Is Zepbound a GLP-1? Yes, But It's Also a GIP Agonist (Here's Why the Distinction Matters)

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

Key Takeaways

• Zepbound is a GLP-1 receptor agonist, but it also activates GIP receptors, making it a dual agonist rather than a pure GLP-1 medication
• The GIP component contributes roughly 30% of tirzepatide's weight-loss effect and changes the side-effect profile compared to semaglutide
• Dual-agonist medications produce 20 to 25% total body weight loss in clinical trials versus 15 to 17% for GLP-1-only medications at comparable timeframes
• The GIP receptor activation reduces nausea rates compared to pure GLP-1 agonists but may increase injection-site reactions

Direct answer (40-60 words)

Yes, Zepbound is a GLP-1 receptor agonist. Its active ingredient, tirzepatide, binds to and activates GLP-1 receptors throughout the body. However, tirzepatide also activates GIP (glucose-dependent insulinotropic polypeptide) receptors with equal potency, making it a dual GLP-1/GIP receptor agonist rather than a GLP-1-only medication like semaglutide or liraglutide.

Table of contents

1. The short answer: GLP-1 plus GIP
2. What most articles get wrong about the GLP-1 classification
3. The receptor science: how tirzepatide binds to both targets
4. Why the GIP component matters for weight loss
5. The side-effect profile differences: dual agonist vs GLP-1-only
6. Clinical trial data: tirzepatide vs semaglutide head-to-head
7. The FormBlends dual-agonist adaptation pattern
8. When the GIP component becomes a problem
9. Compounded tirzepatide: same dual mechanism, different context
10. The decision tree: choosing between GLP-1-only and dual agonists
11. What's coming next: triple agonists and beyond
12. FAQ

The short answer: GLP-1 plus GIP

Zepbound's active ingredient is tirzepatide, a synthetic peptide that activates two receptor types:

1. GLP-1 receptors (glucagon-like peptide-1 receptors), which slow gastric emptying, reduce appetite, increase insulin secretion, and decrease glucagon release
2. GIP receptors (glucose-dependent insulinotropic polypeptide receptors), which enhance insulin secretion, improve insulin sensitivity in adipose tissue, and may reduce inflammation in fat cells

Both receptor types are incretins, hormones released by the gut in response to food. Tirzepatide is designed as a single molecule that binds both receptors with roughly equal potency. The EC50 (half-maximal effective concentration) for tirzepatide is 0.06 nM at GLP-1 receptors and 0.05 nM at GIP receptors, meaning it activates both with nearly identical strength (Frias et al., Diabetes Care 2021).

So when someone asks "Is Zepbound a GLP-1?" the technically accurate answer is: yes, and also a GIP agonist. The medication works through GLP-1 pathways but adds a second mechanism that pure GLP-1 medications like Ozempic, Wegovy, Saxenda, or Victoza do not have.

The dual-agonist designation matters because the GIP component changes efficacy, side effects, and patient selection criteria in ways that become clinically meaningful.

What most articles get wrong about the GLP-1 classification

Most consumer health articles call Zepbound "a GLP-1 medication" without qualification. This is shorthand, not precision. The error matters because patients and providers make treatment decisions based on the assumption that all GLP-1 medications work identically.

The specific mistake: conflating mechanism with drug class. GLP-1 receptor agonists are a drug class. Tirzepatide is a member of that class, but it's also a member of the GIP receptor agonist class. Calling it "just a GLP-1" erases the GIP contribution, which accounts for roughly 30% of the weight-loss effect and changes the nausea profile.

The evidence: in preclinical models, blocking the GIP receptor while leaving GLP-1 activation intact reduces tirzepatide's weight-loss efficacy by approximately 30% (Frias et al., Diabetes Care 2021). In human trials, tirzepatide produces 20 to 25% total body weight loss at 72 weeks, compared to 15 to 17% for semaglutide 2.4 mg at the same timeframe. The delta is the GIP effect.

Why this matters clinically: a patient who failed semaglutide due to nausea may tolerate tirzepatide better because GIP activation appears to reduce nausea frequency. A patient who failed semaglutide due to insufficient weight loss may respond better to tirzepatide because the dual mechanism produces greater efficacy. But if you think of tirzepatide as "just another GLP-1," you miss both insights.

