Individualized pharmacotherapy: background and development

Introduction

Most drug prescriptions are still based on empiricism and not on solid biological data, which often results in considerable patient-to-patient variability and, in some cases, low patient benefits (1,2). For several widely used drugs in disease areas such as cancer, asthma, cardiology, and psychiatry, it was estimated that only 25–60% of patients derived clinically meaningful benefits from treatment (2). Over the past few decades, advancements in molecular medicine have increased our understanding of pathophysiology and drug mechanisms of action, fostering the development of different types of predictive biomarkers. These predictive biomarkers assist in predicting the effects and side effects of several drugs based on pharmacokinetic and pharmacodynamic parameters (1,3). In particular, two types of predictive biomarker tests have been integrated into the clinical setting: companion diagnostic (CDx) and pharmacogenetic (PGx) tests. Both are deemed essential for the individualization and optimization of pharmacotherapy (4).

Traditionally, pharmacotherapy has been categorized into small molecule drugs and biologics. However, within the framework of individualized pharmacotherapy, it is imperative to include advanced therapy medicinal products (ATMPs). This is a relatively new type of therapy that involves medicines based on genes, tissues, or cells designed for individualized application (5,6). This mini review aims to describe the overall development and current options for individualizing pharmacotherapy, with a primary focus on the predictive biomarkers used for therapy individualization and optimization with respect to the choice of the right drug and dosing.

Background

For centuries and even further back, healthcare providers have recognized the importance of tailoring therapies to individual patients. As early as the ancient Greek era, around the 5^th century BC, Hippocrates commented that treatment should be customized to meet the specific needs and characteristics of each patient. It was further noted that every human is unique and responds differently to treatment; therefore, applying the same treatment universally would be incorrect (7). Based on these principles, pharmacists have been engaged in compounding medications tailored to individual patients for centuries. Taking a big jump in time to the end of the 19th century, one of the fathers of modern medicine, Sir William Osler, expressed the issue of patient variability as follows: “If it were not for the great variability among individuals, medicine might as well be a science and not an art” (8). This statement expresses the need to individualize therapy, which was further outlined more than half a century later in the principles of rational use of drugs or rational pharmacotherapy (9). Here, the goal was that individual patients should receive medications appropriate to their clinical needs to optimize the benefits and minimize harm. Subsequently, these principles were translated into “the right drug for the right patient in the right dose at the right time”. In fact, the United Sates (US) Food and Drug Administration (FDA) has integrated this saying into its description of precision medicine, and on their homepage, the following is stated: “The goal of precision medicine is to target the right treatments to the right patients at the right time” (10). Consequently, one might argue that individualized pharmacotherapy was already introduced in the 1960s. However, a significant difference between then and now lies in our increased molecular understanding of the pathophysiology, including disease heterogeneity and drug mechanisms of action. This understanding has been crucial for implementing individualized pharmacotherapy and developing various predictive biomarkers to guide therapy optimization.

Individualized pharmacotherapy

Individualized pharmacotherapy can be regarded as a method of adapting drug choice and dosing to the specific biological and clinical characteristics of a single patient to meet their clinical needs. For several drugs and biologics, molecular diagnostic tools, such as CDx and PGx assays, are available to individualize therapies. However, when discussing individualized pharmacotherapy, factors such as patient preferences, age, concomitant therapy and diseases are important aspects that also must be considered when making treatment decisions.

Despite ATMPs being prepared for individual use and frequently being autologous, they form a distinct category owing to the nature of the treatment, in which predictive biomarkers have a relatively limited role. Based on this premise, various small molecule drugs and biologics can be classified into three groups according to the availability of predictive diagnostic tools, as shown in Figure 1, with ATMPs representing a distinct category of therapies. However, it is important to remember that a substantial number of small molecule drugs and biologics currently do not have an associated CDx or PGx assay, which limits the potential for therapy individualization.

Figure 1 Small molecule drugs and biologics associated with CDx and/or PGx assays, as well as ATMPs, are the major elements of individualized pharmacotherapy. ATMP, advanced therapy medicinal product; CDx, companion diagnostic; PGx, pharmacogenetic.

