Compounds › Verified against primary sources

Kidney disease

From zero to six drugs in four and a half years — and five of them were approved on a number that is not the one that matters to the patient

Partially approvedVerified against primary sources

Experimental material. Read before using anything from here.

Nothing on this page is a medical recommendation, prescription or treatment plan. It is an organized translation of protocols circulating in research communities and, where it exists, of what published trials tested. The two are marked differently — and they are not equivalent.

Most of the compounds here have no FDA approval for human use. Several are sold labeled "research use only", which means they have not gone through purity, sterility or dosage controls for human consumption. A community-reported dose is not a validated dose: it is what someone reported having done.

Talk to a licensed health professional before considering any of these compounds. If you already use one and feel anything unexpected, seek care — do not wait for the next routine test.

Specific caution for this compound: Nothing on this page is applicable on one's own: these are six prescription drugs, several with mandatory monitoring programs for hepatotoxicity or immunosuppression. And there is a point that runs through the whole site: reduced kidney function changes the risk of anything eliminated by the kidneys. This page does not provide dose adjustment for renal impairment, and the absence is deliberate — that adjustment is a clinical decision with lab results in hand.

Summary

IgA nephropathy had no approved drug until December 2021. Today it has six, all by the FDA. This page enters the reference as a yardstick: it shows what an evidence base looks like when it truly exists — multicenter phase 3, placebo, hundreds of patients, an agency demanding confirmation — and, at the same time, shows the price of that. Five of the six approvals rested on proteinuria, which is a surrogate outcome; only three have already converted to full approval by showing an effect on kidney function, and the trial that will answer that for atrasentan only closes data collection in April 2028. In Brazil, the sweep of the 43,491 records in open data found two of the six: Vanrafia, registered on August 31, 2026, and Fabhalta, on January 27, 2025. The ClinicalTrials.gov search for peptides in this reference in kidney disease returned two records, and in neither is the peptide the treatment.

Why this page exists on a peptide site

Because nephrology has just done, in four and a half years, what this site spends all its time demanding: going from no approved drug to six, with phase 3 trials, agency registration and a package insert. It is the exact opposite of the situation of most compounds catalogued here — and that is why it serves as a yardstick.

But the yardstick has two marks, not one. Five of these six approvals rested, at first, on a number that is not what matters to the patient: the amount of protein in the urine. Only later — and not yet in every case — did the proof appear that the kidney actually stops getting worse. The distance between those two things is the subject of this page, and it is the same distance that separates "the marker improved" from "the person improved" in any table on this site.

And there is one finding that closes the loop. I searched ClinicalTrials.gov for trials using the peptides in this reference — BPC-157, Epitalon, Thymalin, GHK-Cu, Ipamorelin, MOTS-c, Humanin — in kidney disease. The search returned two records, and neither tests the peptide as a treatment: in one, Humanin and MOTS-c are measured as markers in an anesthesia study in kidney transplantation; in the other, Humanin is assayed in plasma as a possible marker of acute kidney injury. Zero interventional trials. It is the entire contrast in one line.

From zero to six, in four and a half years

The disease is IgA nephropathy — the most common primary glomerulopathy in the world, also known as Berger's disease. Until December 2021 there was not a single drug approved specifically for it anywhere: it was treated with renin-angiotensin system blockade and, in a flare, systemic corticosteroids.

Today there are six, all approved by the FDA. The column that matters is the last one.

Drug	Active ingredient	Mechanism	1st FDA approval	On which outcome
Tarpeyo	delayed-release budesonide	locally acting corticosteroid in the Peyer's patches, where the abnormal IgA is produced	December 2021 — accelerated	proteinuria
Filspari	sparsentan	dual antagonist: endothelin A receptor and angiotensin II AT₁ receptor	February 17, 2023 — accelerated	proteinuria
Fabhalta	iptacopan	oral factor B inhibitor — alternative complement pathway	August 2024 — accelerated	proteinuria
Vanrafia	atrasentan	selective endothelin A receptor antagonist	April 2, 2025 — accelerated	proteinuria at 36 weeks
Voyxact	sibeprenlimab	anti-APRIL monoclonal antibody	November 25, 2025 — accelerated	proteinuria at 9 months
Trutakna	atacicept	fusion protein that blocks BAFF and APRIL at the same time — first in class	July 7, 2026 — accelerated	proteinuria at 9 months

What "accelerated approval" means, in practice

It is a pathway in which the agency accepts a surrogate outcome — a number believed to predict the real benefit — in exchange for a commitment to prove the real benefit later, in a confirmatory trial. If the confirmation does not come, the registration can be withdrawn.

