The short version of synthetic heptapeptide fits in a sentence. The long version — which is the one that helps — is below.
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Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It is described in the literature as an analogue of the ACTH(4–10) fragment, a short N-terminal portion of adrenocorticotropic hormone that retains some neurotropic activity without the full hormonal effects of the parent peptide. The molecule carries a methionine residue at the N-terminus and two proline residues near the C-terminus, features that shape both its interactions with receptor systems and its chemical stability. The free peptide corresponds to the formula C37H51N9O10S and a molecular mass near 813.9 Da.
The compound was developed in the 1980s at the Institute of Molecular Genetics in Moscow, where it emerged from research on short ACTH fragments and their effects on the central nervous system. Russian pharmaceutical listings describe it as a nootropic and neuroprotective agent, most often formulated as nasal drops. It is not a marketed medicine in the United States or the European Union, and no pharmacopoeial monograph covers it. Consequently, most published clinical experience with the substance originates from a small number of research centres, mainly in Russia and neighbouring countries.
Pharmacological accounts link semax to melanocortin signalling and to modulation of neurotrophic factor expression, particularly brain-derived neurotrophic factor and nerve growth factor. Much of this evidence comes from rodent studies using intranasal delivery, a route chosen because it allows peptides to reach the central nervous system with limited systemic exposure. Whether the same mechanisms operate in humans at comparable magnitude remains an open question. The precise receptor or receptors responsible for the reported behavioural and neuroprotective effects have not been conclusively identified.
Semax is a synthetic heptapeptide whose sequence is Met-Glu-His-Phe-Pro-Gly-Pro. The first four residues correspond to the ACTH(4-10) fragment, while the terminal Pro-Gly-Pro extension was added to improve metabolic stability. Its molecular formula is C37H51N9O10S and its monoisotopic mass is approximately 813.9 Da. The compound is classified as a peptide research chemical and as a registered pharmaceutical product in Russia, but it does not hold marketing approval in the European Union or the United States. Naming conventions vary across supplier catalogs.
Development of the compound took place in the Soviet Union during the 1980s, largely through peptide research groups affiliated with the Shemyakin-Ovchinnikov Institute and Moscow State University. Investigators screened fragments of adrenocorticotropic hormone for activity on the central nervous system while attempting to separate cognitive effects from hormonal ones. The shortened sequence was selected because it retained behavioral activity in animal models without stimulating corticosteroid release. Early publications described the molecule as an ACTH(4-10) analog.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C37H51N9O10S | Free acid form of the heptapeptide; depends on terminal groups |
| Molecular mass | About 813.9 g/mol | Average mass used for mass spectrometry confirmation |
| Appearance | White to off-white solid | Supplied as a lyophilised powder; hygroscopic |
| Solubility class | Freely soluble in aqueous media | Water, saline, and phosphate buffers; limited organic solubility |
| Typical storage temperature | -20 degrees Celsius | Long term and dry; short working periods may use 2 to 8 degrees Celsius |
Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It was derived from the ACTH(4-10) fragment, a short segment of adrenocorticotropic hormone that lacks the hormonal activity associated with the full-length peptide. Researchers at the Institute of Molecular Genetics in Moscow developed the compound during the 1980s. It has been registered as a pharmaceutical product in Russia and several neighbouring countries, where it is supplied as a nasal solution, and it is also sold internationally as a research chemical.
The proposed mechanism centres on neurotrophic signalling rather than direct receptor activation. Semax is reported to increase expression of brain-derived neurotrophic factor and nerve growth factor in several brain regions, and to shift the balance between excitatory and inhibitory neurotransmitter systems. Interaction with melanocortin receptors has been suggested because of the parent ACTH fragment. Many of these findings come from rodent studies, and the extent to which they translate to human physiology remains an open question.
After the Indo-Pakistani war of 1947–1948, three distinct areas of the princely state of Jammu and Kashmir were under Indian control: Muslim-majority Kashmir Valley, Hindu-majority Jammu region, and Buddhist-dominated Ladakh district. These regions were constituted as Jammu and Kashmir state and accorded special status by Article 370 of the Constitution of India, adopted in 1950. In contrast to other states of India, Jammu and Kashmir established its own constitution, flag, and administrative autonomy. In 1954, Article 35A was introduced via a Presidential Order under Article 370, empowering the Jammu and Kashmir Legislature to define permanent residents and bar Indian citizens from other states from purchasing property. From the early 1950s, Jammu and Kashmir used the titles of Prime Minister and Sadr-e-Riyasat for its executive heads, as permitted under Article 370 and formalised in the Delhi Agreement of 1952. The Constituent Assembly, tasked with drafting the constitution and deciding Article 370's future, adopted the constitution of Jammu and Kashmir in 1957 and then dissolved without recommending 370's abrogation, leading to the provision's indefinite continuation. In 1953, Sheikh Abdullah, the first Prime Minister of Jammu and Kashmir, was dismissed and jailed by the Indian government over charges of conspiracy, accused of espousing the creation of an independent country.
