$89.99
Buy Trinity-X Peptide Online from SourceTides. GLP-1R + GIPR + GCGR triple agonist | 39 amino acids | ≥99% HPLC | Endotoxin <1 EU/mg (LAL) | Full CoA (full-length MS confirmed) | Lyophilised | Dry-ice cold chain.
Trade-name tri-agonist research compound. Same mechanistic class as Retatrutide (LY3437943; NEJM Phase 2; 24.2% weight loss at 48 weeks). Simultaneous GLP-1R (satiety/insulin), GIPR (incretin/adipose), and GCGR (hepatic fat oxidation/energy expenditure) activation in one molecule. No independently published clinical data under Trinity-X name — use Retatrutide Phase 2 data as class benchmark. Not WADA-prohibited. For in-vitro laboratory research use only. Not for human consumption.
Buy Trinity-X Peptide Online | GLP-1 + GIP + Glucagon Tri-Agonist | Research Grade | ≥99% Purity | CoA | SourceTides
Buy Trinity-X Peptide Online from SourceTides.
Trinity-X is a synthetic 39-amino acid peptide engineered as a tri-agonist simultaneously activating three metabolic hormone receptors: the GLP-1 receptor (GLP-1R), the GIP receptor (GIPR), and the glucagon receptor (GCGR).
Trinity-X is a trade-name research compound in the same mechanistic class as Retatrutide (LY3437943) — the Eli Lilly Phase 2 triple agonist that demonstrated up to 24.2% body weight reduction at 48 weeks in the landmark NEJM trial.
Trinity-X and Retatrutide share the same three-receptor agonism strategy; the specific molecular design and pharmacokinetic modifications of Retatrutide (including its C20 fatty diacid albumin-binding chain) are the product of Eli Lilly’s proprietary development programme.
The tri-agonist class represents a fundamentally different approach from all prior metabolic peptides.
Semaglutide activates one receptor (GLP-1R).
Tirzepatide activates two (GLP-1R + GIPR).
Trinity-X activates three simultaneously — GLP-1R for satiety and insulin secretion, GIPR for insulinotropic and adipose effects, and GCGR for hepatic fat oxidation and energy expenditure.
This triple receptor convergence produces metabolic effects that no single- or dual-agonist can replicate.
Trinity-X provides a single-molecule research tool for studying all three pathways simultaneously — enabling streamlined protocols for obesity, metabolic syndrome, NAFLD/NASH, type 2 diabetes, and body composition research without requiring separate compounds for each receptor axis.
Every SourceTides vial is lyophilised, tested at ≥99% HPLC purity, and ships with a full lot-specific Certificate of Analysis.
For in-vitro laboratory research use only. Not for human consumption.
Trinity-X Peptide — Technical Specifications
| Parameter | Specification |
|---|---|
| Trade Name | Trinity-X™ |
| Mechanistic Class | Triple receptor agonist: GLP-1R + GIPR + GCGR (same class as Retatrutide/LY3437943) |
| Peptide Length | 39 amino acids; synthetic; modified backbone |
| Receptor Targets | GLP-1R (Glucagon-Like Peptide-1 Receptor; Gs-coupled GPCR) + GIPR (Glucose-dependent Insulinotropic Polypeptide Receptor; Gs-coupled) + GCGR (Glucagon Receptor; Gs-coupled) |
| Downstream Signalling | All three receptors: Gs→adenylyl cyclase→cAMP→PKA cascade; downstream: insulin secretion (GLP-1R, GIPR); glucagon suppression (GLP-1R); hepatic glucose output suppression (GCGR); adipose lipolysis/energy expenditure (GCGR); gastric emptying delay (GLP-1R) |
| Class Comparators | Retatrutide (LY3437943; Eli Lilly; Phase 2 NEJM trial; up to 24.2% weight loss at 48 weeks); most directly comparable clinical reference for tri-agonist class |
| Evidence Base Note | Trinity-X is a trade-name research compound with no independently published clinical trial data of its own. Its biological rationale derives from the triple GLP-1R/GIPR/GCGR agonist class literature — primarily Retatrutide Phase 2 data (NEJM 2023) and preclinical tri-agonist pharmacology studies |
| Physical Form | White lyophilised powder; hygroscopic |
| Purity | ≥99% (RP-HPLC); identity confirmed by ESI-MS |
| Endotoxin | <1 EU/mg (LAL chromogenic assay) |
| Solubility | Soluble in sterile water and PBS pH 7.4; 1 mg/mL stock recommended; no organic solvent required for standard aqueous use |
| Storage — Lyophilised | −20°C long-term (stable 18–24 months); 2–8°C short-term; protect from moisture and light; equilibrate sealed vial to room temperature before opening |
| Storage — Reconstituted | 2–8°C for up to 7 days; −20°C for longer; aliquot for single use; avoid freeze-thaw |
| Certificate of Analysis | Lot-specific CoA with every order; HPLC chromatogram + ESI-MS identity + endotoxin result |
| Regulatory Status | Not FDA, EMA, TGA, or Health Canada approved; not a controlled substance; research compound only; not for human consumption |
| WADA Status | Not listed on 2024–2025 WADA Prohibited List; not prohibited |
What Is Trinity-X? The Tri-Agonist Class Explained
Trinity-X is a trade-name research peptide in the GLP-1R/GIPR/GCGR triple agonist class.
