Sema 10 mg

What is Sema? (GLP-1)
Sema is a synthetic peptide analog of human glucagon-like peptide-1 (GLP-1), designed to mimic the effects of this naturally occurring incretin hormone. Incretin hormones are a group of metabolic peptides released by the gut in response to food intakeparticularly glucose and fat. The main role of incretin hormones and their analogs, such as sema, is to stimulate insulin secretion from the pancreas in a glucose-dependent manner, meaning they help regulate blood sugar without triggering excessive insulin release when glucose levels are low.
The two primary incretin hormones are:

GLP-1 (glucagon-like peptide-1)
GIP (glucose-dependent insulinotropic polypeptide)

These hormones support metabolic balance by stimulating insulin secretion, inhibiting glucagon release (which would otherwise raise blood sugar), slowing gastric emptying (to help regulate the pace of digestion), and promoting a feeling of fullness or satiety, which can reduce overall food intake.
Why Use Sema in Your Research?
In research settings, sema is studied for its ability to modulate these mechanisms that are of interest in metabolic and obesity-related studies.
Being a GLP-1 analog, sema is a modified peptide that includes specific substitutions and a fatty acid side chain, which enhances its binding to albumin and significantly extends its half-life. These modifications make it more stable and resistant to enzymatic degradation compared to native GLP-1, allowing for prolonged activity in vitro and in vivo models.
Researchers value Sema for its:

High stability under standard storage and handling conditions
Excellent solubility in common research-grade diluents
Consistency across experiments due to its chemical design and long half-life

Studies have shown that Sema demonstrates strong GLP-1 receptor agonism, supporting its relevance in research focused on glucose homeostasis, appetite regulation, and weight management pathways.
Important: This product is offered strictly for research use only. It is not approved by the FDA for human or veterinary use. It must not be used for any form of clinical or diagnostic application.
Sema Mechanism of Action (Based on Research)
Sema is a GLP-1 receptor agonist, which means it binds to and activates the same receptor that natural GLP-1 does. However, unlike endogenous GLP-1, which breaks down rapidly in the body, Sema has been chemically modified to be long-acting and resistant to enzymatic degradation.
In research, Sema mimics and amplifies the actions of GLP-1, making it especially relevant in studies focused on:

Glucose regulation
Appetite control and energy balance
Obesity and metabolic disorders

The effects of sema have been observed across multiple metabolic and hormonal pathways in preclinical and non-clinical studies. The primary mechanisms involve the following:
Appetite Regulation
Sema has been shown to influence appetite control centers in the brain, particularly within the hypothalamus. Research suggests it may reduce food intake by enhancing satiety signals and lowering hunger levels through GLP-1 receptor activity in the central nervous system (CNS).
In rodent models, chronic administration led to significant decreases in caloric intake and body weight without signs of tolerance development.
Functional MRI data show that Sema alters activation in brain regions involved in reward and motivation, including the insula, putamen, and orbitofrontal cortex, which are associated with food cue reactivity and cravings.
Participants exhibited reduced neural response to high-calorie food images, suggesting a shift in food-related attention and motivationmechanisms that may contribute to sustained appetite suppression and reduced caloric intake in research contexts.
Blood Sugar Modulation
Sema enhances glucose-dependent insulin secretion and suppresses glucagon release, both of which contribute to improved glycemic control in research settings. These actions support a more stable postprandial (after-meal) blood glucose profile.
Importantly, the sema peptide does not typically stimulate insulin when blood glucose is low, reducing the risk of hypoglycemia in research models.
In addition to its pancreatic effects, Sema has been shown to improve the efficiency of glucose disposal in peripheral tissues, enhancing overall glycemic regulation in experimental systems.
Studies suggest that sema helps lower both fasting and postprandial glucose levels by improving insulin sensitivity, reducing hepatic glucose output, and delaying gastric emptying, which collectively help flatten glucose spikes after meals. These mechanisms make it particularly relevant in research focused on insulin resistance, beta-cell function, and type 2 diabetes modeling.
Hormonal Pathways
GLP-1 receptor activation also affects broader hormonal networks. Sema has been observed to slow gastric emptying, influencing gut-brain signaling and the timing of nutrient absorption. These effects are tied to changes in gut-derived hormones, which may further modulate insulin dynamics, satiety, and energy balance.
Recent findings also suggest that Sema may influence neuroendocrine circuits involved in food-related stress regulation and energy homeostasis.
Studies have observed interactions between GLP-1 receptor pathways and the hypothalamic-pituitary-adrenal (HPA) axis, hinting at potential roles in modulating cortisol levels, feeding behavior under stress, and central energy-sensing mechanisms.
While these findings are still under investigation, they point to Sema’s broader relevance in endocrine-focused research beyond metabolic control alone.
Research Applications (Sema Benefits)
Sema has been the subject of a wide range of non-clinical and preclinical studies exploring its effects on energy regulation, glucose metabolism, and hormonal pathways. As a GLP-1 receptor agonist with enhanced stability and bioavailability, it has become a valuable tool in controlled research environments.
Below are key areas where Sema has been investigated:
Weight Management
Sema has been widely studied for its role in body weight regulation, especially in the context of appetite modulation and caloric intake reduction. In various non-clinical models, including rodent and primate studies, sema peptide has been observed to reduce body weight through mechanisms involving central satiety pathways and food-motivated behavior.
One comprehensive study on this mode is The STEP 1 trial, a randomized, double-blind study published in The New England Journal of Medicine. Participants receiving 2.4 mg of Sema weekly, alongside lifestyle modifications, experienced an average 14.9% reduction in body weight over 68 weekssubstantially more than the placebo group.
These reductions were attributed primarily to decreased appetite, lower food cravings, and reduced energy intake, aligning with earlier findings in animal models.
Important: Although the study involved human subjects, its outcomes are not intended to imply any therapeutic claims. The study provided insight into how Sema influences energy balance in controlled conditions.
A related study published in Nature Metabolism further supported these observations. The research showed that Sema influences not only homeostatic hunger circuits but also hedonic pathways associated with reward-based eating.
Functional MRI data revealed decreased activity in brain regions tied to high-calorie food stimuli, reinforcing the idea that Sema may alter both physiological hunger and food-related motivation.
Together, these findings suggest that Sema’s ability to engage central appetite-regulating networksparticularly in the hypothalamus, brainstem, and reward centersmakes it a valuable compound for ongoing research into obesity, energy regulation, and neuroendocrine control of eating behavior.
Metabolic Studies
Sema is frequently used in metabolic research to investigate glucose homeostasis, insulin dynamics, and lipid metabolism. Its ability to enhance glucose-dependent insulin secretion while suppressing glucagon release makes it particularly relevant in models of type 2 diabetes and insulin resistance.
In particular, research has highlighted improvements in postprandial glucose control, hepatic glucose output, and peripheral glucose uptakekey endpoints in studies of metabolic disease progression.
In one trial, subjects with type 2 diabetes who were administered Sema experienced significant reductions in fasting plasma glucose, postprandial glucose excursions, and mean glucose levels compared to placebo.
The same study also showed that Sema markedly reduced glucose area under the curve (AUC) over a standardized meal test, highlighting its ability to improve glycemic response through coordinated pancreatic and gastrointestinal effects. These findings further underscore its utility as a research agent for exploring both acute and long-term glucose regulation.
Hormonal Research
Beyond glucose and appetite pathways, Sema has been studied for its impact on neuroendocrine signaling. It may influence the gut-brain axis, HPA (hypothalamic-pituitary-adrenal) axis, and broader hormonal loops involved in energy balance and stress response.
Emerging evidence points to its effects on thyroid hormone pathways. In rodent models, Sema has been shown to activate GLP-1 receptors in the hypothalamus, indirectly affecting TSH (thyroid-stimulating hormone) levels and downstream thyroid hormone regulation.
These findings suggest relevance in research beyond metabolism alone, particularly in exploring endocrine feedback mechanisms.
Sema Peptide Characteristics

