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How does BPC-157 help balance dopamine, cardiovascular function, and healing?

By Nemo 3 days ago

Multi-Organ Membrane Repair and Dopamine Balancing.

"Pentadecapeptide BPC 157 antagonises the incidence of a series of gastrointestinal lesions, it has a positive impact on the healing processes of various wounds, a proven angiogenic effect, protective effect on endothelium and it modulates synthesis of NO." (1)

"Apart from the effects on various gastrointestinal lesions, the potentially beneficial effect on pancreas, liver injuries, endothelium and heart damage, i.e. dysrhythmias following reoxygenation, and blood pressure, along with effect on experimental acute/chronic inflammation, wound and fracture (pseudoarthrosis) healing are described. It appears that these beneficial effects all together provide a particular network reflecting activity of a special peptidergic defence system." (4)

"In support of this concept, it appears that there are interactions of this pentadecapeptide with many important systems (namely, dopamine-, NO-, prostaglandin-, somatosensory neurone-systems), that could provide a basis for the observed protective effects. Moreover, since disturbance of these systems' functions (i.e. dopamine-, NO-, somatosensory neuronal-system) which manifest either over-activity or as inhibition, may contribute to the multiple lesions in different organs. The reported evidence that this pentadecapeptide is able to counteract both their over-action, and their inhibition, may suggest this pentadecapeptide as a new, but most probably essential physiological defence system and that should be further investigated." (4)

File:Gastric Ulcer.png

Read More Posted in: BPC-157

Can viral replication be reduced with MOTS-c and FOXO4-DRI by killing zombie (senescent) cells?

By Nemo 8 days ago

Senescent cells increase replication of a DNA virus in vitro.

“A significant increase in viral replication efficiency was detected by replicative senescence during IFV and VZV infection. ... As one of possible mechanisms for the increase in viral replication in senescent cells, a reduction in interferon (IFN) response after viral infection may account for it.” (2)

The concentration of this DNA virus in senescent cells is 300% more infected than non-senescent cells.

300% increase of viral infection in senescent cells

"Similarly, Andrew et al. showed that by increasing SASP phenotype, MOTS-c could make senescent cells more easily detected and then cleaned by the immune system, thus protecting normal cells."

How does Thymosin Alpha 1 improve anti-viral immune responses?

By Nemo 16 days ago

Antigen, Antibody, and Lymphocytic White Blood Cell Recruitment.

“Importantly, Ta1 acts without overstimulation of cytokine production and is generally well tolerated; it has an excellent safety profile and does not appear to induce the side effects and toxicities commonly associated with agents in this class such as interferon alpha and interleukin-2.” (1)

“Clinical trials using Ta1 in the treatment of patients with immunodeficiency or cancer indicate that this agent is nontoxic, enhances immune responsiveness and augments specific lymphocyte functions, including lymphoproliferative responses to mitogens, maturation of T-cells, antibody production, and T-cell-mediated cytotoxicity” (5)

• Increased Natural Killer (NK) activity

• A shift of T helper (Th or CD4) cells to the Th1 cell subset

• Increased expression of Th1 type cytokines such as Interleukin (IL) 2, and Interferon (IFN)-alpha

• Increased levels of Cytotoxic T (Tc1 or CD8) cells

Thymalin boosts immune system while mitigating fever and excess cell death induced by cytokine storms.

By Nemo 21 days ago

Immune Paralysis Following "cytokine storm" may be reversed by Thymalin.

"Uncontrolled development of the initial [cytokine storm] stage inevitably leads to immune imbalance, which increases the probability of secondary infections, such as pneumonia, and activation of latent herpes virus (including cytomegalovirus) infections." (2)

"Over the last decade, preclinical and clinical studies have definitively shown that sepsis leads not only to hyperinflammation, but also impaired immunity, including dysfunction of the adaptive immune system. Certain investigators and clinical practitioners believe that the main cause of the failure of sepsis therapy involves the development of severe immunodeficiency..." (2)

“Administration of Thymalin to old mice led to an increase of the titer of FTS in the blood, the restoration of disturbed circannual rhythm, the number of CD4+ cells in the bone marrow, and the concentration of corticosterone in the blood.” (4) “Both natural and synthetic pharmaceuticals activated T-cell differentiation, T-cell recognition of peptide-MHC complexes, induced the changes in intracellular composition of cyclic nucleotides and cytokine [interleukin (IL-2), interferon (IFN)] excretion of blood lymphocytes.” (3)