To understand it, you need to understand the progression of metabolic peptide research over the past decade — from single receptor activation to dual, to the triple agonism that defines this class.
The metabolic hormone system regulates energy balance through three closely related Class B GPCRs.
GLP-1R responds to gut-derived GLP-1, driving insulin secretion, suppressing glucagon, slowing gastric emptying, and signalling satiety in the hypothalamus.
GIPR responds to gut-derived GIP, enhancing insulin secretion in a glucose-dependent manner, modulating adipose tissue metabolism, and influencing bone turnover.
GCGR responds to pancreatic glucagon, driving hepatic glucose output, stimulating fat oxidation in liver and adipose, and increasing energy expenditure.
GLP-1 and Semaglutide activate only GLP-1R — producing powerful appetite suppression and insulin secretion but leaving GIPR and GCGR untouched.
Tirzepatide added GIPR activation to GLP-1R, and the combination produced substantially more weight loss than GLP-1R alone — confirming the synergistic value of multi-receptor activation.
Retatrutide (LY3437943) extended this to all three receptors, and its Phase 2 NEJM data showed up to 24.2% body weight reduction at 48 weeks — surpassing everything that came before it.
Trinity-X operates in this same tri-agonist class, providing a research tool for studying the combined GLP-1R + GIPR + GCGR signalling network in metabolic disease models.
The Three Receptors: How Each Contributes
GLP-1R Activation: Satiety, Insulin Secretion, and Gastric Emptying
GLP-1R is the most validated of the three targets.
Endogenous GLP-1 is released from intestinal L-cells in response to food intake — particularly fats and complex carbohydrates.
It acts on pancreatic beta cells to drive glucose-dependent insulin secretion, on the hypothalamus and brainstem to signal satiety and reduce food intake, on the stomach to slow gastric emptying (extending meal-related satiety), and on GLP-1R-expressing neurons in the reward system to reduce the hedonic drive to eat.
GLP-1R activation also suppresses glucagon secretion from pancreatic alpha cells — the hormone that drives hepatic glucose output.
This dual action (insulin↑, glucagon↓) from a single receptor activation is why GLP-1R agonists produce such robust glycaemic control.
Approved GLP-1R agonists include Semaglutide (Wegovy/Ozempic) and liraglutide.
The GLP-1R component of Trinity-X provides these same mechanisms within the triple agonist framework.
The clinical reference population for isolated GLP-1R effects is the extensive Semaglutide trial programme.
GIPR Activation: Insulinotropic Enhancement and Adipose Biology
GIPR responds to gastric inhibitory polypeptide (GIP) released from duodenal K-cells.
Its primary established role is augmenting glucose-dependent insulin secretion synergistically with GLP-1R — the two incretins together drive approximately 50–70% of post-meal insulin release, a phenomenon called the incretin effect.
Beyond the pancreas, GIPR is expressed on adipocytes, osteoblasts, and several CNS regions.
In adipose tissue, GIP signalling modulates lipid uptake, storage, and release.
The GIPR component was added to GLP-1R activation in Tirzepatide, producing greater weight loss than GLP-1R alone — confirming that GIPR activation in the adipose context adds to the therapeutic effect beyond incretin augmentation.
The precise mechanism by which GIPR contributes to weight loss beyond insulinotropic enhancement is still under active research.
GIPR on central neurons (hypothalamus, VTA) may contribute to appetite regulation independently of the pancreatic role.
This makes GIPR a particularly interesting target for CNS-metabolic axis research in the tri-agonist context.
GCGR Activation: Hepatic Fat Oxidation and Energy Expenditure
Glucagon receptor (GCGR) activation is the component that most distinguishes the triple agonist class from all prior metabolic peptides.
