Ocedurenone (KBP-5074): A Comprehensive Report on its Development, Clinical Profile, and Discontinuation

I. Introduction to Ocedurenone

A. Overview of Ocedurenone (KBP-5074)

Ocedurenone, identified by the investigational name KBP-5074, is a novel, orally administered small molecule pharmaceutical agent.[1] It was engineered as a third-generation non-steroidal mineralocorticoid receptor antagonist (nsMRA).[3] This classification is significant, as it positions Ocedurenone in a therapeutic class aiming to improve upon older, steroidal MRAs, such as spironolactone and eplerenone, and to compete with other contemporary nsMRAs like finerenone. The development of third-generation nsMRAs generally seeks to optimize the balance of efficacy and safety, particularly concerning side effects common to earlier MRAs.

B. Initial Therapeutic Promise and Targeted Indications

Ocedurenone was primarily developed and investigated for the treatment of uncontrolled hypertension. A particular focus was placed on patients with advanced chronic kidney disease (CKD), specifically those with stage 3b or stage 4 CKD.[5] This patient demographic represents a substantial unmet medical need, as managing hypertension in the presence of advanced CKD is challenging due to the high risk of cardiovascular complications and the limitations of existing antihypertensive treatments, especially concerning the risk of hyperkalemia.[7]

The development trajectory of Ocedurenone was substantially influenced by this critical unmet need. The potential to offer an effective and safer antihypertensive option for individuals with advanced CKD, a group where traditional MRAs are often used with caution or are contraindicated due to the risk of hyperkalemia, was a primary driver for its advancement. Beyond hypertension in CKD, there was also an expectation that Ocedurenone could have broader applications in other cardiovascular diseases and heart failure.[2] The drug was envisioned to possess "best-in-class potential" [2], suggesting ambitions for it to become a leading treatment in its intended indications.

C. Originator and Subsequent Acquisition

Ocedurenone was originated and its initial development was conducted by KBP Biosciences, a clinical-stage biotechnology company.[1] Based on promising early-phase clinical data, Ocedurenone attracted significant interest, leading to its acquisition by Novo Nordisk in October 2023.[1] This acquisition by a major pharmaceutical company underscored the perceived high therapeutic and commercial potential of Ocedurenone at that stage of its development.

II. Pharmacological Profile

A. Mechanism of Action

Ocedurenone exerts its pharmacological effects as a selective and potent antagonist of the mineralocorticoid receptor (MR).[1] The MR, a nuclear hormone receptor, plays a crucial role in the regulation of electrolyte and fluid balance, primarily through the actions of its endogenous ligand, aldosterone. Overactivation of the MR by aldosterone is a key pathophysiological mechanism contributing to hypertension, sodium and water retention, inflammation, fibrosis, and subsequent damage to cardiovascular and renal tissues.[5]

By competitively inhibiting the binding of aldosterone to the MR, Ocedurenone aims to mitigate these detrimental downstream effects.[5] A central tenet of Ocedurenone's design was its high selectivity for the MR over other steroid hormone receptors (e.g., glucocorticoid, androgen, progesterone receptors).[5] This selectivity was anticipated to minimize the risk of off-target side effects commonly associated with less selective, steroidal MRAs, such as gynecomastia, menstrual irregularities, and other hormonal disturbances.[5]

Further supporting its distinct profile, Ocedurenone was described as having different binding properties to the MR, involving cofactors and gene activation pathways, compared to spironolactone. These differences were hypothesized to contribute to a lower propensity for inducing hyperkalemia, a significant dose-limiting side effect of older MRAs.[13] Ocedurenone also demonstrated a higher binding affinity for the MR in comparison to steroidal MRAs like spironolactone and eplerenone.[11]

Beyond its direct effects on blood pressure via MR antagonism in epithelial tissues (like the kidney), preclinical data and mechanistic understanding suggested that Ocedurenone might also possess anti-inflammatory and antifibrotic properties.[5] These potential pleiotropic effects could contribute to its overall therapeutic benefit by directly addressing pathological processes involved in the progression of cardiovascular and renal disease, independent of, or in addition to, blood pressure reduction. This broader mechanistic potential aimed to position Ocedurenone as a more comprehensive treatment for cardiorenal conditions.

B. Pharmacokinetics (PK)

The pharmacokinetic profile of Ocedurenone was characterized through various clinical studies:

• Administration and Absorption: Ocedurenone was designed for oral administration.[2] Following oral intake, it demonstrated steady absorption, with the median time to reach peak plasma concentration (Tmax) observed to be between 3 and 4 hours in clinical studies.[15]
• Distribution: In plasma, Ocedurenone is highly protein-bound, with studies indicating greater than 99.7% binding to plasma proteins.[15] Investigations in subjects with moderate hepatic impairment suggested that this condition did not significantly alter the extent of plasma protein binding or the fraction of unbound (free) drug.[15]
• Metabolism and Elimination: The elimination of Ocedurenone from the plasma appeared to follow a biphasic pattern.[15] A key characteristic of Ocedurenone's PK profile is its long plasma half-life (t1/2​). Reports indicate a t1/2​ of approximately 60 hours [14], with more specific geometric mean values of 65.7 hours in individuals with normal hepatic function and 75.6 hours in those with moderate hepatic impairment.[3] This extended half-life supports the feasibility of once-daily dosing, which is advantageous for patient adherence in chronic conditions.
• Effect of Hepatic Impairment: A dedicated study in subjects with moderate hepatic impairment (Child-Pugh Class B) found that systemic exposure to Ocedurenone, as measured by the area under the plasma concentration-time curve (AUC), was 23.5-26.6% lower, and the maximum plasma concentration (Cmax) was 41.2% lower, compared to subjects with normal hepatic function. Despite these observed differences, it was concluded that dose adjustment for Ocedurenone would not be warranted in patients with moderate hepatic impairment, likely due to its long half-life and the therapeutic window established in other studies.[13]
• Drug-Drug Interactions (DDI): Studies were conducted to assess the potential for drug-drug interactions. Co-administration of Ocedurenone with itraconazole, a strong inhibitor of the cytochrome P450 3A4 (CYP3A4) enzyme, resulted in a less than 2-fold change in Ocedurenone's Cmax and AUC. This suggested a weak interaction, and co-administration with CYP3A4 inhibitors was generally considered safe.[13] The effect of rifampin, a strong CYP3A inducer, was also investigated, and while detailed quantitative results are not fully provided, it was noted to have an effect on Ocedurenone's pharmacokinetics.[13]
• Chemical Properties: Ocedurenone has a molecular weight of 504.02 g/mol, a molecular formula of C28​H30​ClN5​O2​, and its Chemical Abstracts Service (CAS) Registry Number is 1359969-24-6.[16]

The combination of oral administration, a long half-life facilitating once-daily dosing, and the absence of a need for dose adjustment in patients with moderate hepatic impairment suggested a generally favorable and convenient pharmacokinetic profile for the long-term management of chronic diseases such as hypertension and CKD.

