The question nobody else answers
Can you actually tell if it's working?
Every peptide site tells you what a compound is claimed to do. Almost none tell you whether you could ever confirm it's doing anything in your own body. So we did that for all 42. For each one: is there a blood marker that reads the drug's action, is it only a proxy, or can no routine lab tell you at all? We show the marker and the timing where one exists, and we say "you can't test this" where it's true. We sell nothing either way.
6
Directly testable
9
Testable by proxy
27
Not testable by bloodwork
27 of 42can't be verified by any blood test. That is the honest state of this field, and it is the number the rest of the internet leaves out.
Directly testable
6A routine blood marker reads the drug's action. A number tells you it engaged.
| Peptide | Evidence | Marker to watch | When to retest | Safety lab (accumulation / harm) |
|---|---|---|---|---|
| Semaglutide | A | HbA1c · Fasting plasma glucose | ~12 weeks (after titration to maintenance dose and long enough for HbA1c to re-equilibrate over the ~120-day RBC lifespan); fasting glucose can move by 4-8 weeks | Lipase · fasting glucose |
| Tirzepatide | A | HbA1c · Fasting plasma glucose · Fasting insulin (with HOMA-IR) · Triglycerides | 8-12 weeks, drawn after the user has reached and held a stable therapeutic maintenance dose (titration runs several weeks, so retesting mid-titration understates effect). | Lipase · fasting glucose |
| MK-677 (Ibutamoren) | B | IGF-1 · IGFBP-3 | 4-8 weeks. IGF-1 often begins rising within 1-2 weeks and plateaus by ~2-4 weeks, so a 4-8 week retest reliably captures the steady-state effect. | IGF-1 ceiling · fasting glucose / HbA1c |
| Sermorelin | B | IGF-1 · IGFBP-3 | 6-8 weeks on a stable dose (4-8 weeks acceptable), drawn at a consistent interval after the prior dose | IGF-1 ceiling · fasting glucose / HbA1c |
| GHRP-2 | C | IGF-1 · IGFBP-3 | 4-8 weeks on stable, adequate dosing (IGF-1 plateaus within ~2 weeks of consistent exposure). | IGF-1 ceiling · fasting glucose / HbA1c |
| CJC-1295 (no-DAC / Modified GRF 1-29) | D | IGF-1 | 6-8 weeks. The DAC version plateaus by roughly 4 weeks; short-acting no-DAC / Mod-GRF 1-29 needs weeks of consistent multi-daily dosing to accumulate. Draw at a consistent time of day and hydration state; IGF-1 does not require fasting but keep conditions matched to baseline. | IGF-1 ceiling · fasting glucose / HbA1c |
Testable by proxy
9A marker moves, but it confirms the drug is active — not that it delivered the outcome you want. Read it as target engagement, not success.
| Peptide | Evidence | Marker to watch | When to retest | Safety lab (accumulation / harm) |
|---|---|---|---|---|
| Tesamorelin | A | IGF-1 | IGF-1 at 4-8 weeks (a rise can appear within ~2 weeks) | IGF-1 ceiling · fasting glucose / HbA1c (GH is diabetogenic) |
| Thymosin Alpha-1 | A | Absolute lymphocyte count (ALC) · CD4+ and CD8+ T-cell counts | 4-6 weeks (T-cell reconstitution takes weeks); draw at the same time of day and not during an acute illness. | — none established |
| Cagrilintide | B | HbA1c | 12 weeks (HbA1c reflects ~3 months of glycemia, so it needs the full window to register the change) | Fasting glucose |
| Ipamorelin | B | IGF-1 | 6-8 weeks | IGF-1 ceiling · fasting glucose / HbA1c |
| Kisspeptin | B | LH (luteinizing hormone) · Total testosterone (men) · FSH (follicle-stimulating hormone) · Estradiol (women) | Timed post-dose, same session: LH at ~30-45 min, testosterone at ~2-4 hr. This is an acute challenge test, NOT a weeks-later retest. Chronic daily dosing desensitizes KISS1R, so a flat LH measured weeks in cannot distinguish "not working" from receptor downregulation. | — none established |
| Retatrutide | B | HbA1c · Fasting glucose · Triglycerides · ALT / AST · Fasting insulin (with HOMA-IR) | 8-12 weeks (HbA1c needs at least 8-12 weeks to move given the ~3-month RBC lifespan; fasting glucose, insulin, and triglycerides shift within 2-4 weeks but are best retested together at the 12-week mark) | Lipase · fasting glucose |
| Survodutide | B | ALT / AST · HbA1c | ~12 weeks, after the slow titration reaches maintenance dose; liver enzymes may keep drifting down out to ~24 weeks | Lipase · fasting glucose · LFTs |
| GHRP-6 | C | IGF-1 | 4-8 weeks | IGF-1 ceiling · fasting glucose / HbA1c |
| Hexarelin | C | IGF-1 | 3-4 weeks, drawn on the early side. Any transient IGF-1 rise fades as GHS-receptor desensitization sets in within days-to-weeks; human data show IGF-1 is commonly flat by later weeks, so an early retest is the only realistic window to catch a signal. | IGF-1 ceiling · fasting glucose / HbA1c |
Not testable by bloodwork
27No routine lab confirms it's working. The effect is local, subjective, or intracellular. Judge it by outcomes — how you feel, heal, or perform — not a blood proxy.
