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  • Pyrazole: A Promising Agent for The Ovarian and Prostate Cancer Therapy

  • Photo Mahek Patel* Photo Hit Ghodasara Photo Sanmey Pradhan Photo Riddhi Trivedi

  • 123Department of Chemistry, Faculty of Medicinal Chemistry, Sal College of Pharmacy, Ahmedabad-380060, Gujarat, India

    4Department of Pharmaceutics, Sal College of Pharmacy,Ahmedabad—380060,Gujarat,India

Abstract

Pyrazole-based derivatives have become an important chemo-type in modern anticancer drug discovery because of their ability to modulate key molecular pathways involved in tumor initiation and progression. Darolutamide, a nonsteroidal anti-androgen, and niraparib, a selective PARP inhibitor, are prominent clinically validated examples demonstrating the therapeutic relevance of the pyrazole scaffold. [1–5]In darolutamide, the pyrazole core serves as a crucial pharmacophoric element that facilitates noncompetitive interaction with the androgen receptor (AR). Its distinct structural features enable high-affinity binding, inhibit AR nuclear translocation, and overcome resistance commonly associated with first- and second-generation AR antagonists. This structural robustness underlies its marked efficacy, in patients with metastatic(non) castration resistant prostate cancer. Mechanistically, darolutamide selectively antagonizes AR signaling, thereby suppressing androgen-driven proliferation of prostate cancer cells.In niraparib, the pyrazole ring plays a pivotal role in achieving potent and selective inhibition of poly(ADP-ribose) polymerase (PARP) enzymes. This strategy exploits synthetic lethality in tumors exhibiting defects in homologous recombination repair (HRR). The nitrogen atoms of the pyrazole ring and their electronic characteristics are essential for productive binding within the PARP catalytic site. PARP inhibition by Niraparib leads to the cluster of unrepaired DNA impairment in HRR-deficient tumor cells. Clinically, this mechanism has produced significant benefits in ovarian cancers with BRCA mutations and, when it combined with abiraterone acetate, it improves the outcomes in metastatic castration-resistant prostate cancer.Overall, pyrazole-containing agents such as darolutamide and niraparib exemplify rational, target-directed therapeutic design. Their integration into treatment regimens highlights the value of pathway-specific modulation, and continued clinical investigation is warranted to optimize combinations and improve patient outcomes.

Keywords

Pyrazole, Darolutamide, Niraparib, Ovarian Cancer, Prostate Cancer, Targeted Therapy, Androgen Receptor Antagonist, PARP Inhibitor

Introduction

Cancer remains a serious worldwide health concern, with incidence rates rising alongside improvements in living standards. It is characterized by the uncontrolled proliferation of cells and represents a complex set of diseases resulting from accumulated genetic and epigenetic disruptions. These alterations disrupt normal cellular regulation, enabling unchecked growth and survival. According to estimates from the International Agency for Research on Cancer (IARC), an estimated 12.7 million new cancer cases are diagnosed annually worldwide, accompanied by approximately 7.6 million cancer-associated deaths each year.  [6]Over the last century, treatment paradigms have evolved but remain centered on surgery, chemotherapy, and radiotherapy. Individually or in combination, these modalities aim to reduce tumor burden or achieve remission. Systemic chemotherapy, designed to target rapidly dividing cells throughout the body, has shown efficacy in several malignancies; however, its therapeutic benefits are often limited by significant side effects such as myelosuppression, alopecia, gastrointestinal toxicity, and fatigue, which can impair patient quality of life. In parallel, stem cell–based interventions, including hematopoietic stem cell transplantation for hematological cancers and regenerative therapies to repair cytotoxic damage, are gaining traction as complementary approaches.Heterocyclic scaffolds, particularly pyrazole, have attracted considerable interest in medicinal chemistry due to their versatile electronic and binding properties. Pyrazole is a five-membered aromatic heterocycle with two adjacent nitrogen atoms. Its aromatic stabilization arises from a six-π-electron conjugated system in which four carbon atoms and one nitrogen atom each contribute a single electron, while the second nitrogen donates a lone pair of electrons into the conjugated system. This delocalization confers significant electronic stability and aromatic character. [7–12]The reactivity of the pyrazole ring is position-specific: electrophilic substitution generally occurs at the 4-position, while the 3- and 5-positions exhibit reduced reactivity due to the electron-withdrawing influence of the ring nitrogen atoms, making these sites somewhat more susceptible to nucleophilic attack. Substituent effects on the pyrazole core substantially influence physicochemical properties and biological activity. N-unsubstituted pyrazoles display amphoteric behavior, with the pyrrolic nitrogen capable of donating a proton and the pyridinic nitrogen capable of accepting one. Electron-donating groups can modulate this behavior by stabilizing the conjugate base and increasing acidity.In drug design, the hydrogen-bond donor and acceptor capabilities of N-unsubstituted pyrazoles facilitate favorable interactions with biological targets. In contrast, substitution at the pyrrolic nitrogen abolishes its hydrogen-bond donating ability and alters its acidic/basic character, with subsequent effects on binding affinity and pharmacokinetic profiles. Compared with similar heterocycles such as imidazole, thiazole, and oxazole, which are more prone to cytochrome P450-mediated oxidative metabolism, pyrazole frameworks generally exhibit enhanced metabolic stability due to their electron delocalization and relative resistance to oxidative cleavage. Nevertheless, in N-substituted pyrazoles, metabolic pathways often involve removal of the substituent attached to nitrogen.

