Abiraterone
Beschreibung
Historical Development and Discovery
The historical development of this compound traces its origins to fundamental observations made by Dr. Charles Huggins in 1941, who demonstrated that surgical castration could lead to prostate cancer regression through androgen depletion, work that ultimately earned him the 1966 Nobel Prize for Physiology or Medicine. This foundational understanding established the principle that prostate cancer depends on male hormones for growth and survival, setting the stage for subsequent therapeutic interventions targeting the androgen axis.
The direct precursor to this compound development began in the early 1990s when researchers at The Institute of Cancer Research (ICR) and The Royal Marsden Hospital initiated a systematic search for more effective androgen synthesis inhibitors. The research team, led by Professor Mike Jarman, Dr. Elaine Barrie, and Professor Gerry Potter, recognized the limitations of existing treatments and sought to develop compounds that could more effectively block androgen production throughout the body. Their initial work focused on ketoconazole, an antifungal agent that had demonstrated some activity against prostate cancer through its ability to inhibit CYP17, albeit with significant limitations including low potency, poor selectivity, and concerning side effects.
The breakthrough came when Professor Potter and Dr. Barrie designed and synthesized a novel chemical entity designated CB7598, which they subsequently named this compound. This compound was specifically engineered to irreversibly block the CYP17 enzyme, preventing androgen synthesis not only in the testes and adrenal glands but also within the tumor microenvironment itself. The team filed their first patent application in 1992, followed by a second patent in 1993 covering the compound's synthesis, and published their seminal research findings in 1994.
Early preclinical studies demonstrated that this compound effectively blocked androgen synthesis in animal models and cancer cell cultures, leading to decreased hormone levels and reduced tumor growth. However, the compound's development faced significant challenges, including concerns about potential adrenal insufficiency and skepticism within the medical community about the effectiveness of androgen suppression in late-stage prostate cancer, which was then commonly referred to as "hormone-refractory" disease.
The development trajectory changed dramatically in 2003 when Professor Johann de Bono joined the ICR team with a renewed vision for this compound's potential. Professor de Bono challenged the prevailing paradigm, arguing that late-stage prostate cancer should be considered "castration-resistant" rather than "hormone-refractory," suggesting that these tumors remained dependent on androgens but had developed mechanisms to access testosterone from alternative sources. This conceptual shift, combined with emerging evidence that children born with CYP17 deficiency do not suffer from adrenal insufficiency, provided the scientific rationale for pursuing this compound's clinical development.
Structural Classification and Nomenclature
This compound belongs to the chemical class of synthetic androstane steroids and represents a sophisticated modification of the natural steroid scaffold. The compound is systematically classified as a derivative of androstadienol (androsta-5,16-dien-3β-ol), an endogenous androstane pheromone, with specific structural modifications that confer its unique pharmacological properties. The most significant structural feature is the incorporation of a pyridine ring at the C17 position, which distinguishes this compound from naturally occurring steroids and is crucial for its inhibitory activity against the CYP17 enzyme.
The complete chemical nomenclature of this compound follows IUPAC conventions as (3S,8R,9S,10R,13S,14S)-10,13-dimethyl-17-(pyridin-3-yl)-2,3,4,7,8,9,11,12,14,15-decahydro-1H-cyclopenta[a]phenanthren-3-ol. This systematic name reflects the complex three-dimensional architecture of the molecule, including the specific stereochemical configuration at multiple chiral centers that is essential for biological activity. The molecular formula C₂₄H₃₁NO indicates the presence of 24 carbon atoms, 31 hydrogen atoms, one nitrogen atom (within the pyridine ring), and one oxygen atom (the hydroxyl group at the C3β position).
In clinical practice, this compound is administered as its acetate ester, this compound acetate, which serves as a prodrug to improve oral bioavailability and stability. The acetate formulation has the molecular formula C₂₆H₃₃NO₂ and molecular weight of 391.55 Da, representing the attachment of an acetyl group to the C3β hydroxyl position. This esterification is crucial for therapeutic effectiveness, as the parent this compound molecule exhibits poor oral absorption and is susceptible to hydrolysis by esterases.
