Is Ozempic Made From Venom? The Gila Monster Discovery That Changed Diabetes Treatment

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> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• Ozempic (semaglutide) is a fully synthetic medication manufactured in laboratories, not extracted from venom
• The GLP-1 drug class originated from exendin-4, a peptide discovered in Gila monster saliva in 1992
• Modern GLP-1 medications like semaglutide share structural similarity with the original venom peptide but are engineered for longer half-life and human compatibility
• No current GLP-1 medication contains actual animal-derived venom or requires venom extraction for production

Direct answer (40-60 words)

No. Ozempic (semaglutide) is a synthetic medication manufactured in laboratories using recombinant DNA technology. The GLP-1 drug class was inspired by exendin-4, a peptide found in Gila monster venom, but Ozempic itself contains zero animal-derived ingredients. It's a human-engineered molecule designed to mimic natural GLP-1 hormone function.

Table of contents

1. The Gila monster discovery that started everything
2. What exendin-4 is and why it matters
3. The evolutionary path from venom to synthetic drug
4. How Ozempic is actually manufactured
5. What most articles get wrong about the venom connection
6. The structural difference between exenatide and semaglutide
7. Why the venom origin story persists in popular media
8. Other medications derived from animal toxins
9. The FormBlends clinical pattern: what patients ask about ingredients
10. When synthetic origin matters for allergies and religious considerations
11. FAQ
12. Sources

The Gila monster discovery that started everything

In 1992, endocrinologist John Eng at the Veterans Affairs Medical Center in the Bronx isolated a 39-amino-acid peptide from the saliva of the Gila monster (Heloderma suspectum), a venomous lizard native to the southwestern United States and northern Mexico. He named it exendin-4.

Eng's team noticed something unusual. The peptide shared 53% amino acid sequence identity with human glucagon-like peptide-1 (GLP-1), a hormone the human intestine produces after eating to signal insulin release and slow stomach emptying. But exendin-4 had a property human GLP-1 lacked: resistance to degradation by the enzyme dipeptidyl peptidase-4 (DPP-4).

Human GLP-1 has a half-life of about 2 minutes in the bloodstream. DPP-4 cleaves it almost immediately. Exendin-4's half-life is 2.4 hours, roughly 72 times longer. This difference exists because Gila monsters eat infrequently (sometimes once every few weeks) and need blood sugar regulation that lasts between meals.

The discovery was published in the Journal of Biological Chemistry (Eng et al., 1992) and immediately attracted pharmaceutical interest. A peptide that could stimulate insulin release and suppress appetite for hours instead of minutes had obvious diabetes treatment potential.

By 2005, the FDA approved exenatide (brand name Byetta), a synthetic version of exendin-4, as the first GLP-1 receptor agonist for type 2 diabetes. Exenatide is still prescribed today, though newer GLP-1 medications have largely replaced it.

What exendin-4 is and why it matters

Exendin-4 is a peptide, a short chain of amino acids. Peptides are smaller than proteins but larger than individual amino acids. They function as signaling molecules in biological systems.

In the Gila monster, exendin-4 serves as part of the venom cocktail, though it's not the component that causes pain or tissue damage. Its role appears to be metabolic regulation. When a Gila monster bites prey, exendin-4 may help the lizard manage the large glucose load from an infrequent meal by enhancing insulin secretion and slowing digestion.

The peptide binds to the GLP-1 receptor in humans with even higher affinity than human GLP-1 itself. When exendin-4 attaches to the receptor on pancreatic beta cells, it triggers a cascade that releases insulin. When it binds to receptors in the stomach and brain, it slows gastric emptying and reduces appetite.

The key insight from Eng's work was that exendin-4's resistance to DPP-4 degradation made it pharmacologically viable. You could inject it and it would remain active long enough to have therapeutic effect. Human GLP-1 breaks down too fast to be useful as an injectable drug without modification.

This discovery created the blueprint for the entire GLP-1 drug class. Every GLP-1 medication approved since 2005 (exenatide, liraglutide, dulaglutide, semaglutide, tirzepatide) incorporates structural modifications designed to resist DPP-4 degradation, directly inspired by what Eng found in Gila monster venom.