Endogenous glucagon from pancreatic alpha cells drives hepatic glucose output (glycogenolysis and gluconeogenesis) — the mechanism that raises blood glucose between meals.
This is why glucagon was historically considered a target to block, not activate, in metabolic disease.
The insight that unlocked GCGR as a weight loss target is that glucagon also drives hepatic fat oxidation (beta-oxidation), stimulates brown adipose tissue thermogenesis, and increases energy expenditure — effects that are independent of its glucose-raising action.
In the tri-agonist context, the concomitant GLP-1R activation suppresses the glucagon-driven glucose rise (GLP-1R suppresses hepatic glucose output and stimulates insulin), while the GCGR-driven fat oxidation and energy expenditure effects are retained.
The result is fat burning without hyperglycaemia — the defining pharmacological innovation of the triple agonist class.
In NASH/NAFLD research, GCGR activation is particularly relevant because hepatic fat reduction is the primary endpoint.
Glucagon alone reduces liver fat in preclinical models; in a tri-agonist background, this hepatic fat reduction is amplified by GLP-1R-mediated insulin sensitisation and adipose GIPR effects.
This makes Trinity-X relevant to liver research protocols in addition to systemic obesity research.
The Clinical Evidence Base for the Triple Agonist Class
Retatrutide Phase 2 Trial (NEJM 2023): The Triple Agonist Benchmark
The landmark Phase 2 trial of Retatrutide — published in the New England Journal of Medicine in 2023 — is the most important clinical data for understanding the triple agonist class.
The trial enrolled participants with obesity (BMI ≥30) and assessed 24- and 48-week outcomes at multiple doses.
At 48 weeks, the highest-dose group (12 mg weekly) achieved 24.2% mean body weight loss — the largest weight reduction ever reported in a randomised controlled trial for any pharmacological intervention at that timepoint.
Longer-term follow-up data extended this to 28.7% body weight reduction at 68 weeks in some cohorts.
Key mechanistic findings from the trial: weight loss was continuous throughout the 48-week period (no plateau by 48 weeks, unlike Semaglutide which shows flattening); liver fat was substantially reduced (particularly relevant for NAFLD/NASH models); glycaemic markers improved robustly; and the weight loss appeared to be predominantly fat mass rather than lean mass.
The Tri-Agonist Superiority over Dual Agonism
Tirzepatide (GLP-1R + GIPR) was itself a step beyond Semaglutide — achieving 22.5% body weight loss in the SURMOUNT-1 trial.
The Retatrutide data suggests adding GCGR as the third target produces further improvement.
The additional weight loss from the third receptor (GCGR) is attributed primarily to the energy expenditure and hepatic fat oxidation effects.
The GLP-1R + GIPR combination dominates satiety and insulin secretion; GCGR adds metabolic rate enhancement and liver-fat reduction that GLP-1R/GIPR alone does not produce.
For research design, this hierarchy — single agonist → dual → triple — provides a natural dose-escalation and receptor-attribution framework.
Comparing Trinity-X effects against Semaglutide (GLP-1R only) and Tirzepatide (GLP-1R + GIPR) in identical metabolic models directly measures the marginal contribution of GCGR to the triple agonist effect.
Trinity-X Research Evidence and Evidence Hierarchy
| Research Domain | Evidence Level | Key Finding | Source / Note |
|---|---|---|---|
| Triple agonist class — body weight reduction | Phase 2 RCT (Retatrutide; NEJM 2023; class reference) | 24.2% mean body weight reduction at 48 weeks (highest dose; 12 mg weekly); 28.7% at 68 weeks; largest weight reduction ever reported in a pharmacological obesity RCT; weight loss continuous at 48 weeks with no plateau | Jastreboff AM et al. 2023 — NEJM — PMID: 37366315 |
