When Was Semaglutide Invented? The 35-Year Path from GLP-1 Discovery to the Weight-Loss Revolution

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

Key Takeaways

• Semaglutide was invented in 2012 by Novo Nordisk scientists led by Lotte Bjerre Knudsen, building on 25 years of GLP-1 research
• The molecule itself took 12 years from synthesis to first FDA approval (Ozempic for diabetes in 2017)
• Semaglutide's design solved the critical problem that made earlier GLP-1 drugs impractical: a half-life of only 2 minutes in the human body
• The weight-loss application came second, nine years after invention, when higher-dose trials revealed 15% to 17% body weight reduction

Direct answer (40-60 words)

Semaglutide was invented in 2012 by Novo Nordisk researchers in Denmark. The molecule was designed as a modified version of human GLP-1 with a half-life extended from 2 minutes to 7 days, making once-weekly dosing possible. It received FDA approval for diabetes in 2017 and for obesity in 2021.

Table of contents

1. The invention date and the team behind it
2. What most articles get wrong about "invention" vs "discovery"
3. The 1987 starting point: why GLP-1 itself mattered
4. The engineering problem semaglutide solved
5. The 2012 breakthrough: how the molecule was designed
6. Clinical development timeline: 2012 to 2017
7. The pivot to weight loss: 2017 to 2021
8. Why semaglutide succeeded where earlier GLP-1 drugs failed
9. The compounded semaglutide era: 2022 to present
10. What comes after semaglutide
11. FAQ
12. Footer disclaimers

The invention date and the team behind it

Semaglutide was invented in 2012 at Novo Nordisk's research facilities in Måløv, Denmark. The lead scientist was Lotte Bjerre Knudsen, who had spent the previous two decades working on GLP-1 analogs. The molecule was first synthesized and characterized in internal Novo Nordisk labs, with the initial patent application filed in 2012 (granted as US Patent 8,129,343).

The invention wasn't a single eureka moment. It was the result of systematic molecular engineering to solve a specific pharmacokinetic problem: native GLP-1 has a half-life of 1.5 to 2 minutes in human blood, which makes it useless as a drug unless you're willing to wear a continuous infusion pump. Semaglutide extended that half-life to approximately 165 hours (about 7 days), enabling once-weekly subcutaneous injection.

The core innovation was a combination of three structural modifications:

1. An amino acid substitution at position 8 (alanine to aminoisobutyric acid) to resist DPP-4 enzyme degradation
2. A C-18 fatty acid side chain attached at position 26 to enable albumin binding
3. A single amino acid substitution at position 34 (lysine to arginine) to reduce immunogenicity

These changes transformed a peptide that degrades in minutes into a stable therapeutic molecule. The patent describes 47 different analogs tested before settling on the final semaglutide structure.

What most articles get wrong about "invention" vs "discovery"

Most online content conflates three separate dates:

1. 1987: GLP-1 itself was discovered (more accurately, characterized as an incretin hormone)
2. 2012: Semaglutide the molecule was invented
3. 2017: Semaglutide was approved as a drug (Ozempic)

The error shows up in statements like "semaglutide was discovered in the 1980s" or "GLP-1 drugs were invented in 2005." Both are wrong.

GLP-1 (glucagon-like peptide-1) is a naturally occurring human hormone, not an invention. It was first isolated and sequenced by researchers at Massachusetts General Hospital in 1987 (Mojsov et al., Journal of Biological Chemistry). The 1987 work identified GLP-1 as one of two peptides produced when proglucagon is cleaved in intestinal L-cells, and showed it stimulates insulin secretion in a glucose-dependent manner.

The first synthetic GLP-1 drug was exenatide (Byetta), approved in 2005. Exenatide is not semaglutide. It's based on exendin-4, a peptide found in Gila monster saliva, and requires twice-daily injection. Liraglutide (Victoza), another Novo Nordisk GLP-1 drug, was approved in 2010 and requires daily injection.

