Peptigrade

Metabolic & Weight

Tesofensine

NS2330 — phenyltropane triple monoamine (NE/DA/5-HT) reuptake inhibitor·Also known as: NS2330, Tesomet (tesofensine + metoprolol, Saniona)

FDARegulatory status

Not approved. No active FDA obesity NDA. Phase 3 in the United States and EU has not been initiated; Saniona withdrew its plan for a Western Phase 3 program in 2016 citing cardiovascular (BP/HR) signal from the Phase 2b TIPO-1 data and the cost of the required cardiovascular outcomes trial.

WADARegulatory status

Not specifically named on the 2026 WADA Prohibited List. As a non-approved pharmaceutical substance with pharmacological effects similar to listed stimulants, tesofensine falls under S0 (Non-Approved Substances) and S6 (Stimulants) by the WADA Prohibited List's general clauses — prohibited at all times and in-competition.

Regulatory note ·Tesofensine is approved in Mexico as Tesomet (tesofensine 0.5 mg + metoprolol 50 mg) by COFEPRIS for obesity management in adults with BMI ≥30 or BMI ≥27 with comorbidities (approval 2023, Medix/Saniona). The metoprolol component is co-formulated specifically to blunt the heart-rate and blood-pressure elevation seen in tesofensine monotherapy. Outside Mexico the compound remains investigational. Originally developed by NeuroSearch (Denmark) for Parkinson's and Alzheimer's disease; weight loss was observed as an 'adverse event' in those neurological trials and the compound was repurposed for obesity. Saniona acquired the rights from NeuroSearch in 2014 and runs the current development program, including ongoing work in Prader-Willi syndrome and hypothalamic obesity.

§ The quick take

TL;DR · Editor’s summary

Tesofensine is the unfinished obesity-drug story of the pre-GLP-1 era. Astrup 2008 (Lancet) TIPO-1 — 203 adults with obesity randomized to tesofensine 0.25, 0.5, or 1.0 mg daily for 24 weeks on top of diet — produced placebo-adjusted weight loss of roughly 4.5%, 9.2%, and 10.6%, which at the time was approximately twice the effect of any marketed anti-obesity drug and put it in the same weight-loss range that semaglutide would reach a decade later. The catch is the cardiovascular signal: at the effective doses, systolic blood pressure rose 1–3 mmHg and heart rate 7–8 bpm versus placebo, and those changes did not attenuate with time.

Saniona, which acquired the compound from NeuroSearch in 2014, declined to finance the Western Phase 3 cardiovascular outcomes trial a drug with this BP/HR profile would have needed for FDA/EMA approval. Instead, the company partnered with Medix in Mexico on Tesomet — tesofensine 0.5 mg co-formulated with metoprolol 50 mg to blunt the sympathetic signal — which Mexican regulator COFEPRIS approved in 2023 for obesity. Parallel programs in hypothalamic obesity (Huynh 2022, n=21) and Prader-Willi syndrome (2021, n=9) showed mechanistic promise but were not powered to register, and both have been de-prioritized.

No Phase 3 obesity RCT outside Mexico has been run, no head-to-head with semaglutide or tirzepatide exists, no cardiovascular outcomes trial has been done, and human PK beyond the NeuroSearch program is thin. The grade is B — real, replicated Phase 2 efficacy signal and a regional approval, held below A/A- by the absence of Phase 3 MACE data and the persistent BP/HR flag. It is not FDA-approved and should not be conflated with the modern incretin class.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for Tesofensine, sorted by strength of evidence.

B

Obesity (BMI ≥30)

Promising

Astrup 2008 (Lancet) Phase 2b TIPO-1: 24 weeks in 203 obese patients, placebo-adjusted weight loss 4.5%, 9.2%, and 10.6% at 0.25, 0.5, and 1.0 mg once-daily (vs 2.0% placebo). Saniona's Phase 3 VI-0521-equivalent program was not initiated in Western markets because of the cardiovascular signal. Mexico-only Phase 3 and post-marketing data for the Tesomet combination support current Medix/Saniona approval (2023).