C. Pharmacodynamics (PD)

The primary pharmacodynamic effect of Ocedurenone is the potent antagonism of the mineralocorticoid receptor, leading to a reduction in blood pressure.[5] This blood pressure-lowering effect was anticipated to translate into a reduced risk of adverse cardiovascular and renal outcomes in patients with conditions like heart failure and chronic kidney disease.[5]

By blocking the effects of aldosterone at the MR, Ocedurenone was expected to inhibit pro-inflammatory and pro-fibrotic signaling pathways.[5] These pathways are critically involved in the pathogenesis and progression of structural and functional damage in the heart and kidneys. The overactivation of MR is recognized as a central element in the pathophysiology of hypertension, promoting sodium retention, inflammation, fibrosis, and ultimately contributing to end-organ damage in cardiorenal syndromes.[5] Ocedurenone's mechanism directly targets this pivotal pathway.

The pharmacodynamic rationale for Ocedurenone thus extended beyond simple hemodynamic effects. The anticipated modulation of inflammatory and fibrotic processes suggested the potential for direct tissue-protective benefits in the cardiovascular and renal systems. This aligns with contemporary therapeutic strategies for CKD and heart failure, which increasingly focus on agents that can offer pleiotropic effects targeting multiple facets of the disease process, rather than solely addressing a single symptom like elevated blood pressure.

Table 1: Key Pharmacological and Developmental Characteristics of Ocedurenone

Feature	Description
Generic Name	Ocedurenone
Investigational Name	KBP-5074
Chemical Class	Non-steroidal Mineralocorticoid Receptor Antagonist (nsMRA), Small Molecule
Originator	KBP Biosciences
Acquirer	Novo Nordisk
Mechanism of Action	Selective and potent antagonist of the mineralocorticoid receptor (MR), reducing effects of aldosterone; potential anti-inflammatory and antifibrotic properties.
Key Pharmacokinetic Features	Oral administration; Tmax ~3-4 hours; Plasma half-life ~60-76 hours; Plasma protein binding >99.7%.
Highest Development Phase	Phase III (CLARION-CKD trial, terminated)
Primary Targeted Indications	Uncontrolled hypertension in advanced Chronic Kidney Disease (CKD); potential for broader cardiovascular and kidney diseases.

III. Clinical Development Program

The clinical development of Ocedurenone involved several studies, progressing from early phase to Phase III, before its eventual termination.

A. Phase IIb Study (BLOCK-CKD - NCT03574363)

The BLOCK-CKD trial was a crucial study that provided the initial evidence for Ocedurenone's efficacy and safety in its target population.

• Study Design: This was an international, multicenter, randomized, double-blind, placebo-controlled, parallel-group study.[18] The trial's design and rationale were peer-reviewed and published, for instance, in Hypertension.[19]
• Patient Population: A total of 162 patients were randomized into the study, although the initial plan was for approximately 240 participants.[14] Eligible patients were adults with stage 3b/4 CKD, defined by an estimated glomerular filtration rate (eGFR) between ≥15 and ≤44 mL/min/1.73 m2, and uncontrolled or resistant hypertension. Uncontrolled hypertension was defined as a resting trough-cuff seated systolic blood pressure (SBP) between ≥140 and ≤179 mm Hg, despite treatment with two or more antihypertensive medications at stable doses.[18] A significant proportion of the enrolled patients (approximately 39.5% overall, with 35.2% in the 0.5 mg arm) had stage 4 CKD (eGFR <30 mL/min/1.73 m2).[18]
• Treatment Arms: Patients were randomized in a 1:1:1 ratio to receive once-daily oral treatment with either placebo, Ocedurenone 0.25 mg, or Ocedurenone 0.5 mg, administered in addition to their existing antihypertensive medication regimen.[18]
• Primary Endpoint: The primary efficacy endpoint was the change in trough cuff seated SBP from baseline to day 84 of treatment.[18]
• Key Efficacy Outcomes: The BLOCK-CKD trial successfully met its primary endpoint.[9] Ocedurenone demonstrated a clinically meaningful and statistically significant dose-dependent reduction in SBP when compared to placebo.[18] Specifically, the 0.5 mg dose of Ocedurenone resulted in a placebo-adjusted SBP reduction of -10.6 mm Hg.[18] Subgroup analyses indicated that these SBP reductions were consistent across various demographic groups and comorbid conditions. For example, in Hispanic patients, the placebo-adjusted SBP reduction was -9.9 mm Hg with the 0.5 mg dose. In patients with CKD stage 4, the reduction was -10.4 mm Hg for the 0.5 mg dose, and in patients with diabetes, it was -11.6 mm Hg for the 0.5 mg dose.[18]
• Safety and Tolerability Profile: Ocedurenone was generally reported to be safe and well-tolerated in the BLOCK-CKD study.[18]
• Hyperkalemia: An increased incidence of mild hyperkalemia was observed with Ocedurenone treatment. The percentage of subjects with at least one maximum serum potassium level ≥5.6 mmol/L (measured by central lab) was 8.8% (5 out of 57) in the placebo group, 9.8% (5 out of 51) in the Ocedurenone 0.25 mg group, and 13.0% (7 out of 54) in the Ocedurenone 0.5 mg group.[14] Importantly, no cases of severe hyperkalemia (defined as serum potassium ≥6.0 mmol/L) or acute kidney injury were reported in association with Ocedurenone treatment during this study.[18]
• Discontinuations due to Adverse Events: There are conflicting reports regarding discontinuations due to hyperkalemia. Some sources state that no cases of hyperkalemia required intervention or resulted in study discontinuation.[18] However, detailed safety tables from another publication of the BLOCK-CKD results indicate that 2 patients (3.7%) in the Ocedurenone 0.5 mg group and 2 patients (3.5%) in the placebo group discontinued due to hyperkalemia.[14] The overall rate of adverse events leading to withdrawal was 5.3% for placebo, 2.0% for Ocedurenone 0.25 mg, and 7.4% for Ocedurenone 0.5 mg.[14]

The positive outcomes of the BLOCK-CKD Phase IIb trial were pivotal. They provided the foundational evidence that supported further development and were instrumental in KBP Biosciences securing the $1.3 billion acquisition agreement with Novo Nordisk.[9] This success generated considerable optimism and momentum for Ocedurenone. However, the subsequent failure of the Phase III CLARION-CKD trial, which reportedly employed similar inclusion criteria to BLOCK-CKD [22], presents a significant paradox. This stark contrast in outcomes raises profound questions regarding the robustness or predictive value of the Phase IIb findings. Alternatively, it could point to potential unidentified issues in the Phase IIb data or its interpretation, or flaws in the execution or design of the Phase III trial. These questions gained further complexity in light of subsequent legal allegations by Novo Nordisk, which claimed that KBP Biosciences had withheld negative Phase 2 data from 2022 and concealed issues at an investigational site that produced anomalous positive results.[23] If these allegations were substantiated, it would suggest that the perceived success of BLOCK-CKD might have been based on incomplete or potentially misrepresented information.

