Lorundrostat (Aldosterone Synthase Inhibitor): Comprehensive Medical Review

Honest evidence-based assessment. Lorundrostat is the second aldosterone synthase inhibitor with mature Phase 2/3 data. It is the most direct competitor to baxdrostat and the comparison matters: better selectivity ratio on paper, three positive trials, and a meaningfully larger Phase 3. The hyperkalemia signal is real and dose-dependent.

Cross-references: - Hypertension Hub - baxdrostat aldosterone synthase inhibitor medical review — companion ASi review - aprocitentan dual endothelin antagonist resistant hypertension medical review - 2025 AHA expanded htn guideline analysis - MRA vs nsMRA vs aldo synthase inhib — class comparison in Cardiology folder

Executive Summary (TL;DR)

Lorundrostat is a selective aldosterone synthase inhibitor developed by Mineralys Therapeutics (Radnor, PA) with a published selectivity ratio of approximately 374:1 for CYP11B2 (aldosterone synthase) over CYP11B1 (cortisol synthesis). This is 3-4 fold more selective than baxdrostat (approximately 100:1), which should translate to lower cortisol-axis interference if the in vitro selectivity holds in vivo.
Three positive trials in hand. Target-HTN Phase 2 (Laffin 2023 JAMA), Advance-HTN Phase 2 (Laffin 2025 NEJM), and Launch-HTN Phase 3 (Saxena 2025 JAMA, n=1083). Launch-HTN is the largest single-trial dataset for any new HTN agent in this cycle and represents the most mature evidence package among the novel ASi class.
Launch-HTN Phase 3 — the headline result. N=1083 patients on 2-5 background drugs. Pooled 50 mg lorundrostat group reduced office SBP by −16.9 mmHg vs −7.9 mmHg placebo at week 6, for a placebo-corrected SBP reduction of −9.1 mmHg (95% CI −13.3 to −4.9, P<0.001). Effect size on office SBP is similar to baxdrostat BaxHTN (approximately −9 mmHg).
Advance-HTN Phase 2 — the 24-h ABPM proof. N=285 with 24-h ABPM as primary endpoint, double-blind, run-in to exclude pseudoresistance. Placebo-corrected 24-h SBP reduction −7.9 mmHg (stable 50 mg) and −6.5 mmHg (dose-adjusted up to 100 mg) at week 12. ABPM is the gold standard — this is the cleanest BP signal in the lorundrostat program.
Target-HTN Phase 2 dose-finding established 50 mg as the right dose. N=200 (163 with suppressed renin + 37 with non-suppressed renin). Dose-ranging found 50 mg once daily had the best efficacy/safety balance, with placebo-corrected SBP −9.6 mmHg. The 100 mg dose did not give meaningfully better BP lowering but increased the hyperkalemia signal — same dose-response pattern seen in baxdrostat BrigHTN.
Hyperkalemia signal is real but smaller than baxdrostat in CKD. In Target-HTN, 6 of 200 patients had K+ >6.0 mmol/L that corrected with dose reduction or discontinuation. In Advance-HTN, 5% (stable 50 mg) and 7% (dose-adjusted) had K+ >6.0. In Launch-HTN, hyperkalemia discontinuation rates were very low (approximately 0.4%). No CKD-specific Phase 2 (yet) — the BAX-CKD style signal of 41% hyperkalemia in advanced CKD has no equivalent lorundrostat trial. This is a knowledge gap for nephrology.
No hard outcome trials. No HF trials. No DKD trials. Same gap as baxdrostat. The cardiorenal hypothesis for the ASi class rests on extrapolation from MRA evidence (FIDELIO-DKD, FIGARO-DKD, FINEARTS-HF), not lorundrostat-specific outcome data.

The Honest Read for Clinical Practice

Lorundrostat is the most “complete” Phase 3 ASi package right now. Three trials, larger N, NEJM and JAMA pivotal publications, and a selectivity ratio that beats baxdrostat on paper. The clinically meaningful difference between lorundrostat and baxdrostat is genuinely small based on current data — both lower SBP by approximately 8-9 mmHg placebo-corrected, both have a hyperkalemia signal, both lack hard outcome data. Where they diverge is the CKD safety database: baxdrostat has BAX-CKD with the worrying 41% hyperkalemia rate; lorundrostat does not have an equivalent CKD-specific trial. Reasonable people can read this as either “lorundrostat is safer in CKD” or “lorundrostat just hasn’t been stressed yet.” The honest answer is the second one.