 

The human body is composed of billions of microscopic units known as cells. They aggregate to form tissues and organs, each specialized for distinct physiological functions. 

There are over 200 distinct types of cancer identified in humans.

Cancers can be classified in two principal ways:

  1. By the anatomical location where the malignancy originates (e.g., breast cancer, lung cancer).
  2. By the specific type of cell from which the cancer arises.

Major Cancer Classifications by Cell Origin

On the basis of cellular origin, cancers are broadly categorized into five primary groups:

Carcinomas – Cancer begins in epithelial cells that lines organs and tissues.It can    develop in the skin or in the cells that cover internal organ such as liver or kidney.

Sarcomas – Cancers that develops in connective tissues, including bone cartilage, muscle, fat, vascular tissues.

Leukemia – Hematologic cancers originating in the bone marrow and affecting blood-forming tissues, leading to abnormal white blood cell proliferation.

Lymphomas – Cancers of the lymphatic system, primarily affecting lymphocytes, a type of immune cell.

Myelomas – Malignancies that develop in plasma cells, a subset of white blood cells involved in antibody production.

Cancer patient data of India: [36–38]

The estimated number of incident cancer cases in India for the year 2022 was 14,61,427 and in the same year, the mortality-to-incidence ratio was found to be 64.47%. This implies that nearly 3 out of 5 individuals diagnosed with cancer in India ultimately died from the diseases in that year.  

 In India 1 in every 9 individuals is likely to develop cancer at some point during their lifetime. Among males lung cancer represents the most prevalent site of malignancy, whereas among females breastcancer was the leading diagnosis. Among paediatric(0-14yr) lymphoid leukaemia emerged as most frequently reported malignancy. 

The incidence of cancer cases is estimated to increase by 12.8 per cent in 2025 as compared to 2020. Among all the cancer, In female Ovarian cancer is one of the most lethal gynecologic malignancies due to its typically asymptomatic progression and late stage diagnosis. In male Prostate cancer is the most frequently diagnosed malignancy.

 

TABLE 1: CANCER PATIENT(S) DATA.

Cancer Type

Country/Region

Cases(in 2022)

Deaths(in 2022)

Ovarian

Worldwide

324,603

206,956

Prostate

Worldwide

14,67,854

397,430

Ovarian

India

47,333

32,978

Prostate

India

37,948

18,386

 

TABLE 2: MECHANISM OF ANTI-CANCER ACTIVITY. [13–20]

MECHANISM

CHARACTERIZATION

Kinase Inhibition

Pyrazole derivatives inhibit kinases like JAK, EGFR, and VEGFR, blocking cell proliferation signaling.

Tubulin Polymerization Inhibition

Disrupts mitotic spindle formation, arresting cancer cells in metaphase.

Topoisomerase Inhibition

Prevents DNA unwinding, causing replication failure and cell death.