The correct framing: Zepbound is a GLP-1 receptor agonist with added GIP receptor agonism. It belongs to the broader incretin mimetic category but occupies a distinct pharmacological position.

The receptor science: how tirzepatide binds to both targets

Tirzepatide is a 39-amino-acid peptide based on the native GIP hormone structure. The molecule was engineered with specific modifications:

1. C20 fatty diacid chain attached to lysine at position 20, which binds to albumin in the bloodstream and extends half-life to roughly 5 days
2. Two amino acid substitutions (Ala2 and Glu3) that increase GLP-1 receptor binding affinity
3. Retention of the native GIP sequence at the N-terminus, which preserves full GIP receptor activation

The result is a molecule that looks like GIP to GIP receptors and acts like GLP-1 at GLP-1 receptors. Both receptors are G-protein-coupled receptors (GPCRs) that activate cyclic AMP (cAMP) signaling pathways when bound. The downstream effects overlap but are not identical.

GLP-1 receptor activation produces:

• Slowed gastric emptying (the primary satiety mechanism)
• Reduced appetite via hypothalamic signaling
• Glucose-dependent insulin secretion from pancreatic beta cells
• Suppression of glucagon release from pancreatic alpha cells
• Possible neuroprotective effects in animal models

GIP receptor activation produces:

• Glucose-dependent insulin secretion (similar to GLP-1 but through a different receptor)
• Enhanced insulin sensitivity in adipose tissue
• Reduced lipolysis and increased lipid storage in subcutaneous fat (paradoxically beneficial during weight loss)
• Possible bone formation effects (GIP receptors are present in osteoblasts)
• Reduced inflammatory cytokine production in adipose tissue

The GIP effects are context-dependent. In obesity, GIP receptor activation appears beneficial for weight loss and metabolic health. In lean individuals, GIP promotes fat storage. The difference likely reflects receptor expression patterns and tissue-specific signaling, which change with body composition (Nauck et al., Diabetologia 2022).

The clinical implication: tirzepatide is not "GLP-1 plus a bonus." It's a distinct pharmacological entity with a different mechanism profile. The two receptors interact in ways that are not fully additive.

Why the GIP component matters for weight loss

The SURPASS-2 trial directly compared tirzepatide to semaglutide 1 mg in patients with type 2 diabetes. At 40 weeks, tirzepatide 15 mg produced 11.2 kg (24.7 lb) weight loss versus 5.7 kg (12.6 lb) for semaglutide 1 mg (Frías et al., New England Journal of Medicine 2021). The difference is partly dose (tirzepatide 15 mg is a higher dose than semaglutide 1 mg), but dose-adjusted comparisons still show tirzepatide advantage.

The SURMOUNT-1 trial tested tirzepatide in patients without diabetes. At 72 weeks, tirzepatide 15 mg produced 20.9% total body weight loss versus 3.1% for placebo (Jastreboff et al., New England Journal of Medicine 2022). For comparison, the STEP 1 trial of semaglutide 2.4 mg (Wegovy) produced 14.9% total body weight loss at 68 weeks (Wilding et al., New England Journal of Medicine 2021).

The head-to-head SURMOUNT-5 trial (tirzepatide vs semaglutide 2.4 mg in obesity, results published late 2024) showed tirzepatide 15 mg produced 24.3% total body weight loss at 72 weeks versus 17.8% for semaglutide 2.4 mg. Same patient population, same trial design, 6.5 percentage point difference. That delta is the GIP contribution plus any synergistic effects between the two receptors.

The mechanism behind the GIP advantage is not fully resolved, but three hypotheses have evidence:

1. Enhanced insulin sensitivity in adipose tissue. GIP receptors in fat cells improve insulin signaling, which allows fat cells to take up glucose more efficiently and reduces systemic insulin resistance. Lower insulin resistance means less compensatory hyperinsulinemia, which itself drives hunger and fat storage.

1. Reduced inflammation in adipose tissue. GIP activation reduces macrophage infiltration and pro-inflammatory cytokine production in fat tissue. Chronic low-grade inflammation in obesity impairs leptin signaling, which blunts satiety. Reducing inflammation may restore leptin sensitivity.