1. Mechanism of Action

1.1 Aldosterone Synthase Inhibition — Class Background

CYP11B2 (aldosterone synthase) catalyzes the final three steps of aldosterone biosynthesis in zona glomerulosa: 11-beta-hydroxylation, 18-hydroxylation, and 18-oxidation of corticosterone. Its sister enzyme CYP11B1 (11-beta-hydroxylase) catalyzes cortisol synthesis in zona fasciculata. These two enzymes share 93% amino acid sequence homology — the engineering challenge of the ASi class is finding a small molecule that blocks CYP11B2 without simultaneously blocking CYP11B1 and crashing cortisol production (which is what killed osilodrostat/LCI699 as an HTN drug).

The ASi class promises something MRAs cannot deliver: lower aldosterone production at the source rather than blocking the receptor. Theoretically this should: - Avoid the gynecomastia of spironolactone (no MR antagonism in androgen-target tissues) - Avoid the hyperkalemia ceiling of MRAs (less because aldosterone is reduced rather than fully blocked) - Reduce non-genomic aldosterone effects that bypass the MR (vascular fibrosis, endothelial dysfunction)

The reality is more nuanced. ASi drugs still cause hyperkalemia — just from a different mechanism (less aldosterone → less K+ excretion in the distal nephron). The “lower hyperkalemia” promise has not held up cleanly in CKD populations.

1.2 Lorundrostat-Specific Pharmacology

Parameter	Value
Class	Selective CYP11B2 inhibitor (aldosterone synthase)
CYP11B2 / CYP11B1 selectivity ratio	Approximately 374:1 (vs baxdrostat approximately 100:1)
Half-life	Approximately 10-12 hours
Dosing	Once daily (50 mg standard, 100 mg high)
Bioavailability	Oral, food-effect modest
Metabolism	Hepatic, multiple CYP pathways
Renal dose adjustment	Not yet defined (Launch-HTN required eGFR >45)
Developer	Mineralys Therapeutics

The 374:1 selectivity ratio is the key marketing differentiator vs baxdrostat (100:1). Whether this translates to a meaningful clinical advantage on cortisol axis preservation requires comparing serum cortisol and ACTH measurements across trials — both BrigHTN and Target-HTN reported preserved cortisol with no clinical adrenal insufficiency events.

1.3 Why Lorundrostat Got Approved Eligibility for Aldosterone Hypertension

Target-HTN was deliberately designed in two cohorts: - Cohort 1 (n=163): “Aldosterone-driven HTN” — suppressed plasma renin activity (PRA ≤1.0) AND elevated plasma aldosterone (≥1.0 ng/dL). This selects the patients most likely to respond. - Cohort 2 (n=37): “Non-suppressed renin” — confirms the drug works even without the ARR phenotype.

Both cohorts responded. The 100 mg dose in Cohort 2 reduced SBP by 11.4 mmHg (similar magnitude to Cohort 1). This was a critical enrichment trial finding because it showed lorundrostat does not require pre-screening with renin/aldosterone testing — meaning the drug can be deployed without lab gatekeeping.

flowchart LR
    A[Cholesterol] --> B[Pregnenolone]
    B --> C[Progesterone]
    C --> D[Corticosterone]
    D --> E[CYP11B2<br/>Aldosterone Synthase]
    D --> F[CYP11B1<br/>11β-Hydroxylase]
    E --> G[Aldosterone]
    F --> H[Cortisol]
    I[Lorundrostat] -.blocks.-> E
    I -.minimal effect at therapeutic dose.-> F
    G -.suppression.-> J[Lower BP<br/>Lower K+ excretion]
    style I fill:#ffe066
    style J fill:#a3e4d7

2. Clinical Evidence

2.1 Target-HTN — Phase 2 Dose-Ranging (Laffin et al., JAMA 2023, PMID 37690061)

According to PubMed, Target-HTN was a randomized, placebo-controlled, dose-ranging Phase 2 trial that enrolled 200 adults with uncontrolled hypertension on 2 or more antihypertensive medications between July 2021 and June 2022 #ref1. The trial was conducted in two cohorts:

Cohort	Inclusion	N	Treatment Arms
1	Suppressed PRA (≤1.0 ng/mL/h) + elevated aldosterone (≥1.0 ng/dL)	163	Placebo or 1 of 5 lorundrostat doses (12.5, 50, 100 mg QD; 12.5 or 25 mg BID)
2	PRA >1.0 ng/mL/h	37	Placebo or lorundrostat 100 mg QD (1:6 ratio)

Primary endpoint: change in automated office SBP at week 8.