ROS Generation

Metal pyrazole complexes increase oxidative stress, leading to Apoptosis.

PI3K/Akt/mTOR Pathway Inhibition

Supresses survival signals in tumor cells, promoting apoptosis.

 

TABLE 3: EXAMPLES OF PYRAZOLE BASED ANTI-CANCER COMPOUNDS. [21–28]

Compound Name

Mechanism

Target Cancer Type

Status

Ruxolitinib

JAK1/JAK2 Kinase Inhibitor

Myelofibrosis, leukemia

FDA Approved

Crizotinib

ALK/ROS1

Inhibitor

NSCLC

FDA Approved

Diarylpyrazoles

Tubulin inhibition

Colon, breast, leukemia

Preclinical

Pyrazole Thiazoles

DNA intercalation

Cervical, lung cancer

Investigational

Metal Pyrazole Complexes

ROS generation

Liver, lung cancer

In vitro studies

BRAF targeted Pyrazole

BRAF V600E mutuation

Inhibition

Melanoma

Clinical Trials

 

Role of Pyrazole in anti-cancer activity: [29–35]

As cancer remains a multifaceted and adaptive disease, the pyrazole ring continues to offer immense potential in the development of nextgeneration anti-cancer therapies that address resistance mechanisms, improve therapeutic windows, and provide more personalized treatment options.

 

TABLE 4: ROLE OF PYRAZOLE AND IMPACT IN ANTI-CANCER DRUGS.

 

Aspect

Role of pyrazole

Impact in Anti-cancer Drugs

Example

Structural Scaffold

Provides rigidity, stability & act as a bioisostere for other rings.

Enhances drug design flexibility, allowing substituiton at C3,,C4 ,C 5 to tune activity.

Ruxolitinib, Crizotinib.

Hydrogen Bonding Ability

It can form multiple hydrogen bonds with protein active sites or cofactors.

Improves binding affinity & selectivity Celecoxib. for cancer-related

enzymes(Kinases, PARP,COX-2)

Celecoxib

Pharmacokinetic properties

Increase lipophilicity, improves BBB and penetration. Provides metabolic stability against rapid degradation.

Better oral bioavalibility longer half life.

Several pyrazole based kinase inhibitors in trials.

Substitution versatility

At position 3,4,5 can attach aryl, heteroaryl, alkyl, halogen etc.

Improve potency, solubility, toxicity and spectrum of activity.

Numerous synthetic

derivatives under

study.

Electronic effects

Aromatic system allows π-π stacking with amino residues(Phe, Tyr,Trp).

Electron rich N atoms modulates electrostatic interaction.

Strengthens drug target interaction, increases selectivity for cancer proteins vs normal proteins

 

Pyrazole PARP inhibitors(ovarian cancer& prostate cancer research)

 

Drugs used in the treatment of ovarian and prostate cancer: [39–41]

  1. Ovarian cancer;

i)First-line / cytotoxic chemotherapy 

Carboplatin, cisplatin, paclitaxel (standard front-line regimens; carboplatin + paclitaxel is the most commonly used)

      1. Targeted therapy — PARP inhibitor(s)

Olaparib (Lynparza), Niraparib (Zejula), Rucaparib (Rubraca) — used as treatment and as maintenance therapy for epithelial ovarian cancer, especially in patients with BRCA or other homologous-recombination defects.

      1. Anti-angiogenic therapy

 Bevacizumab (Avastin) — used in combination with chemotherapy and sometimes as maintenance therapy.

  1. Prostate cancer;
    1. Androgen-deprivation therapy (ADT)

Luteinizing hormone-releasing hormone (LHRH) agonists/antagonists: leuprolide, goserelin, degarelix — foundational for most advanced prostate cancers.

 

    1. Androgen receptor signaling inhibitors (ARSi) / antiandrogens

Enzalutamide (Xtandi), Apalutamide (Erleada), Darolutamide (Nubeqa) — used in non-metastatic and metastatic settings depending on indication. Abiraterone acetate (Zytiga) inhibits androgen synthesis and is often used with steroids.

    1. Chemotherapy

 Docetaxel (first-line chemo for many metastatic cases), Cabazitaxel (used after docetaxel progression).