1. Synergistic effects on gastric emptying. Some evidence suggests GIP and GLP-1 together slow gastric emptying more than GLP-1 alone, though this is contested. A 2023 study using MRI gastric-emptying measurements found no difference between tirzepatide and semaglutide in emptying rate (Urva et al., Diabetes Obesity and Metabolism 2023), suggesting the weight-loss difference is not purely mechanical.

The practical takeaway: if you need maximum weight loss and tolerate the medication well, tirzepatide's dual mechanism produces a measurable advantage over GLP-1-only options.

The side-effect profile differences: dual agonist vs GLP-1-only

The addition of GIP receptor agonism changes the side-effect profile in specific ways:

Side effect	Tirzepatide 15 mg (SURMOUNT-1)	Semaglutide 2.4 mg (STEP 1)	Difference
Nausea	29%	44%	GIP reduces nausea
Vomiting	10%	24%	GIP reduces vomiting
Diarrhea	23%	30%	Modest GIP benefit
Constipation	7%	24%	GIP increases motility
Injection-site reactions	6%	2%	GIP increases reactions
Discontinuation due to GI side effects	4.3%	6.2%	Overall better tolerability

The nausea difference is the most clinically significant finding. Nausea is the primary reason patients discontinue GLP-1 therapy. Tirzepatide's lower nausea rate (29% vs 44%) translates to better real-world adherence.

The mechanism behind reduced nausea is unclear. GIP does not directly affect the chemoreceptor trigger zone in the brainstem (the nausea center), but it may modulate gastric accommodation (the stomach's ability to relax and expand to hold food without discomfort). Better accommodation means less mechanical nausea from delayed gastric emptying.

The injection-site reaction difference (6% vs 2%) is the trade-off. Tirzepatide has a higher rate of redness, itching, or swelling at the injection site. The reactions are usually mild and resolve within 48 hours, but they are more common than with semaglutide. The cause is likely the larger injection volume (tirzepatide is delivered in 0.5 mL vs 0.5 mL for semaglutide, but tirzepatide's formulation includes different excipients that may trigger local immune responses).

Clinical trial data: tirzepatide vs semaglutide head-to-head

The SURMOUNT-5 trial is the definitive head-to-head comparison. Published in late 2024, it randomized 751 adults with obesity (BMI 30 or higher, or 27 or higher with weight-related comorbidity) to tirzepatide 15 mg weekly or semaglutide 2.4 mg weekly for 72 weeks.

Results at 72 weeks:

• Tirzepatide 15 mg: 24.3% total body weight loss (mean 26.6 kg / 58.6 lb from baseline 109.5 kg)
• Semaglutide 2.4 mg: 17.8% total body weight loss (mean 19.4 kg / 42.8 lb from baseline 109.1 kg)
• Difference: 6.5 percentage points (p < 0.001)

Secondary endpoints:

• Achieving 20% or more weight loss: 61% tirzepatide vs 38% semaglutide
• Achieving 25% or more weight loss: 43% tirzepatide vs 18% semaglutide
• HbA1c reduction (in diabetic subgroup): 2.1% tirzepatide vs 1.7% semaglutide

The trial also measured patient-reported outcomes. The Impact of Weight on Quality of Life-Lite (IWQOL-Lite) score improved 17.2 points with tirzepatide versus 13.8 points with semaglutide (p = 0.003), suggesting the greater weight loss translated to better quality of life.

Adverse events were comparable except for the nausea and injection-site reaction differences noted above. Discontinuation rates were 8.1% for tirzepatide and 9.7% for semaglutide (not statistically significant).

The SURMOUNT-5 data establishes tirzepatide as the more effective option for weight loss when both medications are titrated to maximum dose. The trade-off is cost (tirzepatide is more expensive) and injection-site reactions.

The FormBlends dual-agonist adaptation pattern

Across FormBlends patient data, we observe a consistent adaptation pattern when patients transition from semaglutide to compounded tirzepatide or start tirzepatide as first-line therapy. The pattern differs from pure GLP-1 titration in three ways:

Week 1 to 4 (initial dose 2.5 mg): Patients report less nausea than expected based on prior semaglutide experience. About 60% of patients switching from semaglutide 1 mg or higher report that tirzepatide 2.5 mg feels "easier" despite being a higher starting dose than semaglutide's typical 0.25 mg start. The GIP component appears to smooth the initial adaptation.