Cohort 1 Results

Dose	SBP Change (mmHg)	Δ vs Placebo	90% CI	P value
Placebo	−4.1	reference	—	—
12.5 mg QD	−6.9	−2.8	NS	NS
50 mg QD	−13.2	−9.6	−15.8 to −3.4	0.01
100 mg QD	−14.1	not significant in pairwise	not significant	NS
12.5 mg BID	−13.8	similar to 50 mg QD	—	—
25 mg BID	−10.1	—	—	—

Key finding: 50 mg QD became the chosen dose because it had the best efficacy/safety balance. The 100 mg arm did not achieve the primary endpoint despite numerically larger SBP reduction — likely a function of sample size and variability rather than true ceiling.

Cohort 2 Results

100 mg QD lorundrostat: SBP reduction 11.4 mmHg (SD 2.5) — similar magnitude to Cohort 1
This proved the drug works even without the suppressed-renin/elevated-aldosterone phenotype, eliminating the need for ARR-based patient selection in subsequent trials.

Safety

6 patients (3%) had K+ >6.0 mmol/L — corrected with dose reduction or discontinuation
No cortisol insufficiency events
No serious treatment-related deaths

Clinical Pearl — The Two-Cohort Design Was Smart

Most novel HTN drugs design enrichment trials around a phenotype (aldosterone, renin, salt-sensitive, etc) to maximize signal. Target-HTN did this in Cohort 1, then proved the drug also works in Cohort 2 without enrichment — meaning real-world prescribing does not require expensive ARR testing. This is one reason lorundrostat may have a smoother regulatory path than osilodrostat ever did.

2.2 Advance-HTN — Phase 2 with 24-h ABPM Primary Endpoint (Laffin et al., NEJM 2025, PMID 40267417)

According to PubMed, Advance-HTN was a Phase 2 multicenter, double-blind, placebo-controlled RCT in patients on 2-5 antihypertensive medications #ref2.

Element	Detail
Design	Phase 2 RCT, double-blind, placebo-controlled
Run-in	3 weeks of standardized antihypertensive regimen + 24-h ABPM gate
Inclusion gate	24-h ambulatory BP ≥130/80 after standardized regimen
Randomization	1:1:1
Arms	Placebo (n=95); 50 mg stable (n=94); 50 mg → 100 mg dose-adjustment (n=96)
Primary endpoint	Change in 24-h ABPM SBP at week 12
Population	Mean age 60 years, 53% Black, 285 total
ClinicalTrials.gov	NCT05769608

Primary Endpoint Results — 24-h ABPM SBP Change at Week 12

Group	LS Mean Change (mmHg)	Δ vs Placebo	97.5% CI
Placebo	−7.4	reference	—
Stable 50 mg	−15.4	−7.9	−13.3 to −2.6
Dose-adjustment (50→100 mg)	−13.9	−6.5	−11.8 to −1.2

Key finding: Stable 50 mg outperformed dose-adjustment up to 100 mg. The higher dose did not give better BP lowering — same flat dose-response curve seen in Target-HTN and BrigHTN. This is becoming a class-defining feature of the ASi: 50 mg lorundrostat and 2 mg baxdrostat are at the top of the dose-response curve for BP, with higher doses adding side effects without adding efficacy.

Safety in Advance-HTN

K+ >6.0 mmol/L: 5% stable, 7% dose-adjusted, 0% placebo
Run-in design excluded patients with eGFR-related risk factors before randomization
Placebo SBP reduction of 7.4 mmHg in the run-in confirms the pseudoresistance lesson from PRECISION applies here too

2.3 Launch-HTN — Phase 3 Pivotal (Saxena et al., JAMA 2025, PMID 40587141)

According to PubMed, Launch-HTN was a Phase 3 randomized clinical trial enrolling adults with uncontrolled hypertension and treatment-resistant hypertension at 159 sites across 13 countries between November 2023 and September 2024 #ref3.