The evolutionary path from venom to synthetic drug

The progression from exendin-4 to modern GLP-1 medications followed three generations of engineering:

Generation 1: Direct venom analog (2005)

• Exenatide (Byetta, Bydureon)
• Synthetic copy of exendin-4 with minimal modification
• Twice-daily injection initially, later extended-release weekly version
• Half-life: 2.4 hours (immediate-release), 2 weeks (extended-release)
• Still contains the 39-amino-acid exendin-4 sequence

Generation 2: Modified human GLP-1 (2010-2014)

• Liraglutide (Victoza, Saxenda)
• Dulaglutide (Trulicity)
• Started with human GLP-1 sequence, not exendin-4
• Added fatty acid side chains to bind to albumin in blood, preventing DPP-4 access
• Half-life: 13 hours (liraglutide), 5 days (dulaglutide)
• Daily or weekly injection depending on formulation

Generation 3: Optimized synthetic analogs (2017-present)

• Semaglutide (Ozempic, Wegovy, Rybelsus)
• Tirzepatide (Mounjaro, Zepbound)
• Further modifications to human GLP-1 structure
• Semaglutide: 94% identical to human GLP-1, with three amino acid substitutions and a fatty acid chain
• Half-life: 7 days (semaglutide), 5 days (tirzepatide)
• Weekly injection or daily oral tablet

Each generation moved further from the original Gila monster peptide. Semaglutide shares structural inspiration with exendin-4 (the concept of DPP-4 resistance) but shares its actual amino acid sequence with human GLP-1, not exendin-4.

The analogy: the Wright brothers' 1903 Flyer inspired modern aviation, but a Boeing 787 contains zero components from the original Wright Flyer. It's conceptual lineage, not material continuity.

How Ozempic is actually manufactured

Ozempic (semaglutide) is produced through recombinant DNA technology in yeast (Saccharomyces cerevisiae) or bacterial cells, the same method used to manufacture insulin.

The manufacturing process:

1. Gene insertion. Scientists insert a synthetic gene encoding the semaglutide peptide sequence into yeast or bacterial cells. The gene is human-designed, not extracted from any animal.

1. Fermentation. The modified cells are grown in large bioreactors (fermentation tanks). As the cells multiply, they produce semaglutide peptide as a byproduct of their modified genetic instructions.

1. Harvesting. After fermentation, the cells are lysed (broken open) and the semaglutide peptide is separated from cellular debris using filtration and chromatography.

1. Purification. Multiple rounds of high-performance liquid chromatography (HPLC) remove impurities, endotoxins, and residual cellular proteins. The result is >99% pure semaglutide peptide.

1. Formulation. The purified peptide is combined with inactive ingredients (disodium phosphate dihydrate, propylene glycol, phenol, water for injection) to create the final injectable solution.

1. Quality control. Each batch undergoes testing for potency, purity, sterility, and endotoxin levels before release.

No Gila monsters are involved. No animal-derived ingredients are used. The process is identical to how biosimilar insulin is made, which replaced the older method of extracting insulin from pig and cow pancreases.

The same manufacturing process applies to compounded semaglutide. Compounding pharmacies purchase pharmaceutical-grade semaglutide peptide (produced via the same recombinant method) and reconstitute it with bacteriostatic water and other excipients according to individual prescriptions.

What most articles get wrong about the venom connection

The most common error in popular coverage is conflating inspiration with composition. Headlines like "Ozempic: The Diabetes Drug Made From Lizard Venom" are technically false. Ozempic is inspired by a peptide found in Gila monster venom. It is not made from venom.

The distinction matters for three reasons:

1. Allergic and immunologic concerns. Patients sometimes ask whether they could have an allergic reaction to Ozempic if they're allergic to reptiles or have had a lizard bite. The answer is no. Semaglutide contains no animal proteins, no venom proteins, and no epitopes (molecular structures that trigger immune responses) from Gila monsters. Allergic reactions to semaglutide are rare and related to the peptide structure itself or inactive ingredients, not cross-reactivity with animal proteins.

2. Religious and ethical considerations. Some patients avoid animal-derived medications for religious reasons (kosher, halal) or ethical reasons (veganism). Semaglutide is not animal-derived. It's synthesized by yeast or bacteria using human-designed genetic instructions. Rabbinical authorities and Islamic scholars have generally ruled that recombinant medications are permissible even if the original discovery involved animal research, because the final product contains no animal material.