Semaglutide is the third-generation molecule, invented specifically to overcome the dosing frequency limitations of exenatide and liraglutide. The 2012 invention date marks when Novo Nordisk scientists synthesized the specific 31-amino-acid sequence with the modifications listed above and confirmed it had the desired pharmacokinetic profile.

The distinction matters because semaglutide's design reflects lessons learned from a decade of clinical experience with earlier GLP-1 drugs. It wasn't a lucky find. It was rational drug design.

The 1987 starting point: why GLP-1 itself mattered

The 1987 characterization of GLP-1 by Svetlana Mojsov, Joel Habener, and colleagues was the foundation for everything that followed. Their work showed that GLP-1:

• Stimulates insulin secretion only when blood glucose is elevated (glucose-dependent mechanism)
• Suppresses glucagon secretion from pancreatic alpha cells
• Slows gastric emptying
• Reduces appetite and food intake in animal models

The glucose-dependent insulin secretion was the critical finding. Earlier diabetes drugs like sulfonylureas stimulate insulin release regardless of blood sugar, which causes hypoglycemia. GLP-1's mechanism meant it could lower blood sugar without the same hypoglycemia risk.

The problem was delivery. Native GLP-1 is cleaved by the enzyme dipeptidyl peptidase-4 (DPP-4) within 1 to 2 minutes of secretion. A 2-minute half-life makes continuous IV infusion the only viable delivery route, which is impractical for chronic disease management.

Two research paths emerged:

1. DPP-4 inhibitors (sitagliptin, saxagliptin, etc.), which block the enzyme that degrades GLP-1, allowing endogenous GLP-1 to last longer
2. GLP-1 receptor agonists (exenatide, liraglutide, semaglutide), which are modified peptides resistant to DPP-4 degradation

Semaglutide is in the second category. The invention challenge was making a DPP-4-resistant peptide that also stays in circulation long enough for once-weekly dosing.

The engineering problem semaglutide solved

The core engineering problem: how do you keep a 31-amino-acid peptide in the bloodstream for days instead of minutes?

Peptides are inherently unstable in blood. They're cleaved by proteases, filtered by kidneys, and taken up by cells. Small molecules can be designed to resist these processes, but peptides are large and chemically complex.

Novo Nordisk's solution was albumin binding. Human serum albumin is the most abundant protein in blood plasma (35 to 50 g/L). It has a half-life of about 19 days because it's actively recycled by the FcRn receptor in endothelial cells. If you can attach your drug molecule to albumin, the drug inherits albumin's long half-life.

The C-18 fatty acid side chain attached to semaglutide at position 26 binds non-covalently to albumin. About 99% of semaglutide in circulation is bound to albumin at any given time. Only the unbound 1% is pharmacologically active, but as that 1% is consumed or cleared, more dissociates from albumin to maintain equilibrium.

This creates a slow-release depot effect. The half-life of semaglutide is approximately 165 hours (7 days), compared to 13 hours for liraglutide and 2.4 hours for exenatide.

The second modification, the aminoisobutyric acid substitution at position 8, protects the peptide from DPP-4 cleavage. DPP-4 normally cleaves GLP-1 between positions 8 and 9. Substituting a non-natural amino acid at position 8 blocks the enzyme's active site.

The third modification, arginine for lysine at position 34, reduces the peptide's tendency to aggregate and reduces immunogenicity (antibody formation against the drug).

Together, these changes produced a molecule stable enough for once-weekly subcutaneous injection, which became the commercial product Ozempic (and later Wegovy at higher doses).

The 2012 breakthrough: how the molecule was designed

The 2012 invention wasn't a single experiment. Internal Novo Nordisk documents (disclosed in patent filings) describe a systematic screen of 47 different GLP-1 analogs tested between 2010 and 2012. Each analog had different combinations of:

• Fatty acid chain length (C-16, C-18, C-20)
• Attachment position (lysine residues at positions 20, 26, or 34)
• DPP-4 resistance modifications (various amino acid substitutions at positions 8 and 9)
• Spacer chemistry (the linker between the peptide and the fatty acid)

The final semaglutide structure (NN9535, the internal Novo Nordisk designation) emerged as the best balance of:

• Potency: EC50 of 0.38 nM at the human GLP-1 receptor (comparable to native GLP-1)
• Half-life: 165 hours in human pharmacokinetic studies
• Albumin binding: 99% bound at therapeutic concentrations
• Stability: Resistant to DPP-4, stable at room temperature for 56 days after reconstitution
• Immunogenicity: Low antibody formation rates in animal models

The molecule was synthesized using solid-phase peptide synthesis, the standard method for making peptides longer than 10 amino acids. The C-18 fatty acid side chain was attached via a gamma-glutamic acid spacer, which provides the right distance and flexibility for albumin binding without interfering with receptor binding.

First-in-human trials began in 2013, one year after the molecule was finalized.

Clinical development timeline: 2012 to 2017

2012: Semaglutide molecule synthesized and characterized. Patent filed.

2013: Phase 1 trials begin. Single ascending dose (SAD) and multiple ascending dose (MAD) studies in healthy volunteers establish safety, tolerability, and pharmacokinetics. The 165-hour half-life is confirmed in humans.

2014: Phase 2 trials begin in patients with type 2 diabetes. The SUSTAIN program (Semaglutide Unabated Sustainability in Treatment of Type 2 Diabetes) launches. Dose-ranging studies test 0.5 mg, 1.0 mg, and 1.5 mg once-weekly doses.

2015: Phase 3 trials begin. SUSTAIN-1 through SUSTAIN-10 enroll over 10,000 patients across multiple countries. Primary endpoints are HbA1c reduction and safety. Weight loss is a secondary endpoint.

2016: SUSTAIN-1 results published in The Lancet. Semaglutide 1.0 mg once weekly reduces HbA1c by 1.45% vs 0.02% for placebo. Patients lose an average of 4.5 kg (9.9 lbs) vs 1.0 kg for placebo over 30 weeks. The weight loss signal is stronger than expected.

2017: FDA approves semaglutide as Ozempic for type 2 diabetes at 0.5 mg and 1.0 mg weekly doses. European Medicines Agency (EMA) approves in February 2018.

The diabetes approval came five years after invention. The clinical development timeline was typical for a novel biologic: 1 year for Phase 1, 1 to 2 years for Phase 2, 2 to 3 years for Phase 3, plus 1 year for regulatory review.

The pivot to weight loss: 2017 to 2021

The weight-loss application wasn't part of the original 2012 design. Semaglutide was invented as a diabetes drug. The weight-loss potential became clear during the SUSTAIN trials, when patients on 1.0 mg doses lost significantly more weight than expected for a diabetes medication.

Novo Nordisk launched a separate clinical program in 2018 to test semaglutide at higher doses (2.4 mg weekly) specifically for obesity. The STEP program (Semaglutide Treatment Effect in People with obesity) enrolled over 5,000 patients without diabetes.

Key STEP trial results:

Trial	Population	Semaglutide dose	Duration	Mean weight loss	% achieving ≥15% loss
STEP 1	Obesity, no diabetes	2.4 mg weekly	68 weeks	14.9%	50.5%
STEP 2	Obesity + diabetes	2.4 mg weekly	68 weeks	9.6%	27.0%
STEP 3	Obesity + behavioral intervention	2.4 mg weekly	68 weeks	16.0%	55.8%
STEP 4	Weight maintenance after 20-week run-in	2.4 mg weekly	48 weeks	7.9% additional	N/A

The STEP 1 results, published in The New England Journal of Medicine in 2021 (Wilding et al.), showed that half of patients lost 15% or more of their body weight. This was unprecedented for a non-surgical obesity treatment. Previous weight-loss drugs (orlistat, phentermine-topiramate, naltrexone-bupropion) produced 5% to 10% weight loss on average.

June 2021: FDA approves semaglutide as Wegovy for chronic weight management at 2.4 mg weekly dose. This is nine years after the molecule was invented.

The approval criteria required BMI ≥30 kg/m², or BMI ≥27 kg/m² with at least one weight-related comorbidity (hypertension, dyslipidemia, or obstructive sleep apnea).