Darolutamide:

Darolutamide is a second generation nonsteroidal anti androgen approved for the treatment of non-metastatic castration resistant prostate cancer. It is androgen receptor (AR) antagonist with a distinct molecular structure compared to the other next generation AR antagonist enzalutamide and apalutamide. This compound possesses of two pharmacologically active compounds ([S,R]darolutamide and [S,S]-darolutamide) which metabolized into active metabolite keto-darolutamide. Darolutamide act as a complete AR-inhibitor that blocks the AR translocation into the nucleus of cell and testosterone-induced downstream effects of DNA activation, cell growth and survival. However, darolutamide exhibits several notable pharmacological difference compared to other AR antagonist. It has higher AR inhibition potency in preclinical studies as demonstrated by the lower inhibitory constant (Ki) and maximal inhibitory concentration (IC50) values compared to enzalutamide and apalutamide. Darolutamide does not induce activation of mutant AR variants such as AR(F877L), AR(W742L) and AR(T878A) which lead to promiscuous activation. Darolutamide has negligible blood-brain barrier penetration as demonstrated in mouse PK studies, with a brain/plasma ratio of about 2% compared to 25% for enzalutamide. However, it is important to note that despite these differences, current available data do not clearly demonstrate better clinical outcomes with darolutamide compared to enzalutamide or apalutamide.  [42–46]

  • Dose: 600 mg taken orally (bid) for total daily dose of 1200 mg, Dose should be adjusted on your specific health condition.
  • Administration: Tablet should be swallowed whole with food.
  • Combination therapy: It is used in combination with docetaxel.
  • Development companies: 1) Orion corporation 2) Bayer AG
  • Approved by the US-FDA in July 2019

Niraparib:

Niraparib is an orally administered, highly selective inhibitor of PARP1 and PARP2, that is approved for use as maintenance therapy in patients with recurrent ovarian cancer following a response to platinum-based chemotherapy, which shows clinical efficacy in both BRCA-mutated and non-mutated tumors. [47–51]

The poly(ADP-ribose) polymerase (PARP) family consists of enzymes that are essential for repairing damaged DNA, particularly single-strand breaks (SSBs), mainly through the base excision repair (BER) pathway. PARP1, the most active member of this family, recognizes SSBs and binds to the damaged DNA. Upon binding, it catalyzes the addition of ADP-ribose chains to itself and associated proteins, a process known as PARylation. This modification allows PARP1 to detach from DNA, enabling other DNA repair proteins, recruited via ADP-ribose chains, to access and repair the damage. PARP2 contributes to this process to a lesser extent, accounting for approximately 10% of the repair activity.

Inhibition of both PARP1 and PARP2 prevents proper DNA repair. PARP inhibitors block the formation of ADP-ribose chains, causing PARP1 to remain trapped at sites of DNA damage. This trapping hinders the repair of SSBs, which can subsequently convert into double-strand breaks (DSBs) during cell division. DSBs require repair through the homologous recombination (HR) pathway. When HR is defective, as in patients with BRCA1 or BRCA2 mutations, DNA damage accumulates, leading to cell death. This mechanism exemplifies synthetic lethality, in which the loss of either BRCA or PARP alone is tolerable, but simultaneous loss of both is lethal.

Other HR-related genes, such as FANC, ATM, CHEK2, MRE11A, and RAD51, also exhibit synthetic lethality when PARP is inhibited. Deficiencies in these genes, collectively referred to as homologous recombination deficiency (HRD), can serve as predictive biomarkers to identify tumors likely to respond to PARP inhibitor therapy.

  • Dose: 100 mg taken orally once a day.
  • Administration: Capsule should be swallowed with/without food.
  • Development companies : TESARO (Brand name – Zejula)
  • Approved by the US-FDA in March 2017.

 

 

TABLE 5: COMPARISON OF BIOLOGICAL DATA OF DAROLUTAMIDE WITH OTHER DRUG. [52–53]

Feature

Darolutamide (ODM-201)

Apalutamide (ARN-509)

Enzalutamide (MDV3100)

Chemical Structure

Contains a pyrazole ring fused to a benzene ring, with a unique N,N-dimethyl group.