In IgA nephropathy the surrogate is proteinuria. The real outcome is the estimated glomerular filtration rate (eGFR) — how much the kidney still filters, and how fast that falls. Nobody dies of proteinuria; people die of a kidney that stopped.

It is not my interpretation: it is written in each one's package insert. I went and fetched the current text of all six from the FDA labels endpoint, on September 4, 2026, and the division appears on its own.

Product	Current indication	Does the package insert declare accelerated approval?
Vanrafia (atrasentan)	reduce proteinuria in adults with primary IgAN at risk of rapid progression, generally with a urine protein-to-creatinine ratio ≥ 1.5 g/g	Yes. "This indication is approved under accelerated approval based on a reduction in proteinuria. It has not been established whether VANRAFIA slows kidney function decline"
Voyxact (sibeprenlimab)	reduce proteinuria in adults with primary IgAN at risk of progression	Yes. Same formula: "it has not been established whether it slows kidney function decline in the long term"
Trutakna (atacicept)	reduce proteinuria in adults with primary IgAN at risk of progression	Yes. Same formula, with the same caveat
Tarpeyo (budesonide DR)	*reduce the loss of kidney function* in adults with primary IgAN at risk of progression	No. The accelerated approval sentence no longer appears
Filspari (sparsentan)	*slow the decline of kidney function* in adults with primary IgAN; and reduce proteinuria in FSGS without nephrotic syndrome, from 8 years of age onward	No, in neither of the two indications
Fabhalta (iptacopan)	*slow the decline of kidney function* in adults with primary IgAN at risk of progression (in addition to PNH and C3 glomerulopathy)	No.

Those that have already moved beyond the surrogate — with the published numbers

Three of the six converted accelerated approval into full approval, and the trials that support this are published. Below are the numbers as they appeared in the peer-reviewed article, not as they appeared in the manufacturer's announcement — the difference between the two showed up in the check and is recorded at the end of this page.

Drug	Trial	Effect on eGFR	Hard outcome of kidney failure
Fabhalta (iptacopan)	APPLAUSE-IgAN, NCT04578834 — New England Journal of Medicine, 2026. 477 patients in the final analysis	Annualized decline of −3.10 against −6.12 mL/min/1.73 m²/year on placebo over 24 months (difference 3.02; 95% CI 2.02 to 4.01; P<0.001)	21.4% against 33.5% on placebo (hazard ratio 0.57; 95% CI 0.40 to 0.81; P=0.003). It is the only one of the three with a significant reduction in a hard outcome. Serious infections in 6.7% against 2.1%; no deaths
Tarpeyo (budesonide DR)	NefIgArd, NCT03643965 — The Lancet, 2023. 364 patients, 9 months of treatment and 15 of observation	Time-weighted mean eGFR over 2 years: benefit of 5.05 mL/min/1.73 m² (95% CI 3.24 to 7.38; p<0.0001) — −2.47 with Nefecon against −7.52 with placebo	Was not a study outcome. Most frequent adverse effects: peripheral edema (17% against 4%), hypertension (12% against 3%), cramps and acne
Filspari (sparsentan)	PROTECT, NCT03762850 — The Lancet, 2023. 406 patients, head-to-head comparison with irbesartan over 110 weeks	Chronic eGFR slope (weeks 6 to 110): −2.7 against −3.8 mL/min/1.73 m²/year (difference 1.1; 95% CI 0.1 to 2.1; p=0.037). The total slope, from day one to week 110, gave a difference of 1.0 with a CI of −0.03 to 1.94 and p=0.058 — not significant	Kidney failure composite in 9% against 13% (relative risk 0.7; 95% CI 0.4 to 1.2). The interval crosses 1: not significant

The honest reading of this table

Only one of the three significantly reduced kidney failure. Iptacopan took the composite outcome from 33.5% to 21.4%. That is what converting a surrogate outcome into a real outcome should always look like — and it is not what the other two showed.
In PROTECT, the result depends on which slope you look at. The chronic slope was significant by a narrow margin (p=0.037); the total slope was not (p=0.058). They are two cuts of the same data, and the current package insert kept the favorable reading. I record both.
Preserving eGFR is not the same as preventing kidney failure. NefIgArd did not even measure it, and in PROTECT the difference was not significant. A better slope is a good sign, not a promise kept.
And the price shows. In the iptacopan arm there were three times as many serious infections (6.7% against 2.1%). None of these drugs is free.

