Of note, in rats with spinal cord injury, there is permanent reperfusion. Once BPC 157 is administered 10 minutes post-compression injury, there is continuous protection and no spontaneous spinal cord injury-induced disturbances reappear.All spinal cord injuries immediately provoke hemorrhage, with subsequent death of neurons and oligodendrocytes.

Hence, it is conceivable that early hemostasis may be beneficial and enable functional recoveryafter spinal cord contusion in rats. However, the effect exerted by BPC 157 is likely different from the simple hemostatic effect that would attenuate spinal cord injury, because BPC 157 also markedly improves thrombocyte function in rats without affecting coagulation factors. During recovery from spinal cord injury, BPC 157 also directly protects the endothelium, alleviates peripheral vascular occlusion disturbances, rapidly activates alternative bypass pathways, and counteracts venous occlusion–induced syndromes. Thus, assuming that there is a substantial venous contribution to the spinal cord compression, it is conceivable that the reestablished blood flow mediated by BPC 157 may undoubtedly contribute to the rapid recovery effect. Furthermore, considering that BPC 157 promotes permanent reperfusion after spinal cord compression, it should be noted that when BPC 157 is given during reperfusion, it counteracts stroke induced by bilateral clamping of the common carotid arteries. BPC 157 resolves neuronal damage and prevents memory, locomotor, and coordination deficits. BPC 157 apparently exerts these effects by altering gene expression in the hippocampus .

In conclusion, BPC 157 exerts beneficial effects on stroke, schizophrenia, and spinal cord injury .
Researchers have consistently demonstrated that BPC 157 exerts a myriad of beneficial effects throughout the body. There is no reason to indicate that the benefits of BPC 157 are limited by the validity of the utilized models and/or methodology limitations. Indeed, we can argue that the effectiveness, easy applicability, safe clinical profile and mechanism of BPC 157 represent an alternative, likely successful, future therapeutic direction for neurological conditions. Therefore, additional studies are needed to clarify how potential BPC 157 therapy would specifically deal with a mechanism of action that involves multiple subcellular sites in the CNS. The influence on the function of most, if not all, neuronal systems at the molecular, cellular, and systemic levels should be explored. Some visceral repetitive relay of the CNS or circumventricular organs, one of the few regions in the brain without the blood-brain barrier, is a known pathway by which a systemically administered peptide can exert a central effect. Thus, it must act within the gut-brain axis, regardless of whether this action is direct or indirect.

When protein is extracted from broken cells, proteases can be released, which need to be rapidly inhibited to keep protein from being degraded. In the process of protein extraction, protease inhibitors need to be added to prevent proteolysis. Protease inhibitor broadly refers to a substance that binds to some groups on the active center of protease molecules, so that the protease activity decreases or even disappears, but does not denature the enzyme protein. The sensitivity of various proteases to different protein is different, so it is necessary to adjust the concentration of various proteases. Because the solubility of protease inhibitor in liquid is extremely low, it should be paid special attention to that protease inhibitor should be fully mixed in the buffer to reduce the precipitation of protease inhibitor. Pepstantin A can inhibit acid proteases such as pepsin, angiotensin, collagenase, cathepsin D and chymosin.

Figure 1. Homology model of cagrilintide (23) bound to AMY3R. (A) N-terminal part of 23 (blue) is formed by an amphipathic a-helix, deeply buried in the TM domain of AMY3R, while the C-terminal part is predicted to adopt an extended conformation that binds the extracellular part of the receptor. (29,30) The fatty acid attached to the N-terminus of 23, proline residues (which minimize fibrillation), and the C-terminal amide (essential for receptor binding) are highlighted in stick representations. AMY3R is formed by CTR (gray) bound to RAMP3 (receptor-activity modifying protein 3; orange). The structural model was created using the following template structures: a complex structure of CGRP (calcitonin receptor-like receptor; pdb code 6E3Y) and an apo crystal structure of the 23 backbone (pdb code 7BG0). (B) Zoom up of 23 highlighting the N-terminal disulfide bond, an internal salt bridge between residue 14 and 17, a “leucine zipper motif,” and an internal hydrogen bond between residues 4 and 11. (adapted from Kruse T, Hansen JL, Dahl K, Schäffer L, Sensfuss U, Poulsen C, Schlein M, Hansen AMK, Jeppesen CB, Dornonville de la Cour C, Clausen TR, Johansson E, Fulle S, Skyggebjerg RB, Raun K. Development of Cagrilintide, a Long-Acting Amylin Analogue. J Med Chem. 2021 Aug 12;64(15):11183-11194.)

