Tirzepatide (5mg & 10mg)


Tirzepatide peptides are Synthesized and Lyophilized in the USA.

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Tirzepatide Peptide

Tirzepatide is an analog peptide to the glucose-dependent insulinotropic polypeptide (GIP). Gastric inhibitory peptide (GIP) is a hormone produced by the duodenum and small intestine. It appears to act as an incretin, stimulating the production of insulin. Unlike GIP, which is made of 42 amino acids, Tirzepatide has a modified amino acid chain consisting of 39 amino acids which are additionally lipidated to improve the peptide’s uptake into cells and its stability during metabolism.[1] Tirzepatide is being investigated for its potential impact in research within the context of research related to type 2 diabetes, obesity, bone metabolism, the pancreas, and the central nervous system.


Molecular Formula: C225H348N48O68

Molecular Weight: 4813.45 g/mol


Tirzepatide Research

Tirzepatide Mechansim of Action
Tirzepatide is a GIP-analog that appears to activate both the GLP-1 and GIP receptors. Generally, the peptide is reported to be a potential activator for GIP than GLP-1 receptors. Both of those receptors may be found in the pancreas but also in other organs. Usually, the small intestine produces GLP-1 and GIP when certain nutrients are in its lumen. For example, researchers posit that GIP is triggered by the hyperosmolarity of glucose that enters the duodenum after caloric intake.[2] The GIP and GLP-1 peptides may then be released in the blood and travel to the corresponding receptors. Activating either of those receptors in the pancreas may stimulate the beta-cells to produce insulin in a glucose-dependent manner. However, the action is glucose-dependent, so GIP or GIP analogs like Tirzepatide do not appear to trigger insulin secretion if glucose levels are low or average, and this reduces the risk of hypoglycemia. GIP receptors may also be found in the gut, adipose tissue, heart, pituitary, and inner layers of the adrenal cortex.[3] GLP-1 receptors have also been discovered in cell models of the gut, exocrine pancreas, brain, heart, lung, and kidney.[4]

Tirzepatide and Glycemic Control
The main influence of Tirzepatide is posited to be in the reduction of blood sugar levels and improved glucose control, as exhibited in conditions of type 2 diabetes. Studies suggest that due to this dual agonist behavior, Tirzepatide may have a high potency for  improving glycemic control compared to anti-diabetic compounds such as GLP-1 agonists, SGLT-2 inhibitors, or DPP-4 inhibitors.[5] Moreover, Tirzepatide may potentially support insulin sensitivity and beta-cell function in conditions of type 2 diabetes. Studies note that the peptide appeared to reduce insulin resistance in animal models as measured by the HOMA2-IR index, and the action was more remarkable when compared to GLP-1 agonists. Thomas et al. explained that the improvement appeared to be primarily independent of weight reduction and noted that “weight loss explained only 13% and 21% of improvement in HOMA2-IR with Tirzepatide.” [6]

Tirzepatide and Weight Loss
A meta-analysis of 9 clinical studies that covered more than 7,000 models of type 2 diabetes reported that Tirzepatide may lead to more weight loss than GLP-1 agonists such as Semaglutide.[7] The duration of the studies ranged from 8 to 52 weeks, with a reported 5kg average loss. Moreover, Tirzepatide appeared to exhibit better glycemic control than Semaglutide and insulin. Permana et al. concluded, “Tirzepatide has shown superiority in glycemic control and weight reduction … [in conditions of] T2D.” Tirzepatide has been suggested to induce weight loss with or without the precondition of diabetes. In a clinical trial with 2,539 models of obesity and at least one related complication (excluding diabetes),Tirzepatide exposure was reported to lead to a dramatic reduction in weight.[8] In 72 weeks of exposure, findings indicated at least a 20% reduction in weight or more, compared to only 3% weight loss in the control group for the same period.

Tirzepatide and Hepatoprotection
Tirzepatide has been reported to potentially improve markers of liver function in research models of non-alcoholic fatty liver disease (NAFLD).[9] Apart from reducing liver enzymes such as ALT and AST, the peptide also appeared to lower markers of liver cell death, such as K-18, and markers of liver fibrosis, such as Pro-C3.[10] The results of another trial suggests that Tirzepatide may also lead to a significant reduction in liver fat content, which is another direct marker for NAFLD.[11] In 52 weeks, the peptide appeared to lead to an average 8% reduction in liver fat.