"Adequate zinc is essential for T-cell division, maturation, and differentiation. Zinc itself is a cofactor for thymulin, a best known zinc-dependent thymic hormone crucial for T-cell formation and maturation which exists in two forms, a zinc-bound active one, and a zinc-free inactive form. What’s more, zinc may also prevent the programmed death (apoptosis) of precursor T-cell populations and mature CD4+T cells through various enzymatic mechanisms and through chronic production of glucocorticoids. Thymulin and thymopentin restore antibody avidity in aged or thymectomized animals, enhance antibody production in aging mice... Additionally, thymulin reduces induced hyperalgesia in rats and mice.” (7)


Thymulin: An Emerging Anti-Inflammatory Molecule

MOTS-c Vascular Calcification and Insulin Resensitization

By Nemo 27 days ago

AMPK Activation Targets Vascular Calcification and Metabolic Homeostasis

"Recently, MOTS-c, a novel bioactive mitochondrial-derived peptide, has been demonstrated to activate the AMPK pathway to promote metabolic homeostasis... Our findings provide evidence that MOTS-c may act as an inhibitor of VC [Vascular Calcification] by activating the AMPK signaling pathway and suppressing the expression of the AT-1 and ET-B receptors." (1)

"Angiotensin II type 1 (AT-1) and endothelin B (ET-B) have been found to be involved in the AMPK pathway by binding to the AT-1 and ET-B receptors, respectively. A decreased level of the AT-1 receptor plays roles in reducing oxidative stress and preventing the development of myocardial contractile dysfunction, while a high level of the AT-1 receptor induces myocardial fibrosis and cardiac dysfunction. AT-1 can induce the relocation and suppression of the AMPK pathway via the AT-1 receptor in the development of diabetic proteinuria. After treatment with metformin, AMPK signaling is activated and AT-1 levels are decreased in the kidney. In epithelial ovarian carcinoma, ET-1 plays a role in epithelial-mesenchymal transition. A decrease in ET-1 receptor activation is beneficial in attenuating biventricular remodeling, and the overexpression of ET-1 causes sustained blood pressure elevation and vascular and renal injury. The activation of the AMPK pathway can also upregulate the ET-B receptor to inhibit autophagy in vascular smooth muscle cells under high glucose conditions." (1)

"Previous reports have shown that MOTS-c can amplify glucose uptake, inhibit the folate cycle and de novo purine biosynthesis following metabolic stress, and regulate nuclear gene expression in an AMPK-dependent manner. MOTS-c treatment dramatically reduced the number of disordered elastic fibers and significantly improved vascular wall structure (Fig. 2c). Moreover, MOTS-c also significantly reduced VDN [Vitamin D3 plus Nicotine] induced calcium phosphate salt deposition in the calcified aortas, as detected by alizarin red S staining and von Kossa staining... Our results showed that MOTS-c reverses VDN-induced AMPK downregulation. In mice with hypoxia-induced pulmonary hypertension, the activation of the AMPK pathway can effectively improve right ventricular systolic pressure and right ventricular hypertrophy due to treatment with liraglutide." (1)

Read More Posted in: MOTS-c

Potential Synergy of MOTS-c or Humanin with Senolytics

By Nemo 29 days ago

FOXO4-DRI senescent cell remover is potentiated by SASP factors

"SASP factors as IL-6 may be the cause for the observed loss in renal function, and we wondered how FOXO4-DRI would function under such high SASP conditions. In vitro experiments showed FOXO4-DRI to be more potent against senescent cells in which SASP wastransiently boosted by recombinant IL1a/b or lipopolysaccharide (LPS), whereas an IL1 receptor antagonist or the general anti-inflammatory drug cortisol reduced its potency (Figures 6H and 6I). Thus, FOXO4-DRI actually is most effective against senescent cells expressing high levels of SASP and could as such be particularly effective against loss of renal function. Excitingly, while not substantially influencing total body nor kidney weight (Figure S6G), FOXO4-DRI treatment normalized the percentage of tubular cells lacking LMNB1 (Figure 6G), the tubular IL-6 elevation (Figure 6J), and the elevations in plasma urea levels (Figure 6K)." (4)