The structural relationship between this compound and its acetate ester can be represented in the following table:
| Compound | Molecular Formula | Molecular Weight (Da) | CAS Registry Number | Key Structural Features |
|---|---|---|---|---|
| This compound | C₂₄H₃₁NO | 349.51 | 154229-19-3 | Free hydroxyl at C3β position |
| This compound Acetate | C₂₆H₃₃NO₂ | 391.55 | 154229-18-2 | Acetate ester at C3β position |
The pyridine substituent at C17 represents the most innovative aspect of this compound's design, as this heterocyclic aromatic ring system provides the molecular interactions necessary for tight binding to the CYP17 enzyme active site. The nitrogen atom within the pyridine ring can coordinate with the heme iron of CYP17, resulting in irreversible enzyme inhibition. This mechanism contrasts with reversible inhibitors and provides sustained pharmacological effect even after the compound has been cleared from circulation.
Importance in Steroid Chemistry
The development of this compound has had profound implications for the field of steroid chemistry, establishing new paradigms for rational drug design and demonstrating the potential for creating highly selective enzyme inhibitors based on steroid scaffolds. The compound represents a successful example of structure-based drug design, where detailed understanding of the target enzyme's active site enabled the creation of a molecule with exquisite selectivity for CYP17 over other cytochrome P450 enzymes. This selectivity was crucial for avoiding the toxicities associated with earlier, less specific inhibitors like ketoconazole.
From a synthetic chemistry perspective, this compound has driven significant advances in steroid modification techniques and has established efficient synthetic routes that can be scaled for commercial production. The original synthesis route developed by the ICR team involved complex multi-step processes starting from prasterone acetate (dehydroepiandrosterone acetate), utilizing sophisticated coupling reactions to install the pyridine ring at the C17 position. Subsequent process improvements have focused on optimizing yields, reducing impurities, and developing more cost-effective manufacturing approaches suitable for large-scale production.
The success of this compound has validated the concept of androgen biosynthesis inhibition as a therapeutic strategy, leading to increased research interest in developing additional CYP17 inhibitors and related compounds targeting the androgen synthesis pathway. This has resulted in a new class of therapeutic agents collectively known as second-generation antiandrogens, which includes compounds like enzalutamide and apalutamide that target different aspects of androgen signaling. The mechanistic insights gained from this compound development have informed the design of these subsequent agents and have established a framework for understanding resistance mechanisms and combination therapy approaches.
The compound's clinical success has also demonstrated the value of targeting peripheral androgen synthesis rather than focusing solely on androgen receptor antagonism. This approach recognizes that castration-resistant prostate cancer often develops through mechanisms that maintain androgen signaling despite low circulating testosterone levels, including intratumoral androgen synthesis. By blocking androgen production at the source, this compound addresses this resistance mechanism and has established the therapeutic rationale for combination approaches that simultaneously target multiple components of the androgen axis.
The intellectual property landscape surrounding this compound has created substantial value for research institutions and has demonstrated the importance of early patent protection for enabling subsequent commercial development. The ICR's patent portfolio for this compound has generated significant royalty streams that have been reinvested into further cancer research, creating a sustainable model for translating academic discoveries into therapeutic benefits for patients. This success story has influenced how research institutions approach intellectual property management and technology transfer, emphasizing the importance of strategic patenting decisions in maximizing the impact of scientific discoveries.