According to incomplete statistics, the incidence of pain in the world is about 35% ~ 45% at present, and the incidence of pain in the elderly is relatively high, about 75% ~ 90%. An American survey shows that the incidence of migraine increased from 23.6 million in 1989 to 28 million in 2001. In the investigation of chronic pain in six cities in China, it is found that the incidence of chronic pain in adults is 40%, and the rate of medical treatment is 35%; The incidence of chronic pain in the elderly is 65% ~ 80%, and the rate of seeing a doctor is 85%. In recent years, the medical expenses for pain relief are increasing year by year.
From 2013 to July 2015, the Pain Research Center in the United States and several medical institutions conducted a long-term, multi-center and observational study on intrathecal injection of ziconotide in 93 adult white female patients with severe chronic pain. The pain digital score scale and the overall sensory score of patients with intrathecal injection of ziconotide and without injection of ziconotide were compared Among them, 51 patients used intrathecal injection of ziconotide, while 42 patients did not. The baseline pain scores were 7.4 and 7.9, respectively. The recommended dose of intrathecal injection of ziconotide was 0.5-2.4 mcg/ day, which was adjusted according to the patient’s pain response and side effects. The average initial dose was 1.6 mcg/ day, 3.0 mcg/ day at 6 months and 2.5 at 9 months. At 12 months, it was 1.9 mcg/ day, and after 6 months, the decrease rate was 29.4%, the contrast increase rate was 6.4%, and the improvement rate of overall sensory score was 69.2% and 35.7% respectively. After 12 months, the decrease rate was 34.4% and 3.4% respectively, and the improvement rate of overall sensory score was 85.7% and 71.4% respectively. The highest side effects were nausea (19.6% and 7.1%), hallucination (9.8% and 11.9%) and dizziness (13.7% and 7.1%). The results of this study once again confirmed the effectiveness and safety of ziconotide recommended as a first-line intrathecal injection.

The preliminary study on ziconotide can be traced back to the 1980s, when the potential therapeutic application of rigid and protein-like peptides in conus venom was explored for the first time. These conotoxins are small peptides rich in disulfide bonds, usually 10-40 residues in length, to target various ion channels, GPCR and transporter proteins efficiently and selectively. Ziconotide is a 25-peptide derived from Conus magus, which contains three disulfide bonds, and its short β-fold is spatially arranged into a unique three-dimensional structure, which allows it to selectively inhibit CaV2.2 channels.

Linaclotide is a novel and effective medication for patients with CC and IBS-C who have not responded well to conventional therapies. It works by mimicking the action of endogenous peptides that regulate intestinal function and sensation. Linaclotide can improve bowel habits, reduce abdominal pain, and enhance quality of life for these patients.

As we all know, botulinum toxin is a beauty product that needs injection. It is extremely dangerous to use, and needs to be used by professionals. The dosage should be strictly controlled, but it still cannot avoid various side effects such as facial stiffness and facial paralysis.

Argireline was verified in the human experiments of cosmetics manufacturers: the average wrinkle depth decreased by 16.9% and 27.0% after 15 and 30 days with 10% Argireline solution, and the wrinkle volume decreased by 20.6% and the wrinkle length decreased by 15.9% after only 7 days with 2% Argireline solution. It can be seen that the effect of achillerin on wrinkles is very significant.