| GCGR hepatic fat oxidation in tri-agonist context | Preclinical + Phase 2 data (class evidence) | Liver fat substantially reduced in Retatrutide trial; GCGR-driven hepatic beta-oxidation confirmed in animal models; NASH/NAFLD application supported by both preclinical and emerging clinical data | NEJM Phase 2 data; GCGR NAFLD preclinical literature |
| Tri-agonist cryo-EM structural characterisation | Structural biology (cryo-EM; Retatrutide–GLP-1R, –GIPR, –GCGR complexes) | Cryo-EM structures of Retatrutide in complex with all three receptors determined at 2.68–3.26 Å resolution; structural basis of simultaneous tri-receptor agonism characterised; confirms single molecule can physically engage all three GPCRs | PMC11255275 — Cryo-EM tri-agonist structural data |
| GIPR contribution to weight loss (beyond GLP-1R) | Phase 3 RCT (Tirzepatide SURMOUNT-1); mechanistic preclinical data | Tirzepatide (GLP-1R + GIPR) achieved 22.5% body weight loss vs ~15% for Semaglutide (GLP-1R only) — confirms GIPR adds substantial weight loss beyond GLP-1R alone; GIPR adipocyte signalling implicated in the difference | Jastreboff AM et al. 2022 — NEJM SURMOUNT-1 — PMID: 35658024 |
| Trinity-X compound specific evidence | No independently published clinical or animal trial data under the Trinity-X name | Trinity-X is a trade-name research compound; its mechanistic rationale is derived from the published GLP-1R/GIPR/GCGR tri-agonist class literature; no peer-reviewed studies have been published specifically characterising Trinity-X as a distinct compound | Researcher note: use Retatrutide Phase 2 data as the class benchmark; design Trinity-X studies to contribute compound-specific pharmacodynamic characterisation |
The GLP-1/GIP/Glucagon Agonist Spectrum: Choosing the Right Compound
| Compound | Receptors | Peak Weight Loss (published) | Evidence Base | Best Research Use | SourceTides |
|---|---|---|---|---|---|
| GLP-1 (native) | GLP-1R | Minimal (very short half-life ~2 min) | Strongest — endogenous; decades of mechanistic data; receptor pharmacology gold standard | GLP-1R receptor pharmacology reference; GLP-1R signalling assay positive control; incretin biology | Buy GLP-1 |
| Semaglutide | GLP-1R | ~15% (STEP trials; 68 weeks) | FDA-approved; Phase 3 RCT gold standard; most published weight loss data | GLP-1R monotherapy benchmark; obesity RCT comparator; T2D/cardiovascular research; the reference for single-receptor activation | Buy Semaglutide |
| Glucagon | GCGR | Not an obesity drug standalone | Endogenous; GCGR pharmacology well characterised; glucagon emergency use data | GCGR pharmacology reference; hepatic fat oxidation; hypoglycaemia models; GCGR contribution dissection in tri-agonist protocols | Buy Glucagon |
| Tirzepatide | GLP-1R + GIPR | ~22.5% (SURMOUNT-1; 72 weeks) | FDA-approved; Phase 3 SURMOUNT-1 data; dual agonist gold standard | Dual agonist benchmark; GIPR contribution vs GLP-1R alone; diabetes + obesity combination; pre-triple-agonist comparator | Buy Tirzepatide |
| Retatrutide | GLP-1R + GIPR + GCGR | 24.2% (Phase 2; 48 weeks); 28.7% (68 weeks) | Phase 2 NEJM RCT; most extensive published data for triple agonist class; the clinical reference benchmark | Triple agonist clinical reference; GCGR contribution vs dual agonist; NASH/liver fat; the most powerful published comparator for Trinity-X class research | Buy Retatrutide |
| Trinity-X (this product) | GLP-1R + GIPR + GCGR | No published standalone data | Trade-name tri-agonist; class evidence from Retatrutide/tirzepatide literature | Single-molecule tri-agonist tool; streamlined multi-receptor metabolic research; comparison vs mono/dual agonists in same protocol | Buy Trinity-X |
What Is Trinity-X Used for in Research?
