Senior Researcher, Fundación de Investigación del Hospital de la Princesa in Madrid, since June. My role is to support research projects and provide technical and scientific advice in other functions of the Clinical Pharmacology Service, such as: expert reports on drugs, bioequivalences ...
Previous experience: In the 12 years working in the pharmaceutical industry, I have held various positions, from head of research and development of generic drugs, different positions in medical and training departments, to being the head of a business unit, reporting directly from the departments of marketing, sales, and medical, and with reporting international projection.
Therapeutic areas:Experience in: Phase I clinical trials in healthy volunteers and patients: pharmacokinetics, pharmacodynamics, dose-ranging, bioequivalence, more than 80 studies that was performed starting in 1997; Phase II and III clinical trials in: Women´s health, hormones and drugs for fertility treatments, pharmacogeneti
EDUCATION
Degree in Biology Science 1996, Masters in Clinical Trial Monitoring 2000, Doctor of Medicine -pHd (area of Pharmacology) 2003, and Master in Fertility and Embryology.
RESEARCH INTERESTS
Farmacogenetic, Drug Clinical Trials, Bioequivalence
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Scopus Publications
Scopus Publications
Genomic and Sex Contributions to Interindividual Variability in Pitavastatin Bioavailability Eva González‐Iglesias, Sofía Moreno‐Pérez de Villar, Dolores Ochoa, Manuel Román, Jesús Novalbos, Samuel Martín‐Vilchez, Alejandro de Miguel, Francisco Abad‐Santos Basic and Clinical Pharmacology and Toxicology, 2026 Aim This study investigates pharmacogenetic determinants of pitavastatin disposition using a candidate‐gene approach. Methods In 48 healthy volunteers, 138 variants across 40 genes involved in drug metabolism and transport were analysed to assess their relationship with pitavastatin pharmacokinetics, alongside the influence of sex and biogeographical origin. Results Women exhibited 35% higher AUC and C max values than men; however, these differences disappeared after adjusting for the dose/weight (DW) ratio, with only a 22% increase in t 1/2 remaining. The most prominent finding was the 50%–65% increase in AUC/DW and C max /DW observed in decreased function (DF) individuals compared with increased function (IF) and normal function (NF) carriers of SLCO1B1 phenotype, reinforcing its role as the primary hepatic uptake transporter for pitavastatin. Additional variants in efflux transporters such as ABCB1 , ABCC3 and ABCG2 may also contribute to interindividual variability, albeit to a lesser extent. Among drug‐metabolising enzymes, CYP4F2 emerged as a candidate for further investigation, given the 36% reduction in AUC 48h /DW associated with the rs3093200 variant. No significant associations were detected for CYP2D6 or CYP2C9 genes. Evidence to date does not indicate a meaningful impact of UGT enzymes on pitavastatin pharmacokinetics. Conclusion Overall, these findings highlight several genetic factors that may modulate pitavastatin disposition, warranting confirmation through functional studies or larger population cohorts.
Impact of CYP and ABCB1 Polymorphisms on Bortezomib-Induced Adverse Events in Multiple Myeloma Antonio Sanz-Solas, Noelia Pérez-Gómez, Jorge Labrador, Beatriz Cuevas, María Victoria Cuevas, Francisco Javier Díaz-Gálvez, Gerardo Hermida, Rodolfo Álvarez-Nuño, Gonzalo Benzo, Cristina Alonso-Madrigal, María González-Oter, Natalia García-Sancha, Raquel Vinuesa, Andrea Rodríguez-Lopez, Jesús Novalbos, Natalia Busto, Raquel Alcaraz, Francisco Abad-Santos, Miriam Saiz-Rodríguez Biomedicines, 2026 Purpose: Bortezomib (BTZ) is widely used in multiple myeloma (MM), but its toxicity shows marked interindividual variability. This study aimed to identify pharmacogenetic and clinical factors associated with BTZ-related adverse drug reactions (ADRs). Methods: A retrospective and prospective observational study was conducted in 127 MM patients treated with BTZ-based regimens. Polymorphisms in CYP enzymes and ABCB1 were genotyped using qPCR. Associations between genetic variants, treatment response, and ADRs were assessed using univariate and multivariate analyses with Benjamini–Hochberg correction. Results: ADRs occurred in 98.4% of patients, most commonly gastrointestinal toxicity (49%), general toxicity (46%), and peripheral neuropathy (39%). Women showed higher rates of gastrointestinal toxicity and non-peripheral neurotoxicity. Multivariate analysis identified the ABCB1 C1236T A/G genotype as protective against gastrointestinal toxicity, while the CYP3A4 intermediate metabolizer phenotype was associated with increased psychiatric toxicity. TP53 mutations were independently associated with hematologic and renal toxicity. Kaplan–Meier analysis showed earlier onset of peripheral neuropathy and respiratory toxicity in CYP3A4 intermediate and poor metabolizers. Conclusions: Genetic variation in ABCB1 and CYP3A4, together with clinical factors such as TP53 mutation and sex, may contribute to interindividual variability in BTZ safety in MM. These findings should be considered exploratory given the sample size and require confirmation in larger cohorts. Nonetheless, they suggest a potential role for pharmacogenomics in supporting future approaches to treatment personalization.