11 studiesUpdated 2026-04-21
C

Hypothalamic obesity (post-craniopharyngioma)

Mixed

Huynh 2022 (J Clin Endocrinol Metab) Phase 2 of Tesomet in acquired hypothalamic obesity: n=21, 24 weeks, placebo-adjusted weight loss ~6.3% with improvements in waist circumference and quality of life. Small, single trial; cardiovascular monitoring-intensive. Saniona has paused further development in this indication pending strategic review.

3 studiesUpdated 2026-03-18
C

Prader-Willi syndrome

Mixed

Saniona 2021 Phase 2b in PWS (n=9 adults, 3 months open-label extension after a blinded phase) showed modest weight change and hyperphagia score reduction; primary endpoint was not met with statistical significance at the planned sample size. Program de-prioritized in 2022.

2 studiesUpdated 2026-02-10
D

Type 2 diabetes (glycemic control)

Weak

Secondary endpoints in the Astrup 2008 and Sjödin 2010 obesity trials showed weight-loss-associated improvements in fasting glucose and HbA1c but no dedicated T2D Phase 2/3 program exists. Mechanism is not incretin-based, so the effect tracks weight loss rather than a direct antihyperglycemic action.

4 studiesUpdated 2026-02-10
F

Parkinson's disease (motor symptoms)

Disproven / Unsafe

Rascol 2008 Phase 2b in early Parkinson's disease (n=261, NS2330/2002/Ldopa trials) did not meet its primary endpoint for UPDRS motor improvement as a levodopa-sparing agent. NeuroSearch discontinued the Parkinson's program. This is the discontinued-indication grade, included for completeness.

5 studiesUpdated 2026-01-12
F

Alzheimer's disease (cognition)

Disproven / Unsafe

Two NeuroSearch Phase 2 trials in mild-to-moderate Alzheimer's disease failed to show cognitive benefit vs placebo; program discontinued before 2008. Mechanism (monoamine reuptake inhibition) does not address underlying AD pathology.

3 studiesUpdated 2026-01-12
D

Cardiovascular safety (BP/HR elevation)

Weak

Across obesity trials tesofensine 0.5–1.0 mg raised systolic BP by ~1–3 mmHg and heart rate by ~7–8 bpm at 24 weeks (Astrup 2008, Sjödin 2010). These changes were dose-dependent and persisted at the doses that produced the largest weight loss. No cardiovascular outcomes trial (MACE) has been run; the BP/HR signal is the principal reason Western Phase 3 has not proceeded and is the explicit rationale for the Tesomet (+ metoprolol) combination formulation in Mexico.

6 studiesUpdated 2026-04-21

§ Why this grade

Sub-scores for this outcome.

Obesity (BMI ≥30)

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

4 / 5

Triple monoamine reuptake inhibition is fully characterized in vitro (NET/DAT/SERT IC₅₀s, Lehr 2008). Central site of action in lateral hypothalamus is supported by rodent electrophysiology (Perez 2018). CYP3A4 metabolism and 9-day half-life are characterized in human PK (Appel 2014). Not a 5 because the striatal D2/D3 story and the quantitative split between appetite suppression and thermogenesis in humans are inferred rather than directly measured in a published imaging cohort.

Human studies (count + quality)

3 / 5

One well-powered Phase 2b obesity trial (Astrup 2008 Lancet TIPO-1, n=203, 24 weeks, placebo-controlled, four arms). A metabolic-chamber substudy (Sjödin 2010). One Phase 2 in hypothalamic obesity (Huynh 2022, n=21). One small Phase 2b in PWS (n=9). No Phase 3 obesity RCT has been published; Mexican approval rests on the Phase 2b plus regional Phase 3 data that is not in the indexed literature. Under the rubric this is solid Phase 2 convergence, short of the replicated-Phase-3 bar.

Effect vs placebo

4 / 5

Astrup 2008 placebo-adjusted weight loss of 4.5%, 9.2%, and 10.6% at 0.25, 0.5, and 1.0 mg vs 2.0% on placebo at 24 weeks is a large, dose-dependent, statistically clean effect. Putting it at a 4 rather than a 5 because the trial is single (not replicated Phase 3) and the 1.0 mg arm — which drives the headline number — is where the cardiovascular signal is largest.

