Tirzepatide is a synthetic 39-residue peptide built on a GIP backbone that activates both the glucose-dependent insulinotropic polypeptide receptor and the GLP-1 receptor — the first dual incretin agonist to be studied at scale. It is often called a twincretin, and it is the standard tool compound when a laboratory needs to probe what happens when two incretin receptors are engaged by one ligand instead of two. We supply research-grade tirzepatide as lyophilized powder in sealed vials for in vitro and preclinical use only.
Human clinical data exist for the approved pharmaceutical built on this molecule. Those data describe a regulated medicine, not the reference material on this page, and nothing here is a human protocol.
What is tirzepatide, precisely
Tirzepatide is a linear 39-amino-acid peptide with a C20 fatty diacid conjugated through a glutamate and two short ethoxy-based spacer units. Its sequence derives from native GIP rather than GLP-1, which surprises people who assume a dual agonist must be a GLP-1 molecule with extras bolted on. It is not. The design started from the GIP scaffold and introduced substitutions that recruit GLP-1 receptor activity onto that backbone. That origin matters experimentally: tirzepatide is a potent, near-native-affinity GIP receptor agonist, while its GLP-1 receptor activity is weaker than a dedicated GLP-1 analog such as semaglutide. It is an imbalanced dual agonist, not a balanced one.
Origin and structure
- Backbone. GIP(1-39)-derived, 39 residues, considerably longer than the 31-residue GLP-1 analogs in the same collection.
- Aib at positions 2 and 13. Alpha-aminoisobutyric acid at position 2 blocks DPP-4 cleavage; the second Aib further rigidifies the helix and has been reported to contribute to the receptor-activity balance.
- C20 fatty diacid at Lys20. A longer lipid than semaglutide carries, attached through a gamma-Glu and two AEEA spacers, driving reversible albumin binding and the extended circulating persistence reported in pharmacokinetic studies.
- C-terminal amidation. The amidated C-terminus removes a negative charge and improves resistance to carboxypeptidases.
Catalog identifiers: CAS 2023788-19-2, molecular formula C225H348N48O68, molecular weight 4813.45 Da. At roughly 4.8 kDa this is one of the heavier molecules in the incretin range, and the mass difference relative to semaglutide is large enough to be diagnostic in a mass spectrometry identity check.
How tirzepatide is thought to work
Reported mechanism rests on simultaneous engagement of two class B G-protein-coupled receptors that both couple to Gs. GLP-1 receptor activation in islet beta cells raises cAMP and amplifies glucose-dependent insulin secretion. GIP receptor activation does the same in beta cells but has additional reported actions absent from GLP-1 signalling: GIP receptors are expressed on adipocytes, where published work has described effects on lipid buffering and blood flow, and on alpha cells, where GIP has been reported to influence glucagon release in a glucose-dependent manner.
Two features of tirzepatide pharmacology recur throughout the in vitro literature. First, signal bias — the molecule has been reported to recruit beta-arrestin poorly at the GLP-1 receptor relative to native GLP-1, producing less receptor internalisation and more sustained cAMP output, a property several groups have proposed as an explanation for its potency in whole-animal models. Second, receptor imbalance — potency at the GIP receptor exceeds that at the GLP-1 receptor, so at low occupancy the molecule behaves more like a GIP agonist and the GLP-1 component becomes prominent only as occupancy rises. Any concentration-response design that ignores this will conflate two different pharmacologies.
What research has examined
- Receptor and cell studies. cAMP accumulation and binding assays in cells expressing human GIPR and GLP-1R, beta-arrestin recruitment, receptor trafficking imaging, and knockout or antagonist experiments designed to isolate which receptor carries which effect.
- Rodent work. Diet-induced obesity models reporting reduced food intake and altered adiposity, studies of hepatic lipid content, brown adipose thermogenesis experiments, and receptor-knockout mice used to attribute observed changes to GIPR versus GLP-1R signalling. The relative contribution of the GIP arm remains genuinely contested in this literature, and researchers should not treat it as settled.