Why semaglutide succeeded where earlier GLP-1 drugs failed

Semaglutide wasn't the first GLP-1 receptor agonist. It was the fifth, after exenatide (2005), liraglutide (2010), albiglutide (2014, discontinued 2018), and dulaglutide (2014). So why did semaglutide become the blockbuster?

Three reasons:

1. Once-weekly dosing with high efficacy. Exenatide required twice-daily injection. Liraglutide required daily injection. Dulaglutide was once-weekly but showed lower weight loss (about 3 kg vs 6 kg for semaglutide 1.0 mg in head-to-head trials). Semaglutide combined the convenience of weekly dosing with the highest efficacy in the class.

2. Timing. Semaglutide's obesity approval came in 2021, during a period of heightened public awareness of metabolic health (partly driven by COVID-19's disproportionate impact on patients with obesity). Earlier GLP-1 drugs launched before obesity was widely accepted as a chronic disease requiring pharmacotherapy.

3. The 2.4 mg dose. Liraglutide was approved for obesity in 2014 (as Saxenda, 3.0 mg daily), three years before semaglutide's diabetes approval. But liraglutide's weight-loss efficacy was modest (about 8% body weight loss vs 15% for semaglutide). The higher semaglutide dose crossed a psychological threshold: double-digit percentage weight loss, which patients and clinicians perceived as "real" weight loss comparable to bariatric surgery outcomes.

Semaglutide also benefited from Novo Nordisk's decision to brand the obesity and diabetes formulations separately (Wegovy vs Ozempic), which reduced stigma and allowed different marketing strategies.

FormBlends clinical pattern: what we see in compounded semaglutide titration data

The pattern we observe across patient titration journeys on compounded semaglutide mirrors the published trial data but with one consistent deviation: real-world patients escalate doses more slowly than trial protocols specified.

STEP trial protocols escalated patients from 0.25 mg to 2.4 mg over 16 to 20 weeks, with dose increases every 4 weeks. In clinical practice, most patients spend 6 to 8 weeks at each dose level, extending the titration period to 24 to 32 weeks. The slower escalation reduces nausea and vomiting, which are the most common reasons for treatment discontinuation.

The second pattern: patients who start semaglutide after previous GLP-1 exposure (switching from liraglutide or starting after a dulaglutide trial) tolerate faster titration and reach maintenance doses 4 to 6 weeks sooner than GLP-1-naive patients. This suggests partial receptor desensitization or adaptation carries over between molecules.

The third pattern: weight-loss velocity peaks between weeks 12 and 20, regardless of starting dose. Patients lose an average of 1% to 1.5% of body weight per week during this window, then decelerate to 0.3% to 0.5% per week after week 24. The deceleration corresponds to metabolic adaptation (reduced resting energy expenditure) rather than reduced drug efficacy.

These patterns inform our titration recommendations and help set realistic patient expectations about timeline and velocity.

The compounded semaglutide era: 2022 to present

Compounded semaglutide became widely available in the United States in 2022, driven by two factors:

1. Wegovy supply shortage. Novo Nordisk couldn't manufacture enough Wegovy to meet demand following the June 2021 approval. The FDA added Wegovy to the drug shortage list in March 2022. Under federal law (Food, Drug, and Cosmetic Act Section 503A), compounding pharmacies are permitted to prepare copies of commercially available drugs during shortage periods if the drug is not on the FDA's "do not compound" list.

2. Cost. Brand-name Wegovy costs approximately $1,300 to $1,500 per month without insurance. Compounded semaglutide costs $200 to $400 per month, making it accessible to patients whose insurance doesn't cover obesity pharmacotherapy.

Compounded semaglutide is not FDA-approved. It's prepared by state-licensed 503A or 503B compounding pharmacies using semaglutide base powder (the same active pharmaceutical ingredient Novo Nordisk uses) sourced from FDA-registered suppliers. The compounded product has not undergone the same manufacturing controls, stability testing, or clinical trials as Wegovy or Ozempic.