Furthermore, despite the primary narrative from BLOCK-CKD emphasizing the absence of severe hyperkalemia, the data clearly indicated a dose-dependent increase in the incidence of mild hyperkalemia (serum potassium ≥5.6 mmol/L) with Ocedurenone.[14] While not meeting the predefined threshold for a severe event in this particular trial, any elevation in serum potassium is a notable concern for MRAs, especially within a vulnerable CKD population. This persistent hyperkalemia signal, even if categorized as mild, is a classic safety consideration for this drug class that would necessitate careful management and monitoring in larger and longer-duration clinical trials. The conflicting information regarding study discontinuations specifically due to hyperkalemia [14] further complicates a clear interpretation of this critical safety aspect from the Phase IIb data.

Table 2: Summary of BLOCK-CKD (Phase IIb - NCT03574363) Key Findings

Feature	Description
Study Design	International, multicenter, randomized, double-blind, placebo-controlled, parallel-group.
Patient Population (N=162)	Stage 3b/4 CKD (eGFR ≥15-≤44 mL/min/1.73 m2), uncontrolled/resistant hypertension (SBP ≥140-≤179 mm Hg on ≥2 antihypertensives).
Treatment Arms (Day 84)	Placebo QD; Ocedurenone 0.25 mg QD; Ocedurenone 0.5 mg QD.
Primary Efficacy Endpoint	Change in trough cuff seated Systolic Blood Pressure (SBP) from baseline to Day 84.
Key Efficacy Result (0.5 mg vs. Placebo)	Statistically significant placebo-adjusted SBP reduction of -10.6 mm Hg.18
Key Safety Finding - Hyperkalemia (K+ ≥5.6 mmol/L, central lab)	Placebo: 8.8% (5/57); Ocedurenone 0.25 mg: 9.8% (5/51); Ocedurenone 0.5 mg: 13.0% (7/54).14
Key Safety Finding - Severe Hyperkalemia (K+ ≥6.0 mmol/L)	0 cases reported in any group.14
Key Safety - AE-related Withdrawals (due to Hyperkalemia)	Placebo: 2 (3.5%); Ocedurenone 0.25 mg: 0; Ocedurenone 0.5 mg: 2 (3.7%).14 Note: This conflicts with other sources stating no discontinuations for hyperkalemia.18

B. Phase III Study (CLARION-CKD - NCT04968184)

Following the encouraging results from BLOCK-CKD, Ocedurenone advanced to Phase III investigation in the CLARION-CKD trial.

• Study Design and Initiation: CLARION-CKD was designed as a global, multicenter, randomized, double-blind, placebo-controlled Phase III study.[2] The first patient in this pivotal trial was dosed at the end of 2021.[2] The trial was initiated and conducted by KBP Biosciences, continuing under their management during the period leading up to and immediately following the acquisition by Novo Nordisk.[3]
• Patient Population: The trial aimed to enroll over 600 patients across more than 150 sites located in the US, Europe, and Asia.[2] The target population consisted of patients with uncontrolled hypertension and advanced CKD (moderate to severe, Stage 3b/4).[2] The inclusion criteria for CLARION-CKD were reported to be similar to those used in the preceding BLOCK-CKD study.[22] KBP Biosciences announced the completion of enrollment for this study in November 2023.[20]
• Primary Endpoint: The primary efficacy endpoint for CLARION-CKD was the change in SBP from baseline to week 12 of treatment.[3]
• Interim Futility Analysis and Premature Termination: The CLARION-CKD trial protocol included a prespecified interim analysis to be conducted by an independent data monitoring committee (IDMC). This analysis was planned to occur after all enrolled trial participants had completed 12 weeks of treatment.[3] In June 2024, Novo Nordisk announced a critical development: the IDMC had reviewed the interim data and concluded that the trial met the prespecified futility criteria.[3] This determination meant that the trial had failed to demonstrate efficacy on its primary endpoint – a significant change in SBP from baseline to week 12.[3] The finding that the trial met futility criteria signifies that there was a very low probability of achieving a statistically significant positive result for the primary endpoint even if the trial were to continue to its planned completion. Such a conclusion from an IDMC is a strong directive to halt a trial, primarily to prevent further exposure of patients to an apparently ineffective investigational treatment and to conserve resources. As a direct consequence of this interim futility analysis, Novo Nordisk made the decision to stop the CLARION-CKD trial prematurely.[3]
• Reported Reasons for Failure: The explicitly stated reason for the trial's failure and subsequent termination was its inability to meet the primary endpoint related to SBP reduction at the 12-week interim analysis, as determined by the futility criteria.[3] Beyond this top-line announcement of primary endpoint failure, detailed efficacy or comprehensive safety data from the terminated CLARION-CKD trial were not made publicly available in the reviewed information. This lack of detailed disclosure from the terminated Phase III trial creates an information vacuum. While the failure on SBP is clear, the absence of data on secondary endpoints (such as effects on albuminuria or eGFR) or a full safety profile up to the point of termination limits a complete scientific understanding of Ocedurenone's performance in this larger, more definitive study. Such detailed information, even if negative, is valuable for the broader medical and scientific community but is often not fully disseminated for drug development programs that are discontinued.

Table 3: Overview of CLARION-CKD (Phase III - NCT04968184) and Termination

Feature	Description
Study Design	Global, multicenter, randomized, double-blind, placebo-controlled.
Patient Population (Planned >600; Enrollment Completed)	Uncontrolled hypertension and advanced (Stage 3b/4) CKD.2
Treatment Arms	Assumed to be similar to Phase IIb (Placebo, Ocedurenone 0.25 mg QD, Ocedurenone 0.5 mg QD), though specific Phase III doses were not detailed in the provided information.
Primary Efficacy Endpoint	Change in Systolic Blood Pressure (SBP) from baseline to Week 12.3
Outcome of Prespecified Interim Analysis (June 2024)	Failed to meet primary endpoint; trial met prespecified futility criteria.3
Consequence	CLARION-CKD trial stopped by Novo Nordisk (June 2024).3 Ocedurenone development program completely terminated by Novo Nordisk (announced November 2024).6

C. Studies in Special Populations (beyond primary efficacy trials)

In addition to the main efficacy trials, Ocedurenone was evaluated in studies designed to understand its behavior in specific patient populations and potential drug interaction scenarios. These are standard components of a comprehensive drug development program.