An Overview of Endometriosis and Potential Pharmacogenetic Targets Noelia Pérez-Gómez, María Ángeles Martínez-Zamora, Francisco Carmona, Jesús Novalbos, Francisco Abad-Santos, Dora Koller, Miriam Saiz-Rodríguez Pharmaceutical Research, 2026 Background Endometriosis is a chronic inflammatory disease characterized by the presence of endometrial-like tissue outside the uterine cavity. It affects approximately 10–15% of women of reproductive age globally and is characterized by heterogeneous symptoms with chronic pelvic pain, dysmenorrhea, and infertility being the most common. Although pharmacological treatments are available to manage its symptoms, many women either do not respond to these therapies or experience adverse drug reactions (ADRs) that outweigh the original symptoms of endometriosis. Rationale/Objectives The aim of this review is to provide a comprehensive overview of endometriosis and to identify pharmacogenetic markers that might influence drug response in its treatment and management. Outcomes Current research highlights a critical gap in pharmacogenetic biomarkers for endometriosis treatment, limiting the potential for personalized therapeutic strategies. Wider Implications Integrative multi-omics approaches combining genetic, inflammatory, and hormonal profiles may enhance patient stratification and optimize individualized care.
Apixaban kinetics could be influenced by sex, cytochrome P450 enzymes and SLC6A2 transporter Eva González-Iglesias, Dolores Ochoa, Houwaida Abbes, Gonzalo Villapalos-García, Manuel Román, Sergio Luquero, Samuel Martín-Vilchez, Jesús Novalbos, y Francisco Abad-Santos Biomedicine and Pharmacotherapy, 2025 Apixaban is an oral anticoagulant that directly inhibit the coagulation pathway by binding to factor Xa, making it the best alternative to vitamin K inhibitors. Currently, there are no pharmacogenetic markers related to its kinetics or safety, so the objective of this study was to carry out a candidate gene study that would allow us to study 118 variants in 36 genes related to drug transport or metabolism and thus expand the existing knowledge on the pharmacogenetics of apixaban. This study included 75 healthy volunteers from three apixaban bioequivalence trials conducted at the Clinical Trials Unit of Hospital Universitario de La Princesa (UECHUP). DNA was genotyped using a ThermoFisher OpenArray of our own design. An increase in C max/ DW (dose/weight adjusted) was observed in women ( p = 0.048). No significant differences were observed based on biogeographic origin or clinical trial. An increase in t 1/2 was observed in carriers of the ABCC2 rs2273697 variant ( p = 0.031), an increase in T max in carriers of rs72552763 of SLC22A1 ( p = 0.028) and a decrease in both AUC and C max /DW in carriers of the SLC6A2 rs3785143 variant ( p = 0.020, p = 0.029, p = 0.002, respectively). Of these, only the decrease in C max /DW associated with the SLC6A2 gene was maintained in the multivariate analysis ( p multivariate(mv) = 0.027). An increase in C max /DW was observed in carriers of rs2740574 variant in CYP3A4 ( p = 0.040) and in poor metabolizers of CYP3A5 ( p = 0.022, p mv =0.027). Carriers of the rs3093200 variant in CYP4F2 showed a decrease in C max /DW ( p = 0.049, p mv =0.020). Further studies are needed to understand the involvement of these genes in apixaban kinetics. • Analysis of 118 variants in 36 genes in relation to the kinetics of apixaban. • Women show an 11 % increase in C max /DW (dose/weight adjusted) compared to men. • Poor metabolizers for CYP3A5 show a 14 % increase in C max /DW. • Carriers of SLC6A2 rs3785143 variant show a slight decrease in AUC and Cmax.