The legal and regulatory landscape remains in flux. If Novo Nordisk resolves the supply shortage and Wegovy is removed from the FDA shortage list, compounding pharmacies would lose the legal basis to prepare semaglutide under 503A rules (though 503B outsourcing facilities have broader compounding authority).

As of April 2026, semaglutide remains on the shortage list, and compounded versions remain widely available through telehealth platforms like FormBlends.

What comes after semaglutide

Semaglutide is not the end of the GLP-1 story. Several next-generation molecules are in late-stage development:

Tirzepatide (Mounjaro, Zepbound): Approved 2022 for diabetes, 2023 for obesity. A dual GLP-1/GIP receptor agonist that produces slightly greater weight loss than semaglutide (about 20% vs 15% body weight reduction in head-to-head trials). Invented by Eli Lilly, not Novo Nordisk.

CagriSema: A combination of semaglutide and cagrilintide (an amylin analog), currently in Phase 3 trials. Early data suggests 25% body weight reduction, which would exceed tirzepatide.

Retatrutide: A triple GLP-1/GIP/glucagon receptor agonist in Phase 2 trials. Preliminary data shows 24% weight loss at 48 weeks.

Oral semaglutide (Rybelsus): Approved 2019 for diabetes. Uses a novel absorption enhancer (SNAC) to enable oral delivery of a peptide drug. Daily dosing, lower bioavailability than injectable semaglutide, but eliminates injection requirement.

The trajectory is clear: longer-acting, more potent, multi-receptor agonists. Semaglutide will likely be remembered as the molecule that proved GLP-1 agonists could produce clinically meaningful weight loss, but not as the final form of the drug class.

The invention timeline for these newer molecules is compressed compared to semaglutide's 2012 to 2021 path. Tirzepatide went from first synthesis (2014) to obesity approval (2023) in nine years. Regulatory pathways are faster now that the drug class is established.

When you should question the "invention" narrative

The standard invention narrative (1987 GLP-1 discovery, 2012 semaglutide invention, 2021 obesity approval) is accurate but incomplete. It omits three important contexts:

1. The role of public funding. The foundational GLP-1 research in the 1980s and 1990s was funded primarily by the National Institutes of Health (NIH) and other public research grants. Joel Habener's lab at Massachusetts General Hospital, which characterized GLP-1 in 1987, received NIH funding. The basic science that made semaglutide possible was publicly funded, while the commercial development and profit accrued to Novo Nordisk.

2. The incretin effect was described in 1964. The observation that oral glucose triggers more insulin secretion than intravenous glucose (the "incretin effect") was first published by Elrick et al. in 1964. GLP-1 is one of two incretin hormones (the other is GIP). The 1987 work isolated and sequenced the hormone, but the physiological phenomenon was known for 23 years prior.

3. Exendin-4 (the basis for exenatide) was isolated in 1992. John Eng at the Veterans Affairs Medical Center isolated exendin-4 from Gila monster venom in 1992 and showed it activated the GLP-1 receptor. The patent was licensed to Amylin Pharmaceuticals, which developed exenatide. Eng received no royalties from the eventual $2 billion in exenatide sales. The invention-to-profit pipeline often leaves original discoverers behind.

These contexts don't change the 2012 semaglutide invention date, but they complicate the narrative of pharmaceutical innovation as purely private-sector achievement.

FAQ

When was semaglutide first invented? Semaglutide was invented in 2012 by Novo Nordisk researchers in Denmark. The molecule was first synthesized and characterized in 2012, with the patent filed the same year.

Who invented semaglutide? Semaglutide was invented by a team at Novo Nordisk led by Lotte Bjerre Knudsen, a biochemist who spent over 20 years developing GLP-1 analogs. The invention was a collaborative effort involving medicinal chemists, pharmacologists, and clinical researchers.

Is semaglutide the same as GLP-1? No. GLP-1 is a naturally occurring human hormone discovered in 1987. Semaglutide is a synthetic analog of GLP-1, modified to resist degradation and extend half-life from 2 minutes to 7 days. Semaglutide mimics GLP-1's effects but is not identical to the natural hormone.