• Hepatic Impairment Study: A dedicated clinical trial assessed the pharmacokinetics, safety, and tolerability of a single 0.5 mg oral dose of Ocedurenone in subjects with moderate hepatic impairment (Child-Pugh Class B) compared to individuals with normal hepatic function. The study found that Ocedurenone was safe and well-tolerated in both groups. Although subjects with moderate hepatic impairment exhibited lower systemic exposure (AUC was 23.5-26.6% lower) and lower peak plasma concentrations (Cmax was 41.2% lower) compared to those with normal hepatic function, it was concluded that a dose adjustment for Ocedurenone would not be necessary in this population. This conclusion was based on Ocedurenone's long half-life and the established efficacy and safety of the 0.25 mg and 0.5 mg doses in other clinical studies.[13] The results of this study were published in the European Journal of Drug Metabolism and Pharmacokinetics.[15]
• Severe CKD and Hemodialysis: A single-dose pharmacokinetic study indicated that KBP-5074 (Ocedurenone) was well-tolerated in patients with severe CKD, including those requiring hemodialysis. It was also reported that the drug's half-life was not significantly affected by the hemodialysis procedure.[14]
• Drug-Drug Interaction Study: The potential for drug-drug interactions was investigated in a study involving healthy subjects. This study assessed the pharmacokinetics and safety of a single 0.5 mg dose of Ocedurenone when administered alone or in combination with itraconazole (a strong CYP3A4 inhibitor) or rifampin (a strong CYP3A4 inducer). Ocedurenone was reported to be well-tolerated in these scenarios. The co-administration of itraconazole had a weak effect on the pharmacokinetic parameters of Ocedurenone.[13]

The findings from these supporting studies generally suggested that Ocedurenone could be manageable in diverse patient conditions and with common co-medications. For instance, not requiring a dose adjustment in moderate hepatic impairment would have simplified prescribing. However, the relevance of these findings became largely academic following the failure of the primary efficacy trial, CLARION-CKD.

IV. Commercial and Regulatory History

A. Origin and Development by KBP Biosciences

Ocedurenone, also known by its investigational designation KBP-5074, was discovered and its initial clinical development was spearheaded by KBP Biosciences PTE., Ltd..[1] KBP Biosciences is a global, clinical-stage biotechnology company headquartered in Singapore, with a focus on the discovery and development of novel small-molecule therapeutics for serious cardiorenal and infectious diseases that have significant unmet medical needs.[13]

KBP Biosciences successfully navigated Ocedurenone through preclinical development and multiple phases of clinical trials. This included the design and execution of the Phase IIb BLOCK-CKD study, which yielded positive results, and the subsequent initiation and progression of the global Phase III CLARION-CKD trial.[2] This systematic advancement of Ocedurenone through the clinical development pipeline rendered it an attractive asset for larger pharmaceutical companies seeking to bolster their portfolios in the cardiorenal space. The trajectory of KBP Biosciences with Ocedurenone, up to the initiation of Phase III, exemplifies a common strategy within the biotechnology sector: a smaller, innovation-focused company develops a novel drug candidate to a significant value inflection point (typically mid-to-late-stage clinical proof-of-concept), thereby de-risking the asset to an extent that it becomes appealing for partnership or acquisition by a larger pharmaceutical entity possessing the extensive resources required for late-stage development, regulatory approval, and global commercialization.

B. Acquisition by Novo Nordisk

In October 2023, Novo Nordisk A/S, a major global pharmaceutical company, announced an agreement to acquire Ocedurenone from KBP Biosciences.[1] The deal was valued at up to $1.3 billion, a figure indicative of the high expectations for Ocedurenone's therapeutic and commercial success.[1]

Novo Nordisk's strategic rationale for this significant investment was multifaceted. The company stated that Ocedurenone, based on its "expected benefit-risk profile," was perceived to have "best-in-class potential" for the treatment of uncontrolled hypertension.[2] It was anticipated to address a major unmet medical need, particularly in patients living with cardiovascular disease and chronic kidney disease.[2] The acquisition was also intended to complement and strengthen Novo Nordisk's existing development programs in the cardiovascular and chronic kidney disease therapeutic areas.[9] Furthermore, Ocedurenone was viewed as a potential competitor to Bayer's already approved non-steroidal MRA, Kerendia (finerenone), suggesting Novo Nordisk's ambition to secure a significant position in this evolving market.[26] This acquisition represented a calculated strategic bet by Novo Nordisk, heavily influenced by the positive data from the Phase IIb BLOCK-CKD study and the allure of developing a leading MRA therapy.

C. Termination of Development and Financial Impact

The promising trajectory of Ocedurenone under Novo Nordisk's stewardship took a decisive downturn in June 2024. Following the interim futility analysis of the CLARION-CKD Phase III trial, which concluded that the trial failed to meet its primary endpoint for SBP reduction, Novo Nordisk promptly halted the study.[3]

Although initial statements after the trial halt suggested that Novo Nordisk was evaluating the potential for further development of Ocedurenone in other indications [3], these considerations did not materialize into a continued program. After conducting a further analysis of the "detailed trial data" from CLARION-CKD, Novo Nordisk announced in its third-quarter earnings report (around November 2024) the complete termination of the entire Ocedurenone development program.[6]

This clinical failure had substantial financial repercussions for Novo Nordisk. The company recognized an impairment loss amounting to DKK 5.7 billion (approximately $816.5 million to $821 million USD at the time) related to the intangible asset Ocedurenone.[3] This significant write-down adversely impacted Novo Nordisk's operating profit growth outlook for the 2024 fiscal year.[3] The substantial impairment loss vividly illustrates the inherent and considerable financial risks associated with late-stage pharmaceutical development and acquisitions based on mid-stage data. Even with promising earlier clinical results, the failure of a pivotal Phase III trial can lead to the complete write-off of multi-billion dollar investments, underscoring the unpredictable nature of drug development. The rapid shift from evaluating other indications to complete termination suggests the detailed data from CLARION-CKD were unequivocally negative regarding the drug's core efficacy or overall profile.

With the discontinuation of Ocedurenone, Novo Nordisk's pipeline in chronic kidney disease primarily features semaglutide. Semaglutide, the active ingredient in Ozempic and Wegovy, has demonstrated success in a Phase III study by reducing the risk of kidney disease progression in patients with Type 2 diabetes.[26] This highlights the contrasting fortunes within a pharmaceutical pipeline and the importance of diversified approaches in drug development.