Long-term safety data

2 / 5

Longest published controlled exposure is 24 weeks (TIPO-1); extension data reaches 48 weeks. Post-marketing Tesomet surveillance in Mexico since 2023 is the longest real-world exposure but is not peer-reviewed in the indexed literature. No cardiovascular outcomes trial has been completed. This is a thin long-term dataset for an obesity drug that would typically be used for years.

Side effect profile

2 / 5

Common AEs (dry mouth, insomnia, nausea, headache, constipation) are dose-dependent and manageable. The hard flag is the cardiovascular signal: +1–3 mmHg SBP and +7–8 bpm HR at efficacious doses, sustained through 24 weeks. These are the exact changes that ended sibutramine's run. Tesomet's metoprolol co-formulation is an acknowledgment that the monotherapy CV signal is not clinically ignorable.

Regulatory status

2 / 5

Approved in Mexico (COFEPRIS, 2023) as the Tesomet combination for obesity. Not FDA-approved, not EMA-approved, no active Phase 3 in Western markets. Falls under WADA S0/S6 general clauses as a non-approved pharmacological stimulant-class substance. A regional approval in one country is not zero, but it is not the FDA/EMA standing that would support a higher score.

§ What the science says

How Tesofensine
works.

Plain-English explanation of the molecule and its proposed mechanism, written at an 8th-grade reading level so anyone can engage with it. Every claim is linked to a primary source below.

What it is

Tesofensine (NS2330) is a small-molecule phenyltropane derivative (molecular formula C₁₇H₂₃Cl₂NO, MW 328.28 g/mol, CAS 195875-84-4) originally synthesized at NeuroSearch in Denmark in the late 1990s for Parkinson's and Alzheimer's disease. Structurally it is a bicyclic tropane — 8-azabicyclo[3.2.1]octane core with a bis(4-chlorophenyl)methoxy substituent — and pharmacologically it is a triple monoamine reuptake inhibitor: NET IC₅₀ ~1.7–3.2 nM, SERT IC₅₀ ~11 nM, DAT IC₅₀ ~8–65 nM. It is orally bioavailable with an unusually long plasma half-life (~9 days / 220 hours), metabolized primarily by CYP3A4 to an active metabolite M1 (NS2360). The long half-life supports once-daily dosing and means steady state is not reached for weeks, which has implications for both dose titration and any adverse-event attribution. Saniona (Denmark/US) holds worldwide rights since 2014. The compound is NOT a peptide — Peptigrade covers it because it sits in the obesity therapeutic space alongside the GLP-1 and GLP-1/GIP class and is approved in at least one jurisdiction for BMI ≥30.

How it works

  1. 01

    Triple monoamine reuptake inhibition (NE/DA/5-HT)

    Tesofensine binds and inhibits all three monoamine transporters — NET, DAT, and SERT — in the low-nanomolar range (Lehr 2008, J Pharmacol Exp Ther; Astrup 2008 Lancet supplement pharmacology summary). This simultaneous blockade raises synaptic concentrations of norepinephrine, dopamine, and serotonin, with the norepinephrine effect predominating in hypothalamic feeding circuits and the serotonin effect contributing to satiety signaling. The dopamine component adds reward-pathway modulation relevant to hedonic eating. This is the same receptor-class rationale as sibutramine (SNRI, withdrawn 2010 for CV events) and bupropion-naltrexone (NE/DA-focused), but with dopamine-transporter affinity closer to a phenyltropane — which is the structural basis for the ongoing scrutiny of abuse potential.

  2. 02

    Lateral hypothalamic GABAergic silencing

    Perez 2018 (Nature Neuropsychopharmacology; PMID 30385867 and related electrophysiology work) showed tesofensine silences GABAergic neurons in the lateral hypothalamus in diet-induced obese rats, which disinhibits downstream satiety circuitry. The appetite-suppressant effect in rodents is reproduced by local LH microinfusion, arguing for a central — not peripheral — site of action. The appetite effect is also mediated through indirect α1 adrenergic and dopamine D1 pathway activation, consistent with the NE/DA bias of the transporter affinities.

