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acebutolol + HCTZ (Sectral Plus / Secadrex / acebutolol + HCTZ)

✓ Approved

Sanofi S.A · ADRB1 · Small Molecule

What is acebutolol + HCTZ?

acebutolol + HCTZ is a small molecule developed by Sanofi S.A. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesSectral Plus, Secadrex, acebutolol + HCTZ
CompanySanofi S.A
Drug ClassSmall Molecule
Molecular TargetADRB1, SLC12A3
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Sanofi S.A

Mechanism of Action

Molecular Targets

acebutolol + HCTZ acts on 2 molecular targets:

ADRB1adrenoceptor beta 1 (B1AR, RHR)
SLC12A3solute carrier family 12 member 3 (NCCT, NCC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

acebutolol + HCTZ is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedLuminescence : the journal of biological and chemical luminescence2026-08-24

Micellar Enhanced Second Derivative Spectrofluorimetric Determination of Hydrochlorothiazide, Amlodipine, and Telmisartan in Fixed Dose Combination and Spiked Human Plasma.

Yenduri Suvarna S, H Shashank S, K Naga Prashant NP

A very sensitive and eco-friendly second-derivative spectrofluorimetric method was developed for simultaneous analysis of hydrochlorothiazide (HCTZ), amlodipine besylate (AML), and telmisartan (TEL) in pharmaceutical products and human plasma. Native fluorescence of HCTZ (λex267/λem295 nm), AML (λex362/λem415 nm), and TEL (λex292/λem369 nm) was used together with fluorescence enhancement achieved through sodium lauryl sulfate micelles at optimum excitation/emission wavelengths for all other analytes being analyzed. Overlap of spectroscopic data was able to be resolved through second-derivative spectrofluorimetry without prior separation. Method validation was performed according to ICH Q2(R1) guidelines; results showed excellent linearity (R2 > 0.999) across a concentration range of 3-18, 2-10, and 10-50 ng/mL for HCTZ, AML, and TEL, respectively. Accuracy, precision and robustness were demonstrated with %RSD values below two. Application of the method to pharmaceutical product and spiked plasma samples gave satisfactory recoveries with minimal matrix interference. Assessment of method greenness was conducted using AGREE Prep, MoGAPI, AGSA, SAMI, Ma Tool, CACI, and WECA metrics, all of which indicate superior environmental sustainability. The proposed method is simple, fast, low-cost, ultra-sensitive, and suitable for routine quality control and/or bioanalytical analysis.

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PubMedFrontiers in pharmacology2026-08-06

Drug-associated psoriasis: a pharmacovigilance study based on the FAERS database.

Yi Sha S, Liu Aimei A, Huoshen Wuda W, Xia Dengmei D et al.

Drug-induced psoriasis has been increasingly recognized, but the spectrum of potential triggering medications remains incompletely characterized. We aimed to identify the drugs potentially associated with psoriasis using a large-scale and real-world pharmacovigilance analysis. Firstly, disproportionality analyses were used to detect psoriasis-related drug signals. Furthermore, Multivariable logistic regression and Bayesian shrinkage models were applied to evaluate the consistency of the detected associations after adjustment for available demographic and reporting-related factors. Finally, stratified analyses by sex, age, and reporter type were conducted to assess signal robustness. A total of 30 drugs showed significant associations with psoriasis. These signals involved several pharmacological categories, including anti-infective agents (e.g., Abacavir, Fluconazole, Moxifloxacin, Sulfamethoxazole), anti-inflammatory and immunomodulatory drugs (e.g., Celecoxib, Tofacitinib), cardiovascular agents (e.g., Acebutolol, Telmisartan, Clonidine), neuropsychiatric drugs (e.g., Nortriptyline, Temazepam, Zopiclone, Wellbutrin), hormonal agents (e.g., Progesterone, Prometrium), and respiratory medications (e.g., Ventolin). Bayesian correction generally attenuated extreme effect estimates but confirmed the robustness of most signals. The stratified analysis also approve the above results. Our findings suggest that multiple drug classes are associated with psoriasis signals in pharmacovigilance data. These results highlight the importance of early recognition of drug-associated psoriasis and may assist clinicians in medication review and risk stratification in routine practice.

PMID 42558881
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PubMedPharmacogenomics2026-07-31

Association of ACE I/D polymorphism with blood pressure response to valsartan-hydrochlorothiazide combination therapy in hypertensive patients from Khyber Pakhtunkhwa, Pakistan.

Ullah Aftab A, Rahim Abdur A, Jan Asif A, Khan Muhammad M et al.