D. Regulatory Status and Designations

During its development, Ocedurenone was classified as a New Molecular Entity (NME), reflecting its novel chemical structure.[1] It did not hold Orphan Drug Status.[1] While some search results juxtaposed news about Ocedurenone with information on orphan drug designations for other compounds [21], the specific regulatory information for Ocedurenone indicates it was not designated as such. This is consistent with its primary target indications of hypertension and chronic kidney disease, which are prevalent conditions and do not typically qualify for orphan drug designation, even if the initial clinical focus was on a specific sub-population with advanced CKD.

As Ocedurenone did not successfully complete Phase III development, no marketing authorization applications (such as a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) or a Marketing Authorisation Application (MAA) to the European Medicines Agency (EMA)) were filed.

Table 4: Timeline of Key Events in Ocedurenone Development and Post-Acquisition Trajectory

Date	Event
End of 2021	KBP Biosciences doses first patient in the Phase III CLARION-CKD trial for Ocedurenone.2
October 16, 2023	Novo Nordisk announces agreement to acquire Ocedurenone from KBP Biosciences for up to $1.3 billion.1
November 2, 2023	KBP Biosciences announces completion of patient enrollment for the CLARION-CKD Phase 3 study.20
June 26, 2024	Novo Nordisk announces that the CLARION-CKD Phase 3 trial is stopped due to failure to meet its primary endpoint at a prespecified interim futility analysis. Company announces DKK 5.7 billion impairment loss.3
November 6, 2024 (approx.)	Novo Nordisk, in its Q3 earnings report, confirms the complete termination of the Ocedurenone development program after analyzing detailed trial data from CLARION-CKD.6
February 2025 (approx.)	Novo Nordisk files a lawsuit against KBP Biosciences and its founder, alleging data misrepresentation related to the Ocedurenone acquisition.23
February 28, 2025	KBP Biosciences issues a public statement indicating its intention to contest an injunction obtained by Novo Nordisk in relation to the lawsuit.20

V. Post-Termination Developments: The Novo Nordisk vs. KBP Biosciences Litigation

The discontinuation of Ocedurenone's development was followed by significant legal action initiated by Novo Nordisk against KBP Biosciences.

A. Allegations by Novo Nordisk

Novo Nordisk filed a lawsuit in the Singapore International Commercial Court against KBP Biosciences PTE., Ltd., and its founder, Dr. Zhenhua Huang.[23] In this lawsuit, Novo Nordisk is seeking damages amounting to $830 million, which corresponds to a significant portion of the impairment loss it incurred following the Ocedurenone program's failure.[23]

The central allegation made by Novo Nordisk is that it was misled into the $1.3 billion acquisition of Ocedurenone due to material data misrepresentation by KBP Biosciences.[23] Specific claims detailed in the lawsuit include accusations that KBP knowingly failed to disclose interim data from a Phase 2 clinical trial that dated back to 2022. According to Novo Nordisk, this undisclosed 2022 data allegedly indicated that Ocedurenone was unlikely to demonstrate efficacy in later-stage trials.[23] This point is particularly critical as it suggests that negative signals may have existed prior to the acquisition agreement in October 2023.

Furthermore, Novo Nordisk alleged that KBP Biosciences concealed quality and compliance issues at one of the clinical investigation sites involved in the Ocedurenone trials. This site purportedly produced "anomalous positive results," which, if true, could have improperly skewed the overall data package reviewed by Novo Nordisk during its due diligence process.[23] Dr. Zhenhua Huang, who served as KBP's founder, executive chairman, and was a 40% shareholder in the company, is also named in the lawsuit, with allegations that he knew of and participated in these misrepresentations.[23]

These allegations by Novo Nordisk fundamentally shift the narrative surrounding Ocedurenone's failure. Instead of being a case of straightforward clinical trial failure – an inherent risk in pharmaceutical R&D – the lawsuit posits a scenario of potential fraud and deliberate concealment of critical negative data by the seller, KBP Biosciences. If these claims are proven, they would have severe implications for KBP Biosciences and could also cast a spotlight on the thoroughness and integrity of due diligence processes in pharmaceutical mergers and acquisitions.

B. Legal Proceedings and Asset Freeze

The legal dispute is complex, with the lawsuit filed in Singapore, while the underlying Asset Purchase Agreement (APA) stipulates that disputes are to be resolved by arbitration administered by the International Chamber of Commerce (ICC), seated in New York, and governed by New York law.[24]

In a significant early development in the legal proceedings, the Singapore International Commercial Court granted Novo Nordisk's application for a Mareva injunction (an asset freezing order) against KBP Biosciences and Dr. Huang.[23] The presiding judge granted this request based on being satisfied that Novo Nordisk had demonstrated a "good arguable case for fraud under New York law" and that there was a "real risk of dissipation of assets" by KBP that could frustrate the enforcement of an anticipated arbitral award.[24]

The court's concern about asset dissipation was reportedly heightened by financial transactions undertaken by KBP around the time the acquisition deal with Novo Nordisk closed. It was noted that KBP had transferred a substantial sum, $339.1 million, to its holding company and had also declared $578.5 million in dividends.[23] The court viewed these actions as lacking a clear commercial rationale and suggestive of an intention on Dr. Huang's part to move assets out of Novo Nordisk's reach in anticipation of a potential claim.[24] The granting of a worldwide Mareva injunction is a serious legal measure, not undertaken lightly, and indicates that Novo Nordisk presented a sufficiently compelling preliminary case regarding both the alleged fraud and the tangible risk of KBP attempting to make its assets inaccessible. The timing and magnitude of KBP's fund transfers appear to have been key factors in the court's decision.

C. KBP Biosciences' Stated Defense

In response to these legal actions and public allegations, KBP Biosciences issued a statement on February 28, 2025.[20] In this statement, the company announced its intention to "vigorously defend their legal rights" and to contest the injunction, which, it emphasized, had been obtained by Novo Nordisk on an ex parte basis – meaning without KBP's prior knowledge or opportunity to be heard at that initial stage.[27]

Dr. Zhenhua Huang, founder and chairman of KBP Biosciences, was quoted as stating, "The serious allegations made by Novo Nordisk are completely unfounded and the truth will vindicate us in time to come." He also expressed disappointment with Novo Nordisk's approach in seeking the injunction without prior notice to KBP.[27] Despite the legal challenge and the termination of Ocedurenone's development by Novo Nordisk, KBP Biosciences reiterated its belief in the "tremendous potential in Ocedurenone".[27]

KBP's response effectively draws the battle lines for a contentious legal dispute. Their defense strategy appears to focus on the procedural fairness concerning the ex parte injunction while preparing a substantive rebuttal to Novo Nordisk's allegations. The core of this legal conflict will undoubtedly revolve around the evidence presented concerning what KBP Biosciences knew about Ocedurenone's clinical trial data, the timing of this knowledge, and the nature and completeness of the disclosures made to Novo Nordisk during the due diligence process leading up to the acquisition. The outcome of this litigation could have significant implications for how pharmaceutical companies approach due diligence and manage transparency in M&A transactions.