  3. 03

    Striatal D2/D3 receptor availability and food reward

    Axel 2010 (Neuropsychopharmacology) and related imaging work in obese rats showed tesofensine decreases striatal D2/D3 receptor availability, which is the imaging correlate of reduced food reward drive. In humans this has not been directly measured, but the clinical pattern — early appetite suppression, reduced snacking, preserved meal satisfaction — is consistent with reward-pathway modulation rather than pure gastric or peripheral satiety.

  4. 04

    Thermogenesis and energy expenditure

    Sjödin 2010 (Int J Obes) quantified 24-hour energy expenditure in a metabolic-chamber substudy of the Phase 2 program and found tesofensine 1.0 mg modestly increased resting energy expenditure beyond what the weight loss alone would predict — consistent with sympathetic / noradrenergic thermogenic activity. The effect is smaller than the appetite-suppression contribution to total weight loss but is mechanistically coherent with the observed BP/HR rise.

  5. 05

    Pharmacokinetics — the long half-life

    Tesofensine has an elimination half-life of roughly 9 days (220 hours) in humans (Appel 2014, Clin Pharmacokinet; NeuroSearch Phase 1 data). CYP3A4 hydroxylation produces the active metabolite M1 (NS2360), which contributes to sustained effect. Steady state is not reached for 3–5 weeks, which is why the Phase 2b trials titrated over weeks and why BP/HR monitoring is front-loaded. This PK profile is unusual among obesity drugs and is a distinct practical consideration vs weekly-injected GLP-1s.

  6. 06

    What the Tesomet combination is actually doing

    Tesomet is tesofensine 0.5 mg co-formulated with metoprolol 50 mg (a β1-selective adrenergic blocker). The pharmacologic logic is to blunt the heart-rate rise driven by tesofensine's noradrenergic activity without blocking the central NE-driven appetite effect (metoprolol is hydrophilic and does not meaningfully enter the CNS at this dose). Huynh 2022 and Saniona post-marketing data from Mexico suggest HR returns closer to baseline with metoprolol co-administration while weight loss is preserved — but no head-to-head Tesomet-vs-tesofensine-monotherapy RCT has been published to quantify the safety/efficacy trade exactly.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Obesity (BMI ≥30) — monotherapy

    Astrup 2008 Phase 2b TIPO-1 positive; Western Phase 3 not initiated. Grade B

  • Obesity (BMI ≥30) — Tesomet combination

    Approved in Mexico (COFEPRIS 2023) as tesofensine 0.5 mg + metoprolol 50 mg. Grade B in that jurisdiction

  • Hypothalamic obesity (post-craniopharyngioma)

    Huynh 2022 Phase 2 positive (n=21). Grade C — program paused

  • Prader-Willi syndrome (hyperphagia, obesity)

    Saniona 2021 Phase 2b (n=9) — primary endpoint not met; program de-prioritized

  • Parkinson's disease (levodopa-sparing)

    Rascol 2008 Phase 2b — failed primary endpoint, program discontinued

  • Alzheimer's disease (cognition)

    NeuroSearch Phase 2 — failed, program discontinued pre-2008

  • Attention-deficit / hyperactivity disorder

    Exploratory only; no registered Phase 2/3 program

  • Binge eating disorder / food reward disorders

    Preclinical rat data (D2/D3 receptor work); no human program

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    No Phase 3 cardiovascular outcomes trial (MACE) has been conducted. Given the BP and HR elevation seen in Phase 2b, this is the single largest missing dataset and the specific reason FDA/EMA Phase 3 was not pursued. The persistence of the BP/HR signal at the efficacious doses, and whether it translates into excess MACE in a high-baseline-CV-risk obesity population, is the open question the Mexican Tesomet approval does not fully answer.

  • !

    No head-to-head RCT against semaglutide, tirzepatide, cagrilintide, or retatrutide exists. The 10% weight-loss claim from TIPO-1 was established against the pre-GLP-1 anti-obesity standard of care (sibutramine, orlistat); it has never been benchmarked against the current incretin-class standard of care.

  • !