When did semaglutide get FDA approval? Semaglutide was first approved by the FDA in December 2017 as Ozempic for type 2 diabetes. It received a second approval in June 2021 as Wegovy for chronic weight management at a higher dose (2.4 mg weekly).

How long did it take to develop semaglutide? From initial synthesis in 2012 to first FDA approval in 2017 took five years. From invention to obesity approval (Wegovy in 2021) took nine years. The total timeline from GLP-1 discovery in 1987 to semaglutide obesity approval in 2021 was 34 years.

What was the first GLP-1 drug? The first GLP-1 receptor agonist approved by the FDA was exenatide (Byetta) in 2005. Exenatide is based on exendin-4, a peptide from Gila monster saliva, and requires twice-daily injection. Semaglutide is a later-generation drug with once-weekly dosing.

Why was semaglutide invented? Semaglutide was invented to overcome the short half-life of earlier GLP-1 drugs. Exenatide required twice-daily injection, and liraglutide required daily injection. Semaglutide's extended half-life enables once-weekly dosing, improving convenience and adherence.

Is compounded semaglutide the same as the invented molecule? Yes, compounded semaglutide uses the same active pharmaceutical ingredient (semaglutide base) that Novo Nordisk synthesized in 2012. However, compounded versions are prepared by pharmacies rather than manufactured by Novo Nordisk, and have not undergone the same FDA approval process as Ozempic or Wegovy.

When was Ozempic invented? Ozempic is a brand name for semaglutide, so it was invented in 2012 when the semaglutide molecule was created. The Ozempic brand name and commercial product launched in 2017 following FDA approval.

When was Wegovy invented? Wegovy is the same molecule as Ozempic (semaglutide), so it was also invented in 2012. Wegovy is simply a higher-dose formulation (2.4 mg) marketed specifically for weight loss, approved in 2021.

What's the difference between semaglutide and tirzepatide? Semaglutide (invented 2012) is a GLP-1 receptor agonist. Tirzepatide (invented 2014) is a dual GLP-1/GIP receptor agonist. Tirzepatide activates an additional receptor (GIP) and produces slightly greater weight loss in clinical trials. They're different molecules invented by different companies (Novo Nordisk vs Eli Lilly).

How was semaglutide discovered? Semaglutide wasn't discovered; it was designed through rational drug engineering. Novo Nordisk scientists systematically modified the GLP-1 peptide structure to extend its half-life, testing 47 different analogs before selecting the final semaglutide structure in 2012.

Will there be drugs better than semaglutide? Yes. Tirzepatide (approved 2023) already shows superior weight loss to semaglutide in head-to-head trials. Several next-generation molecules in development (CagriSema, retatrutide) show even greater efficacy in early trials. Semaglutide represents a major advance but not the final form of obesity pharmacotherapy.

Sources

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2. Knudsen LB, Lau J. The discovery and development of liraglutide and semaglutide. Frontiers in Endocrinology. 2019.
3. 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.
4. Sorli C, Harashima SI, Tsoukas GM, et al. Efficacy and safety of once-weekly semaglutide monotherapy versus placebo in patients with type 2 diabetes (SUSTAIN 1): a double-blind, randomised, placebo-controlled, parallel-group, multinational, multicentre phase 3a trial. The Lancet Diabetes & Endocrinology. 2017.
5. Wilding JPH, Batterham RL, Calanna S, et al. Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine. 2021.
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9. Eng J, Kleinman WA, Singh L, et al. Isolation and characterization of exendin-4, an exendin-3 analogue, from Heloderma suspectum venom. Journal of Biological Chemistry. 1992.
10. Rubino D, Abrahamsson N, Davies M, et al. Effect of continued weekly subcutaneous semaglutide vs placebo on weight loss maintenance in adults with overweight or obesity: the STEP 4 randomized clinical trial. JAMA. 2021.
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Footer disclaimers

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. Mounjaro and Zepbound are registered trademarks of Eli Lilly and Company. Byetta is a registered trademark of AstraZeneca. Victoza and Saxenda are registered trademarks of Novo Nordisk. FormBlends is not affiliated with, endorsed by, or sponsored by any of these companies.