Molecular Formula: CHNO
CAS Number: 910463-68-2
Amino Acid Sequence: HAEGTFTSDVSSYLEGQAAKEFIAWLVRGRG

(Note: Sequence includes chemical modifications to enhance half-life and receptor binding)

Synonyms: GLP-1(7-37) analog, NN9535,Molar Mass: ~4113.58 g/mol
Recommended Storage:

Lyophilized powder: Store at -20C or lower for long-term stability
Reconstituted solution: Store at 28C for 30-60 days. Avoid repeated freeze-thaw cycles and exposure to strong light.

Note: For research use only. Not for human or veterinary use.

Sema vs Tirz vs Reta (Comparison)
The landscape of GLP-1based therapies continues to evolve rapidly, with each new compound building upon the mechanisms of its predecessors.
Here’s how the three leading incretin-based compounds compare in terms of structure, function, and research progress:

Feature
Sema
Tirz
Reta

Type
Single agonist (GLP-1)
Dual agonist (GLP-1, GIP)
Triple agonist (GLP-1, GIP, Glucagon)

Targets
Appetite suppression, blood sugar control
Appetite suppression, blood sugar control
Appetite suppression, blood sugar control, energy expenditure

Mechanism Complexity
Simplest (single pathway)
Moderate (dual pathways)
Most complex (triple pathways)

Research Stage
FDA Approved
FDA Approved
Early-stage trials (preclinical and phase 1)

Weight Loss Potential (Research)
High clinically validated
Very high clinically validated
Potentially highest based on early data

Impact on Glucose Regulation
Strong
Strong
Strong promising in early studies

Additional Effects
Cardiovascular benefits (documented in trials)
Enhanced insulin sensitivity
Increased energy expenditure (in animal studies)

–
–
–
–

Approval Status
Approved prescription medication under certain brand names
Approved prescription medication under certain brand names
Research use only

Disclaimer
Compounded sema is not approved for human use; research only
Compounded sema is not approved for human use; research only
Not approved for human use; research only

Certificate of Analysis (COA)
All Sema peptide batches offered by Evolve Peptides undergo rigorous third-party testing to confirm identity, purity, and consistency. A Certificate of Analysis (COA) is available for each lot, providing detailed results from independent analytical labs.
Researchers may request a copy of the COA by contacting our support team, or by referencing the batch number included with each order. COAs include test results for purity (HPLC), mass spectrometry, and microbial screening, ensuring confidence in the quality of each vial.
Sample COAs may be made available for review upon request.
Disclaimer
This product is intended for laboratory research purposes only and is not approved for human or veterinary use.