VI. Comprehensive Safety and Tolerability Assessment

A thorough evaluation of Ocedurenone's safety and tolerability is constrained by the premature termination of its Phase III program, but data from earlier studies provide some insights.

A. Overview of Adverse Events from Clinical Trials

• BLOCK-CKD (Phase IIb): In this study, Ocedurenone was generally described as well-tolerated.[18] The most frequent adverse events (AEs) reported in the Ocedurenone 0.5 mg arm, other than hyperkalemia, included hypertensive urgency (5.6%), headache (5.6%), and diarrhea (5.6%).[14] Serious adverse events (SAEs) were reported in 7.0% of patients receiving placebo, 2.0% of those receiving Ocedurenone 0.25 mg, and 3.7% of those receiving Ocedurenone 0.5 mg.[14] Two deaths occurred during the study, both in the placebo group.[14] Adverse events leading to study withdrawal were reported in 5.3% of placebo patients (3 patients, of whom 2 cited hyperkalemia), 2.0% of Ocedurenone 0.25 mg patients (1 patient), and 7.4% of Ocedurenone 0.5 mg patients (4 patients, of whom 2 cited hyperkalemia).[14]
• Hepatic Impairment Study: A single 0.5 mg dose of Ocedurenone was found to be safe and well-tolerated in subjects with moderate hepatic impairment as well as in those with normal hepatic function.[13]
• Drug-Drug Interaction Study: Ocedurenone was also reported as well-tolerated when administered as a single 0.5 mg dose alone or in combination with itraconazole or rifampin in healthy subjects.[13]
• Early Clinical Development: Initial preclinical studies and earlier phase clinical trials had generally indicated a promising efficacy and safety profile for Ocedurenone.[5]
• CLARION-CKD (Phase III): Crucially, no detailed adverse event data from the terminated Phase III CLARION-CKD trial are available in the provided information. This absence of comprehensive safety data from a larger, longer-duration study represents a significant gap in the overall safety assessment of Ocedurenone.

While the Phase IIb and pharmacokinetic studies suggested that Ocedurenone was generally well-tolerated, the lack of complete safety information from the pivotal Phase III CLARION-CKD trial prevents a definitive conclusion regarding its overall safety profile in the intended patient population over a longer treatment duration. The numerically higher rate of withdrawals due to adverse events in the Ocedurenone 0.5 mg arm in the Phase IIb study (7.4%) compared to placebo (5.3%) [14] was a signal that would have warranted careful monitoring and further investigation in the Phase III program. Without the Phase III data, it is unknown whether new safety concerns emerged or if known AEs, such as hyperkalemia, became more problematic or frequent with broader exposure.

B. Focus on Hyperkalemia Risk Management

Hyperkalemia (elevated serum potassium levels) is a well-recognized and clinically significant adverse effect associated with all mineralocorticoid receptor antagonists. This risk often limits their therapeutic use, particularly in patients with chronic kidney disease, who are already predisposed to potassium dysregulation.[5] Ocedurenone, as a non-steroidal MRA, was specifically developed with the objective of offering a reduced risk of hyperkalemia compared to older, steroidal MRAs like spironolactone and eplerenone.[5] This improved potassium safety profile was a key element of its anticipated clinical value.

Findings from the BLOCK-CKD (Phase IIb) study related to hyperkalemia were as follows:

• A dose-dependent increase in serum potassium levels was observed with Ocedurenone treatment. The incidence of investigator-reported hyperkalemia, specifically defined as serum potassium levels between 5.6 and 5.9 mmol/L, was 3.5% (2 patients) in the placebo group, 7.8% (4 patients) in the Ocedurenone 0.25 mg group, and 12.9% (7 patients) in the Ocedurenone 0.5 mg group.[14]
• A critical positive finding was that no cases of severe hyperkalemia (defined as serum potassium ≥6.0 mmol/L) were reported in any treatment group during this study.[18]
• As previously noted, there is conflicting information regarding study discontinuations specifically attributed to hyperkalemia. Some sources assert that "No cases of hyperkalemia required intervention or resulted in study discontinuation".[18] However, detailed safety tables from another publication of the BLOCK-CKD results [14] list hyperkalemia as the reason for withdrawal for 2 patients in the placebo group and 2 patients in the Ocedurenone 0.5 mg group.
• Changes in serum potassium levels were reported to be generally similar across various patient subgroups, including those stratified by baseline eGFR, diabetes status, or the degree of albuminuria.[18]

While Ocedurenone appeared to avoid inducing severe hyperkalemia in the Phase IIb setting, it was associated with a notable and dose-dependent increase in the incidence of mild-to-moderate hyperkalemia. The critical question, which the CLARION-CKD Phase III trial might have definitively answered had it been completed, was whether this potassium-sparing profile was sufficiently differentiated and manageable in a broader clinical context to offer a true advantage over existing therapies, particularly if its antihypertensive efficacy was not demonstrably superior. The discrepancy in the reported data concerning discontinuations due to hyperkalemia in Phase IIb further clouds a clear assessment of this specific risk from that stage of development.

C. Comparison with Other MRAs (based on available information)

• Steroidal MRAs (Spironolactone, Eplerenone): The clinical utility of these first-generation MRAs is often constrained by the risk of hyperkalemia and undesirable hormonal side effects, such as gynecomastia in males and menstrual disturbances in females. These limitations are particularly pronounced in patients with advanced CKD.[7] Ocedurenone was developed with the aim of overcoming these specific drawbacks.[32]
• Finerenone (Kerendia - another nsMRA): Finerenone is a non-steroidal MRA approved for slowing the progression of CKD and reducing cardiovascular events in patients with type 2 diabetes. Large clinical trials such as FIDELIO-DKD and FIGARO-DKD demonstrated its renal and cardiovascular benefits.[12] However, finerenone treatment is also associated with an increased risk of hyperkalemia. For instance, in the FIDELIO-DKD trial, hyperkalemia leading to discontinuation of the trial regimen occurred in 2.3% of patients receiving finerenone compared to 0.9% in the placebo group. Similarly, in the FIGARO-DKD trial, these rates were 1.2% for finerenone and 0.4% for placebo.[12] This indicates that while nsMRAs may offer an improved profile over steroidal agents, hyperkalemia remains a relevant consideration.
• Esaxerenone: This nsMRA is approved for the treatment of hypertension and diabetic nephropathy in Japan, based on Phase III clinical trials conducted exclusively in Japanese patients. This limited geographic scope of development compromises the external validity of its findings for other populations.[7]