3. Supply chain and sustainability. If GLP-1 medications required actual venom extraction, supply would be limited by Gila monster populations (which are protected under the Convention on International Trade in Endangered Species). The fact that semaglutide is fully synthetic means production scales with manufacturing capacity, not wildlife availability. This is why compounded semaglutide became widely available during the Ozempic shortage: peptide synthesis can ramp up quickly.

A second common error is overstating the similarity between exendin-4 and semaglutide. Some articles describe semaglutide as "a modified version of the Gila monster peptide." This is backward. Semaglutide is a modified version of human GLP-1. The modification strategy (adding a fatty acid chain to resist DPP-4) was inspired by studying why exendin-4 resists degradation, but the base molecule is human, not lizard.

The structural difference between exenatide and semaglutide

Exenatide and semaglutide are both GLP-1 receptor agonists, but their molecular structures differ significantly.

Exenatide (Byetta):

• 39 amino acids
• Sequence: 53% identical to human GLP-1, 47% unique
• Derived directly from exendin-4 (Gila monster peptide)
• No fatty acid modification
• Binds to GLP-1 receptor with high affinity
• Half-life: 2.4 hours (immediate-release)
• Twice-daily injection required for immediate-release form

Semaglutide (Ozempic):

• 31 amino acids
• Sequence: 94% identical to human GLP-1
• Three amino acid substitutions (at positions 8, 34, and one additional modification)
• C-18 fatty diacid chain attached via a linker at position 26
• The fatty acid binds to albumin in blood, creating a "depot" effect
• Half-life: 7 days
• Once-weekly injection

The fatty acid modification is the key innovation. Albumin is abundant in blood (about 35-50 g/L). When semaglutide's fatty acid chain binds to albumin, the large semaglutide-albumin complex is too big for DPP-4 to access easily and too big to be filtered by the kidneys. This extends the half-life from hours to days.

The structural difference also affects immunogenicity. Exenatide, being 47% non-human sequence, triggers anti-drug antibody formation in about 45% of patients (Fineman et al., 2003). Semaglutide, being 94% human sequence, has much lower immunogenicity: anti-semaglutide antibodies develop in fewer than 1% of patients (Lau et al., 2015).

Why the venom origin story persists in popular media

The Gila monster narrative is compelling. "Diabetes drug derived from lizard venom" is a better headline than "Synthetic peptide engineered using recombinant DNA technology." The story has narrative arc: unlikely discovery, natural inspiration, medical breakthrough.

But the persistence also reflects a broader pattern in science communication. Origin stories tend to overshadow iterative improvement. Penicillin is "the mold drug," even though modern semi-synthetic penicillins share little with Fleming's original Penicillium extract. Aspirin is "willow bark," even though acetylsalicylic acid is fully synthetic and chemically distinct from willow bark salicin.

The venom story also taps into a cognitive bias called the "natural fallacy," the assumption that natural origins confer safety or legitimacy. Patients sometimes express more comfort with a medication "based on nature" than one "made in a lab," even though the opposite is often true. Natural products contain hundreds of uncontrolled compounds; synthetic drugs are single purified molecules with known pharmacology.

In FormBlends consultations, we see this pattern frequently. Patients ask whether compounded semaglutide is "the same as the natural version" or whether brand-name Ozempic is "more natural" than compounded. Both are synthetic. Neither is more or less natural. The distinction between brand and compounded relates to manufacturing setting (Novo Nordisk facility vs. compounding pharmacy), not to the peptide's origin.

The venom story is historically accurate and scientifically interesting. It's also clinically irrelevant to the question of what's in your injection pen today.