=== Cell death === A cancer cell can die in three ways: apoptosis, necrosis, and autophagy. Excessive ROS can induce apoptosis through both the extrinsic and intrinsic pathways. In the extrinsic pathway of apoptosis, ROS are generated by Fas ligand as an upstream event for Fas activation via phosphorylation, which is necessary for subsequent recruitment of Fas-associated protein with death domain and caspase 8 as well as apoptosis induction. In the intrinsic pathway, ROS function to facilitate cytochrome c release by activating pore-stabilizing proteins (Bcl-2 and Bcl-xL) as well as inhibiting pore-destabilizing proteins (Bcl-2-associated X protein, Bcl-2 homologous antagonist/killer). The intrinsic pathway is also known as the caspase cascade and is induced through mitochondrial damage which triggers the release of cytochrome c. DNA damage, oxidative stress, and loss of mitochondrial membrane potential lead to the release of the pro-apoptotic proteins mentioned above stimulating apoptosis. Mitochondrial damage is closely linked to apoptosis and since mitochondria are easily targeted there is potential for cancer therapy. The cytotoxic nature of ROS is a driving force behind apoptosis, but in even higher amounts, ROS can result in both apoptosis and necrosis, a form of uncontrolled cell death, in cancer cells. Numerous studies have shown the pathways and associations between ROS levels and apoptosis, but a newer line of study has connected ROS levels and autophagy.
Coca herbal infusion (also referred to as coca tea) is used in coca-leaf producing countries much as any herbal medicinal infusion would elsewhere in the world. The free and legal commercialization of dried coca leaves under the form of filtration bags to be used as "coca tea" has been actively promoted by the governments of Peru and Bolivia for many years as a drink having medicinal powers. In Peru, the National Coca Company, a state-run corporation, sells cocaine-infused teas and other medicinal products and also exports leaves to the U.S. for medicinal use. The effects of drinking coca tea are mild stimulation and mood lift. In 1986 an article in the Journal of the American Medical Association revealed that U.S. health food stores were selling dried coca leaves to be prepared as an infusion as "Health Inca Tea". While the packaging claimed it had been "decocainized", no such process had actually taken place. The article stated that drinking two cups of the tea per day gave a mild stimulation, increased heart rate, and mood elevation, and the tea was essentially harmless.
Sources: en.wikipedia.org
==== Kidnapping and extortion ransoms ==== Colombia is a country in which many people are or have been kidnapped. Kidnapping, as one of the manifestations that underlie armed conflict, carries both direct and indirect costs. The former consists mainly of the payment of ransoms and the expenses assumed by the State to control and prevent kidnapping. Indirect costs include, "[...] the loss of human capital for the duration of the detention and for the death of the kidnapped during his captivity". There are two types of kidnapping:
=== Systemic lupus erythematosus === The role of Th22 cells in systematic lupus erythematous (SLE) is still unclear. In some patients levels of Th22 cells and interleukin-22 (IL-22) were increased, which correlated with disease activity, but decreased levels of interleukin-22 (IL-22) and Th22 cells were also reported. Interleukin-22 (IL-22) is a cytokine involved in recruiting neutrophils in response to microbe invading, and in the case of lupus, it seems that interleukin 22 (IL-22) is involved in inflammatory and pathological processes via recruiting of immune cells. On the other hand, Th22 cells might be a better predictor of systematic lupus erythematous (SLE) development than Th17 cells.
The two substrates of this enzyme are indan-1-ol and oxidised nicotinamide adenine dinucleotide (NAD+). Its products are 1-indanone, reduced NADH and a proton. The enzyme can use the alternative cofactor, nicotinamide adenine dinucleotide phosphate. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is indan-1-ol:NAD(P)+ 1-oxidoreductase.
Sources: en.wikipedia.org
It is described as a synthetic analogue of the ACTH(4–10) fragment, a short segment of adrenocorticotropic hormone. Its sequence differs from that fragment and includes two proline residues, which influence stability and behaviour in solution.
It appears in Russian pharmaceutical listings as a nasal formulation, but it is not an authorised medicine in the United States or the European Union. Outside those markets it is normally encountered as a research chemical rather than a prescription product.
Laboratory and animal work points to melanocortin signalling and changes in neurotrophic factor levels, especially brain-derived neurotrophic factor. The exact receptor targets and the degree to which these findings transfer to humans are still unresolved.
It is a synthetic peptide of seven amino acids. Its backbone corresponds to a fragment of adrenocorticotropic hormone extended at the carboxyl end. The material is distributed as a lyophilized solid for laboratory use.