Eigenschaften
IUPAC Name |
(3S,8R,9S,10R,13S,14S)-10,13-dimethyl-17-pyridin-3-yl-2,3,4,7,8,9,11,12,14,15-decahydro-1H-cyclopenta[a]phenanthren-3-ol |
Source
|
|---|---|---|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI |
InChI=1S/C24H31NO/c1-23-11-9-18(26)14-17(23)5-6-19-21-8-7-20(16-4-3-13-25-15-16)24(21,2)12-10-22(19)23/h3-5,7,13,15,18-19,21-22,26H,6,8-12,14H2,1-2H3/t18-,19-,21-,22-,23-,24+/m0/s1 |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
InChI Key |
GZOSMCIZMLWJML-VJLLXTKPSA-N |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Canonical SMILES |
CC12CCC(CC1=CCC3C2CCC4(C3CC=C4C5=CN=CC=C5)C)O |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Isomeric SMILES |
C[C@]12CC[C@@H](CC1=CC[C@@H]3[C@@H]2CC[C@]4([C@H]3CC=C4C5=CN=CC=C5)C)O |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
Molecular Formula |
C24H31NO |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
DSSTOX Substance ID |
DTXSID80879993 |
Source
|
| Record name | Abiraterone | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID80879993 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
Molecular Weight |
349.5 g/mol |
Source
|
| Source | PubChem | |
| URL | https://pubchem.ncbi.nlm.nih.gov | |
| Description | Data deposited in or computed by PubChem | |
CAS No. |
154229-19-3 |
Source
|
| Record name | Abiraterone | |
| Source | CAS Common Chemistry | |
| URL | https://commonchemistry.cas.org/detail?cas_rn=154229-19-3 | |
| Description | CAS Common Chemistry is an open community resource for accessing chemical information. Nearly 500,000 chemical substances from CAS REGISTRY cover areas of community interest, including common and frequently regulated chemicals, and those relevant to high school and undergraduate chemistry classes. This chemical information, curated by our expert scientists, is provided in alignment with our mission as a division of the American Chemical Society. | |
| Explanation | The data from CAS Common Chemistry is provided under a CC-BY-NC 4.0 license, unless otherwise stated. | |
| Record name | Abiraterone [INN:BAN] | |
| Source | ChemIDplus | |
| URL | https://pubchem.ncbi.nlm.nih.gov/substance/?source=chemidplus&sourceid=0154229193 | |
| Description | ChemIDplus is a free, web search system that provides access to the structure and nomenclature authority files used for the identification of chemical substances cited in National Library of Medicine (NLM) databases, including the TOXNET system. | |
| Record name | Abiraterone | |
| Source | DrugBank | |
| URL | https://www.drugbank.ca/drugs/DB05812 | |
| Description | The DrugBank database is a unique bioinformatics and cheminformatics resource that combines detailed drug (i.e. chemical, pharmacological and pharmaceutical) data with comprehensive drug target (i.e. sequence, structure, and pathway) information. | |
| Explanation | Creative Common's Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/legalcode) | |
| Record name | Abiraterone | |
| Source | EPA DSSTox | |
| URL | https://comptox.epa.gov/dashboard/DTXSID80879993 | |
| Description | DSSTox provides a high quality public chemistry resource for supporting improved predictive toxicology. | |
| Record name | (1S,2R,5S,10R,11S,15S)-2,15-dimethyl-14-(pyridin-3-yl)tetracyclo[8.7.0.0²,�.0¹¹,¹�] heptadeca-7,13-dien-5-ol | |
| Source | European Chemicals Agency (ECHA) | |
| URL | https://echa.europa.eu/information-on-chemicals | |
| Description | The European Chemicals Agency (ECHA) is an agency of the European Union which is the driving force among regulatory authorities in implementing the EU's groundbreaking chemicals legislation for the benefit of human health and the environment as well as for innovation and competitiveness. | |