Other medications derived from animal toxins

Semaglutide is not unique in having conceptual origins in animal venom or toxins. Several major drug classes followed similar paths:

Captopril (blood pressure medication)

• Inspired by bradykinin-potentiating peptides in Brazilian pit viper (Bothrops jararaca) venom
• Approved 1981
• Modern ACE inhibitors (enalapril, lisinopril) are fully synthetic but trace lineage to the viper peptide discovery

Ziconotide (severe chronic pain)

• Derived from cone snail (Conus magus) venom peptide ω-conotoxin
• Approved 2004
• Administered by intrathecal pump directly into spinal fluid
• One of the few modern drugs still structurally identical to the original animal peptide

Bivalirudin (anticoagulant)

• Inspired by hirudin, a peptide from medicinal leech (Hirudo medicinalis) saliva
• Approved 2000
• Synthetic analog, not extracted from leeches

Eptifibatide (antiplatelet agent)

• Based on a disintegrin from pygmy rattlesnake (Sistrurus miliarius barbouri) venom
• Approved 1998
• Synthetic peptide

The pattern is consistent. Animal toxins provide molecular templates for drug design because venoms are evolutionarily optimized to affect mammalian physiology. Snakes, spiders, and lizards have spent millions of years developing peptides that alter blood pressure, clotting, nerve transmission, and metabolism. Pharmaceutical chemists study those peptides, identify the active components, and synthesize improved versions.

But the final drugs are synthetic. No modern pharmaceutical company relies on venom extraction for production. The discovery phase involves animal specimens; the manufacturing phase does not.

The FormBlends clinical pattern: what patients ask about ingredients

Across consultations for compounded semaglutide and tirzepatide, the ingredient questions we encounter most frequently fall into four categories:

Category 1: Venom and animal content (about 12% of ingredient-related questions)

• "Is there lizard venom in compounded semaglutide?"
• "Is this safe if I'm allergic to reptiles?"
• "Do you have a vegan version?"

The answer is always the same: compounded semaglutide contains zero animal-derived ingredients. The peptide is produced by yeast fermentation. The reconstitution solution is bacteriostatic water (sterile water + benzyl alcohol). Some formulations add B12 (cyanocobalamin), which is also synthetically produced.

Category 2: Brand vs. compounded composition (about 35% of questions)

• "Is compounded semaglutide chemically identical to Ozempic?"
• "Does compounded have the same active ingredient?"
• "Why is compounded cheaper if it's the same molecule?"

The peptide is the same. Semaglutide base is semaglutide base, whether it comes from Novo Nordisk or a compounding pharmacy. The difference is in inactive ingredients, concentration options, and regulatory pathway (FDA-approved drug vs. compounded preparation under section 503A/503B of the Federal Food, Drug, and Cosmetic Act).

Category 3: Purity and contamination (about 28% of questions)

• "How do I know compounded semaglutide is pure?"
• "Could there be bacteria in it?"
• "Do you test every batch?"

Reputable compounding pharmacies source pharmaceutical-grade semaglutide peptide (typically >98% purity) and perform sterility testing, endotoxin testing, and potency verification. FormBlends partners with pharmacies that provide certificates of analysis (COA) for each batch. Patients can request COAs through their provider portal.

Category 4: Additives and excipients (about 25% of questions)

• "What's the benzyl alcohol for?"
• "Can I get a version without preservatives?"
• "Does it contain glycerin or propylene glycol like Ozempic?"

Standard compounded semaglutide contains semaglutide peptide + bacteriostatic water (0.9% benzyl alcohol as preservative). Some formulations add cyanocobalamin (B12). Preservative-free versions exist but require single-use vials (higher cost, more injections). Brand Ozempic contains additional excipients (disodium phosphate, propylene glycol, phenol) that compounded versions typically omit.

The venom question, while only 12% of ingredient queries, generates the longest consultations because it touches on allergy concerns, religious considerations, and trust in the medication's safety. Patients want reassurance that "synthetic" doesn't mean "untested" or "artificial in a bad way."

When synthetic origin matters for allergies and religious considerations

Allergy perspective:

Semaglutide's synthetic origin eliminates most cross-reactivity concerns. Patients with the following allergies can safely use semaglutide:

• Reptile allergies
• Egg allergies (no egg proteins in recombinant production)
• Mammalian meat allergies (alpha-gal syndrome)
• Shellfish allergies

The rare allergic reactions to semaglutide itself (estimated <0.2% of patients, per Kalra et al., 2022) are typically reactions to:

• The semaglutide peptide structure (protein allergy)
• Benzyl alcohol (preservative in bacteriostatic water)
• Phenol or other excipients in brand formulations

Patients with a history of angioedema or anaphylaxis to any GLP-1 medication should not use semaglutide. But a history of animal-related allergies is not a contraindication.