Tirzepatide and Lipid Metabolism
Tirzepatide is currently being researched for its potential impact on cardiovascular system, the kidneys, and the heart.[12] In models of type 2 diabetes, Tirzepatide might slow the decline of kidney function and the progression of chronic kidney disease.[13] Furthermore, researchers hypothesize that Tirzepatide exposure may improve lipid profiles in such instances. After 26 weeks, one study by Wilson et al. reported that the peptide appeared to decrease apoB, apoC-III, LDL levels, and triglycerides. Wilson et al. indicated that “At 26 weeks, change in apoC-III, but not body weight, was the best predictor of changes in triglycerides with Tirzepatide, explaining up to 22.9% of their variability.”[14] The researchers also noted that the improvement in the lipid profile of the models appeared partially independent of weight.

Tirzepatide and Metabolic Rate
Tirzepatide may regulate metabolic rates by modulating the activity of GIP receptors. This hypothesis is supported by studies using heterozygous transgenic murine models (Het GIP Tg mice), engineered to express extra GIP genes.[15] On a high-fat diet, these mice appeared to have gained less weight and accumulated less body fat compared to their wild-type (WT) counterparts, who lacked the transgene. Furthermore, the Het GIP Tg mice may have maintained better insulin sensitivity and glucose tolerance, suggesting improved pancreatic β-cell function. In these mice, adipose tissue appeared to have exhibited reduced macrophage presence and lower hepatic fat deposits. This reduction may reflect decreased expression of genes critical to fat metabolism and inflammation, such as ATP citrate lyase (Acly) and interleukin 4 receptor alpha (IL4ra).

Tirzepatide and Gastric Motility
In murine models, acute exposure to Tirzepatide appeared to delay gastric emptying and motility, showing a similar action to other long-acting GLP-1 receptor agonists.[16] Thus, this likely involves interactions with neural pathways using GLP-1 receptors in both the central and peripheral nervous systems.[17] The process might begin with an engagement of GLP-1 receptors on enteroendocrine cells in the intestinal lining. These cells, which release GLP-1 in response to caloric intake, might be simulated by Tirzepatide to enhance the hormone’s actions. Activated GLP-1 receptors may then relay signals through the enteric nervous system, controlling gastrointestinal movements and functions. This interaction may lead to reduced stomach contractions and delayed release of stomach contents into the small intestine. Furthermore, Tirzepatide might also impact gastric motility through signals sent to the central nervous system via the vagal nerve, potentially modifying autonomic responses that regulate stomach functions and further slow gastric emptying. Notably, this inhibitory action on gastric emptying and motility seemingly vanished after two weeks of exposure, suggesting a transient influence of Tirzepatide in these conditions. These results might indicate that Tirzepatide might initially slow gastric motility, potentially contributing to its glucose-lowering actions, although this appears to diminish with continued exposure. The diminishing action of Tirzepatide on gastric emptying and motility over time, observed in murine models, suggests a potential tachyphylaxis—the gradual diminishment of response to a compound after repeated exposure.

Tirzepatide and Appetite Suppression
Tirzepatide appears to have a potent influence on appetite suppression which appears to be related to a potential dual function as an agonist for both GIP and GLP-1 receptors. For example, the GIP signaling pathway in the central nervous system might influence hypothalamic centers that regulate feeding, potentially leading to decreased food consumption and improved glucose metabolism.[18,19] The agonism of GIP receptors is thought to activate hypothalamic neurons that suppress appetite, with data from studies where chemogenetic activation of hypothalamic Gipr+ neurons reduced food intake. Additionally, GIP receptor activation might increase the blood-brain barrier’s permeability, potentially enhancing the delivery of GLP-1RAs and other appetite-regulating signals to their brain targets, based on Gipr+ expression in cells influencing the neurovascular unit. Consequently, stimulating GLP-1 receptors in brain areas linked to reward might further influence hunger perceptions associated with GLP-1 receptor agonists like Tirzepatide.[20] These agonists are thought to interact with neurons in the arcuate nucleus of the hypothalamus, considered crucial for neuroendocrine control. Such interactions are suspected to initiate a complex neurochemical pathway that integrates energy status signals, possibly affecting behavioral and physiological responses to hunger. Neurons in this area might regulate hunger, possibly expressing both proopiomelanocortin and cocaine- and amphetamine-regulated transcript (POMC/CART), which are believed to hold significant roles in appetite suppression. Activating these POMC/CART-expressing neurons might promote satiety and indirectly reduce the release of appetite-stimulating peptides like neuropeptide Y (NPY) and agouti-related peptide (AgRP). Moreover, GLP-1 receptor agonists like Tirzepatide may help maintain levels of circulating free leptin—a hormone linked to satiety—and may raise levels of peptide YY (PYY) 3-36, a hormone associated with reduced food intake and increased fullness.[21] Thus, Tirzepatide’s role in appetite suppression might involve intricate interactions between neurochemical and hormonal signals.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing. Bodily introduction of any sort is strictly prohibited by law. All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.



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Dr. Usman

Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.

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