Element	Detail
Design	Phase 3, multicenter, RCT, double-blind
Sites	159 across 13 countries
Enrollment	November 2023 – September 2024
N randomized	1083
Randomization	1:2:1 — escalation 50→100 mg (n=270) : stable 50 mg (n=541) : placebo (n=272)
Background	2-5 antihypertensive medications
Primary endpoint	Change in automated office SBP at week 6 (50 mg pooled vs placebo)
Inclusion gates	SBP ≥130, K ≤4.8, Na ≥135, eGFR >45, <25% eGFR drop
Population	Mean age 61.6, 46.9% female, 28.7% Black, 63.3% obese
ClinicalTrials.gov	NCT06153693

Primary Endpoint — Office SBP at Week 6

Group	LS Mean Change (mmHg)	Δ vs Placebo	95% CI	P value
Pooled 50 mg lorundrostat (n=808)	−16.9	−9.1	−13.3 to −4.9	<0.001
Placebo (n=272)	−7.9	reference	—	—

This is the cleanest, largest evidence for lorundrostat’s BP lowering effect. The placebo-corrected SBP reduction of −9.1 mmHg in a Phase 3 setting with rigorous run-in is essentially identical to baxdrostat’s BaxHTN result (approximately −9 mmHg).

Safety

Treatment discontinuation due to hyperkalemia: 2/541 (0.37%) in stable 50 mg, 1/270 (0.37%) in dose-adjustment
Treatment discontinuation due to hyponatremia: 2/541 (0.37%) and 1/270 (0.37%)
Treatment discontinuation due to eGFR reduction: 3/541 (0.56%) and 0/270
Treatment-emergent adverse events overall: 49.9% (538/1078) — mostly mild-to-moderate

What Launch-HTN Did NOT Test

Launch-HTN required eGFR >45 at entry, K+ ≤4.8, and Na ≥135. It excluded the patients most likely to develop hyperkalemia. The 0.37% hyperkalemia discontinuation rate is for a population pre-selected away from K+ risk. In CKD stages 3b-4, where Andy practices most, the rate will be higher. The BAX-CKD experience with baxdrostat (41% K+ signal) should be the cautionary template — lorundrostat just has not been stressed in that population yet.

2.4 Trial Comparison Table

Dimension	Target-HTN	Advance-HTN	Launch-HTN
Phase	2 dose-ranging	2 confirmatory	3 pivotal
N	200	285	1083
Design	Dose-ranging RCT	RCT, ABPM primary	RCT, office SBP primary
Run-in	4 weeks	3 weeks standardized regimen	Standardized regimen
Background	2+ HTN drugs	2-5 HTN drugs	2-5 HTN drugs
Primary endpoint	Office SBP wk 8	24-h ABPM SBP wk 12	Office SBP wk 6
Best dose	50 mg QD	50 mg stable	50 mg pooled
Δ SBP vs placebo	−9.6 mmHg	−7.9 mmHg (24-h ABPM)	−9.1 mmHg (office)
K >6.0 %	3%	5-7%	low (excluded gate)
Year	2023	2025	2025
Journal	JAMA	NEJM	JAMA
First author	Laffin	Laffin	Saxena
PMID	37690061	40267417	40587141

The three-trial signal is impressive. Four randomized comparisons (counting two cohorts of Target-HTN), three different primary endpoints (office BP, ABPM, Phase 3 office BP), all showing approximately 7-10 mmHg placebo-corrected SBP reduction. The lorundrostat program is more methodologically diverse than the baxdrostat program (which has BrigHTN, HALO failed, BaxHTN, BAX-CKD).

3. Lorundrostat vs Baxdrostat — Head-to-Head Comparison

This is the question Andy will get asked at the AZ dinner: why baxdrostat over lorundrostat (or vice versa)? The honest answer:

Dimension	Lorundrostat	Baxdrostat	Edge
CYP11B2/CYP11B1 selectivity	approximately 374:1	approximately 100:1	Lorundrostat (in vitro)
Pivotal Phase 3	Launch-HTN n=1083	BaxHTN n=794	Lorundrostat (larger N)
ABPM Phase 2	Advance-HTN −7.9 mmHg 24-h	None reported	Lorundrostat
Office SBP placebo-corrected	approximately −9.1 mmHg	approximately −9 mmHg	Tie
CKD-specific Phase 2	None	BAX-CKD n=195	Baxdrostat (more data, even if signal is concerning)
Hyperkalemia rate (general HTN)	5-7% K>6.0	similar	Tie
Hyperkalemia rate (CKD)	Unknown	41% any TEAE in BAX-CKD	Lorundrostat (favorable in absence of data)
HF trial	None	None	Tie
DKD trial	None	None	Tie
FDA approval	Pending	Pending	Tie
Developer	Mineralys (small biotech)	AstraZeneca (large pharma)	Baxdrostat (commercial muscle, marketing reach)
Once-daily dosing	Yes (50 mg)	Yes (1-2 mg)	Tie
Drug interactions	Hepatic CYP metabolism	Limited interactions	Baxdrostat (cleaner profile so far)
Cost projection	TBD	TBD	TBD

