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NCT Number: NCT07748975

Decode the Environment Variation of Targeted Aldosterone Inducer and siLencer

Clinical outcome to identify and analyze the epigenetic, phenotypic, protein variation, metabolites of CYP450 Family 11 Subfamily B, both 1 and 2, human-associated aldosterone protein release, and signaling inhibitory pathways post-aldosterone-mineralocorticoid interaction.

We will include clinical studies (RCTs, cohort, case-control/series/report) from fresh human specimens. We will exclude animal studies, studies generated from cell culture, and aldosterone synthesis.

To systematically review and synthesize the literature on the main 2 questions Question 1: Which environment induces CYP11B1 or CYP11B2 activation causing hyperaldosteronemia in hypertension patients? Question 2: Which intracellular signal silences aldosterone-MR activity? For Individual Participant Data Meta-analysis, data will be extracted from final analysis articles from the framework of the data selection process only; the effect measurement and multi-variable model meta-analysis will be performed.

Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure.

Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone

Secondary Objective 2:

Sub-group analysis effect measurement following;

* Proposed mechanisms, biological markers, or pathways that contribute to failure to regulate aldosteronemia * Treatment-related permanent normotensive post-hyperaldosteronemia. Primary Objective 2: Identify possible intracellular signal inhibit aldosterone action * Analyze possible mechanisms of signal that are silent aldosterone-MR activity * Differentiation of free aldosterone and attached aldosterone

Secondary Objective 2:

● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone

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Key information

Age range

18 year–100 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

About this study

Primary Objective1: to identify CYP450 Family 11 Subfamily B and Aldosterone in hypertension patients following; By structure ● Evidence confirms Epigenetic profile of CYP450 Family 11 Subfamily B, Aldosterone, Signal in hypertension patients, both random and treated from any DNA sequencing method Protein synthesis evidence of aldosterone protein induces hypertension from Western blot or LC-MS By function Metabolomic profile: the substrate or product refers to aldosterone interaction causing end-organ cell line dysfunction or impaired structure.

Inhibitory signaling profiling of hypertension patients compared to non-hypertension patients, which negatively feedback to CYP450 Family 11 Subfamily B or Aldosterone

Secondary Objective 2:

Sub-group analysis effect measurement following;

  • Proposed mechanisms, biological markers, or pathways that contribute to failure to regulate aldosteronemia
  • Treatment-related permanent normotensive post-hyperaldosteronemia. Primary Objective 2: Identify possible intracellular signal inhibit aldosterone action
  • Analyze possible mechanisms of signal that are silent aldosterone-MR activity
  • Differentiation of free aldosterone and attached aldosterone

Secondary Objective 2:

● Sensitivity and specificity of outcomes of hypertension patients who underwent estimate substrate associated aldosterone circulation Plasma CYP450 Family 11 Subfamily B Urine CYP450 Family 11 Subfamily B Plasma Aldosterone (active form) Plasma Aldosterone (metabolite form) Urine Aldosterone Axin-CK1-GSK3-APC-Beta-catenin complex

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Human birth in all sex chromosomes; evidence of systemic arterial hypertension, both treated and untreated.
  • Evidence of living with owned systemic/arterial hypertension by one of the following;
  • Quantitative: Blood pressure number higher than the normal range by each protocol in mmHg unit in any arm of study.
  • Qualitative: Clarify whether both retrospective, observational, or intervention study of blood pressure, and clearly clarify the number of hypertension participants in the article.

Exclusion criteria

  • Under 18 years old
  • Specimens of studies not from humans or human specimens but not from an actual living hypertension patient, such as cell culture, in vitro synthesis from laboratory synthesis
  • No evidence of hypertension in the main study
  • Study of imaging confirms adrenal tumor in all types of histopathology results.

Treatment and study plan

Aldosterone circulation

Diagnostic Test

Evidence of synthesis of aldosterone and/or degradation of inactive forms of aldosterone, which focuses on

  • CYP450 Family 11 Subfamily B
  • Aldosterone protein
  • Beta-catenin
  • Axin-CK1-GSK3-APC complex

medication

Drug

Medical treatment that interferes with free aldosterone levels and reports systolic blood pressure deviation

Operation

Procedure

The non-medical intervention includes MIS, Open surgery, and intravascular guide treatment aim to treat hypetension and lower aldosterone level.

Primary outcomes

  1. Aldosterone circulation profile

    Time frame: 12 months

    The result, both qualitative and quantitative, from aldosterone synthesis to degradation and elimination via urine.

  2. Aldoseterone synthesis profile

    Time frame: 12 months

    Focus on both quantitative and qualitative evidence of aldosterone, CYP11B1, andand CYP11B2 protein

Secondary outcomes

  1. Degradation Profile

    Time frame: 12 months

    Focus on the ratio of degradation activity of the inactive form of aldosterone and the inhibitory competitor inhibits the cell product from the aldosterone-mineralocorticoid receptor. Axin-CK1-GSK3-APC complex profile is indicated

Study contacts

Contact information is provided by the study sponsor or research team.

Nathaphong Dejthida, Medical Degree

CONTACT

[email protected]

+66819220662

Sponsors and collaborators

Lead sponsor

DejthidaNathaphong

Other

Registry information

Acronym: DETAIL

Important dates

Study start
2026
Primary completion
2027
Study completion
2028
First posted
Aug 6, 2026
Registry last updated
Aug 6, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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