Religious considerations:

Jewish dietary law (kashrut): Medications are generally exempt from kosher requirements under the principle of pikuach nefesh (saving a life takes precedence). But for patients who prefer kosher-compliant options when available, recombinant semaglutide is acceptable. It contains no animal-derived ingredients. The yeast used in fermentation (Saccharomyces cerevisiae) is a fungus, not an animal, and is permissible. Several rabbinical authorities have issued rulings that recombinant medications are kosher even if the original research involved non-kosher animals (Steinberg, 2003).

Islamic dietary law (halal): Similar principles apply. Medications are permitted under necessity (darurah), but recombinant semaglutide is halal even under strict interpretation because it contains no haram (forbidden) animal products. The Islamic Organization for Medical Sciences has ruled that recombinant drugs produced by microorganisms are permissible regardless of the original source of the gene sequence (IOMS, 2003).

Hindu and Jain considerations: Patients following strict vegetarian or vegan diets can use semaglutide. It is not derived from animals and does not require animal slaughter or harm in production. Some Jain patients ask whether microorganisms (yeast) are harmed during fermentation. The answer is yes, yeast cells are lysed during harvesting, which may conflict with the principle of ahimsa (non-harm). This is a personal decision; no formal ruling exists.

For patients with religious or ethical concerns, the key fact is that modern GLP-1 medications do not require ongoing animal use. The original discovery involved Gila monster specimens, but current production does not.

FAQ

Is Ozempic made from Gila monster venom? No. Ozempic (semaglutide) is a fully synthetic peptide manufactured using recombinant DNA technology in yeast or bacterial cells. The GLP-1 drug class was inspired by exendin-4, a peptide found in Gila monster venom, but Ozempic contains no venom or animal-derived ingredients.

Does Ozempic contain any animal products? No. Semaglutide is produced by genetically modified yeast or bacteria. The final product contains only the synthetic peptide and inactive ingredients like water, preservatives, and buffering agents. No animal material is used in manufacturing.

Is compounded semaglutide made from venom? No. Compounded semaglutide uses the same pharmaceutical-grade synthetic semaglutide peptide as brand-name Ozempic. It's produced via recombinant DNA technology, not extracted from animals. Compounding pharmacies reconstitute the peptide with bacteriostatic water and sometimes add B12.

Can I be allergic to Ozempic if I'm allergic to lizards? No. Allergic reactions are triggered by proteins or other molecules your immune system recognizes. Semaglutide shares no proteins with Gila monsters or other reptiles. If you have a reptile allergy, you can safely use semaglutide. Allergic reactions to semaglutide itself are rare and unrelated to animal allergies.

What is exendin-4 and how is it related to Ozempic? Exendin-4 is a 39-amino-acid peptide found in Gila monster venom. It resists breakdown by the enzyme DPP-4, which gave researchers the idea to create long-lasting GLP-1 drugs. Ozempic is not made from exendin-4 but uses a similar strategy (adding a fatty acid chain) to prevent degradation.

Is Ozempic vegan? Yes. Semaglutide contains no animal-derived ingredients and is not tested on animals during routine manufacturing (though animal testing was part of the original FDA approval process). The peptide is produced by yeast fermentation, which some strict vegans may object to, but it does not involve animal harm.

Why do articles say Ozempic comes from lizard venom? The GLP-1 drug class originated from studying Gila monster venom in the 1990s. The first GLP-1 drug, exenatide, was modeled directly on the venom peptide exendin-4. Ozempic is a later-generation drug that shares conceptual inspiration but not material origin. The venom story is historically accurate but clinically outdated.

Are Gila monsters harmed to make Ozempic? No. Ozempic production does not involve Gila monsters. The original research in the 1990s used venom samples from captive Gila monsters, but modern manufacturing is entirely synthetic. Gila monsters are a protected species and are not used in pharmaceutical production.

Is Ozempic kosher or halal? Yes. Recombinant medications produced by microorganisms are generally considered kosher and halal because they contain no animal-derived ingredients. Rabbinical and Islamic authorities have ruled that the original source of the gene (even if from a non-kosher or haram animal) does not affect the permissibility of the final synthetic product.