| Research Field | Application | Why Trinity-X |
|---|---|---|
| Obesity and body composition | DIO (diet-induced obesity) rodent models; body weight reduction; fat mass vs lean mass dissection; adiposity endpoints; energy intake and expenditure | Single compound activating all three pathways simplifies DIO protocols — no need to co-administer GLP-1R, GIPR, and GCGR agonists separately; designed to model the maximal pharmacological effect achievable from simultaneous tri-receptor activation; compare against Semaglutide and Tirzepatide in parallel to establish receptor contribution hierarchy |
| NAFLD / NASH research | Hepatic steatosis; liver fat reduction; hepatic insulin resistance; NASH progression models; NAS scoring; hepatic fibrosis | GCGR-driven hepatic beta-oxidation is the unique liver-targeting mechanism that distinguishes triple from dual agonists; combined GLP-1R insulin sensitisation + GCGR fat oxidation + GIPR adipose effects create multi-mechanism hepatic fat reduction; studied alongside LIPO-C for hepatic lipid biology and Glucagon for GCGR-specific hepatic fat comparisons |
| Type 2 diabetes / glycaemic control | Glucose-stimulated insulin secretion; OGTT models; HbA1c reduction; beta-cell function; insulin sensitivity; fasting glucose | GLP-1R + GIPR dual incretin activation provides maximal glucose-dependent insulin secretion; GLP-1R glucagon suppression reduces hepatic glucose output; simultaneous glycaemic control and weight loss in the same compound; the most complete pharmacological tool for T2D multi-mechanism research |
| Receptor contribution dissection | GLP-1R vs GIPR vs GCGR receptor attribution; using selective antagonists to block one receptor at a time; comparing mono-, dual-, and triple-agonist outcomes in identical models | The most scientifically informative Trinity-X study design: use alongside GLP-1, Tirzepatide, and Glucagon in the same protocol, with selective receptor antagonists as blockers, to precisely attribute each metabolic endpoint to its receptor source |
| Metabolic syndrome research | Concurrent obesity + dyslipidaemia + insulin resistance + hepatic steatosis models; metabolic syndrome reversal; multi-endpoint metabolic panels | Metabolic syndrome involves multiple simultaneous pathways; Trinity-X’s three-receptor design addresses adipose (GIPR), pancreatic (GLP-1R/GIPR), and hepatic (GCGR) components simultaneously; studied alongside NAD⁺ (mitochondrial metabolism), AOD-9604 (adipocyte lipolysis), and LIPO-C in comprehensive metabolic syndrome panels |
| Energy expenditure research | Resting metabolic rate; brown adipose thermogenesis; mitochondrial oxidative phosphorylation; UCP-1 expression; respiratory quotient | GCGR activation increases energy expenditure via brown adipose thermogenesis — a mechanism not present in GLP-1R agonists; the incremental energy expenditure contribution of GCGR vs dual agonists is an important research question for the triple agonist class; calorimetry studies comparing Trinity-X to Tirzepatide directly measure GCGR’s energy expenditure contribution |
| GLP-1 axis + complementary peptide panels | Multi-compound metabolic protocols combining triple agonist pharmacology with tissue repair, adipose biology, or GH axis compounds | Trinity-X addresses the hormonal/receptor-signalling axis; AOD-9604 addresses direct adipocyte lipolysis (non-receptor, non-hormonal); Ipamorelin addresses GH/IGF-1 lean mass preservation; Sermorelin drives GH axis for body composition; together these create a comprehensive multi-mechanism weight management and metabolic research protocol |
Trinity-X Pharmacokinetics and Research Design
| Parameter | Value / Notes | Research Implication |
|---|---|---|
| Routes of administration | SC injection (standard for all GLP-1 family peptide research; systemic bioavailability); IV for receptor assays and pharmacokinetic studies | SC is the clinically and preclinically validated route for GLP-1 family peptides; use SC for all in-vivo metabolic endpoint studies; use IV for dose-response and pharmacokinetic characterisation studies |
| In-vitro receptor assay concentration | 1–100 nM for GLP-1R, GIPR, and GCGR cell-based assays (cAMP accumulation, β-arrestin recruitment, receptor internalisation); run dose-response from 0.01 nM to 10 µM | Confirm receptor expression in your cell line before assuming published concentrations apply; HEK293 cells transiently transfected with each receptor individually are the standard characterisation system; include selective antagonists for each receptor as controls |
| Rodent in-vivo dose range (class reference from Retatrutide) | 1–30 nmol/kg SC in DIO mouse/rat models (published triple agonist literature range); body weight and food intake endpoints measurable within 7–14 days | Start at 10 nmol/kg SC in DIO mouse model; measure body weight, food intake, and blood glucose daily for first 2 weeks; collect adipose, liver, and pancreas tissue at endpoint for histology and gene expression; include a vehicle, Semaglutide, and Tirzepatide arm for receptor contribution comparison |
| Key metabolic endpoints | Body weight; food intake; fasting glucose; OGTT; insulin; HOMA-IR; liver weight; liver triglycerides; ALT/AST; adipose tissue mass; histology (H&E, Oil Red O liver) | Measure all six primary metabolic endpoints simultaneously — the tri-agonist’s value is in producing changes across all three receptor-controlled systems; single-endpoint studies miss the integrated nature of the compound’s mechanism |
| Receptor attribution controls | Selective GLP-1R antagonist (Exendin(9-39)); selective GIPR antagonist (GIP(3-42) or GIP(7-30)); selective GCGR antagonist (L-168,049 or des-His¹-[Glu⁹]-glucagon amide) | Include one selective antagonist per experiment group to block each receptor independently; effects that disappear with a specific antagonist are attributable to that receptor; this is the definitive mechanistic design for a tri-agonist compound without its own published receptor attribution data |
Trinity-X Quality Control at SourceTides
Every batch of Trinity-X Peptide from SourceTides undergoes these tests before release.