CDx testing

The first CDx assay developed alongside a pharmaceutical product was an immunohistochemical (IHC) assay designed to detect HER2 protein tumor expression. This assay was associated with the use of the human monoclonal antibody trastuzumab for the treatment of women with HER2 overexpressing breast cancer (11). In an article published in Science in 1987, it was reported that more than 15% of women with breast cancer had ERBB2 amplification, which was associated with poor disease prognosis. The authors proposed that the gene product, the HER2 protein, functioned as a growth factor receptor and plays a role in the pathogenesis of breast cancer. Furthermore, they suggested that the development of a specific antagonist could have significant therapeutic implications for this specific group of breast cancer patients (12). This antagonist later became trastuzumab, and when it entered clinical development, an IHC assay was developed and used to identify HER2 protein expression at the tumor level (11). In the final phase III trial, only patients with metastatic breast cancer who overexpressed the HER2 protein were enrolled. The results of the trial showed that trastuzumab combined with chemotherapy was superior to chemotherapy alone in this specific subgroup of patients with breast cancer (13). In 1998, based on results of this phase III trial, the FDA granted marketing approval for both trastuzumab and its IHC assay, HercepTest, simultaneously, underlining the need for a CDx assay to be accessible at the same time as the drug to determine patient eligibility for treatment.

The FDA defines a CDx assay as an in vitro diagnostic device or an imaging tool that provides information that is essential for the safe and effective use of a corresponding therapeutic product (14). This definition is similar to that issued by other regulatory bodies, including the European Medicines Agency (EMA) (15). In the US, there are currently more than 80 drugs and biologics linked to a CDx assay, with the vast majority being associated with targeted therapies for the treatment of hematologic and oncologic malignancies (14). All these assays are intended to aid in the identification of patients likely to respond to a specific small molecule drug or biologic agent. Before a CDx assay can be used in a clinical setting, it must undergo comprehensive analytical and clinical validation. The validation process typically occurs alongside the development of the associated drug or biologic agent to ensure simultaneous regulatory approval and availability. Over the past 15 years, CDx has evolved from mainly tissue-based single-gene assays to more advanced technologies, such as next-generation sequencing (NGS), multi-gene panels, and liquid biopsies. Currently, the dominant platform for CDx assays is polymerase chain reaction (PCR), followed by NGS, IHC, and in situ hybridization (ISH). The molecular aberrations detected by these platforms are mainly associated with various somatic mutations in genes, such as ALK, EGFR, KRAS, ERBB2, MET and RAS. These genes are crucial in the pathogenesis of several malignant tumors and encode proteins that are targets for a range of small molecule drugs and biologics. Examples of FDA-approved drugs and their associated CDx assays, including biomarker information, are listed in Table 1 (14).

PGx testing

In the second half of the last century, several studies identified a hereditary pattern of variation in the outcomes following treatment with specific drugs often used in daily clinical practice (16,17). Some patients experience a strong therapeutic effect, others encounter side effects, and some show no or minimal response (8). In 1987, as a result of molecular genetic research, CYP2D6 was identified and cloned as the first polymorphic gene involved in drug metabolism. Subsequently, other members of the CYP450 family, such as CYP2C9 and CYP2C19, and other genes involved in drug metabolism and transport, such as SLCO1B1, have been identified. The CYP450 enzymes are primarily expressed in the liver and play a central role in the oxidative biotransformation of 70–80% of all clinically used drugs (17).

Recent advancements in genomic technologies have further enhanced the development and application of PGx testing to identify the pharmacological relationship between a drug and genetic variants of the CYP450 enzymes, often referred to as the ‘drug-gene interaction’ (DGI) (16,18). Based on the DGI activity scores for metabolic activity, these are classified into five different phenotypes: ‘poor metabolizer’ (PM), ‘intermediate metabolizer’ (IM), ‘normal/extensive metabolizer’ (EM), ‘rapid metabolizer (RM), and ultra-rapid metabolizer’ (UM) (16). The same considerations also apply to the SLCO1B1 transporter, and here, PGx testing can identify whether a person has ‘normal function’ (NF), ‘intermediate function’ (IF), or ‘low function’ (LF). Regarding the SCLO1B1 transporter, increased exposure to statins has been observed in individuals with IF and LF, leading to the development of myopathy and rhabdomyolysis, particularly at high dosages (16). With respect to PGx testing, the ethno-geographic origin plays a role in the prevalence of the different genotypes and phenotypes, which varies according to the region. For example, the prevalence of the CYP2D6 PM phenotype is approximately 5.4% among Caucasians and less than 1% among Asians (3). Over the past two decades, extensive development and validation of clinical dosing guidelines for DGI have been performed for various drugs. These dosing guidelines can be assessed through ClinPGx (https://www.clinpgx.org/) and are regularly updated in accordance with the latest evidence and scientific knowledge (19). Moreover, the FDA and EMA have issued PGx-based annotations for a large number of drugs used in clinical practice by general practitioners and other medical specialties. Furthermore, these annotations are also included in the Prescribing Information for the respective drugs and biologics (19,20).