D. Contraindications, Warnings, and Precautions (from available development data)

Specific contraindications, formal warnings, or precautions for Ocedurenone were not fully established as it did not reach the stage of marketing approval. However, based on its mechanism of action as an MRA and data from its clinical development:

• Hyperkalemia would have been a primary concern, necessitating careful potassium monitoring, especially in patients with advanced CKD, those on potassium supplements, or those taking other medications known to increase potassium levels (e.g., ACE inhibitors, ARBs, potassium-sparing diuretics).
• The drug's safety in pregnancy and lactation was not detailed in the provided information.[10] As with many new drugs, its use in these populations would likely have been contraindicated or advised against without specific safety data.
• No specific data on pediatric use were available.[11]
• The hepatic impairment study suggested no dose adjustment was needed for moderate impairment, but use in severe hepatic impairment would likely have required further investigation or caution.[13]

VII. Conclusion

Ocedurenone (KBP-5074) emerged as a promising third-generation non-steroidal mineralocorticoid receptor antagonist, primarily targeting uncontrolled hypertension in the challenging patient population with advanced chronic kidney disease. Its development was underpinned by a strong scientific rationale: the hypothesis that its selective antagonism of the MR, coupled with unique binding properties, would translate into effective blood pressure reduction with an improved safety profile, particularly a lower risk of hyperkalemia and hormonal side effects compared to older steroidal MRAs.

The Phase IIb BLOCK-CKD trial provided initial validation for this hypothesis, demonstrating statistically significant reductions in systolic blood pressure and an absence of severe hyperkalemia, albeit with a dose-dependent increase in milder forms of hyperkalemia. These positive results were sufficiently compelling to attract a $1.3 billion acquisition by Novo Nordisk, a major pharmaceutical company seeking to expand its cardiorenal pipeline.

However, the trajectory of Ocedurenone took a decisive negative turn with the premature termination of the pivotal Phase III CLARION-CKD trial. The trial was halted after an interim analysis concluded it met prespecified futility criteria, failing to achieve its primary endpoint of systolic blood pressure reduction at 12 weeks. This failure led Novo Nordisk to completely discontinue the Ocedurenone development program and incur a substantial financial impairment loss of approximately $816.5 - $821 million.

The story of Ocedurenone is further complicated by the subsequent litigation initiated by Novo Nordisk against KBP Biosciences. Allegations of data misrepresentation and concealment of negative clinical trial data by KBP, if substantiated, would reframe the narrative from a standard late-stage drug development failure to one involving potential breaches of scientific and commercial integrity. These legal proceedings are ongoing.

Several critical points emerge from the Ocedurenone experience:

1. The Challenge of Translating Phase II to Phase III Success: Despite promising Phase IIb results, Ocedurenone failed to replicate its efficacy in Phase III. This underscores the inherent uncertainties and high attrition rates in late-stage drug development, even for mechanisms with strong biological plausibility.
2. The Persistent Issue of MRA-Induced Hyperkalemia: While Ocedurenone aimed to mitigate hyperkalemia, the Phase IIb data still showed a dose-dependent increase in its incidence. Managing this risk effectively while demonstrating superior or comparable efficacy remains a key challenge for all MRAs, especially in vulnerable CKD populations. The conflicting reports on hyperkalemia-related discontinuations in Phase IIb also highlight the complexities in interpreting safety signals from mid-stage trials.
3. Financial Risks and Due Diligence in Pharmaceutical Acquisitions: The significant financial write-down by Novo Nordisk highlights the immense costs associated with late-stage failures. The ensuing lawsuit also brings into sharp focus the critical importance of comprehensive and transparent due diligence processes in pharmaceutical mergers and acquisitions, particularly concerning the integrity and completeness of clinical trial data.
4. Information Gaps from Terminated Trials: The lack of publicly available detailed efficacy and safety data from the terminated CLARION-CKD trial limits a full scientific understanding of Ocedurenone's performance and the precise reasons for its failure beyond the top-line SBP endpoint.

In conclusion, Ocedurenone's journey from a promising therapeutic candidate for a significant unmet medical need to a discontinued program embroiled in legal disputes serves as a salient case study in the complexities, risks, and potential pitfalls of pharmaceutical innovation and commercialization. While its therapeutic promise ultimately remained unfulfilled, the lessons learned from its development and the subsequent events will likely inform future endeavors in the cardiorenal field and in the broader landscape of drug development and acquisition.