- Human trials of the approved drug. Large randomised programmes in type 2 diabetes and obesity, plus published work in sleep apnoea and heart failure with preserved ejection fraction. Again: approved pharmaceutical, prescription setting, not transferable to research-grade powder.
A practical consequence for bench design: because the two receptor arms are pharmacologically separable, most informative tirzepatide experiments include at least one single-receptor comparator. Running tirzepatide alongside a pure GLP-1 receptor agonist lets you subtract the GLP-1 contribution from any observed effect; adding a selective GIP receptor agonist or antagonist arm isolates the remainder. Without those arms, a result obtained with tirzepatide alone can rarely be attributed to a specific receptor, which is the single most common weakness in published dual-agonist comparisons.
One unresolved question drives much of the current mechanistic work: whether GIP receptor agonism or GIP receptor antagonism is the metabolically useful direction. Both agonist and antagonist strategies have shown activity in preclinical models, and reconciling that paradox is an active research theme.
Species differences deserve a mention. GIP receptor pharmacology is not conserved as tightly across species as GLP-1 receptor pharmacology, and potency ratios measured at rodent receptors do not always reproduce at the human receptor. Papers reporting tirzepatide activity should be read with attention to which receptor ortholog the assay used, and cross-species extrapolation of the GIP arm in particular should be read as a hypothesis rather than a given.
Forms and sizes we supply
| Attribute | Specification |
|---|---|
| Form | Lyophilized powder, sealed glass vial |
| Sizes | 10 mg, 20 mg, 30 mg, 60 mg, 100 mg |
| Purity | Greater than or equal to 99% by HPLC, lot-matched COA |
| CAS | 2023788-19-2 |
| Molecular weight | 4813.45 Da |
| Formula | C225H348N48O68 |
| Class | Acylated dual GIP / GLP-1 receptor agonist |
| Intended use | Laboratory research only |
The 60 mg and 100 mg vials exist for multi-arm animal studies and assay panels where a single lot across all conditions removes a variable. For smaller receptor work the 10 mg vial is usually the sensible unit. Current sizes and pricing are on the tirzepatide product page; the wider range is in the GLP-1 and incretin collection.
Reconstitution and storage in a lab context
Reconstitution is a concentration calculation. A 30 mg vial brought up in 3 mL of bacteriostatic water gives 10 mg/mL, or 10,000 mcg/mL; 0.05 mL of that solution contains 500 mcg of peptide. Introduce diluent gently against the vial wall, allow the cake to dissolve without shaking, and inspect for complete clarity before use — acylated peptides at this molecular weight are prone to visible aggregation if agitated.
Store sealed lyophilized material at minus 20 degrees Celsius away from light and moisture; hold reconstituted solution at 2 to 8 degrees Celsius and use it within the study window. Because tirzepatide vials are often large, aliquoting at the moment of reconstitution matters more here than for smaller peptides: every additional freeze-thaw round on a shared stock is measurable purity loss. Our reconstitution guide covers this.
Purity, COA and how to read it
Expect an HPLC trace with the main-peak area percentage, a mass spectrometry result confirming the observed mass against the theoretical 4813.45 Da, net peptide content, lot number and analysis date. For a 39-residue synthetic peptide the impurity profile is informative in itself: deletion sequences and incompletely deprotected intermediates elute close to the main peak, so a chromatogram showing a clean baseline and well-resolved shoulders tells you more about synthesis quality than a single headline percentage. Match the lot on the certificate to the lot on your vial. See how to read a peptide COA.
Regulatory status
The pharmaceutical form of tirzepatide is an approved prescription medicine in the United States and elsewhere. Research-grade tirzepatide is a laboratory reference chemical, sold research use only, not approved or formulated for administration to humans or animals, and not a substitute for a prescribed product in any circumstance. See research use only, explained.
Related peptides and comparisons
The natural comparators are the single-receptor agonist semaglutide and the triple agonist retatrutide, covered in semaglutide vs tirzepatide and retatrutide vs tirzepatide. For glucagon-receptor-containing duals see survodutide.