Pharmacogenomic biomarkers in drug labeling

The list compiled by the FDA contains different types of annotations included in the regulatory labeling of various therapeutic products approved in the US (20). As of April 2026, this list contained data on 678 specific genomic variants associated with 433 drugs and biologics, including information on germline and somatic gene variants, variations in gene expression, chromosomal abnormalities, and specific protein biomarkers. For example, for the antidepressant citalopram, information is available for patients with CYP2C19 PM, recommending a maximum daily dose of 20 mg, which is half the maximum dose suggested for adults with normal enzyme activity (20). Furthermore, according to the ClinPGx dosing guidelines, individuals who are CYP2C19 PM or CYP2C19 UM should consider alternative medications instead of citalopram, or if citalopram is clinically appropriate, dose alterations are recommended (19). The consumption of 28 drugs with PGx dosing guidelines for CYP2C9, CYP2C19, CYP2D6, and SLCO1B1 was measured in Scandinavian countries (16). For patients treated with citalopram, the number of users per 1,000 individuals ranged from 2.3 to 11.0. The similar numbers for atorvastatin and metoprolol were 73.6–94.7 and 50.5–55.3, respectively. This demonstrates that a relatively high number of patients taking these drugs can potentially be affected by their inherited genotypes.

For some drugs, information on multiple genomic variants is available, such as for the anticancer drug entrectinib, a multikinase inhibitor that targets TRK, ROS1, and ALK. This drug has demonstrated clinical benefits in patients with ROS1-positive metastatic non-small cell lung cancer (NSCLC) and solid tumors harboring NTRK gene fusions (21).

An example in which both CDx and PGx testing might be beneficial is with respect to the EGFR-targeting drug gefitinib, which is indicated for treating metastatic NSCLC. Gefitinib is a tyrosine kinase inhibitor that targets EGFR-activating mutations, specifically exon 19 deletions or exon 21 (L858R) substitutions. For patients who are PM of CYP2D6, treatment with gefitinib may lead to adverse drug reactions because of increased drug exposure (20). In contrast, for CYP2D6 UM, it is recommended to determine the plasma concentration of gefitinib and increase the dose if necessary (19). The gefitinib case illustrates how CDx testing for somatic mutations and PGx testing for germline variations can effectively complement each other.

ATMPs

ATMPs refer to different categories of biological products intended for human use based on genes, tissues, and cells. These therapies are designed for individual applications and can be autologous or allogeneic, with the intention of treating or preventing diseases by repairing, replacing, or regenerating human cells, tissues, or genes (22). The EMA divides ATMPs into gene therapy, somatic cell therapy, tissue-engineered medicine, and combined ATMPs. However, this term and classification are specific to Europe, whereas the FDA classifies these therapies differently in the US. Some fall under the category of “human cell, tissue, and cellular and tissue-based product” (HCT/P), while others are classified as gene therapy (23). ATMPs and HCT/Ps are primarily indicated for treating various rare diseases with significant unmet medical needs.

In 2009, the EMA approved the first ATMP for Europe, which was the tissue-engineered product ChondroCelect, indicated for the repair of single symptomatic cartilage defects of the femoral condyle of the knee (24). In the US, the first HCT/P to receive FDA approval was Provenge in 2010, an autologous cellular immunotherapy designed for the treatment of metastatic castrate-resistant prostate cancer (25). By April 2026, 31 ATMPs were approved for use in the Europe, with gene therapy medical products being the major part (26). By the end of 2025, the FDA had approved a total of 48 products in the US related to cellular and gene therapy, with gene therapy medical products again making up the majority (27).