As a 39-amino acid peptide, synthesis purity confirmation and sequence integrity are the critical QC checkpoints.
| Test | Method | Specification | Why It Matters |
|---|---|---|---|
| Purity | RP-HPLC (C18; UV 220 nm) | ≥99% peak area purity | 39-amino-acid peptides have more opportunity for deletion sequences and synthetic by-products than short tripeptides; ≥99% HPLC ensures the active full-length sequence dominates and truncation fragments (which would have reduced receptor activity) are below detection |
| Identity | ESI-MS with charge-state distribution | Full-length 39-AA sequence confirmed by molecular ion mass; multi-charge states (+4 through +7) resolve the 4,000+ Da mass range accurately | Full-length mass confirmation distinguishes intact Trinity-X from truncated species that would show as incomplete ions; the 39-AA length requires MS charge state deconvolution for accurate MW determination — this is reported explicitly on the CoA |
| Endotoxin | LAL chromogenic assay | <1 EU/mg | LPS activates inflammatory signalling in adipocytes, hepatocytes, and pancreatic beta cells — all primary target cell types for Trinity-X metabolic research; endotoxin would confound insulin secretion, hepatic fat, and adipose gene expression endpoints |
| Appearance | Visual inspection | White lyophilised powder; no discolouration or clumping | Discolouration or aggregation in large peptides can indicate oxidation of Met or Trp residues; clumping indicates hygroscopic moisture uptake and dosing inaccuracy |
| Certificate of Analysis | Lot-specific PDF | HPLC + MS (39-AA full-length confirmed; charge state deconvolution) + endotoxin + dates | The charge-state deconvolution MS confirmation is the unique CoA element for large peptides; confirms full-length integrity that cannot be inferred from HPLC alone for 39-AA compounds |
Trinity-X Regulatory Status
| Jurisdiction | Status | Notes |
|---|---|---|
| USA (FDA) | Not approved; not a DEA controlled substance; research compound only | Trinity-X is not an FDA-approved drug and has no IND filing. The triple agonist class compound with Phase 2 data is Retatrutide (Eli Lilly), not Trinity-X. SourceTides supplies for laboratory research use only. |
| EU / UK / Australia / Canada | Not approved in any jurisdiction; not a controlled substance; research compound | No regulatory approval in any jurisdiction. Not a controlled substance. Research-grade laboratory access. See the SourceTides shipping policy for jurisdiction-specific information. |
| WADA | Not listed on 2024–2025 WADA Prohibited List; not prohibited | No performance-enhancing classification. Verify at wada-ama.org annually. |
Peer-Reviewed References (Triple Agonist Class)
| # | Citation | Link |
|---|---|---|
| 1 | Jastreboff AM, Kaplan LM, Frías JP et al. (2023). Triple hormone receptor agonist retatrutide for obesity. N Engl J Med. 389:514–526. PMID: 37366315. [Phase 2 RCT; 24.2% weight loss at 48 weeks; primary clinical reference for triple agonist class] | PubMed PMID: 37366315 — NEJM 2023 |
| 2 | Jastreboff AM, Aronne LJ, Ahmad NN et al. (2022). Tirzepatide once weekly for the treatment of obesity. N Engl J Med. 387:205–216. PMID: 35658024. [SURMOUNT-1; 22.5% weight loss; dual agonist benchmark; GIPR contribution established] | PubMed PMID: 35658024 — SURMOUNT-1 |
| 3 | Cryo-EM structural characterisation of Retatrutide–GLP-1R, –GIPR, –GCGR complexes. Nat Commun. PMC11255275. [Structural basis of simultaneous tri-receptor agonism at atomic resolution] | PMC11255275 — Cryo-EM tri-agonist |
| 4 | Wilding JPH, Batterham RL, Calanna S et al. (2021). Once-weekly Semaglutide in adults with overweight or obesity. N Engl J Med. 384:989–1002. PMID: 33567185. [STEP-1; ~15% weight loss; GLP-1R monotherapy benchmark] | PubMed PMID: 33567185 — STEP-1 |
| 5 | Wikipedia: Retatrutide. LY3437943; triple agonist structure; mechanism; clinical development; comparison to Semaglutide and Tirzepatide. | Wikipedia: Retatrutide |
Frequently Researched Alongside Trinity-X
These compounds are most commonly studied alongside Trinity-X in metabolic, obesity, NAFLD, and GLP-1 axis research panels:
- Retatrutide — The Phase 2 NEJM benchmark for the triple agonist class; Trinity-X’s direct mechanistic comparator; 24.2% weight loss at 48 weeks; studying Trinity-X alongside Retatrutide in identical DIO protocols establishes cross-compound performance comparison within the same receptor class
- Tirzepatide — FDA-approved GLP-1R + GIPR dual agonist; the most important comparator for measuring GCGR’s marginal contribution — comparing Trinity-X (all three receptors) vs Tirzepatide (two receptors) in identical models directly quantifies what GCGR adds to dual agonism
- Semaglutide — FDA-approved GLP-1R mono-agonist; the foundational comparator for the incremental GIPR + GCGR contributions; studies comparing Trinity-X vs Semaglutide measure the full additive effect of two additional receptors over the GLP-1R baseline
- Glucagon — The endogenous GCGR agonist; used as the selective GCGR pharmacology reference; comparing glucagon alone vs Trinity-X in hepatic fat assays isolates GCGR’s contribution to the overall tri-agonist liver-fat reduction; essential for mechanistic GCGR attribution studies
- GLP-1 — Endogenous GLP-1R agonist; the receptor pharmacology reference for the GLP-1R arm of Trinity-X; used in incretin biology assays and receptor attribution protocols
- AOD-9604 Peptide — hGH fragment; direct adipocyte lipolysis via β₃-AR (non-receptor, non-hormonal fat-burning mechanism); studied alongside Trinity-X to combine receptor-mediated appetite suppression + energy expenditure (Trinity-X) with direct adipocyte triglyceride hydrolysis (AOD-9604) in comprehensive fat-loss research protocols
- LIPO-C Injectable — Multi-nutrient lipotropic with hepatic fat clearance and beta-oxidation support; studied with Trinity-X in NAFLD/NASH protocols combining hormonal hepatic fat reduction (Trinity-X GCGR component) and nutritional lipotropic support (LIPO-C)
- Ipamorelin 10 mg — Selective GHS-R1a GH secretagogue; GH/IGF-1 preserves lean muscle mass during weight loss; studied alongside Trinity-X in body composition protocols to investigate whether GH axis support prevents the lean mass loss that can accompany rapid weight loss from GLP-1 family compounds
- Sermorelin 10 mg — GHRH agonist; GH axis support for lean mass; studied with Trinity-X in obesity + sarcopenia research protocols combining appetite/fat reduction (Trinity-X) and lean mass maintenance (Sermorelin/GH axis)
- MK-677 Ibutamoren — Oral GHS-R1a agonist; elevates IGF-1; studied with Trinity-X in metabolic research panels where GH/IGF-1 anabolic support (MK-677) is combined with tri-receptor metabolic control (Trinity-X) — noting MK-677’s insulin resistance effect as a confounder to be controlled
- NAD⁺ Injectable — Sirtuin substrate; mitochondrial metabolism; SIRT1 and SIRT3 regulate hepatic lipid metabolism and adipose biology through pathways partially overlapping with GCGR-driven energy expenditure; studied with Trinity-X in comprehensive metabolic ageing and NAFLD panels
- Kisspeptin-10 10 mg — GnRH pulse generator; reproductive neuroendocrinology; studied with GLP-1 family in neuroendocrine-metabolic intersection research where energy availability signalling (GLP-1R) and reproductive hormone axis (Kisspeptin/GnRH) converge
- BPC-157 — Tissue repair; studied with Trinity-X in NAFLD research combining hepatic fat reduction (Trinity-X GCGR) and hepatic tissue repair/cytoprotection (BPC-157 VEGFR2/NO pathway)
Frequently Asked Questions
You can buy Trinity-X Peptide (GLP-1R/GIPR/GCGR triple agonist; 39 amino acids) directly from SourceTides.
Every order includes a lot-specific Certificate of Analysis with the RP-HPLC chromatogram (≥99% purity), ESI-MS identity confirmation (full-length 39-AA sequence confirmed by charge-state deconvolution), and LAL endotoxin result (<1 EU/mg).
All vials are lyophilised white powder and dispatched on dry-ice cold chain. See the SourceTides shipping policy for dispatch details.
Trinity-X and Retatrutide (LY3437943) are both GLP-1R/GIPR/GCGR triple agonists. The mechanistic class is the same. The differences are in origin, documentation, and chemical design specifics.