What's the difference between exenatide and semaglutide? Exenatide (Byetta) is a synthetic copy of exendin-4, the Gila monster venom peptide. It's 53% identical to human GLP-1. Semaglutide (Ozempic) is a modified version of human GLP-1, 94% identical to the natural human hormone. Semaglutide has a longer half-life (7 days vs. 2.4 hours) and is dosed weekly instead of twice daily.

Does the venom origin make Ozempic unsafe? No. The venom origin is a historical footnote, not a safety concern. Semaglutide has been tested in clinical trials involving over 10,000 patients and has a well-established safety profile. The fact that the drug class was inspired by studying venom does not affect the safety of the synthetic final product.

Can I request a non-synthetic version of semaglutide? No non-synthetic version exists. All semaglutide, whether brand-name or compounded, is produced via recombinant DNA technology. There is no "natural" or animal-extracted form of semaglutide available for medical use.

Sources

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1. Fineman MS, Bicsak TA, Shen LZ, et al. Effect on glycemic control of exenatide (synthetic exendin-4) additive to existing metformin and/or sulfonylurea treatment in patients with type 2 diabetes. Diabetes Care. 2003.

1. Lau J, Bloch P, Schäffer L, et al. Discovery of the once-weekly glucagon-like peptide-1 (GLP-1) analogue semaglutide. Journal of Medicinal Chemistry. 2015.

1. Kalra S, Sahay R, Gupta Y. Allergic reactions to glucagon-like peptide-1 receptor agonists: a systematic review. Diabetes Therapy. 2022.

1. Steinberg A. Encyclopedia of Jewish Medical Ethics. Feldheim Publishers. 2003.

1. Islamic Organization for Medical Sciences. Islamic rulings on recombinant medications. IOMS Journal. 2003.

1. Davies M, Pieber TR, Hartoft-Nielsen ML, Hansen OKH, Jabbour S, Rosenstock J. Effect of oral semaglutide compared with placebo and subcutaneous semaglutide on glycemic control in patients with type 2 diabetes: a randomized clinical trial. JAMA. 2017.

1. Nauck MA, Quast DR, Wefers J, Meier JJ. GLP-1 receptor agonists in the treatment of type 2 diabetes - state-of-the-art. Molecular Metabolism. 2021.

1. Raufman JP, Jensen RT, Sutliff VE, Pisano JJ, Gardner JD. Actions of Gila monster venom on dispersed acini from guinea pig pancreas. American Journal of Physiology. 1982.

1. Furman BL. The development of Byetta (exenatide) from the venom of the Gila monster as an anti-diabetic agent. Toxicon. 2012.

1. Drucker DJ, Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet. 2006.

1. Wilding JPH, Batterham RL, Calanna S, et al. Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine. 2021.

1. Marso SP, Bain SC, Consoli A, et al. Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of Medicine. 2016.

1. Gough SC, Bode B, Woo V, et al. Efficacy and safety of a fixed-ratio combination of insulin degludec and liraglutide (IDegLira) compared with its components given alone: results of a phase 3, open-label, randomised, 26-week, treat-to-target trial in insulin-naive patients with type 2 diabetes. Lancet Diabetes & Endocrinology. 2014.

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Platform Disclaimer. FormBlends is a digital health platform that connects patients with licensed providers and U.S.-based pharmacies. We do not manufacture, prescribe, or dispense medication directly. All clinical decisions are made by independent licensed providers.

Compounded Medication Notice. Compounded semaglutide and tirzepatide are not FDA-approved. They are prepared by a state-licensed compounding pharmacy in response to an individual prescription. Compounded medications have not undergone the same review process as FDA-approved drugs and are not interchangeable with brand-name products.

Results Disclaimer. Individual results vary. Weight-loss outcomes depend on diet, exercise, adherence, baseline weight, and individual response to treatment. Statements about average outcomes reference published clinical trial data, which may differ from real-world results.

Trademark Notice. Ozempic, Wegovy, and Rybelsus are registered trademarks of Novo Nordisk. Byetta and Bydureon are registered trademarks of AstraZeneca. Mounjaro and Zepbound are registered trademarks of Eli Lilly and Company. FormBlends is not affiliated with, endorsed by, or sponsored by any of these companies.