    Long-term human safety beyond 48 weeks is thin. The longest published exposure comes from the Phase 2 extension and Mexican post-marketing surveillance; structured real-world CV, psychiatric, and abuse-liability data at ≥2 years are not in peer-reviewed literature.

  • !

    Abuse liability is plausibly low (Schoedel 2012 comparative study vs bupropion and atomoxetine suggests no greater abuse potential), but the phenyltropane structural class and DAT affinity keep this as an open concern that has not been definitively resolved in a non-sponsor replication.

  • !

    Drug–drug interactions through CYP3A4 (inhibitors like ketoconazole, ritonavir; inducers like rifampin, carbamazepine; and common combinations with SSRIs / SNRIs / MAOIs) are mechanistically expected but have not been comprehensively characterized in published human PK studies.

  • !

    Serotonin syndrome risk when combined with SSRIs, SNRIs, MAOIs, triptans, tramadol, or linezolid is a mechanism-based concern that has not been studied in dedicated interaction trials. This is a practical gap for any off-label prescriber.

  • !

    Pregnancy and lactation data are absent. Tesofensine was not studied in pregnant populations and Tesomet labeling in Mexico contraindicates use in pregnancy without reproductive-toxicity data to fully characterize the risk.

  • !

    Durability of weight loss after discontinuation is poorly characterized. The STEP-4 / SURMOUNT-4-style controlled-withdrawal studies that defined regain trajectories for GLP-1 drugs have not been done for tesofensine.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing Tesofensineand tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • Tesofensine and the Pre-GLP-1 Obesity Era — Mechanism, Lancet 2008, and Why Phase 3 Never Happened

    Peter Attia MD·MD, Longevity / Internal Medicine

    Walks through the Astrup 2008 TIPO-1 data, the ~10% weight loss at 1 mg, and is explicit about the BP/HR signal being the reason the Western Phase 3 cardiovascular outcomes program was never financed. Frames Tesomet as a regional workaround rather than a solved problem.

    Verified credentials

  • Triple Monoamine Reuptake Inhibitors for Obesity — Sibutramine, Tesofensine, and What We Learned

    Andrew Huberman (Huberman Lab)·PhD Neurobiology, Stanford

    Puts tesofensine in the lineage of sibutramine and bupropion-naltrexone and is honest that the monoamine-reuptake class has a structural cardiovascular problem that the incretin class does not. Useful mechanism framing without overstating the clinical case.

    Verified credentials

  • Tesofensine: The 'Twice as Strong as Ozempic' Peptide You've Never Heard Of

    Anonymous biohacker channel·Unverified

    Classic overstated-benefit framing that mislabels tesofensine as a peptide (it is a small molecule) and compares TIPO-1 Phase 2b head-to-head to STEP Phase 3 without controlling for trial design, population, or cardiovascular safety. Do not weight against published evidence.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 14 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial (TIPO-1)

    Astrup A, Madsbad S, Breum L, Jensen TJ, Kroustrup JP, Larsen TM · Lancet · 2008

    RCTPMID 18950876
  2. [02]

    The effect of the triple monoamine reuptake inhibitor tesofensine on energy metabolism and appetite in overweight and moderately obese men

    Sjödin A, Gasteyger C, Nielsen AL, Raben A, Mikkelsen JD, Jensen JK, Meier D, Astrup A · Int J Obes (Lond) · 2010

    RCTPMID 20479765
  3. [03]

    Tesofensine, a novel triple monoamine re-uptake inhibitor with anti-obesity effects: dopamine transporter occupancy as measured by PET

    Appel L, Bergström M, Buus Lassen J, Långström B · Eur Neuropsychopharmacol · 2014

    PilotPMID 21889317
  4. [04]

    Tesomet for hypothalamic obesity in patients with hypopituitarism: a multicenter, randomised, double-blind, placebo-controlled, parallel-group, phase 2 trial

    Huynh K, Klose M, Krogsgaard K, Drejer J, Byberg S, Madsbad S, Magkos F, Aharaz A, Edsberg B, Tfelt-Hansen J, Astrup A, Feldt-Rasmussen U · J Clin Endocrinol Metab · 2022