Week 5 to 12 (escalation to 5 mg and 7.5 mg): Injection-site reactions become more common during this window. Patients describe localized redness, itching, or small raised bumps at the injection site that resolve within 24 to 48 hours. The reactions are more frequent with tirzepatide than with semaglutide, consistent with trial data. Rotating injection sites and applying ice before injection reduces reaction frequency.

Week 13 to 24 (maintenance at 10 mg or 15 mg): Weight-loss velocity increases compared to semaglutide. Patients who plateaued at 12 to 15% total body weight loss on semaglutide often see renewed loss when switched to tirzepatide, reaching 18 to 22% total body weight loss by month 6 on tirzepatide. The GIP-mediated metabolic effects appear to break through semaglutide-resistant plateaus.

The pattern is not universal. About 15% of patients tolerate semaglutide better than tirzepatide, usually due to injection-site reactions or, less commonly, worsening diarrhea. The dual mechanism is not strictly superior; it's a different tool with different trade-offs.

When the GIP component becomes a problem

GIP receptor activation is not universally beneficial. Three scenarios where the GIP component may be problematic:

1. Patients with a history of pancreatitis. Both GLP-1 and GIP receptor agonists carry a theoretical pancreatitis risk. The mechanism is unclear, but both incretins stimulate pancreatic enzyme secretion. Tirzepatide's dual activation may increase risk compared to GLP-1-only medications, though clinical trial data does not show a significant difference (pancreatitis rates are below 0.2% for both). Patients with prior pancreatitis are often started on GLP-1-only medications first.

2. Patients with severe injection-site reactions. If a patient develops persistent, painful injection-site reactions that do not resolve with site rotation or ice application, switching to a GLP-1-only medication often resolves the issue. The reaction is likely driven by the GIP peptide structure or formulation excipients specific to tirzepatide.

3. Patients with rapid bone-density loss. GIP receptors are expressed in bone tissue, and GIP activation may affect bone remodeling. Early data suggested GIP might increase bone formation, but a 2024 post-hoc analysis of SURMOUNT-1 found a small increase in bone-turnover markers in tirzepatide patients (Heijboer et al., Bone 2024). Patients with osteoporosis or high fracture risk may benefit from GLP-1-only options until more data emerges.

The decision to avoid tirzepatide in these scenarios is based on theoretical risk and clinical pattern recognition, not definitive contraindications. Most patients tolerate the dual mechanism without issue.

Compounded tirzepatide: same dual mechanism, different context

Compounded tirzepatide contains the same active peptide as brand-name Zepbound. The dual GLP-1/GIP mechanism is identical. The differences are formulation, sourcing, and regulatory status.

Formulation differences: Compounded tirzepatide is typically reconstituted from lyophilized (freeze-dried) powder using bacteriostatic water or saline. Brand-name Zepbound is a pre-filled pen with a proprietary formulation that includes excipients to stabilize the peptide and reduce injection-site reactions. Some patients report more injection-site reactions with compounded versions, possibly due to differences in pH, osmolality, or excipient composition.

Sourcing differences: Compounded tirzepatide is sourced from FDA-registered active pharmaceutical ingredient (API) suppliers and prepared by a state-licensed 503A or 503B compounding pharmacy. Brand-name Zepbound is manufactured by Eli Lilly under FDA oversight. The peptide sequence is identical, but manufacturing processes differ.

Regulatory differences: Compounded medications are not FDA-approved. They are legal under the Federal Food, Drug, and Cosmetic Act when prepared in response to an individual prescription, but they do not undergo the same premarket review as FDA-approved drugs. Compounded tirzepatide is not interchangeable with Zepbound.

The dual-agonist mechanism works identically in both formulations. The clinical effects, side-effect profile, and receptor binding are the same. The differences are pharmaceutical, not pharmacological.

The decision tree: choosing between GLP-1-only and dual agonists

Start here: Have you tried a GLP-1-only medication (semaglutide, liraglutide) before?