Interindividual variability in antihypertensive response may be partly explained by genetic variation. The angiotensin-converting enzyme insertion/deletion polymorphism (ACE I/D; rs1799752) has been associated with variable response to renin-angiotensin-aldosterone system-targeting therapies, but evidence for valsartan-hydrochlorothiazide (Val-HCTZ) combination therapy remains limited, particularly in South Asian populations. In this multicenter prospective cohort study, 645 hypertensive patients from Khyber Pakhtunkhwa, Pakistan, receiving fixed-dose Val-HCTZ were enrolled; 627 were included in the final analysis after excluding 18 patients with poor adherence (<80%) followed for 3 months. ACE I/D genotyping was performed by polymerase chain reaction with confirmatory testing. The primary analysis evaluated blood pressure reduction across ACE I/D genotypes using regression models adjusted for age, sex, and body mass index. Achievement of target blood pressure (<140/90 mmHg) was analyzed as a secondary outcome. Genotype distribution was in Hardy-Weinberg equilibrium (p = 0.171). Blood pressure reduction differed across genotypes, with the most favorable response observed in DD carriers, an intermediate response in II carriers, and the least favorable response in ID carriers. In the primary analysis of continuous blood pressure reduction, ID carriers showed significantly less reduction compared to II carriers (ΔSBP: adjusted β = -11.2, 95% CI: -16.8 to -5.6, p = 0.002; ΔDBP: adjusted β = -7.4, 95% CI: -11.9 to -2.9, p = 0.004). DD carriers showed greater observed reduction compared to II carriers, but this was not statistically significant (ΔSBP: adjusted β =  +1.8, 95% CI: -4.2 to +7.8, p = 0.561; ΔDBP: adjusted β =  +0.5, 95% CI: -4.1 to +5.1, p = 0.823). In the secondary analysis, response rates were 90.6% for DD, 75.8% for II, and 40.8% for ID. ACE I/D genotype was associated with variation in blood pressure response to fixed-dose Val-HCTZ therapy in this Pakistani cohort, with the most robust finding being poorer response among ID carriers. These findings support further investigation of ACE I/D as a candidate pharmacogenetic marker in genotype-stratified and interventional studies.

PMID 42535691
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PubMedClinical and experimental hypertension (New York, N.Y. : 1993)2026-07-15

Does hydrochlorothiazide-associated hyponatremia in hypertensive individuals have a genetic origin?

Ozkan Gulsum G, Celik Caner C, Tozkir Hilmi H, Asıkovali Semih S et al.

Hyponatremia is one of the most common electrolyte disorders in clinical practice and is frequently observed following thiazide use. Advanced age and female gender are implicated in the etiology of hydrochlorothiazide (HCTZ)-associated hyponatremia. There has also recently been mention of a genetic disposition. This study evaluated the genetic component, and particularly the clinical significance, of variants in the SLC12A3 gene in the development of hyponatremia in hypertensive patients using HCTZ-group diuretics. Ninety-five patients presenting to the Tekirdağ Namık Kemal University nephrology clinic and receiving antihypertensive therapy including HCTZ for at least one month were examined. Peripheral blood specimens were collected from hyponatremic (n = 62) and non-hyponatremic (n = 33) individuals. Variants in the SLC12A3 gene were analyzed using next generation sequencing and were compared with the clinical data. A total of 947 variants were detected in the SLC12A3 gene, the majority of which were classified as of uncertain significance. Hyponatremia was determined at a higher rate in patients with c.506-276A>G (75.00%), c.282+492G>A (85.70%), c.282+499G>C (87.00%), c.282+495G>A (85.00%), and c.505+375G>A (92.30%) variants in particular. The risk of hyponatremia development increased 9.2-fold in the presence of the c.282+492G>A variant (OR = 9.243; 95% CI: 2.259-37.818; p = 0.002). In conclusion, we think that HCTZ-associated hyponatremia cannot be predicted by clinical and biochemical parameters alone, and that genetic factors should also be considered. Further multi-center prospective studies involving larger populations will clarify the clinical significance of variants in SLC12A3 and other genes and will make a significant contribution to individualized therapeutic approaches.

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PubMedSheng wu gong cheng xue bao = Chinese journal of biotechnology2026-06-25

[Mining of ancestral lipases and enzymatic synthesis of amides].