Genetic Polymorphisms in Psoriasis: Investigating Genetic Variations for Precise Profiling of Response to Brodalumab in Real-Life Clinical Practice B. Butrón-Bris, M. Llamas-Velasco, S. Armesto, A. Sahuquillo-Torralba, J. Pujol-Montcusí, R. Ruiz-Villaverde, A. Martínez-López, P. de la Cueva, A. Romero-Maté, G. Roustan, E. Vilarrasa-Rull, M. Ferrán-Farrés, M.C. Ovejero-Benito, C. Palomar-Moreno, M. Navares, J. Novalbos, F. Abad-Santos, E. Daudén, H. de la Fuente Actas Dermo Sifiliograficas, 2025 Numerous studies have investigated the association that exists between genetic variants and the efficacy profile of biologic therapies for the management of psoriasis. However, as far as we know, data on this association for brodalumab are lacking in the currently available scientific literature. To analyze the association of 180 polymorphisms with an optimal response to brodalumab in real-world clinical practice. A total of 119 patients with plaque psoriasis on a 24-regimen of brodalumab recruited from 11 Spanish hospitals were genotyped for 180 polymorphisms. Optimal response was evaluated as absolute (PASI) ≤ 1 at 6 and 12 months. Polymorphisms with false discovery rates < 0.25 were included in a multiple regression model. A total of 68% and 62% of patients achieved PASI ≤ 1 at 6 and 12 months, respectively. Patient weight, history of biological therapy, disease-modifying anti-rheumatic drugs, and psoriatic arthritis were identified as risk factors for failing to achieve PASI ≤ 1. At 12 months, polymorphisms rs495337 (SPATA2), rs6311 (HTR2A), and rs4085613 (LCE3D) were associated with achieving a PASI ≤ 1 regardless of previous use of biologics and DMARDs, psoriatic arthritis, or weight. The genotypes CT-TT for rs6311 (HTR2A) and GT for rs4085613 (LCE3D) were identified as risk factors for lack of optimal response at 12 months, while genotypes AG-AA for rs495337 (SPATA2) increase the probability of response. No polymorphism was associated to brodalumab response at 6 months. This study identified genetic variations associated with the ability to achieve an optimal response to brodalumab, providing potential insights into its efficacy profile for treating plaque psoriasis. No existen estudios sobre el uso de polimorfismos en psoriasis para predecir la respuesta a brodalumab. Analizar la relación de 180 polimorfismos con una respuesta óptima a brodalumab en práctica clínica real. Se incluyeron pacientes con psoriasis en placas tratados con brodalumab durante al menos 24 semanas. Se genotiparon 180 polimorfismos de genes relacionados con la inmunopatogenia de la psoriasis. La respuesta óptima (PASI absoluto ≤ 1) al tratamiento se evaluó a los 6 y 12 meses. En el análisis multivariante se incluyeron los polimorfismos con False Discovery Rate ≤ 0,25. El estudio incluyó 119 pacientes; el 68% y el 62% alcanzaron un PASI ≤ 1 a los 6 y a los 12 meses, respectivamente. Se identificaron como factores de riesgo para no lograr un PASI ≤ 1: el uso previo de biológicos y fármacos antirreumáticos modificadores de la enfermedad, diagnóstico de artritis psoriásica y el peso. El análisis de asociación a los 12 meses reveló que los polimorfismos rs495337 (SPATA), rs6311 (HTR2A) y rs4085613 (LCE3D) se asocian con alcanzar un PASI ≤ 1 independientemente del uso previo de biológicos, artritis psoriásica o el peso. Los genotipos CT-TT para rs6311 y GT para rs4085613 fueron identificados como factores de riesgo para alcanzar PASI ≤ 1, mientras que AG-AA para rs495337 aumentaron la probabilidad de lograr respuesta óptima. Ningún polimorfismo se asoció con la respuesta a los 6 meses. Este estudio identificó variaciones genéticas que podrían predecir la respuesta a brodalumab, permitiendo optimizar su uso en el tratamiento de la psoriasis.