Three things this table teaches, which hold for the whole site

The surrogate can be confirmed — and it was confirmed three times. Whoever treats proteinuria as a useless number errs in the opposite direction. The point is not that the marker is worth nothing; it is that it counts as a bet until someone pays to verify it.
Verification takes years. Atrasentan was approved in April 2025 and the trial that will say whether it preserves the kidney only closes data collection in April 2028. That is three years of legal prescribing supported by a hypothesis — with registration, package insert and reimbursement.
All of this happens in the best possible scenario. Multicenter, randomized, placebo-controlled phase 3, hundreds of patients, an agency demanding confirmation. If even here the distance between marker and outcome still takes years to close, a dose table assembled on a forum is not a footnote away from the evidence — it is off the scale.

The literature survey

Queries run by me on PubMed and ClinicalTrials.gov on September 4, 2026. The query is written out so that anyone can repeat it and check the number.

Evidence base	Query	Result
PubMed	`IgA nephropathy`	13,624 articles
PubMed	`atrasentan`	521 articles
PubMed	`iptacopan`	178 articles
PubMed	`sparsentan`	133 articles
PubMed	`sibeprenlimab`	28 articles
PubMed	`atacicept AND IgA nephropathy`	16 articles
ClinicalTrials.gov	condition `IgA nephropathy`	279 registered studies
ClinicalTrials.gov	phase 3, condition IgAN, with one of the five drugs as intervention	10 records
ClinicalTrials.gov	peptides in this reference (BPC-157, Epitalon, Thymalin, GHK-Cu, Ipamorelin, MOTS-c, Humanin) in kidney disease	2 records, none interventional

The contrast, in numbers

A single kidney disease has 279 registered trials. The entire family of short bioregulators — eleven compounds — has zero. Thymalin, the most studied of that whole school, has 293 articles on PubMed and no registered trial; atrasentan alone has 521 articles and a phase 3 with a set date to answer the question that matters.

This is not about saying one is good and the other bad. It is about showing what an evidence base looks like when it exists — so that its absence, on the other pages, has something to be compared against.

What of this reached Brazil

I swept open drug data — 43,491 records, downloaded on September 4, 2026 — looking for each of the six active ingredients and each trade name. The result:

Active ingredient	Product	Record	Company	Status
atrasentan hydrochloride	VANRAFIA	100681190 · process completed on August 31, 2026	Novartis Biociências S.A. (56.994.502/0001-30)	Active
iptacopan hydrochloride monohydrate	FABHALTA	100681187 · completed on January 27, 2025	Novartis Biociências S.A.	Active
sparsentan	—	no registration found	—	—
sibeprenlimab	—	no registration found	—	—
atacicept	—	no registration found	—	—
delayed-release budesonide for IgAN	—	no registration found under the names Tarpeyo or Kinpeygo	—	—

Two caveats about this table that cannot be omitted

Open data does not give the approved indication. It says FABHALTA has had active registration in Brazil since January 2025 — it does not say for which disease. Iptacopan is also approved for paroxysmal nocturnal hemoglobinuria and for C3 glomerulopathy, and the Brazilian registration could be for any of them. Stating that Brazil has iptacopan approved for IgA nephropathy would be inference, not data. I will not do that.
Absence from the open data is not proof of absence from the country. It means there is no drug registration with that name or active ingredient in the database — which is strong, but does not cover individual importation, compassionate use or a petition under review.

The Brazilian news of August 31, 2026

The registration of Vanrafia (atrasentan hydrochloride) was approved for adults with primary immunoglobulin A nephropathy at risk of progression, by Resolution RE No. 3,416/2026, published in the Diário Oficial da União. It is the newer of the two — and it is, precisely, one of the three that have not yet proven an effect on kidney function. The trial that will answer that closes in 2028.

I record this without irony: approving on a surrogate outcome is a defensible regulatory decision when the disease progresses and there is no alternative. What is not defensible is the news reaching the patient without that half of the sentence.

Outside glomerulopathy: what changed in common chronic kidney disease

Most kidney disease in the world is not IgA nephropathy — it is a consequence of diabetes and hypertension. There, what became established was a combination, not a molecule: renin-angiotensin system blockade, SGLT2 inhibitor, finerenone and, now, GLP-1 agonist.

In Brazil, a new indication was approved on February 2, 2026 for semaglutide: type 2 diabetes with chronic kidney disease, as an adjunct to standard therapy, with reduced progression of kidney failure and fewer deaths from major cardiovascular events. This is put in context by the Brazilian Society of Nephrology's 2024 figure: 29% of dialysis patients in the country have diabetes.

Finerenone — a non-steroidal mineralocorticoid receptor antagonist — has active registration in Brazil as FIRIALTA (Bayer S.A., registration 170560129, process completed on January 16, 2023), according to the same open data.