| Peptide | Evidence | Why you can't | Safety lab (accumulation / harm) |
|---|---|---|---|
| Melanotan I (afamelanotide) | A | Melanotan-1 (afamelanotide) is an alpha-MSH analog and MC1R agonist that drives eumelanin synthesis in skin melanocytes; its therapeutic action is local cutaneous pigmentation/photoprotection, which produces no measurable circulating analyte. In the pivotal EPP randomized trials it did not lower the disease's own biomarker (erythrocyte/plasma protoporphyrin) or alter liver biochemistries, so no routine bloodwork can confirm it is working. | — none established |
| PT-141 (Bremelanotide) | A | PT-141 (bremelanotide) is a centrally-acting melanocortin receptor agonist (primarily MC4R on hypothalamic neurons). Its therapeutic effect is a subjective, CNS-mediated increase in sexual desire/arousal. It does not act on an endocrine or metabolic axis that releases a measurable circulating analyte, so nothing about its efficacy appears in routine bloodwork. | — none established |
| AOD-9604 | B | AOD-9604 is the hGH C-terminal fragment (176-191), engineered to stimulate adipocyte lipolysis while deliberately stripping off the somatotropic/IGF-1 arm; human trials confirmed no rise in IGF-1 and no change in glucose or insulin at any dose, so no routine analyte moves when it acts and the only objective readout is body composition. Note: the exact lipolytic mechanism is unsettled — the animal work often cited for a beta-3 adrenergic pathway actually found the effect is NOT directly beta-3 mediated — but this uncertainty does not change the bloodwork conclusion, since none of the proposed pathways produce a routine analyte shift. | — none established |
| ARA-290 (Cibinetide) | B | Cibinetide (ARA-290) is an 11-amino-acid peptide from EPO's tissue-protective domain that signals only through the innate repair receptor (EPOR/CD131 beta-common heteromer) on injured/inflamed tissue; it was engineered specifically NOT to activate the erythropoietic EPO receptor, so it does not raise hemoglobin, hematocrit, or reticulocytes. Its validated human endpoints (neuropathic pain, small-fiber nerve regeneration) do not register on any routine blood panel, so there is no efficacy proxy in standard bloodwork. | — none established |
| Cerebrolysin | B | Cerebrolysin is a porcine brain-derived neuropeptide mixture that acts centrally by mimicking neurotrophic factors (BDNF/NGF/GDNF/CNTF) on CNS neurons; its therapeutic action is a neurological/cognitive effect that leaves no fingerprint on any routine peripheral blood analyte. | — none established |
| DSIP (Delta Sleep-Inducing Peptide) | B | DSIP is an endogenous nonapeptide that acts centrally to modulate sleep architecture and the stress/HPA response. It has a very short plasma half-life, is not itself an analyte on any routine panel, and controlled human infusion studies show it does not reliably shift cortisol, ACTH, or other pituitary hormones — so it leaves no measurable fingerprint on standard bloodwork. | — none established |
| Selank (N-Acetyl Selank) | B | Selank acts centrally as an anxiolytic/nootropic (GABAergic and serotonin/dopamine modulation, enkephalinase inhibition raising endogenous enkephalins, BDNF upregulation) — CNS effects with no serum readout; its tuftsin-derived immune effects (e.g., IL-6, interferon) are research-only assays, noisy, and do not track symptom relief. | — none established |
| SS-31 (Elamipretide) | B | SS-31 (elamipretide) acts entirely inside the cell at the inner mitochondrial membrane — it binds cardiolipin, stabilizes cristae, improves electron-transport efficiency, and lowers ROS. It creates or alters no circulating hormone or routine serum analyte, so its biological action leaves no fingerprint on a standard blood panel. | — none established |
| VIP (Vasoactive Intestinal Peptide) | B | VIP is an endogenous neuropeptide with a ~1-2 minute plasma half-life that acts locally via VPAC1/VPAC2 receptors and cAMP; it is not measured on any routine panel, and its therapeutic effects (bronchodilation, pulmonary/systemic vasodilation, anti-inflammatory immune modulation, subjective CIRS/mold-illness symptom relief) do not move any standard LabCorp/Quest analyte. | — none established |
