Bayer’s mineralocorticoid receptor antagonist finenerone has already proven its worth in type 2 diabetes patients with severe chronic kidney disease. Now the drug has been shown to decrease cardiovascular outcomes in diabetics with less advanced kidney disease, in the Figaro-DKD study.
However, with these patients often flying under the radar, diagnosing them could be a barrier to increasing adoption. And competition from the SGLT2 inhibitors also looms, although doctors presenting the data at the ESC Congress today believe that a combination approach could be the way forward.
Still, expectations for finenerone have risen since last autumn, when the drug yielded data from its first pivotal study, Fidelio-DKD. At the time, sellside consensus from Evaluate Pharma put 2026 revenues at just $533m. Now finerenone, which was approved under the brand name Kerendia in July, is forecast to bring in $1.2bn that year.
The latest results, presented today and published simultaneously in the NEJM, could boost this figure further. While Fidelio focused predominantly on stage 3 or 4 CKD patients with severely elevated albuminuria and type 2 diabetes, Figaro enrolled diabetics with either stage 2 to 4 CKD and moderately elevated albuminuria, or stage 1 or 2 CKD and severely increased albuminuria.
A high urinary albumin to creatinine ratio (UACR), a marker of kidney damage, comes with an increased risk of cardiovascular events. However, patients with a high UACR but a normal estimated glomerular filtration rate (eGFR) are not always identified because of lack of UACR testing, Professor Bertram Pitt of the University of Michigan School of Medicine told an ESC press conference.
Figaro has therefore found a benefit in patients who “are currently often not diagnosed and therefore not treated”, according to Professor Pitt – and therein could lie the problem for Bayer.
A spokesperson for the company noted that Kerendia's label did not specify eGFR or UACR values. Although she told Evaluate Vantage that UACR testing was the gold standard for identifying kidney damage, she acknowledged that this testing was "not done frequently enough”.
“We are working with key thought leaders to increase education on the importance of UACR in addition to eGFR testing,” the spokesperson concluded.
Another presenter, Professor Gerasimos Filippatos of Athens University Hospital, believes that this could be a chicken-and-egg situation, with a new therapy spurring better diagnosis among this group. “In the past, if we measured [albuminuria], we couldn’t answer the question of what next? Now we have an answer.”
These issues aside, Bayer can celebrate a win with Kerendia in Figaro, which met its primary endpoint of a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalisation for heart failure. Kerendia plus standard of care led to a 13% reduction in the risk of these outcomes versus standard of care alone.
However, this benefit was driven by a 29% decrease in the risk of hospitalisation. Kerendia had no impact on non-fatal MI or stroke; there was a 10% reduction in the risk of cardiovascular death, but this did not reach significance.
The study also did not meet its secondary endpoint, which focused on renal outcomes; namely, kidney failure, a sustained eGFR decrease of at least 40%, or renal death.
On this point, Professor Pitt said: “What’s important to our patients is that we significantly reduce the need for dialysis and progression to end-stage renal disease, and we did that.”
|Figaro-DKD results (N=7,437, NCT02545049)|
|Kerendia + SOC||SOC alone||Stats|
|CV death, nonfatal MI, nonfatal stroke, or HHF*||458 events||519 events||HR=0.87; CI=0.76-0.98; p=0.03|
|CV death**||194 deaths||214 deaths||HR=0.90; CI=0.74-1.09|
|Nonfatal MI**||103 MIs||102 MIs||HR=0.99; CI=0.76-1.31|
|Nonfatal stroke**||108 strokes||111 strokes||HR=0.97; CI=0.74-1.26|
|HHF**||117 hospitalisations||163 hospitalisations||HR=0.71; CI=0.56-0.90|
|Kidney failure, sustained ≥40% deccrease in eGFR, or renal death^||350 events||395 events||HR=0.87; CI=0.76-1.01|
|*Primary endpoint; **component of primary endpoint; ^first seconary endpoint; HHF=hospitalisation for heart failure; MI=myocardial infarction. Source: ESC & Professor Bertram Pitt & NEJM.|
He admitted that not lowering non-fatal stroke or myocardial infarction was “a failing” of Kerendia, but added: “The SGLT2 inhibitors, which are also very useful, have the same limitations – they don’t reduce stroke and hardly reduce myocardial infarction.”
He reckons a better combo might be Kerendia plus a GLP1 agonist, as the latter class has shown a benefit on stroke and myocardial infarction.
However, Professor Filippatos disagreed, saying: “I think that probably most patients will need both finerenone and SGLT2 inhibitors in the near future.”
Still, evidence for this strategy is lacking. In Figaro, only around 8% of patients were receiving either an SGLT2 inhibitor or a GLP1 agonist at baseline. Professor Pitt told Vantage that he was not aware of any ongoing combination studies.
And the spokesperson for Bayer said: "Currently no decision has been taken to investigate the combination of finerenone and SGLT2 inhibitors and/or GLP1 agonists."