Features a pyrazole ring fused to a cyclopropyl group, with a trifluoromethyl group.

Includes a pyrazole ring attached to a 2-cyanopyridine moiety.

Mechanism of Action

AR antagonist; inhibits AR nuclear translocation and DNA binding.

AR antagonist; prevents AR nuclear translocation and DNA binding

AR antagonist; prevents AR nuclear translocation and DNA binding

Selectivity

High selectivity for AR; minimal binding to other steroid hormone receptors.

High selectivity for AR; minimal binding to other steroid hormone receptors.

High selectivity for AR; minimal binding to other steroid hormone receptors.

Half-Life

Approximately 19 hours

Approximately 3 days.

Approximately 5-7 days.

Metabolism

Primarily metabolized by CYP3A4; minimal CYP2C8 involvement.

Metabolized by CYP3A4; minor involvement of CYP2C8.

Metabolized by CYP3A4; minor involvement of CYP2C8.

Drug Interactions

Limited interactions; caution with strong CYP3A4 inhibitors.

Potential interactions with CYP3A4 inhibitors.

Potential interactions with CYP3A4 inhibitors.

Resistance Profile

Effective against AR splice variants and mutations; retains activity in resistant models.

Effective against certain AR splice variants; resistance observed in some cases.

Resistance observed in AR splice variants; efficacy may be reduced.

Clinical Indications

Approved for non-metastatic and metastatic castration-resistant prostate cancer.

Approved for non-metastatic and metastatic castration-resistant prostate cancer.

Approved for metastatic castration-resistant prostate cancer.

Efficacy in Clinical Trials

Demonstrated significant improvement in metastasis-free survival in ARANOTE trial.

Showed significant improvement in metastasis-free survival in SPARTAN trial.

Demonstrated significant improvement in progression-free survival in AFFIRM trial.

Safety Profile

Generally well-tolerated; common adverse events include fatigue and hypertension.

Generally well-tolerated; common adverse events include fatigue and rash.

Generally well-tolerated; common adverse events include fatigue and hot flashes.

 

TABLE 6: COMPARISON OF BIOLOGICAL DATA OF NIRAPARIB WITH OTHER DRUGS. [54–55]

Feature

Niraparib

Olaparib

Rucaparib

Chemical / Structural features

Scaffold: fused aromatic azabicycle (indazole?7?carboxamide), with a pyrazole (indazole has fused pyrazole+benzene) unit. Relies on an intramolecular H-bond between a pyrazole-N and the amide anti?hydrogen.

Uses a cyclic amide / nicotinamide mimic; structure does not include a pyrazole ring. (It is a fused bicyclic amide motif).

Also does not have a classical pyrazole ring; is an azepinoindole scaffold

Potency (PARP1 / PARP2 inhibition, and cell-based)

PARP1 IC?? ~ 3 nM (in enzymatic assays) for its optimized form. Cellular EC?? / potency in PARylation inhibition in HeLa cells ~4 nM.

Also in low nanomolar range (often cited ~5?50 nM depending on assay). Strong PARylation inhibition.

IC?? ~ 1?10 nM for PARP1, similar to olaparib in many in vitro enzyme assays. But some differences in cell trapping potency.

Selectivity / Off?target activity

Highly selective for PARP1 & PARP2. Some off?target binding to other kinases, but to lesser extent.

Moderate; generally good selectivity within PARP family, fewer off?target kinase interactions compared to niraparib/rucaparib.

More promiscuous; rucaparib shows binding to many kinases (37 kinases at 10 µM competition) and others.

Pharmacokinetics / Distribution (in vivo)

Favored tumor distribution: studies show tumor exposure ~ 3.3× plasma exposure in PDX/xenograft models; good blood?brain barrier penetration; large volume of distribution (~1220 L in humans) vs ~158 L for olaparib

More limited volume of distribution; tumor exposure often lower than plasma in certain models; less brain exposure; shorter persistence in certain tissues.

Good oral bioavailability; half?life ~17?19 hours (some sources) in humans; metabolism via multiple CYPs. Some drug?drug interactions.