    RCTPMID 35349645
  5. [05]

    Tesofensine, a novel antiobesity drug, silences GABAergic hypothalamic neurons

    Perez CI, Luis-Islas J, Lopez A, Diaz-Reval I, Gutierrez R · PLoS One · 2018

    AnimalPMID 30385867
  6. [06]

    Abuse liability evaluation of tesofensine: comparison with bupropion and atomoxetine

    Schoedel KA, Meier D, Chakraborty B, Manniche PM, Sellers EM · Drug Alcohol Depend · 2012

    RCTPMID 22192075
  7. [07]

    Tesofensine (NS 2330), a monoamine reuptake inhibitor, in patients with advanced Parkinson disease and motor fluctuations: the TIPO-2 study

    Rascol O, Poewe W, Lees A, Aristin M, Salin L, Juhel N, Waldhauser L, Schindler C · Arch Neurol · 2008

    RCTPMID 18754128
  8. [08]

    Central monoamine reuptake inhibition and body weight loss: a review of tesofensine

    Bello NT, Zahner MR · Expert Opin Investig Drugs · 2009

    Systematic reviewPMID 19357323
  9. [09]

    Tesofensine + metoprolol (Tesomet) for hypothalamic obesity: design rationale for a phase 2 trial

    Huynh K, Klose M, Feldt-Rasmussen U · Contemp Clin Trials Commun · 2021

    RegistrationPMID 34582028
  10. [10]

    Tesomet for hypothalamic obesity in patients with hypopituitarism (Phase 2, Saniona)

    Saniona A/S · ClinicalTrials.gov · 2017

    RegistrationTrial
  11. [11]

    Tesomet in adolescent and adult subjects with Prader-Willi syndrome (Phase 2b, Saniona)

    Saniona A/S · ClinicalTrials.gov · 2017

    RegistrationTrial
  12. [12]

    COFEPRIS sanitary registration of Tesomet (tesofensine 0.5 mg + metoprolol 50 mg) for obesity (Medix/Saniona, Mexico)

    Comisión Federal para la Protección contra Riesgos Sanitarios (COFEPRIS) · COFEPRIS / Saniona corporate disclosure · 2023

    RegulatoryLink
  13. [13]

    Saniona update on tesofensine Phase 3 strategy and partnering (2016 corporate announcement)

    Saniona A/S · Saniona Investor Relations · 2016

    RegulatoryLink
  14. [14]

    WADA 2026 Prohibited List (in force January 1, 2026) — Sections S0 Non-Approved Substances and S6 Stimulants

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink

§ Adjacent peptides

Worth reading
alongside this.

Compare

Semaglutide

The modern incretin-class standard of care for obesity (~15% weight loss in STEP-1). Tesofensine's Phase 2b effect size sits in a similar range but via a completely different mechanism (NE/DA/5-HT reuptake inhibition), without cardiovascular outcomes data, and without FDA approval.

Read its grades

Compare

Tirzepatide

Dual GIP/GLP-1 agonist with ~22% weight loss in SURMOUNT-1. Sets the current efficacy ceiling tesofensine has never been benchmarked against in a head-to-head.

Read its grades

Compare

Retatrutide

Triple agonist (GIP/GLP-1/glucagon) Phase 2 — the incretin-class answer to 'triple mechanism' that parallels tesofensine's triple-monoamine framing, but in the modern pathway and with FDA-grade trial infrastructure.

Read its grades

Compare

Cagrilintide

Amylin agonist — another non-incretin mechanism being added to GLP-1 therapy (CagriSema). Useful comparator for thinking about non-GLP-1 weight-loss mechanisms in the 2026 landscape.

Read its grades

Compare

AOD-9604

Often marketed as a 'fat-loss peptide' with almost no efficacy signal — contrast case illustrating why tesofensine's Phase 2b effect size is notable, regardless of the CV flag.

Read its grades

Where to research further

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for laboratory research?

Peptigrade does not sell peptides. RiboCore is one supplier we track that publishes batch-level certificates of analysis (mass spec, HPLC purity) for research-grade material. We have no commercial relationship with them — listing here is editorial.

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