GHK affects the Gene Expression of COPD, Damaged Protein Clearing, and Nervous System

By Nemo 1 month ago
"GHK (glycyl-l-histidyl-l-lysine) is a human copper-binding peptide with biological actions that appear to counter aging-associated diseases and conditions. GHK, which declines with age, has health promoting effects on many tissues such as chondrocytes, liver cells and human fibroblasts, improves wound healing and tissue regeneration (skin, hair follicles, stomach and intestinal linings, boney tissue), increases collagen, decorin, angiogenesis, and nerve outgrowth, possesses anti-oxidant, anti-inflammatory, anti-pain and anti-anxiety effects, increases cellular stemness and the secretion of trophic factors by mesenchymal stem cells. Studies using the Broad Institute Connectivity Map show that GHK peptide modulates expression of multiple genes, resetting pathological gene expression patterns back to health."
Read More Posted in: GHK-Cu

Hexarelin research and the reduction of cardiac fibrosis

By Nemo 1 month ago

"MMPs, particularly MMP-9 and MMP-2 [collagen degrading enzymes], are involved in cardiac fibrosis. Activities of MMP-2 and MMP-9 in the heart did not show significant differences between SHRs and Wistar rats (Fig. 6). However, hexarelin treatment remarkably increased MMP-2 and MMP-9 activities in SHRs, especially MMP-9 activity, in a GHS-R-dependent manner, since blockade of GHS-R abolished the hexarelin-induced increase in MMP-2 and MMP-9 activities (Fig. 6A). mRNA expression of TIMP-1, the inhibitor of MMPs, was dramatically increased in SHRs compared with Wistar rats and was reduced by hexarelin in SHRs in a GHS-R-dependent manner (Fig. 6B)."

Hexarelin suppressed TIMP-1 mRNA and its inhibition of collagen degrading enzymes in the rat heart, thereby boosting the collagen degrading enzymes MMP-2 and MMP-9.

Humanin Mitochondrial Peptide Prevents Age-related Myocardial Fibrosis in mice

By Nemo 1 month ago

"Humanin (HN) is an endogenous mitochondria-derived peptide that has cytoprotective effects and reduces oxidative stress. The present study aimed to test the hypothesis that chronic supplementation of exogenous HN in middle-aged mice could prevent and reverse cardiac fibrosis and apoptosis in the aging heart."

"HNG treatment significantly increased the ratio of cardiomyocytes to fibroblasts in aging hearts, as shown by the percentage of each cell type in randomly chosen fields after immunofluorescence staining. The percentage of other cell types did not change among these groups... Furthermore, the increased collagen deposition in aged hearts was significantly reduced after HNG treatment, as indicated by picrosirius red staining. HNG treatment also reduced in aging mice cardiac fibroblast proliferation and attenuated transforming growth factor-β1, fibroblast growth factor-2, and matrix metalloproteinase-2 expression. Myocardial apoptosis was inhibited in HNG-treated aged mice."

"Cardiac fibrosis is a biological process that increases with age and contributes to myocardial dysfunction. Humanin is an endogenous mitochondria-derived peptide that has cytoprotective effects and reduces oxidative stress. Here, we demonstrate, for the first time, that exogenous humanin treatment attenuated myocardial fibrosis and apoptosis in aging mice. We also detected upregulated Akt/glycogen synthase kinase-3β pathway in humanin analog-treated mice, which might be the mechanism involved in the cardioprotective effect of humanin analog in aging mice."

Read More Posted in: Humanin

Hexarelin protects heart cells from hypertrophy by stimulating autophagy.

By Nemo 1 month ago

‪"Hexarelin is a synthetic growth hormone-releasing peptide that exerts cardioprotective effects. Regulation of autophagy is known to be cardioprotective so this study examined the role of autophagy and potential regulatory mechanisms in hexarelin-elicited anti-cardiac hypertrophic action in cardiomyocytes subjected to hypertrophy."