Clinical efficacy in ovarian cancer

Approved for maintenance therapy in recurrent, platinum?sensitive epithelial ovarian, fallopian tube, or primary peritoneal cancer; benefits seen in both BRCA mutant and wild?type patients. Improves progression?free survival.

Similarly approved; good PFS prolongation especially in BRCA mutated cases; some efficacy in wild?type cases but less magnitude.

Approved as monotherapy in advanced ovarian cancer with deleterious germline or somatic BRCA mutations; also used as maintenance

Safety / Toxicity profile

Main dose?limiting toxicities include thrombocytopenia, anemia; higher bone marrow exposure possible due to high distribution; but the higher tumor:bone marrow exposure gives therapeutic window.

Similar spectrum: marrow suppression etc.; some GI side effects; drug interactions due to CYP metabolism.

Similar bone marrow toxicity; rucaparib noted for hepatic effects as well; also drug?drug interactions.

PARP?DNA trapping potency

Good trapping capacity; stronger than some (e.g. olaparib) in some models. This contributes to efficacy particularly in tumors with less sensitivity (e.g. BRCA wild type).

Moderate; less trapping than talazoparib but good in many clinical settings.

Similar to olaparib in many models; less than talazoparib.
 

CONCLUSION

Pyrazole has emerged as a privileged scaffold in medicinal chemistry due to its ideal balance of binding specificity, chemical stability, and hydrogen-bonding potential. Its structural adaptability enables the design of derivatives with improved potency and minimized adverse effects. Compared to other heterocyclic rings, pyrazole is particularly effective for targeting androgen receptors (AR) and poly(ADP-ribose) polymerase (PARP), as alternative scaffolds often display lower specificity or metabolic stability, which can limit their therapeutic application.

Among antiandrogen therapies, darolutamide offers significant clinical advantages over enzalutamide and apalutamide. It provides potent AR inhibition while maintaining a favorable safety and tolerability profile, notably reducing central nervous system (CNS) adverse effects and minimizing drug–drug interactions. Its pharmacological attributes, including strong receptor affinity and limited CNS penetration, contribute to its excellent tolerability. With ongoing regulatory approvals, integration into clinical guidelines, and expanding reimbursement options, darolutamide is poised to become an essential treatment in prostate cancer management.

Niraparib, a selective PARP inhibitor, presents unique advantages over other PARP inhibitors, such as olaparib and rucaparib, particularly due to its efficacy in both BRCA-mutated and non-mutated ovarian cancer patients, thereby broadening the eligible patient population. Clinical studies, including the NOVA trial, have demonstrated substantial improvements in progression-free survival across these patient groups. Its once-daily oral regimen enhances patient adherence during long-term maintenance therapy, which is critical for preventing disease recurrence. Favorable pharmacokinetic and pharmacodynamic properties—including good oral bioavailability, metabolic stability, and selective PARP inhibition—further reinforce its clinical effectiveness. Collectively, these characteristics highlight niraparib’s broad applicability, convenience, and therapeutic value in modern ovarian cancer treatment.

ACKNOWLEDGEMENT

We sincerely acknowledge guidance and support of our mentors and collaborators for their valuable suggestions and constant support throughout the preparation of this review article.