Semaglutide already has its own page in this reference, built from the package insert. The difference between what the insert authorizes and what circulates as a protocol is there, not here.

And what failed — which matters as much as what worked

The ZEUS trial tested ziltivekimab — an anti-IL-6 antibody — in 6,376 participants with atherosclerosis, chronic kidney disease and high-sensitivity CRP at or above 2 mg/L. The design and baseline characteristics are published in JAMA Cardiology; the primary outcome was three-point MACE.

The reported result is that there was no reduction in major cardiovascular events: hazard ratio of 0.99 (95% CI 0.88 to 1.11), with total mortality unchanged and more serious infections in the treated group — even though the drug lowered free IL-6 and CRP as expected.

⚠️ Source caveat: on checking, I could not find the main ZEUS article indexed on PubMed. These numbers come from a conference presentation and a manufacturer's announcement, reproduced by the specialized press — not from a peer-reviewed publication. What is published is the trial design.

It is this page's same error, inverted: a marker moved in the right direction and the patient did not follow. It is worth recording here because the anti-inflammatory hypothesis is exactly the kind of mechanistic reasoning that supports half of all peptide claims — it reduces inflammation, therefore it protects. In a trial of 6,300 people, it did not protect.

Kidney failure: what is news and what is treatment

In January 2026, Tim Andrews received a human kidney from a deceased donor after living 271 days without dialysis with a gene-edited pig kidney implanted in January 2025. It is the longest dialysis-free survival ever documented after kidney xenotransplantation in a living person, and the first successful transition from xenotransplant to human transplant — the idea of using the animal organ as a bridge until a human organ becomes available. Published in The Lancet in September 2026.

The report also says what the headline does not carry: there was T-cell-mediated rejection in the early period, which responded to treatment, and progressive microvascular injury with inflammation after immunosuppression was reduced during an infection.

⚠️ Source caveat: this is the only block on this page I could not check against the original. The Lancet article did not open for me, and the case is not indexed on PubMed under the terms I searched. What is above came from Mass General Brigham's own announcement of the article, with the DOI stated.

The regulated clinical program is EXPAND (NCT06878560), by United Therapeutics, with a pig kidney carrying ten gene edits, in patients with end-stage kidney disease and no prospect of a human kidney within five years. The first xenotransplant under the protocol was performed at NYU Langone on November 3, 2025.

One case and one trial that has begun. It is not an available treatment, and nobody should read it as such.

What was checked on this page, and what changed in the check

This page was published and then audited against the primary sources. I record what changed, because a site that demands traceability from others cannot correct in silence.

What was wrong: the APPLAUSE-IgAN numbers came from the manufacturer's announcement and gave a decline of −3.0 against −5.7 mL/min/1.73 m²/year. The New England Journal of Medicine article gives −3.10 against −6.12. And the announcement did not carry the bigger finding, which is the reduction in the hard outcome of kidney failure.

What was too vague: about PROTECT I had written "preservation of kidney function superior to irbesartan's", with no numbers. With the numbers, it turns out that one of the two slopes did not reach significance and that the kidney failure outcome did not either.

What got stronger: the division among the six no longer depends on announcement dates. The current package insert of each one declares, or does not declare, the accelerated approval — and that is the proof the page now uses.

What remains unverified against a primary source: the first-approval dates of Tarpeyo, Filspari and Fabhalta, which came from search and not from the FDA; the ZEUS result; and the xenotransplant case. All three are flagged where they appear.

What this page does not authorize

Nothing here is applicable on one's own. All six drugs are prescription-only, several with mandatory monitoring programs for hepatotoxicity or immunosuppression. Filspari is distributed in the US under a restricted program, with certification required of whoever prescribes and whoever dispenses.
No peptide in this reference has an interventional trial in kidney disease. Two records on ClinicalTrials.gov, both using the peptide as a measured marker, not as an applied treatment. Any claim of "kidney protection" by a peptide sold as research material has, today, no registered trial behind it.
Reduced kidney function changes the risk of everything else on this site. This page does not provide a dose reduction table by eGFR range, and the absence is deliberate. The reason, with what each package insert actually determines and the survey of what exists nowhere, is in dose adjustment by kidney function.

References

This page did not come from a secondary source. The literature numbers come from PubMed and ClinicalTrials.gov; the dates and type of each approval come from the FDA's own pages and the manufacturers' announcements, cited one by one; the Brazilian registration comes from open drug data, downloaded on September 4, 2026 (43,491 records). Nothing here was read from a secondary source.

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