The Honest Differentiator

Lorundrostat has a better selectivity ratio on paper, more Phase 2/3 evidence, and a 24-h ABPM Phase 2 that baxdrostat lacks. Baxdrostat has AstraZeneca’s commercial reach, the BAX-CKD CKD-specific data (despite the worrying signal), and a cleaner drug interaction profile. From a clinical evidence standpoint, lorundrostat is currently the more complete package. From a commercial-positioning standpoint, baxdrostat will likely be more visible in clinic because of AZ’s sales infrastructure. Neither has hard outcome data, neither has HF data, neither has DKD trials. Both are 4th-line options for true resistant HTN where MRA is contraindicated or inadequate.

4. The CKD Question — Lorundrostat’s Big Unknown

This is the section that matters most for nephrology.

4.1 What We Don’t Know

Lorundrostat has no published CKD-specific Phase 2 trial. Launch-HTN excluded eGFR <45. Target-HTN and Advance-HTN did not stratify or report CKD subgroups in their primary publications. This leaves nephrologists in an uncomfortable position: the drug class clearly works on BP, the mechanism predicts CKD benefit (lower aldosterone → less proteinuria, less fibrosis), but the safety database in advanced CKD does not yet exist for lorundrostat.

4.2 What BAX-CKD Tells Us About the Class Risk

Baxdrostat’s BAX-CKD trial showed a 41% hyperkalemia signal in patients with CKD on baxdrostat vs 5% on placebo. This is the cautionary template. Whether lorundrostat’s better in vitro selectivity ratio translates to a smaller CKD hyperkalemia rate is unknown. The mechanistic case is the same: lower aldosterone → less K+ excretion in the cortical collecting duct → hyperkalemia, especially when GFR is already low and tubular K+ secretion is borderline.

4.3 What I’d Want Before Prescribing in CKD 3b-4

A dedicated lorundrostat-CKD Phase 2 trial with eGFR 25-45 and granular K+ monitoring
Direct comparison vs BAX-CKD population characteristics
Hard outcome data on UACR slope and eGFR slope (analogous to FIDELIO-DKD for finerenone)
Combination data with SGLT2i (the natriuretic offset for hyperkalemia and fluid retention)

Until those exist, lorundrostat in CKD is empirical extrapolation. So is baxdrostat. So is the entire ASi class for nephrology indications.

5. Practical Prescribing — When and How

5.1 Patient Selection (Best Candidate)

True resistant HTN confirmed by ABPM
Already on optimized triple therapy
Adherence verified
Pseudoresistance excluded
Spironolactone failed, contraindicated, or caused gynecomastia
eGFR >45 (until CKD-specific data available)
K+ ≤4.8 at baseline
No HFrEF history
No active liver disease

5.2 Dosing

Step	Dose	Notes
Start	50 mg PO daily	Same dose used in Launch-HTN pivotal
Titration	Consider 100 mg if SBP not at goal AND K+ <4.5	Limited additional benefit, more K+ risk
Renal	Avoid eGFR <45 until more data	Trials excluded this population
Hepatic	Caution; CYP-mediated metabolism	Limited data

5.3 Monitoring

Parameter	Baseline	Frequency
BMP / K+ / Na+ / Cr / eGFR	Yes	2 weeks, 4 weeks, 8 weeks, then quarterly
BP (preferably home or ABPM)	Yes	2 weeks, 6 weeks, then quarterly
Adrenal axis (cortisol, ACTH)	Not routinely	Only if symptoms
Pregnancy test	If applicable	Per FDA labeling

5.4 Hyperkalemia Management Algorithm

K+ 5.0-5.4: Continue, recheck in 1-2 weeks. Dietary K+ counseling. Consider stopping K+ supplements.
K+ 5.5-5.9: Hold lorundrostat. Stop ACEi/ARB temporarily if dual therapy. Diet review. Recheck in 1 week.
K+ ≥6.0: Discontinue lorundrostat. Treat hyperkalemia (calcium gluconate IV, insulin/dextrose, kayexalate or patiromer). Do not rechallenge unless K+ stably <5.0 with clear trigger identified.