| BPC-157 | C | BPC-157 acts locally at the injury/gut site via VEGFR2-driven angiogenesis and nitric-oxide signaling, with a plasma half-life under ~30 minutes; its effect is tissue repair at the site, not a systemic shift, so no analyte on a routine panel tracks whether it is working. | — none established |
| GHK-Cu | C | GHK-Cu acts locally: as a copper-carrying tripeptide it drives collagen, elastin, and glycosaminoglycan synthesis in dermal fibroblasts, wound remodeling, and broad gene-expression shifts in the tissue it reaches. That biology plays out in skin, wounds, and hair follicles, not in a systemic analyte. The trace copper it delivers is far too small to reliably move serum copper or ceruloplasmin, and even if it did, that would only prove copper is present, not that the peptide is doing repair work. No routine lab tracks its collagen-stimulating / tissue-repair action in humans. | Copper · ceruloplasmin · zinc (copper accumulation) |
| LL-37 (cathelicidin) | C | LL-37 (cathelicidin) is a host-defense peptide that acts locally as an antimicrobial and immunomodulator at mucosal/tissue surfaces; it has a short systemic half-life and produces no downstream analyte that routine panels capture. Serum LL-37 itself is measurable only by research ELISA (not a LabCorp/Quest order), and a measured level reflects presence/disease-state, not therapeutic action. | — none established |
| Melanotan II | C | Melanotan-2 acts on melanocortin receptors to produce effects that are entirely local (skin melanocyte pigment synthesis), CNS-behavioral (libido, erections), or subjective (appetite suppression); none of these generates a circulating analyte, so no routine serum test can register the drug's efficacy. | — none established |
| NAD+ (injectable) | C | Infused NAD+ is rapidly cleaved extracellularly to nicotinamide and ADP-ribose, so routine chemistry can only register downstream metabolic change; across human RCTs of NAD+ and its precursors, those routine markers do not move. Whole-blood NAD+ itself does rise, but that is a specialty send-out assay measuring presence, not a routine test and not a measure of biological effect. | — none established |
| Semax (N-Acetyl Semax) | C | Semax is an intranasal ACTH(4-10) analog whose action is confined to the CNS (melanocortin-receptor engagement plus BDNF/NGF and TrkB upregulation in hippocampus and cortex, with dopamine/serotonin modulation); it deliberately lacks ACTH's steroidogenic activity, so it moves no cortisol, ACTH, or other peripheral analyte that a routine panel measures. | — none established |
| 5-Amino-1MQ | D | 5-amino-1MQ inhibits NNMT inside adipocytes; its direct pharmacodynamic readouts (intracellular NAD+, SAM, and 1-methylnicotinamide) live inside cells and are not captured by any routine serum panel, and its claimed systemic metabolic effects are unproven in humans. | — none established |
| Cartalax (AED, Ala-Glu-Asp cartilage peptide bioregulator) | D | Cartalax is a Khavinson-type short peptide bioregulator (generally listed as the AED tripeptide, Ala-Glu-Asp) whose proposed action is local modulation of chondrocyte/cartilage gene expression. Given at microgram-to-milligram peptide doses it is rapidly hydrolyzed to constituent amino acids and cleared, and its purported effect is tissue-local, so it produces no systemic analyte that any routine LabCorp/Quest panel measures. | — none established |
| Epitalon (Epithalon) | D | Epitalon (Ala-Glu-Asp-Gly) is a pineal tetrapeptide bioregulator; its claimed actions are hTERT/telomerase upregulation with telomere elongation and restoration of nocturnal melatonin rhythm. None of those map onto a routine LabCorp/Quest analyte, and it has no known dose-dependent effect on any standard CBC, CMP, lipid, or hormone panel value that would predictably rise or fall as it works. | — none established |
| KPV (Lysine-Proline-Valine) | D | KPV is the C-terminal tripeptide of alpha-MSH that is taken up into cells (via PepT1 in gut epithelium/immune cells) and acts locally to suppress NF-kB and MAPK signaling in inflamed mucosa or skin; it has no systemic hormonal, metabolic, or hematologic footprint, so a routine blood panel shows nothing specific to it, and there is zero human pharmacokinetic/pharmacodynamic data. | — none established |
