proteins C-akt MeSH D08.811.913.696.620.682.700.759 – proto-oncogene proteins C-bcr MeSH D08.811.913.696.620.682.700.776 – proto-oncogene proteins C-pim-1 MeSH D08.811.913.696.620.682.700.827 – rhodopsin kinase MeSH D08.811.913.696.620.682.700.862 – ribosomal protein s6 kinases MeSH D08.811.913.696.620.682.700.862.249 – ribosomal protein s6 kinases, 70-kda MeSH D08.811.913.696.620.682.700.862.500 – ribosomal protein s6 kinases, 90-kda MeSH D08.811.913.696.620.682.725 – protein-tyrosine kinase MeSH D08.811.913.696.620.682.725.049 – focal adhesion protein-tyrosine kinases MeSH D08.811.913.696.620.682.725.049.500 – focal adhesion kinase 1 MeSH D08.811.913.696.620.682.725.049.750 – focal adhesion kinase 2 MeSH D08.811.913.696.620.682.725.200 – mitogen-activated protein kinase kinases MeSH D08.811.913.696.620.682.725.200.100 – map kinase kinase 1 MeSH D08.811.913.696.620.682.725.200.200 – map kinase kinase 2 MeSH D08.811.913.696.620.682.725.200.300 – map kinase kinase 3 MeSH D08.811.913.696.620.682.725.200.400 – map kinase kinase 4 MeSH D08.811.913.696.620.682.725.200.500 – map kinase kinase 5 MeSH D08.811.913.696.620.682.725.200.600 – map kinase kinase 6 MeSH D08.811.913.696.620.682.725.200.700 – map kinase kinase 7 MeSH D08.811.913.696.620.682.725.300 – proto-oncogene proteins c-fes MeSH D08.811.913.696.620.682.725.400 – receptor protein-tyrosine kinases MeSH D08.811.913.696.620.682.725.400.020 – fms-like tyrosine kinase 3 MeSH D08.811.913.696.620.682.725.400.024 – receptor, fibroblast growth factor, type 1 MeSH D08.811.913.696.620.682.725.400.037 – receptor, fibroblast growth factor, type 2 MeSH D08.811.913.696.620.682.725.400.043 – receptor, fibroblast growth factor, type 3 MeSH D08.811.913.696.620.682.725.400.046 – receptor, fibroblast growth factor, type 4 MeSH D08.811.913.696.620.682.725.400.050 – proto-oncogene proteins c-kit MeSH D08.811.913.696.620.682.725.400.075 – proto-oncogene proteins c-met MeSH D08.811.913.696.620.682.725.400.087 – proto-oncogene proteins c-ret MeSH D08.811.913.696.620.682.725.400.100 – receptor, epidermal growth factor MeSH D08.811.913.696.620.682.725.400.150 – receptor, erbb-2 MeSH D08.811.913.696.620.682.725.400.175 – receptor, erbb-3 MeSH D08.811.913.696.620.682.725.400.185 – receptor, igf type 1 MeSH D08.811.913.696.620.682.725.400.200 – receptor, insulin MeSH D08.811.913.696.620.682.725.400.500 – receptor, macrophage colony-stimulating factor MeSH D08.811.913.696.620.682.725.400.660 – receptor, trka MeSH D08.811.913.696.620.682.725.400.700 – receptor, trkb MeSH D08.811.913.696.620.682.725.400.800 – receptor, trkc MeSH D08.811.913.696.620.682.725.400.850 – receptors, eph family MeSH D08.811.913.696.620.682.725.400.850.050 – receptor, epha1 MeSH D08.811.913.696.620.682.725.400.850.100 – receptor, epha2 MeSH D08.811.913.696.620.682.725.400.850.150 – receptor, epha3 MeSH D08.811.913.696.620.682.725.400.850.200 – receptor, epha4 MeSH D08.811.913.696.620.682.725.400.850.250 – receptor, epha5 MeSH D08.811.913.696.620.682.725.400.850.300 – receptor, epha6 MeSH D08.811.913.696.620.682.725.400.850.400 – receptor, epha7 MeSH D08.811.913.696.620.682.725.400.850.500 – receptor, epha8 MeSH D08.811.913.696.620.682.725.400.850.600 – receptor, ephb1 MeSH D08.811.913.696.620.682.725.400.850.650 – receptor, ephb2 MeSH D08.811.913.696.620.682.725.400.850.700 – receptor, ephb3 MeSH D08.811.913.696.620.682.725.400.850.750 – receptor, ephb4 MeSH D08.811.913.696.620.682.725.400.850.800 – receptor, ephb5 MeSH D08.811.913.696.620.682.725.400.900 – receptors, platelet-derived growth