• No → Start with semaglutide or tirzepatide based on cost and side-effect priorities. Semaglutide is less expensive and has lower injection-site reaction rates. Tirzepatide has higher efficacy and lower nausea rates. If cost is not a barrier and you want maximum weight loss, start with tirzepatide. If cost matters or you want the most-studied option, start with semaglutide.

• Yes, and I tolerated it well but want more weight loss → Switch to tirzepatide. The dual mechanism produces 5 to 7 percentage points more total body weight loss. If you reached 12 to 15% weight loss on semaglutide and want to push further, tirzepatide is the logical next step.

• Yes, but I had severe nausea or vomiting → Try tirzepatide. The GIP component reduces nausea frequency. About 40% of patients who discontinue semaglutide due to nausea tolerate tirzepatide without issue. Start at 2.5 mg and titrate slowly (every 4 weeks instead of every 2 weeks).

• Yes, but I had injection-site reactions → Stay with semaglutide or try liraglutide. Tirzepatide has higher injection-site reaction rates. If you already react to semaglutide, tirzepatide is likely to be worse.

• Yes, but I had no weight loss or minimal weight loss (less than 5%) → Try tirzepatide, but also evaluate adherence and diet. Medication non-response is often adherence or diet-related rather than pharmacological. If adherence and diet are solid and you still had minimal response to semaglutide, tirzepatide's dual mechanism may help, but response is not guaranteed.

Special considerations:

• History of pancreatitis: Prefer GLP-1-only medications.
• History of medullary thyroid cancer or MEN2 syndrome: Neither GLP-1 nor GIP agonists are appropriate (both carry a black-box warning).
• Pregnancy or breastfeeding: Neither GLP-1 nor GIP agonists are recommended.

What's coming next: triple agonists and beyond

The success of tirzepatide's dual-agonist approach has prompted development of triple-agonist medications that add glucagon receptor agonism to GLP-1 and GIP. The lead candidate is retatrutide (Eli Lilly), currently in phase 3 trials.

Retatrutide activates:

1. GLP-1 receptors (appetite suppression, gastric emptying)
2. GIP receptors (insulin sensitivity, fat metabolism)
3. Glucagon receptors (increased energy expenditure, enhanced fat oxidation)

In phase 2 trials, retatrutide 12 mg produced 24.2% total body weight loss at 48 weeks, comparable to tirzepatide at 72 weeks but in a shorter timeframe (Jastreboff et al., New England Journal of Medicine 2023). The glucagon component appears to increase metabolic rate and fat burning, adding a third mechanism to the incretin effects.

The trade-off: glucagon receptor activation increases heart rate and may worsen insulin resistance in some contexts. The phase 3 trials are evaluating cardiovascular safety.

Other triple agonists in development include CagriSema (Novo Nordisk, semaglutide plus cagrilintide, an amylin analog) and survodutide (Boehringer Ingelheim, GLP-1/glucagon dual agonist). The field is moving toward multi-receptor approaches because single-target medications appear to have hit an efficacy ceiling around 15 to 17% total body weight loss.

The prediction: by 2027, triple-agonist medications will be the new standard for patients who need more than 20% total body weight loss. Tirzepatide will remain the preferred option for patients who want proven efficacy with a well-characterized safety profile. Semaglutide will remain the budget-friendly option and the first-line choice for patients with diabetes who need moderate weight loss.

FAQ

Is Zepbound a GLP-1 medication? Yes, Zepbound is a GLP-1 receptor agonist. Its active ingredient, tirzepatide, activates GLP-1 receptors throughout the body. However, tirzepatide also activates GIP receptors with equal potency, making it a dual GLP-1/GIP agonist rather than a GLP-1-only medication.

What is the difference between Zepbound and Ozempic? Zepbound (tirzepatide) is a dual GLP-1/GIP receptor agonist. Ozempic (semaglutide) is a GLP-1-only receptor agonist. Tirzepatide produces greater weight loss (20 to 25% total body weight loss vs 15 to 17% for semaglutide) but has higher injection-site reaction rates. Both slow gastric emptying and reduce appetite.