| MOTS-c | D | MOTS-c is a 16-aa mitochondrial-derived peptide that acts intracellularly through AMPK as an "exercise mimetic"; its own level is measurable only by a research ELISA (not any routine panel), and it produces no efficacy footprint on standard labs that could be separated from diet, training, or weight. | — none established |
| Pentadeca Arginate (PDA) | D | Pentadeca-arginate is an arginate salt of the BPC-157 pentadecapeptide; its presumed action is local and cytoprotective (angiogenesis via VEGFR2-Akt-eNOS, fibroblast migration and collagen organization, M1-to-M2 macrophage shift at the injury or gut-lining site), not a systemic endocrine, metabolic, or hematologic signal, so it produces no analyte that a routine serum or CBC panel would track for efficacy. | — none established |
| Pinealon | D | Pinealon (Glu-Asp-Arg / EDR) is a short-peptide bioregulator proposed to act as an intranuclear epigenetic regulator of neuronal gene expression in CNS tissue. Its claimed actions are local and transcriptional, so it produces no systemic analyte that a routine blood panel measures. | — none established |
| SNAP-8 (Acetyl Octapeptide-3) | D | SNAP-8 (acetyl octapeptide-3 / acetyl glutamyl heptapeptide-1) is a topical cosmetic peptide that mimics the N-terminal of SNAP-25 to competitively destabilize the SNARE complex and blunt catecholamine/acetylcholine release at the facial neuromuscular junction, softening dynamic expression lines. It acts locally in the skin, is not designed to reach systemic circulation, and produces no systemic analyte that routine bloodwork could track. | — none established |
| TB-500 | D | TB-500 is a synthetic fragment of thymosin beta-4, an actin-sequestering peptide that acts locally at injury sites to promote cell migration, angiogenesis, and tissue repair. It produces no systemic hormone, enzyme, or metabolite that a routine panel measures, so a working dose does not register in standard bloodwork. | — none established |
| Thymulin | D | Thymulin (FTS-Zn) is a zinc-dependent thymic peptide whose action is inducing intrathymic T-cell differentiation. Any blood signal would therefore be a small rise in circulating T-lymphocyte populations — but only from a genuinely lymphopenic/immunosenescent baseline where thymic output is the rate-limiting step. In an immunocompetent adult that effect is buried in normal CBC variation, is abolished entirely in zinc-deficient patients, and cannot be attributed to thymulin rather than to infection, cortisol, CMV status, or regression to the mean. There is no routine blood proxy that tracks thymulin efficacy. | — none established |
| AHK-Cu (Copper Tripeptide-3) | E | One honest line: AHK-Cu is delivered topically at ppm, stays local to the follicle, and has no systemic absorption or circulating pool, so nothing about its efficacy shows up in routine bloodwork. | Copper · ceruloplasmin (if used beyond topical) |
| Dihexa | E | Dihexa is an orally-active, brain-penetrant angiotensin IV analog whose proposed action is potentiating central HGF/c-Met signaling to drive hippocampal dendritic-spine and synapse formation. That effect is confined to neural tissue with a subjective cognitive readout and does not perturb any analyte on a routine serum panel. | — none established |
Two different questions
"Is it working" and "is it hurting me" are not the same test.
A compound can be untestable for efficacy and still very testable for harm. Injected GHK-Cu is the clearest case: no blood test tells you it's helping your skin, but copper, ceruloplasmin and zinc track whether it's accumulating. The GH peptides are testable for engagement (IGF-1) and separately for a cost (glucose creep). We split those columns on purpose, because "there's no efficacy marker" is not the same as "there's nothing to watch."
Have your own labs? The Truth Tracker reads an uploaded panel against these markers and tells you what each result means — or that it means nothing.