“Ang-II induced cardiomyocyte hypertrophy, oxidative stress, apoptosis and decreased cell survival, all of which were significantly suppressed by hexarelin (a growth hormone peptide) treatment which also enhanced autophagy in hypertrophic H9C2 cells.”‬

‪“Conversely, the application of autophagy stimulator rapamycin in H9C2 hypertrophic cells inhibited apoptosis, cell survival and reduced cell size as well. Additionally, hexarelin regulated the upstream signalling of autophagy by inhibiting the phosphorylation of mammalian target of rapamycin(mTOR). We propose that hexarelin plays a novel role of attenuating cardiomyocyte hypertrophy and apoptosis via an autophagy-dependent mechanism associated with the suppression of the mTOR signalling pathway.”‬

Sourcing Study: https://www.ncbi.nlm.nih.gov/pubmed/31526442

Product available for research use only:

Hexarelin


The Research Effects of TB-500 on Tissue Growth

By Logan 4 months ago

TB-500 is also known as thymosin beta 4 (TB4). Thymosin Beta 4 has been found, in animal models, to play a central role in controlling the structure of cells. By improving cell structure, TB-500 is thought to aid in wound healing, improve cell responses to stress, and even help cells to live longer. Scientific animal research studies have shown that TB-500's role in regulating cell structure may eventually make it a leading therapeutic in wound healing, blood vessel repair, and even ocular (eye) repair.

IGF1 LR3 Information

By Carl 4 months ago

IGF1 LR3 (insulin-like growth factor-1 Long R3) is a non-glycosylated, recombinant polypeptide chain made up of 83 amino acids. IGF1 LR3 is the recombinant form of human IGF-1, and as such it contains the entire native amino acid sequence but with two major modifications: substitution of arginine (abbreviated R or arg) at position 3 with glutamic acid (abbreviated E or Glu) hence the label R3; and the extension of the N-terminus of the native sequence by a 13 amino-acid peptide hence the label long. The native form of a polypeptide refers to the naturally occurring amino acid sequence and the resultant conformational structure. The molecular weight of IGF1 LR3 as measured by Mass Spectrometry is 9.116 kD (kiloDaltons). A specifically designed protein expression system is utilized in the production of IGF1 LR3 in Escherichia Coli. Thereafter, chromatographic techniques are used to correctly fold and purify the IGF1 LR3 to the highly-active and functional IGF1 LR3 that can bind to human IGF-1R (insulin-like growth factor-1 receptor).

What is Thymosin Alpha-1

By Becka 4 months ago

Thymosin Alpha-1 is a biologically active peptide derived from prothymosin-alpha. Current hypotheses consider Thymosin Alpha-1 to be the main constituent of Thymosin Fraction-5, and as such it is considered to be the active component that restores the immune function in both athymic animals and animals with dysfunctional thymus glands. Thymosin Alpha-1 was among the first peptide isolates of Thymosin Fraction-5 to be sequenced and thereafter synthetically synthesized.

In humans, the PTMA gene encodes prothymosin-alpha, a 113 amino-acid polypeptide. Thymosin Alpha-1 is a 28 amino-acid fragment of prothymosin-alpha, and research has shown that this fragment derivative enhances the cell-mediated immune component of the human immune system. Its immune actions have enabled it to be used for treating viral infections such as Hepatitis B and Hepatitis C. It has also been incorporated into vaccines as an immune booster. Clinical studies have also shown that Thymosin Alpha-1 can be used to manage neoplasias since they upregulate cytotoxic T-cells which are involved in immune surveillance.

What is Adipotide?

By Carl 4 months ago

Adipotide is a peptidomimetic compound that has been shown to possess pro-apoptotic properties that do cause weight loss in rhesus monkeys and mice. Its sequence is CKGGRAKDC-GG-D(KLAKLAK)2. Studies have shown that its mode of action involves the selective apoptosis of blood vessels supplying the white adipose tissue. Adipotide causes such vessels to undergo atrophy (shrinkage) and eventually apoptosis (cell death), thus cutting off the blood supply to the fat cells. This results in ischemic injury, which is a lack of blood supply and oxygen to the fat cells. The effects are non-reversible, so the fat cells also undergo apoptosis or cell death.

Sermorelin, Sleep and the Brain

By Logan 4 months ago

Fifteen years ago, orexins were identified as central regulators of energy homeostasis. Research indicates that orexins are key modulators of the sleep-wake cycle and that these neuropeptides also affect feelings of satiety and hunger. Given their role in energy homeostasis, it was hypothesized that orexin levels are likely regulated, at least in part, by the growth hormone axis. Recent research supports this fact and suggests that growth hormone releasing hormone analogues, such as sermorelin, may be effective in treating conditions in which orexin release is dysfunctional (e.g. narcolepsy) [1].