Works cited

1. Ocedurenone - Novo Nordisk - AdisInsight - Springer, accessed May 27, 2025, https://adisinsight.springer.com/drugs/800041173
2. Novo Nordisk to Buy Hypertension Treatment from KBP Biosciences - CHEManager, accessed May 27, 2025, https://chemanager-online.com/en/news/novo-nordisk-to-buy-hypertension-treatment-from-kbp-biosciences
3. Novo Nordisk stops the ocedurenone CLARION-CKD trial and recognises impairment loss, accessed May 27, 2025, https://www.novonordisk.com/news-and-media/news-and-ir-materials/news-details.html?id=168529
4. KBP BioSciences PTE. Ltd. - Drug pipelines, Patents, Clinical trials - Patsnap Synapse, accessed May 27, 2025, https://synapse.patsnap.com/organization/63d581bded1baf86f25ded4264582a52
5. What is Ocedurenone used for? - Patsnap Synapse, accessed May 27, 2025, https://synapse.patsnap.com/article/what-is-ocedurenone-used-for
6. Novo Nordisk Drops Ocedurenone After Trial Failure and Financial ..., accessed May 27, 2025, https://www.docwirenews.com/post/novo-nordisk-drops-ocedurenone-after-trial-failure-and-financial-losses
7. Ocedurenone: A Novel Therapy for Uncontrolled Hypertension in Advanced Chronic Kidney Disease - European Medical Journal - EMJ, accessed May 27, 2025, https://www.emjreviews.com/nephrology/article/ocedurenone-a-novel-therapy-for-uncontrolled-hypertension-in-advanced-chronic-kidney-disease-j190123/
8. An evaluation of KBP-5074 in advanced chronic kidney disease with uncontrolled hypertension - PubMed, accessed May 27, 2025, https://pubmed.ncbi.nlm.nih.gov/34595995/
9. Novo Nordisk to acquire ocedurenone for uncontrolled hypertension from KBP Biosciences, accessed May 27, 2025, https://www.globenewswire.com/news-release/2023/10/16/2760508/0/en/Novo-Nordisk-to-acquire-ocedurenone-for-uncontrolled-hypertension-from-KBP-Biosciences.html
10. Evidence for the use of a nonsteroidal mineralocorticoid receptor antagonist for the treatment of chronic kidney disease - Nefrología, accessed May 27, 2025, https://www.revistanefrologia.com/index.php?p=revista&tipo=pdf-simple&pii=S2013251425000355&r=498
11. Ocedurenone (KBP-5074) Featured at ASN Kidney Week: Ocedurenone is a Potential New Treatment Option for Patients with Uncontrolled or Resistant Hypertension and Advanced CKD - PR Newswire, accessed May 27, 2025, https://www.prnewswire.com/news-releases/ocedurenone-kbp-5074-featured-at-asn-kidney-week-ocedurenone-is-a-potential-new-treatment-option-for-patients-with-uncontrolled-or-resistant-hypertension-and-advanced-ckd-301715194.html
12. Non-Steroidal Mineralocorticoid Receptor Antagonists: A Paradigm Shift in the Management of Diabetic Nephropathy | Kidney and Blood Pressure Research | Karger Publishers, accessed May 27, 2025, https://karger.com/kbr/article/doi/10.1159/000545286/923844/Non-steroidal-mineralocorticoid-receptor
13. Ocedurenone (KBP-5074) Featured at ASN Kidney Week: Ocedurenone is a Potential New Treatment Option for Patients with Uncontrolled or Resistant Hypertension and Advanced CKD - BioSpace, accessed May 27, 2025, https://www.biospace.com/ocedurenone-kbp-5074-featured-at-asn-kidney-week-ocedurenone-is-a-potential-new-treatment-option-for-patients-with-uncontrolled-or-resistant-hypertension-and-advanced-ckd
14. Effect of KBP-5074 on Blood Pressure in Advanced Chronic Kidney Disease: Results of the BLOCK-CKD Study | Hypertension - American Heart Association Journals, accessed May 27, 2025, https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.121.17073
15. Pharmacokinetics of the Novel Nonsteroidal Mineralocorticoid ..., accessed May 27, 2025, https://pubmed.ncbi.nlm.nih.gov/38329646/
16. Ocedurenone (KBP-5074) | CAS 1359969-24-6 - AbMole BioScience, accessed May 27, 2025, https://www.abmole.com/products/ocedurenone.html
17. Cardiovascular and emerging therapy areas | Novo Nordisk, accessed May 27, 2025, https://www.novonordisk.com/content/dam/nncorp/global/en/investors/irmaterial/cmd/2024/P7-Cardiovascular-and-Emerging-Therapy-Areas.pdf
18. Efficacy and Safety of Ocedurenone: Subgroup Analysis of the BLOCK-CKD Study - PMC, accessed May 27, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC10570658/
19. BLOCK-CKD Trial - Primary Aldosteronism Foundation, accessed May 27, 2025, https://primaryaldosteronism.org/publication/block-ckd-trial/
20. KBP Biosciences, accessed May 27, 2025, https://www.kbpbiosciences.com/
21. Pharma News | AZs, SELLAS, BMS, MimiVax, Novo Nordisk - DelveInsight, accessed May 27, 2025, https://www.delveinsight.com/blog/pharma-news-for-sellas-bms-mimivax
22. Novo Nordisk stops the ocedurenone CLARION-CKD trial and recognises impairment loss, accessed May 27, 2025, https://www.globenewswire.com/news-release/2024/06/26/2904671/0/en/Novo-Nordisk-stops-the-ocedurenone-CLARION-CKD-trial-and-recognises-impairment-loss.html
23. Novo Nordisk Sues KBP Biosciences Over Alleged Data Misrepresentation in $1.3 Billion Hypertension Drug Deal - AInvest, accessed May 27, 2025, https://www.ainvest.com/news/novo-nordisk-sues-kbp-biosciences-alleged-data-misrepresentation-1-3-billion-hypertension-drug-deal-2502/
24. When licensing deals go bad - Novo sues KBP Bio for $830m - pharmaphorum, accessed May 27, 2025, https://pharmaphorum.com/news/when-licensing-deals-go-bad-novo-sues-kbp-bio-830m
25. Novo Nordisk's ocedurenone Phase III flop costs company $816m - Clinical Trials Arena, accessed May 27, 2025, https://www.clinicaltrialsarena.com/news/novo-nordisk-ocedurenone-flop-816m/
26. Novo Nordisk discards $1.3B kidney drug in wake of phase 3 fail, accessed May 27, 2025, https://www.fiercebiotech.com/biotech/novo-nordisk-discards-kidney-disease-drug-13b-deal-wake-phase-3-fail
27. KBP to Contest Injunction Obtained by Novo Nordisk - PR Newswire, accessed May 27, 2025, https://www.prnewswire.com/apac/news-releases/kbp-to-contest-injunction-obtained-by-novo-nordisk-302388115.html
28. Document 1 - file: caq22024.htm - SEC.gov, accessed May 27, 2025, https://www.sec.gov/Archives/edgar/data/353278/000162828024035364/caq22024.htm
29. Orphan Drug Designation Archives - Page 2 of 3 - DelveInsight, accessed May 27, 2025, https://www.delveinsight.com/blog/tag/orphan-drug-designation/page/2
30. Ocedurenone - Drug Targets, Indications, Patents - Patsnap Synapse, accessed May 27, 2025, https://synapse.patsnap.com/drug/23212eeb60db49f588969dbb88e47686
31. Novo Nordisk A/S v. KBP Biosciences Pte Ltd [2025] SGHC (I) 3 – A Handy Tool in One's Arsenal - Daily Jus, accessed May 27, 2025, https://dailyjus.com/world/2025/05/novo-nordisk-a-s-v-kbp-biosciences-pte-ltd-2025-sghc-i-3-a-handy-tool-in-ones-arsenal
32. An evaluation of KBP-5074 in advanced chronic kidney disease with uncontrolled hypertension - Taylor & Francis Online, accessed May 27, 2025, https://www.tandfonline.com/doi/abs/10.1080/13543784.2021.1985462
33. Impact of P‐gp activity on predicted PK parameters and drug–drug... - ResearchGate, accessed May 27, 2025, https://www.researchgate.net/figure/Impact-of-P-gp-activity-on-predicted-PK-parameters-and-drug-drug-interactions-a-and-b_fig1_355883634
34. New Pharmacologic Therapies for Hypertension on the Horizon in - Kidney News Online, accessed May 27, 2025, https://www.kidneynews.org/view/journals/kidney-news/16/10/11/article-p18_7.xml