| Explanation | Use of the information, documents and data from the ECHA website is subject to the terms and conditions of this Legal Notice, and subject to other binding limitations provided for under applicable law, the information, documents and data made available on the ECHA website may be reproduced, distributed and/or used, totally or in part, for non-commercial purposes provided that ECHA is acknowledged as the source: "Source: European Chemicals Agency, http://echa.europa.eu/". Such acknowledgement must be included in each copy of the material. ECHA permits and encourages organisations and individuals to create links to the ECHA website under the following cumulative conditions: Links can only be made to webpages that provide a link to the Legal Notice page. | |
| Record name | ABIRATERONE | |
| Source | FDA Global Substance Registration System (GSRS) | |
| URL | https://gsrs.ncats.nih.gov/ginas/app/beta/substances/G819A456D0 | |
| Description | The FDA Global Substance Registration System (GSRS) enables the efficient and accurate exchange of information on what substances are in regulated products. Instead of relying on names, which vary across regulatory domains, countries, and regions, the GSRS knowledge base makes it possible for substances to be defined by standardized, scientific descriptions. | |
| Explanation | Unless otherwise noted, the contents of the FDA website (www.fda.gov), both text and graphics, are not copyrighted. They are in the public domain and may be republished, reprinted and otherwise used freely by anyone without the need to obtain permission from FDA. Credit to the U.S. Food and Drug Administration as the source is appreciated but not required. | |
Vorbereitungsmethoden
Synthetic Routes and Reaction Conditions: The synthesis of abiraterone acetate typically involves a four-step process starting from dehydroepiandrosterone . The key steps include:
Condensation: Dehydroepiandrosterone is condensed with hydrazine hydrate in ethanol using sulfuric acid as a catalyst to form a hydrazone intermediate.
Iodination: The intermediate is treated with iodine in the presence of 1,1,3,3-tetramethylguanidine to yield 17-iodoandrosta-5,16-dien-3β-ol.
Suzuki Coupling: The iodinated compound undergoes Suzuki cross-coupling with 3-(diethylboryl)pyridine using a palladium catalyst to form this compound.
Acetylation: Finally, this compound is acetylated to produce this compound acetate.
Industrial Production Methods: Industrial production of this compound acetate involves similar synthetic routes but optimized for large-scale manufacturing. Techniques such as solvent evaporation, direct compaction, and melt granulation are employed to enhance the bioavailability and stability of the final product .
Analyse Chemischer Reaktionen
Arten von Reaktionen: Abirateron unterliegt verschiedenen chemischen Reaktionen, darunter:
Oxidation: Abirateron kann oxidiert werden, um hydroxylierte Derivate zu bilden.
Reduktion: Reduktionsreaktionen können Abirateron in seine entsprechenden Alkohole umwandeln.
Substitution: Abirateron kann an Substitutionsreaktionen teilnehmen, insbesondere in Gegenwart von Halogenen.
Häufige Reagenzien und Bedingungen:
Oxidation: Reagenzien wie Kaliumpermanganat oder Chromtrioxid werden üblicherweise verwendet.
Reduktion: Natriumborhydrid oder Lithiumaluminiumhydrid sind typische Reduktionsmittel.
Substitution: Halogenierungsmittel wie Iod oder Brom werden unter milden Bedingungen verwendet.
Hauptprodukte: Die Hauptprodukte, die aus diesen Reaktionen entstehen, umfassen hydroxyliertes Abirateron, reduzierte Abirateronderivate und halogenierte Abirateronverbindungen .
4. Wissenschaftliche Forschungsanwendungen
Abirateron hat eine breite Palette von wissenschaftlichen Forschungsanwendungen:
Chemie: Es wird als Modellverbindung zur Untersuchung steroidaler Enzyminhibitoren verwendet.
Biologie: Abirateron wird in der Forschung zur Androgenbiosynthese und ihrer Hemmung eingesetzt.
5. Wirkmechanismus
Abirateron entfaltet seine Wirkung, indem es selektiv und irreversibel das Enzym 17α-Hydroxylase/C17,20-Lyase (CYP17) hemmt, das für die Androgenbiosynthese unerlässlich ist . Durch die Blockierung dieses Enzyms reduziert Abirateron die Produktion von Testosteron und anderen Androgenen und hemmt so das Wachstum von androgenabhängigen Prostatakrebszellen . Die molekularen Zielstrukturen umfassen die Nebennieren, Hoden und Prostatatumoren .