The pharmacogenetics of rosuvastatin and implications for treatment: a systematic review Eva González-Iglesias, Jesús Novalbos, Francisco Abad-Santos Pharmacogenomics, 2025 INTRODUCTION: genes. However, there are many other genes whose variation may also affect the treatment. OBJECTIVE: parameters; efficacy, by reduction in lipid levels and carotid intima-media thickness; and safety of rosuvastatin, by the occurrence of adverse events. METHODS: A search of the published literature was conducted in PubMed using the term "rosuvastatin AND pharmacogenetics" (PROSPERO code: CRD420251041953). RESULTS: A total of 37 articles were included, investigating 40 genes. CONCLUSIONS: with efficacy. There are also positive results for other genes that should be studied further to confirm their association with rosuvastatin.
Effect of Genetic Variants on Rosuvastatin Pharmacokinetics in Healthy Volunteers: Involvement of ABCG2, SLCO1B1 and NAT2 Eva González-Iglesias, Clara Méndez-Ponce, Dolores Ochoa, Manuel Román, Gina Mejía-Abril, Samuel Martín-Vilchez, Alejandro de Miguel, Antía Gómez-Fernández, Andrea Rodríguez-Lopez, Paula Soria-Chacartegui, Francisco Abad-Santos, Jesús Novalbos International Journal of Molecular Sciences, 2025 Statins are the primary drugs used to prevent cardiovascular disease by inhibiting the HMG-CoA reductase, an enzyme crucial for the synthesis of LDL cholesterol in the liver. A significant number of patients experience adverse drug reactions (ADRs), particularly musculoskeletal problems, which can affect adherence to treatment. Recent clinical guidelines, such as those from the Clinical Pharmacogenetics Implementation Consortium (CPIC) in 2022, recommend adjusting rosuvastatin doses based on genetic variations in the ABCG2 and SLCO1B1 genes to minimize ADRs and improve treatment efficacy. Despite these adjustments, some patients still experience ADRs. So, we performed a candidate gene study to better understand the pharmacogenetics of rosuvastatin. This study included 119 healthy volunteers who participated in three bioequivalence trials of rosuvastatin alone or in combination with ezetimibe at the Clinical Trials Unit of the Hospital Universitario de La Princesa (UECHUP). Participants were genotyped using a custom OpenArray from ThermoFisher that assessed 124 variants in 38 genes associated with drug metabolism and transport. No significant differences were observed according to sex or biogeographic origin. A significant increase in t1/2 (pmultivariate(pmv) = 0.013) was observed in the rosuvastatin plus ezetimibe trial compared with the rosuvastatin alone trials. Genetic analysis showed that decreased (DF) and poor function (PF) volunteers for the ABCG2 transporter had higher AUC∞/DW (adjusted dose/weight), AUC72h/DW and Cmax/DW compared to normal function (NF) volunteers (pmv< 0.001). DF and PF volunteers for SLCO1B1 showed an increase in AUC72h/DW (pmv = 0.020) compared to increased (IF) and NF individuals. Results for ABCG2 and SLCO1B1 were consistent with the existing literature. In addition, AUC∞/DW, AUC72h/DW and Cmax/DW were increased in intermediate (IA) and poor (PA) NAT2 acetylators (pmv = 0.001, pmv< 0.001, pmv< 0.001, respectively) compared to rapid acetylators (RA), which could be associated through a secondary pathway that was previously unknown.