Retatrutide is Eli Lilly’s proprietary development compound — a 39-amino acid peptide with specific non-standard amino acids (Aib at positions 2 and 20; α-methyl leucine at position 13) and a C20 fatty diacid albumin-binding side chain that extends its plasma half-life to approximately 6 days, enabling once-weekly dosing. It has completed Phase 2 clinical trials (NEJM 2023; 24.2% weight loss at 48 weeks) and is in Phase 3. It has a published CAS number (2381089-83-2), published crystal structures, and an extensive preclinical and clinical literature.
Trinity-X is a trade-name research compound in the same class. It has no independently published clinical or animal trial data under the Trinity-X name, and its specific amino acid sequence and modifications are not publicly disclosed. For research purposes, Retatrutide’s published Phase 2 data is the primary evidence base for what the GLP-1R/GIPR/GCGR triple agonist class can achieve. Trinity-X is best positioned as the preclinical research tool; Retatrutide is the clinical reference comparator.
Tirzepatide is a GLP-1R + GIPR dual agonist — it activates two of the three metabolic receptors that Trinity-X targets. The addition of GCGR is what makes Trinity-X the triple agonist.
For research, the most informative use of both compounds is a direct within-study comparison. Running Trinity-X and Tirzepatide in the same DIO mouse model with identical endpoints measures exactly what GCGR adds to dual agonism: the additional weight loss, the liver fat reduction, the energy expenditure change, and the brown adipose thermogenesis difference. These marginal GCGR effects cannot be isolated any other way.
The Retatrutide Phase 2 data (triple agonist; 24.2% weight loss) vs Tirzepatide SURMOUNT-1 (dual agonist; 22.5% weight loss) suggests GCGR adds modest but real additional weight loss at 48–72 weeks. The liver fat reduction and energy expenditure effects are believed to account for most of the additional benefit. SourceTides supplies both Trinity-X and Tirzepatide for this protocol design.
Glucagon is typically studied as a hormone to suppress in metabolic disease — because it raises blood glucose by driving hepatic glycogenolysis and gluconeogenesis. Including GCGR in a weight loss compound seems counterintuitive. The key is that glucagon has two separable effects: glucose-raising and fat-oxidising.
Glucagon drives hepatic beta-oxidation (fat burning in the liver), stimulates brown adipose tissue thermogenesis, and increases overall energy expenditure. In isolation, these effects come packaged with hyperglycaemia. But in the tri-agonist context, GLP-1R activation simultaneously suppresses hepatic glucose output and stimulates insulin secretion — effectively neutralising the hyperglycaemic risk while retaining the fat-oxidising and energy-expanding effects of GCGR.
This is the pharmacological insight behind the triple agonist class: GLP-1R is the safety net that makes GCGR safe to activate. The result is fat burning and increased energy expenditure without the glucose-raising liability that prevented GCGR-targeted therapy before. GCGR activation also reduces liver fat independently of weight loss — the primary mechanism behind the remarkable NAFLD/NASH data in the Retatrutide Phase 2 trial. See the Glucagon product page for standalone GCGR pharmacology reference.
Trinity-X is a research-grade peptide and is not a controlled substance in any major jurisdiction. It is not DEA-scheduled in the USA, not controlled under the Misuse of Drugs Act 1971 in the UK, and not a CDSA controlled substance in Canada. In Australia, it is not a scheduled substance — verify current TGA status for institutional compliance.
Trinity-X is not WADA-prohibited. It is not an FDA, EMA, TGA, or Health Canada approved drug and has no IND or clinical development filing.
SourceTides supplies for in-vitro laboratory research use only. See the SourceTides shipping policy for jurisdiction-specific details.
SourceTides accepts Visa, Mastercard, American Express, cryptocurrency, and bank transfers for institutional orders. All payments go through secure, encrypted gateways.
For institutional purchase orders, bulk research procurement, or custom quantities, contact the team via the SourceTides contact page. Orders are reviewed for research compliance before dispatch.
All SourceTides products, including Trinity-X Peptide (GLP-1R/GIPR/GCGR triple agonist; 39 amino acids), are for in-vitro laboratory research use only.
They are not approved by the FDA, EMA, TGA, or Health Canada.
Trinity-X is a trade-name research compound with no independently published clinical trial data.
They are not for human consumption.
By purchasing, the buyer confirms authorised researcher status and accepts responsibility for compliance with all applicable regulations.
| Weight | 0.01 lbs |
|---|---|
| Dimensions | 5 × 5 × 5 in |
| Purity | ≥99% HPLC, Full-length 39-AA confirmed (MS charge-state deconvolution) |
| Receptor Targets | |
| Form | Lyophilised Powder |
| Mechanistic Class |
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