factor MeSH D08.811.913.696.620.682.725.400.900.500 – receptor, platelet-derived growth factor alpha MeSH D08.811.913.696.620.682.725.400.900.750 – receptor, platelet-derived growth factor beta MeSH D08.811.913.696.620.682.725.400.925 – receptors, tie MeSH D08.811.913.696.620.682.725.400.925.249 – receptor, tie-1 MeSH D08.811.913.696.620.682.725.400.925.500 – receptor, tie-2 MeSH D08.811.913.696.620.682.725.400.950 – receptors, vascular endothelial growth factor MeSH D08.811.913.696.620.682.725.400.950.100 – vascular endothelial growth factor receptor-1 MeSH D08.811.913.696.620.682.725.400.950.200 – vascular endothelial growth factor receptor 2 MeSH D08.811.913.696.620.682.725.400.950.300 – vascular endothelial growth factor receptor-3 MeSH D08.811.913.696.620.682.725.500 – proto-oncogene proteins c-abl MeSH D08.811.913.696.620.682.725.800 – src-family kinases MeSH D08.811.913.696.620.682.725.800.315 – lymphocyte specific protein tyrosine kinase p56(lck) MeSH D08.811.913.696.620.682.725.800.472 – oncogene protein pp60(v-src) MeSH D08.811.913.696.620.682.725.800.551 – proto-oncogene proteins c-fyn MeSH D08.811.913.696.620.682.725.800.590 – proto-oncogene proteins c-hck MeSH D08.811.913.696.620.682.725.800.610 – proto-oncogene proteins c-yes MeSH D08.811.913.696.620.682.725.800.630 – proto-oncogene proteins pp60(c-src) MeSH D08.811.913.696.620.682.725.900 – zap-70 protein-tyrosine kinase MeSH D08.811.913.696.620.685 – pyridoxal kinase MeSH D08.811.913.696.620.695 – pyruvate kinase MeSH D08.811.913.696.620.750 – thymidine kinase MeSH D08.811.913.696.620.800 – uridine kinase MeSH D08.811.913.696.630 – phosphotransferases (carboxyl group acceptor) MeSH D08.811.913.696.630.025 – acetate kinase MeSH D08.811.913.696.630.050 – aspartate kinase MeSH D08.811.913.696.630.050.050 – aspartokinase homoserine dehydrogenase MeSH D08.811.913.696.630.700 – phosphoglycerate kinase MeSH D08.811.913.696.640 – phosphotransferases (nitrogenous group acceptor) MeSH D08.811.913.696.640.025 – arginine kinase MeSH D08.811.913.696.640.150 – creatine kinase MeSH D08.811.913.696.640.150.500 – creatine kinase, bb form MeSH D08.811.913.696.640.150.625 – creatine kinase, mb form MeSH D08.811.913.696.640.150.750 – creatine kinase, mitochondrial form MeSH D08.811.913.696.640.150.875 – creatine kinase, mm form MeSH D08.811.913.696.645 – phosphotransferases (paired acceptors) MeSH D08.811.913.696.645.700 – pyruvate, orthophosphate dikinase MeSH D08.811.913.696.650 – phosphotransferases (phosphate group acceptor) MeSH D08.811.913.696.650.025 – adenylate kinase MeSH D08.811.913.696.650.150 – atp synthetase complexes MeSH D08.811.913.696.650.150.500 – proton-translocating atpases MeSH D08.811.913.696.650.150.500.249 – bacterial proton-translocating atpases MeSH D08.811.913.696.650.150.500.500 – chloroplast proton-translocating atpases MeSH D08.811.913.696.650.150.500.750 – mitochondrial proton-translocating atpases MeSH D08.811.913.696.650.150.500.875 – vacuolar proton-translocating atpases MeSH D08.811.913.696.650.450 – guanylate kinase MeSH D08.811.913.696.650.550 – nucleoside-diphosphate kinase MeSH D08.811.913.696.650.575 – nucleoside-phosphate kinase MeSH D08.811.913.696.900 – transferases (other substituted phosphate groups) MeSH D08.811.913.696.900.074 – CDP-diacylglycerol—inositol 3-phosphatidyltransferase MeSH D08.811.913.696.900.150 – CDP-diacylglycerol—serine O-phosphatidyltransferase MeSH D08.811.913.696.900.200 – diacylglycerol cholinephosphotransferase MeSH D08.811.913.696.900.250 – ethanolaminephosphotransferase