Pharmacogenetic biomarkers for secukinumab response in psoriasis patients in real-life clinical practice E. Muñoz‐Aceituno, B. Butrón‐Bris, M. C. Ovejero‐Benito, A. Sahuquillo‐Torralba, O. Baniandrés Rodríguez, E. Herrera‐Acosta, R. Rivera‐Diaz, M. Ferran, J. L. Sánchez‐Carazo, J. Riera‐Monroig, J. Pujol‐Montcusí, D. Vidal, P. de la Cueva, M. García‐Bustinduy, R. Ruiz‐Villaverde, F. Ballescà, M. Llamas‐Velasco, M. Navares, I. Palomar‐Moreno, I. Sánchez‐García, J. García‐Martínez, J. Novalbos, P. Zubiaur, F. Abad‐Santos, E. Daudén‐Tello, H. de la Fuente Journal of the European Academy of Dermatology and Venereology, 2024 BackgroundPrediction of the response to a biological treatment in psoriasis patients would allow efficient treatment allocation.ObjectiveTo identify polymorphisms associated with secukinumab response in psoriasis patients in a daily practice setting.MethodsWe studied 180 SNPs in patients with moderate‐to‐severe plaque psoriasis recruited from 15 Spanish hospitals. Treatment effectiveness was evaluated by absolute PASI ≤3 and ≤1 at 6 and 12 months. Individuals were genotyped using a custom Taqman array. Multiple logistic regression models were generated. Sensitivity, specificity and area under the curve (AUC) were analysed.ResultsA total of 173 patients were studied at 6 months, (67% achieved absolute PASI ≤ 3 and 65% PASI ≤ 1) and 162 at 12 months (75% achieved absolute PASI ≤ 3 and 64% PASI ≤ 1). Multivariable analysis showed the association of different sets of SNPs with the response to secukinumab. The model of absolute PASI≤3 at 6 months showed best values of sensitivity and specificity. Four SNPs were associated with the capability of achieving absolute PASI ≤ 3 at 6 months. rs1801274 (FCGR2A), rs2431697 (miR‐146a) and rs10484554 (HLCw6) were identified as risk factors for failure to achieve absolute PASI≤3, while rs1051738 (PDE4A) was protective. AUC including these genotypes, weight of patients and history of biological therapy was 0.88 (95% CI 0.83–0.94), with a sensitivity of 48.6% and specificity of 95.7% to discriminate between both phenotypes.ConclusionWe have identified a series of polymorphisms associated with the response to secukinumab capable of predicting the potential response/non‐response to this drug in patients with plaque psoriasis.
Genetic polymorphisms to identify patients with an optimal response to tildrakizumab in psoriasis patients from real-life clinical practice B. Butrón‐Bris, M. Llamas‐Velasco, M. C. Ovejero‐Benito, J. Santos‐Juanes, A. Martínez‐López, R. Ruiz‐Villaverde, G. Roustan, O. Baniandrés, R. Izu‐Belloso, P. de la Cueva, A. Sahuquillo‐Torralba, A. Gónzalez‐Quesada, E. Vilarrasa‐Rull, J. Pujol‐Montcusí, J. García‐Martínez, M. Navares, I. Palomar‐Moreno, J. Novalbos, F. Abad‐Santos, E. Daudén, H. de la Fuente Experimental Dermatology, 2024 Detecting the association of genetic variants to the response of biological therapy represents an important advance in developing a personalized therapy. The aim of this work was to study the association of polymorphisms with an optimal response to tildrakizumab in patients with psoriasis in a real‐life clinical practice. Ninety patients with plaque psoriasis recruited from—Spanish hospitals receiving tildrakizumab for at least 24 weeks were genotyped for 180 polymorphisms. Optimal response to tildrakizumab was evaluated by absolute PASI ≤1 at 6 and 12 months. Polymorphisms corrected for weight and disease duration with an FDR <0.15 were included in a multiple regression model. Sixty three percent of patients achieved an absolute PASI ≤1 at 6 months, while 71% did so after 12 months. Disease duration (>27 years) and weight (>76 kg) were associated with treatment response; after correcting by these factors, no association (FDR >0.15) was found for any polymorphism and response to tildrakizumab at 6 months. The analysis at 12 months identified the genotype GG for rs610604 (TNFAIP3), CT for rs9373839 (ATG5), and delCTGT/delCTGT for rs72167053 (PDE4D) as risk factors to not achieve an optimal response (PASI ≤1), while CT for rs708567 (IL17RC) was protective, independently of weight and disease duration (FDR <0.15). The final multivariable model at 12 months showed an AUC of 0.90 (95% CI 0.82 to −0.98). We identified a set of polymorphisms that could be helpful to identify psoriatic patients with an optimal response to tildrakizumab at 12 months in real‐world practice conditions.
Meta-analysis of clarithromycin compared to other antibiotics for the treatment of lower respiratory tract infections Revista Espanola De Quimioterapia, 2003
Meta-analysis of clarithromycin compared with other antimicrobial drugs in the treatment of upper respiratory tract infections Revista Espanola De Quimioterapia, 2003
Regulation of bronchial tone in chronic obstructive pulmonary disease (COPD): Role of muscarinic receptors Anales De Medicina Interna, 2003