Ähnliche Verbindungen:
Einzigartigkeit von Abirateron: Die Einzigartigkeit von Abirateron liegt in seinem Wirkmechanismus. Es hemmt die Androgenbiosynthese auf enzymatischer Ebene, während andere Verbindungen wie Bicalutamid und Enzalutamid auf Rezeptor-Ebene wirken . Dies macht Abirateron besonders effektiv in Fällen, in denen Inhibitoren der Androgenrezeptor-Signalgebung weniger wirksam sind.
Wissenschaftliche Forschungsanwendungen
Clinical Applications
1. Metastatic Castration-Resistant Prostate Cancer
Abiraterone was first approved for use in men with metastatic castration-resistant prostate cancer (mCRPC) who had previously received chemotherapy. The pivotal Phase III trial demonstrated that patients treated with this compound plus prednisone had a median overall survival of 14.8 months compared to 10.9 months for those receiving placebo plus prednisone .
2. Newly Diagnosed Metastatic Castration-Sensitive Prostate Cancer
Recent studies have expanded the application of this compound to newly diagnosed metastatic castration-sensitive prostate cancer (mCSPC). In a double-blind, placebo-controlled trial involving 1,199 patients, those receiving this compound alongside standard androgen-deprivation therapy showed significantly improved overall survival (not reached vs. 34.7 months for placebo) and radiographic progression-free survival (33.0 months vs. 14.8 months for placebo) .
Summary of Key Clinical Trials
Real-World Evidence
Recent studies have also investigated the effectiveness of this compound compared to enzalutamide, another androgen receptor inhibitor. A large cohort analysis indicated that patients receiving this compound had a median overall survival of 20.6 months compared to 22.5 months for those on enzalutamide . This suggests that while both drugs are effective, there may be differences in outcomes based on patient demographics and clinical characteristics.
Case Studies
Case Study 1: Efficacy in Older Patients
A retrospective cohort study highlighted that older patients (≥75 years) treated with this compound exhibited shorter median overall survival compared to those treated with enzalutamide, indicating a potential need for personalized treatment approaches based on age and comorbidities .
Case Study 2: Combination Therapy
In another study exploring combination therapies, patients receiving this compound along with enzalutamide showed improved outcomes over those receiving either drug alone, suggesting that dual inhibition of androgen signaling pathways could enhance therapeutic efficacy in select populations .
Wirkmechanismus
Abiraterone exerts its effects by selectively and irreversibly inhibiting the enzyme 17α-hydroxylase/C17,20-lyase (CYP17), which is essential for androgen biosynthesis . By blocking this enzyme, this compound reduces the production of testosterone and other androgens, thereby inhibiting the growth of androgen-dependent prostate cancer cells . The molecular targets include the adrenal glands, testes, and prostate tumors .
Vergleich Mit ähnlichen Verbindungen
Table 1: Structural and Mechanistic Comparison
Pharmacodynamic Efficacy
- CYP17A1 Inhibition : this compound’s IC50 for CYP17A1 (2.9–4 nM) is superior to ketoconazole (historical comparator, IC50 ~100 nM) but less selective than orteronel . It also inhibits CYP21A2 (Kb = 1.4 µM), complicating adrenal steroidogenesis .
- Antitumor Activity : In mCRPC, this compound and enzalutamide show comparable PSA response rates (>50% reduction: 48.4% vs. 69.2%, p=0.171) and median overall survival (30.2 vs. 16.2 months, p=0.734) post-docetaxel . However, this compound demonstrates superior radiosensitization in vitro by impairing DNA repair pathways (NHEJ and HR), unlike enzalutamide .
Pharmacokinetic Profiles
- Food Interaction: this compound acetate’s absorption increases 5- to 10-fold with food, necessitating fasting administration to avoid toxicity . Novel formulations (e.g., oral suspensions) aim to reduce food-dependent variability .
- Metabolism : this compound is primarily excreted in feces (88% of dose), with 55% as unchanged prodrug and 22% as this compound . Enzalutamide, conversely, undergoes CYP2C8/CYP3A4 metabolism, posing drug-drug interaction risks absent in this compound .