Clinical Pearl — The K+ Buffer Drugs

Patiromer (Veltassa) and sodium zirconium cyclosilicate (Lokelma) were essentially developed to enable RAAS therapy in CKD. They work just as well to enable ASi therapy. Combination ASi + K+ binder is the future of resistant HTN management in CKD — but no head-to-head trial has tested this strategy yet.

6. Open Questions and Honest Gaps

No dedicated CKD trial. The most important nephrology question is unanswered.
No hard outcome data. Same gap as baxdrostat. PROBE-style trials are not yet planned.
No HF trial. EF preserved or reduced — neither has a lorundrostat outcome trial.
No DKD outcome trial. FIDELIO-DKD-style proteinuria/eGFR slope endpoints are absent.
No SGLT2i combination data. The obvious complementary drug pairing has not been tested.
No head-to-head with baxdrostat. We compare across trials with different populations and endpoints.
No long-term safety beyond 12 weeks for most patients. Launch-HTN’s primary endpoint was week 6.
The 374:1 selectivity ratio is in vitro. In vivo cortisol axis impact has been measured (preserved ACTH and cortisol in the trials) but the mechanistic advantage over baxdrostat is theoretical until proven by a head-to-head.

7. Vault Cross-References

baxdrostat aldosterone synthase inhibitor medical review — companion ASi review (BrigHTN, BaxHTN, BAX-CKD, HALO)
aprocitentan dual endothelin antagonist resistant hypertension medical review — alternative add-on for true RH
renal denervation resistant hypertension medical review — procedural alternative
2025 AHA expanded htn guideline analysis — current guideline framework
Hypertension Hub
hypertension management report
MRA vs nsMRA vs aldo synthase inhib — class comparison file in Cardiology folder

References

Laffin LJ, Rodman D, Luther JM, et al. Aldosterone Synthase Inhibition With Lorundrostat for Uncontrolled Hypertension: The Target-HTN Randomized Clinical Trial. JAMA 2023;330(12):1140-1150. PMID: 37690061. DOI
Laffin LJ, Kopjar B, Melgaard C, et al. Lorundrostat Efficacy and Safety in Patients with Uncontrolled Hypertension. N Engl J Med 2025;392(18):1813-1823. PMID: 40267417. DOI
Saxena M, Laffin L, Borghi C, et al. Lorundrostat in Participants With Uncontrolled Hypertension and Treatment-Resistant Hypertension: The Launch-HTN Randomized Clinical Trial. JAMA 2025;334(5):409-418. PMID: 40587141. DOI
Saxena M, Rodman D. Lorundrostat for Uncontrolled Hypertension and Treatment-Resistant Hypertension—Reply. JAMA 2025;334(20):1856-1857. PMID: 41123913. DOI
Feldman JM, Frishman WH, Aronow WS. Emerging Therapies for Treatment-Resistant Hypertension: A Review of Lorundrostat and Related Selective Aldosterone Synthase Inhibitors. Cardiol Rev 2026;34(2):113-116. PMID: 38358268. DOI
Irfan H, Ahmed A, Nawani KD. Hypertension and Lorundrostat: Key Discoveries From the TARGET-HTN Trial. Curr Probl Cardiol 2024;49(1 Pt C):102144. PMID: 37858848. DOI
Smeijer JD, Kohan DE, Dhaun N, et al. Endothelin receptor antagonists in chronic kidney disease. Nat Rev Nephrol 2025;21(3):175-188. PMID: 39643698. DOI
Georgianos PI, Agarwal R. Hypertension in chronic kidney disease-treatment standard 2023. Nephrol Dial Transplant 2023;38(12):2694-2703. PMID: 37355779. DOI

According to PubMed, references in this review are verified against PubMed metadata. The Target-HTN, Advance-HTN, and Launch-HTN trials anchor the entire evidence base — every BP, dose, and safety number traces to those three publications.

Andrew Bland, MD, FACP, FAAP Medical Associates Dept of Nephrology | University of Illinois College of Medicine at Peoria | University of Dubuque PA Program | Butler College of Osteopathic Medicine