Sources: en.wikipedia.org

Reference notes

Stachys affinis, commonly called crosne, Chinese artichoke, Japanese artichoke, knotroot, or artichoke betony, is a perennial herbaceous plant of the family Lamiaceae, originating from China. Its rhizome is a root vegetable that can be eaten raw, pickled, dried or cooked.

This is based on the theory that uric acid is a powerful reducing agent and likely an important human antioxidant, in high concentration in blood. Thus, it has been suggested that free radicals, oxidative stress, and reactive oxygen species may play some role in the neuropathology of LNS. However, some evidence suggests against a role for uric acid in the neuropathology of Lesch–Nyhan syndrome:

Scholae: the personal guard of the Emperor, created by Constantine I to replace the Praetorian Guard; Palatinae: "palace troops" were the highest ranked units, created by Constantine I after he disbanded the Praetorian Guard, it was comprised originally of former guardsmen; Comitatenses: regular field units, some were newly-formed, others were descended from Early-Empire legions; Pseudocomitatenses: these were limitanei units diverted into the field army and often kept there; some Early Empire legions became pseudocomitatenses units. These units usually numbered between 300 and 2,000 soldiers and some of them kept their original numbering schemes. The primary source for the legions of this era is the Notitia Dignitatum, a late 4th-century document containing all the civil and military offices of both halves of the Roman Empire (revised in c. 420 for the Western Empire).

=== Dissolving iron and steel === Alum solution has the property of dissolving steels while not affecting aluminium or base metals. Alum solution can be used to dissolve steel tool bits that have become lodged in machined castings.

Recreational cocaine is typically not taken by mouth due to its poor bioavailability, instead it is usually snorted or injected. Cocaine hydrochloride can also be chemically converted into its free base form, crack cocaine, which can be vaporized. Cocaine is a central nervous system stimulant. Its effects can last from 15 minutes to an hour. The duration of cocaine's effects depends on the amount taken and the route of administration. Cocaine can be in the form of fine white powder and has a bitter taste. Crack cocaine is a smokeable form of cocaine made into small "rocks" by processing cocaine with sodium bicarbonate (baking soda) and water. Cocaine use leads to increases in alertness, feelings of well-being and euphoria, increased energy and motor activity, and increased feelings of competence and sexuality. Analysis of the correlation between the use of 18 various psychoactive substances shows that cocaine use correlates with the use of other "party drugs" (e.g., MDMA, amphetamine), as well as with heroin and benzodiazepines use, and can be considered as a bridge between the use of different groups of drugs.

Sources: en.wikipedia.org

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