Discussion

Patients diagnosed with the same disease often respond differently to identical pharmacological treatments. Variability in treatment outcomes is frequently associated with specific biological characteristics caused by different types of genetic aberrations, which may be of germline or somatic origin or a combination of both. In recent decades, advancements in molecular analytical and diagnostic methods have provided valuable insights into this variability. Within cancer research, there has been a growing understanding of the molecular mechanisms that drive tumorigenesis and tumor heterogeneity, insights that are crucial for the possibilities of individualizing and optimizing therapy (28). An increasing number of small molecule drugs and biologics have been designed to target specific oncogenic pathways and signaling mechanisms, and advanced molecular diagnostic methods have enabled the identification of patients who are most likely to respond. Since the turn of the century, CDx testing has been gradually incorporated into clinical practice in oncological and hematological clinics for a growing number of anticancer drugs that have been approved for clinical use. In 2025, a total of 16 new small molecule drugs and biologics for cancer treatment received regulatory approval in the US, with the majority associated with a CDx assay (29). In general, the total number of drugs associated with CDx assays has steadily increased in recent years, and currently, more than 80 small molecule drugs and biologics are linked to this type of assay. Most of these therapeutics are primarily targeted therapies for treating hematologic and oncologic malignancies, where the requirements for CDx testing are part of their regulatory approvals. In the Prescribing Information for these drugs and biologics, instructions for testing are provided in a specific section for patient selection (14). Despite the success of targeted therapies there still seems to be situations where CDx testing is underused and often not comprehensive enough. Surveys have shown that the testing rate for EGFR, ALK, and ROS1 in relation to the treatment of NSCLC ranges from 79% to 99% (30). Discussion in both the US and Europe points towards multiple factors such as inadequate access to biomarker testing, laboratory infrastructure, lack of knowledge, regulatory hurdles, costs, and insufficient reimbursement (30,31).

Similar to CDx testing, integrating PGx testing into clinical practice should be seen as a tool for optimizing and individualizing pharmacotherapy. Although the FDA and EMA have released PGx-based annotations and ClinPGx offers dosing guidelines, along with increasing awareness of the advantages of PGx testing, there are still numerous obstacles that must be overcome to ensure its widespread adoption (3,16,32). One way to do this could be as in the Netherlands, where initiatives have been undertaken to implement a PGx passport, which contains a comprehensive report of readily accessible genetic information, including variants that may influence their response to certain medications (33). The PGx passport is intended to be used by healthcare providers to guide treatment and improve patient outcomes. Documenting the clinical utility of PGx testing is important, and the large-scale PREPARE study, a controlled clinical study in nearly 7000 patients using a 12-gene PGx panel, is important in this respect. This study is part of the U-PGx project, which aims to integrate PGx testing into routine clinical practice across Europe (32,34). The results of the study, published in Lancet in 2023, showed that patients whose drug therapy was adjusted according to their genotype experienced 30% fewer serious adverse drug reactions across multiple medical specialties (32,34). A recent study investigating the distribution of CYP2C9 and CYP2C19 alleles among participants in the Danish Blood Donor Study demonstrated that the Illumina Infinium Global Screening Array may represent a valuable tool for identifying clinically relevant DGIs, in different therapeutic areas e.g. cancer, cardiovascular disease, pain management, and neurological and psychiatric disorders (35). This may further substantiate the clinical utility and broader implementation of PGx testing.

Furthermore, over the last couple of decades, the Prescribing Information and Summaries of Product Characteristics for many medicinal products now include PGx-related information. Despite these initiatives and advancements in PGx implementation, significant barriers continue to hinder the proactive use of PGx testing in routine clinical practice. The primary barriers to broader integration into clinical decision-making are largely related to the lack of education and awareness among healthcare professionals regarding both the potential and limitations of PGx testing (16,32). Despite these obstacles, there appears to be a growing interest in the clinical application of PGx testing in particular pre-emptively panel testing as demonstrated in the PREPARE study and by others (32,34).

Conclusions

In the past decades, progress in pharmacotherapy has been characterized by a shift from a traditional empirical-based treatment approach focusing on the “average patient” to a more individualized strategy. This shift has been facilitated by an increased molecular understanding, allowing tailored drug selection and dosing to meet the specific biological and clinical characteristics of individual patients. These changes have been enabled by the parallel development of molecular analytical methods, such as PCR and NGS, which have provided insights into somatic and germline genetic mutations related to disease pathophysiology and drug metabolism. This knowledge has enabled the development of different types of predictive biomarkers linked to several small molecule drugs and biologics. Despite CDx testing becoming a standard for the treatment of many oncological and hematological patients, improvements are still needed in terms of education, better access to biomarker testing, and reimbursement. Furthermore, PGx testing has provided insights into the germline genetic factors influencing drug metabolism and responses across various therapeutic areas. Although progress has been made, further efforts are needed to fully realize the potential of individualized pharmacotherapy, specifically by integrating PGx testing pre-emptively into routine clinical practice. Looking ahead, artificial intelligence presents a promising avenue for creating sophisticated algorithms capable of managing the complexities associated both with PGx and CDx.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://atm.amegroups.com/article/view/10.21037/atm-2026-0136/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-2026-0136/coif). J.T.J. serves as an unpaid editorial board member of Annals of Translational Medicine from February 2026 to December 2027. J.T.J. has served as consultant and advisory for AstraZeneca and Visiopharm as well as received royalties from Elsevier. The other author has no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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