Table 2: Pharmacokinetic Comparison
Toxicity and Drug Interactions
- Adverse Effects : this compound causes mineralocorticoid excess (hypertension, hypokalemia) due to CYP17A1/CYP21A2 inhibition, requiring co-administration of prednisone. Enzalutamide lacks steroidogenic effects but induces fatigue and seizures .
- Drug Interactions : this compound interacts with CYP3A4 inducers/inhibitors (e.g., rifampicin, ketoconazole), while enzalutamide induces CYP3A4, reducing efficacy of co-administered drugs like warfarin .
Biologische Aktivität
Abiraterone acetate, a selective inhibitor of androgen biosynthesis, has revolutionized the treatment of advanced prostate cancer, particularly metastatic castration-resistant prostate cancer (mCRPC). This article delves into the biological activity of this compound, highlighting its mechanisms of action, clinical efficacy, and emerging research findings.
This compound functions primarily by inhibiting the enzyme CYP17A1, which is crucial for androgen production in the adrenal glands, testes, and prostate tumor cells. This inhibition leads to a significant reduction in serum and intratumoral androgen levels, which are essential for the growth and survival of prostate cancer cells. The compound's action is not limited to androgen suppression; it also exhibits unique biological effects on bone metabolism.
Bone Metabolism Effects
Recent studies have demonstrated that this compound possesses both anabolic and anti-resorptive properties in bone tissue. Specifically, it promotes osteoblast differentiation while inhibiting osteoclast activity. This dual action results in enhanced bone formation and reduced bone resorption, which is particularly beneficial for patients with skeletal metastases.
- In Vitro Findings : this compound treatment resulted in:
- Clinical Observations : In a cohort study involving 49 mCRPC patients treated with this compound:
Clinical Efficacy
This compound has been extensively evaluated in clinical trials, demonstrating substantial benefits for patients with advanced prostate cancer.
Key Clinical Trials
- STAMPEDE Trial : This ongoing multi-arm trial has shown that adding this compound to standard hormone therapy significantly improves overall survival and delays disease progression compared to hormone therapy alone. Notably:
- Phase III Trials : this compound has been compared with other treatments like enzalutamide. In a recent analysis involving over 5,500 patients:
Case Studies
Case Study Example : A patient involved in the STAMPEDE trial reported a dramatic reduction in prostate-specific antigen (PSA) levels from 47 ng/ml at diagnosis to less than 0.1 ng/ml after three months on this compound. The patient experienced manageable side effects and maintained low PSA levels over an extended period .
Emerging Research Findings
Recent studies have explored the potential of combining this compound with other therapies to enhance treatment outcomes:
- Combination Therapy : The addition of drugs like olaparib (a PARP inhibitor) alongside this compound has shown promise in improving radiographic progression-free survival rates in mCRPC patients, regardless of their genetic background .
- Bone Health Studies : Ongoing research aims to further elucidate the mechanisms by which this compound influences bone metabolism and its potential protective effects against skeletal-related events in cancer patients .
Q & A
Q. How to resolve discrepancies between preclinical efficacy and clinical trial outcomes for this compound-based therapies?
- Answer :
- Tumor heterogeneity : Use multi-region sequencing in PDX models to identify resistant subclones.
- Dosing : Compare preclinical doses (mg/kg) to human equivalent doses (HED) using FDA guidelines.
- Biomarker discordance : Validate surrogate endpoints (e.g., PSA) with tissue-based AR-V7 expression .
Retrosynthesis Analysis
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Strategy Settings
| Precursor scoring | Relevance Heuristic |
|---|---|
| Min. plausibility | 0.01 |
| Model | Template_relevance |
| Template Set | Pistachio/Bkms_metabolic/Pistachio_ringbreaker/Reaxys/Reaxys_biocatalysis |
| Top-N result to add to graph | 6 |
Feasible Synthetic Routes
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