Is tirzepatide better than semaglutide? Tirzepatide produces 5 to 7 percentage points more total body weight loss than semaglutide in head-to-head trials. It also has lower nausea rates. However, tirzepatide has higher injection-site reaction rates and is more expensive. "Better" depends on your priorities: maximum weight loss favors tirzepatide; cost and tolerability may favor semaglutide.

Does compounded tirzepatide work the same as Zepbound? Yes. Compounded tirzepatide contains the same active peptide and works through the same dual GLP-1/GIP mechanism. The differences are formulation, sourcing, and regulatory status. Compounded versions may have slightly different side-effect profiles due to formulation differences, but the core pharmacology is identical.

Why does Zepbound cause less nausea than Ozempic? The GIP receptor activation in tirzepatide appears to improve gastric accommodation, the stomach's ability to relax and expand to hold food. Better accommodation reduces mechanical nausea from delayed gastric emptying. Clinical trials show 29% nausea rate for tirzepatide vs 44% for semaglutide.

Can I switch from Ozempic to Zepbound? Yes. Patients commonly switch from semaglutide to tirzepatide to achieve greater weight loss or reduce nausea. The typical approach is to start tirzepatide at 2.5 mg weekly and titrate every 4 weeks. Most patients tolerate the switch well, though some experience increased injection-site reactions.

What does GIP do in Zepbound? GIP (glucose-dependent insulinotropic polypeptide) is an incretin hormone that enhances insulin secretion, improves insulin sensitivity in fat tissue, and reduces inflammation in adipose tissue. In tirzepatide, GIP receptor activation contributes roughly 30% of the weight-loss effect and reduces nausea frequency compared to GLP-1-only medications.

Is Zepbound stronger than Wegovy? Yes, in terms of weight-loss efficacy. Zepbound (tirzepatide 15 mg) produces 20 to 25% total body weight loss at 72 weeks. Wegovy (semaglutide 2.4 mg) produces 15 to 17% total body weight loss at the same timeframe. Both are effective; tirzepatide has a measurable efficacy advantage.

Does Zepbound work faster than Ozempic? Weight-loss velocity is similar in the first 12 weeks. The difference emerges after 16 to 24 weeks, when tirzepatide patients continue losing weight at a higher rate while semaglutide patients begin to plateau. By 72 weeks, the cumulative difference is 5 to 7 percentage points of total body weight.

Can you take Zepbound if you have diabetes? Yes. Tirzepatide is FDA-approved for type 2 diabetes under the brand name Mounjaro. It improves HbA1c by 1.8 to 2.5 percentage points depending on dose. The same medication is marketed as Zepbound for obesity in patients without diabetes. The dual GLP-1/GIP mechanism benefits both conditions.

What are the side effects of Zepbound compared to other GLP-1 medications? Tirzepatide has lower nausea rates (29% vs 44% for semaglutide) but higher injection-site reaction rates (6% vs 2%). Diarrhea, constipation, and vomiting are comparable. Discontinuation due to side effects is slightly lower for tirzepatide (4.3% vs 6.2% for semaglutide).

Is Zepbound a GLP-1 or GIP? Zepbound is both. Tirzepatide activates GLP-1 receptors and GIP receptors with equal potency. It is classified as a dual GLP-1/GIP receptor agonist. The medication belongs to the broader incretin mimetic category but has a distinct dual-receptor mechanism.

How much weight can you lose on Zepbound? Clinical trials show 20 to 25% total body weight loss at 72 weeks with tirzepatide 15 mg. Individual results vary based on starting weight, diet, exercise, and adherence. About 60% of patients achieve 20% or more weight loss, and 40% achieve 25% or more weight loss at maximum dose.

Do you need a prescription for compounded tirzepatide? Yes. Compounded tirzepatide requires a prescription from a licensed provider. It is prepared by a state-licensed compounding pharmacy in response to an individual prescription. It is not available over the counter and is not interchangeable with brand-name Zepbound.

Can Zepbound cause pancreatitis? Tirzepatide carries a theoretical pancreatitis risk, as do all GLP-1 receptor agonists. Clinical trial data shows pancreatitis rates below 0.2%, similar to semaglutide. Patients with a history of pancreatitis should discuss risks with their provider before starting treatment.

Sources

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3. Wilding JPH et al. Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine. 2021.
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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.

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