Zhang Xinxin X, Xu Guochao G

The amide bond plays a crucial role in the synthesis of proteins, pharmaceuticals, and agrochemicals. It is particularly significant in the pharmaceutical field as a key structural unit in many drugs, such as afatinib (an anticancer drug), teriflunomide (used for multiple sclerosis treatment), acebutolol (used for hypertension and arrhythmia treatment), and paracetamol (an antipyretic and analgesic agent). However, chemical synthesis methods usually require harsh reaction conditions (e.g., high temperature, high pressure, or strongly acidic or alkaline environments) and are often accompanied by high energy consumption and environmental pollution issues. In contrast, enzymatic synthesis of amides has attracted widespread attention due to its mild conditions and environmental friendliness. To mine ancestral lipases with high activity and stability and investigate their enzymatic properties, thus achieving efficient enzymatic synthesis of amide bond-containing compounds. Ancestral lipases were screened based on a gene mining strategy employing ancestral sequence reconstruction (ASR), followed by characterization of their enzymatic properties and construction of an enzymatic reaction system for synthesis of the amide bond. Ancestral enzymes ASR-1 and ASR-7 with higher thermal stability were obtained. Substrate spectrum characterization revealed that ASR-1 preferentially catalyzed the synthesis of aromatic amides, while ASR-6 favored the synthesis of aliphatic amides. ASR-1 was purified via nickel-affinity chromatography and characterized for its enzymatic properties, showing an optimal reaction pH in Tris-HCl 7.5 and an optimal reaction temperature of 40 °C. The reaction conditions for amide synthesis were systematically optimized as 10 mg/mL wet cells, water content ≤10% (V/V), n-dodecane as solvent, 20 mmol/L amine substrate, and 10 mmol/L acyl donor. In addition, the enzyme exhibited good tolerance to nonpolar solvents, achieving an amide yield of 73.25%. This study provides a novel strategy for developing efficient and stable enzymatic processes for amide synthesis, demonstrating the promising application potential of ancestral lipases in green biomanufacturing.

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PubMedCombinatorial chemistry & high throughput screening2026-06-24

Exploring the Therapeutic Potential of Plantaginis Herba in Treating Salt-Sensitive Hypertension-Induced Renal Injury: Network Pharmacology Analysis and Experimental Verification.

Zhong Ya Y, Sha Zhongxin Z, Hu Jinxin J, Zhang Jie J et al.

Plantaginis Herba (PH) is a traditional Chinese herb with broad pharmacological effects and has been used to treat hypertension. Salt-sensitive hypertension (SS-HT) is characterized by elevated blood pressure due to a high-salt diet and sodium intake. This study investigates the role and molecular mechanisms of PH in SS-HT-induced renal injury using network pharmacology and in vivo experiments. The components of PH and potential therapeutic targets were identified through network pharmacology. The protein-protein interaction (PPI) network and Herb-CompoundsTargets-Disease-Pathway network were established. GO and KEGG enrichment analyses were performed using DAVID and bioinformatics tools. Active compounds were determined by ultraperformance liquid chromatography- tandem mass spectrometry (UPLC-MS/MS). A SS-HT model was established using male Dahl/SS rats given a high-salt diet, and then treated with lowand high-dose PH, as well as hydrochlorothiazide (HCTZ), upon which kidney injury, urine sodium metabolism-related factors, and PI3K/AKT/Nedd4-2/γ-ENaC pathway-related proteins levels were assessed using histopathological staining, ELISA, and Western blotting. Ninety-nine overlapping genes were identified between PH and SS-HT, with AKT1 highlighted as a hub target in the PPI network. The contents of dinatin, baicalin, baicalein, 6-OHluteolin, β-sitosterol, and stigmasterol in the PH extracts were 1.880, 2.973, 0.210, 1.797, 385.400, and 38.320 ng/mg, respectively. KEGG identified the PI3K-Akt signaling pathway as a core signaling pathway. In vivo experiments showed that PH could improve blood pressure and urinary sodium metabolism, ameliorate kidney histopathological injury, and inhibit apoptosis. Furthermore, PH increased p-PI3K/PI3K, p-AKT/AKT, and Nedd4-2 expression while inhibiting γ-ENaC expression, thereby improving kidney injury and sodium excretion function in SS-HT rats. PH contains multiple bioactive compounds and exerts its effects through multiple targets and pathways, effectively alleviating SS-HT and ameliorating pathological kidney damage, with an efficacy comparable to that of hydrochlorothiazide. PH improves urinary sodium metabolism and mitigates renal injury in SS-HT rats via the PI3K/AKT/Nedd4-2/γ-ENaC pathway. Although PH demonstrates potential as a therapeutic agent for SS-HT, the key functional components in PH and the mechanism by which Nedd4-2 participates in the degradation of γENaC remain to be further studied. PH ameliorates SS-HT-induced renal injury by regulating sodium metabolism and renal function, and by activating the PI3K/AKT/Nedd4-2/γ-ENaC pathway.

PMID 42337900
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