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  44. Kim, T. M., & Lee, D. H. (2016). Efficacy and safety of Crizotinib in advanced NSCLC. Oncology, 91(2), 69-77.
  45. Hantschel, O., & Superti-Furga, G. (2007). Molecular basis of Crizotinib action. Nature Chemical Biology, 3(7), 391-393.
  46. Kotecha, R., & Talpaz, M. (2016). The clinical activity of Ruxolitinib in chronic myelogenous leukemia. Blood Reviews, 30(4), 221-229.
  47. Zarranz, B. J. (2018). The pyrazole core: A privileged motif in medicinal chemistry. Molecules, 23(10), 2678.
  48. Chen, J., & Li, Y. (2019). Pyrazole derivatives as inhibitors of cyclin-dependent kinases (CDKs). European Journal of Medicinal Chemistry, 174, 1-14.
  49. Singh, K., & Kaur, R. (2020). Advances in the design of pyrazole-based BRAF inhibitors for melanoma therapy. Bioorganic & Medicinal Chemistry Letters, 30(23), 127599.
  50. Sani, M. M., & Adam, A. (2023). A review of recent advances in anticancer activity and SAR of pyrazole derivatives. Journal of Advanced Research, 50, 1-20.
  51. Dimmock, J. R., & Sani, M. M. (2017). Pyrazole-containing cytotoxic compounds. Current Topics in Medicinal Chemistry, 17(18), 2055-2070.
  52. Jain, P. K., & Sharma, M. C. (2021). Overview of the therapeutic potential of pyrazole derivatives in oncology. Mini-Reviews in Medicinal Chemistry, 21(5), 415-430.
  53. Lazarevi?, V., Lali?, J., and Novakovi?, T. (2015). Pyrazole-metal complexes: Emerging roles as cytotoxic and antimetastatic agents. Bioorganic & Medicinal Chemistry Letters, 25(17), 3505–3510.
  54. Liu, C. Y., and Zhang, W. F. (2017). Synthesis and anticancer evaluation of pyrazole-linked sulfonamides. European Journal of Medicinal Chemistry, 142, 331–340.
  55. Ahmed, M. S., and El-Kashif, S. S. (2019). Pyrazole-fused compounds targeting BRAF kinase: A structure-activity relationship review. Anti-Cancer Agents in Medicinal Chemistry, 19(10), 1234–1250.

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  45. Hantschel, O., & Superti-Furga, G. (2007). Molecular basis of Crizotinib action. Nature Chemical Biology, 3(7), 391-393.
  46. Kotecha, R., & Talpaz, M. (2016). The clinical activity of Ruxolitinib in chronic myelogenous leukemia. Blood Reviews, 30(4), 221-229.
  47. Zarranz, B. J. (2018). The pyrazole core: A privileged motif in medicinal chemistry. Molecules, 23(10), 2678.
  48. Chen, J., & Li, Y. (2019). Pyrazole derivatives as inhibitors of cyclin-dependent kinases (CDKs). European Journal of Medicinal Chemistry, 174, 1-14.
  49. Singh, K., & Kaur, R. (2020). Advances in the design of pyrazole-based BRAF inhibitors for melanoma therapy. Bioorganic & Medicinal Chemistry Letters, 30(23), 127599.
  50. Sani, M. M., & Adam, A. (2023). A review of recent advances in anticancer activity and SAR of pyrazole derivatives. Journal of Advanced Research, 50, 1-20.
  51. Dimmock, J. R., & Sani, M. M. (2017). Pyrazole-containing cytotoxic compounds. Current Topics in Medicinal Chemistry, 17(18), 2055-2070.
  52. Jain, P. K., & Sharma, M. C. (2021). Overview of the therapeutic potential of pyrazole derivatives in oncology. Mini-Reviews in Medicinal Chemistry, 21(5), 415-430.
  53. Lazarevi?, V., Lali?, J., and Novakovi?, T. (2015). Pyrazole-metal complexes: Emerging roles as cytotoxic and antimetastatic agents. Bioorganic & Medicinal Chemistry Letters, 25(17), 3505–3510.
  54. Liu, C. Y., and Zhang, W. F. (2017). Synthesis and anticancer evaluation of pyrazole-linked sulfonamides. European Journal of Medicinal Chemistry, 142, 331–340.
  55. Ahmed, M. S., and El-Kashif, S. S. (2019). Pyrazole-fused compounds targeting BRAF kinase: A structure-activity relationship review. Anti-Cancer Agents in Medicinal Chemistry, 19(10), 1234–1250.

Photo
Mahek Patel
Corresponding author

Department of Chemistry, Faculty of Medicinal Chemistry, Sal College of Pharmacy, Ahmedabad-380060, Gujarat, India

Photo
Hit Ghodasara
Co-author

Department of Chemistry, Faculty of Medicinal Chemistry, Sal College of Pharmacy, Ahmedabad-380060, Gujarat, India

Photo
Sanmey Pradhan
Co-author

Department of Chemistry, Faculty of Medicinal Chemistry, Sal College of Pharmacy, Ahmedabad-380060, Gujarat, India

Photo
Riddhi Trivedi
Co-author

Department of Pharmaceutics, Sal College of Pharmacy,Ahmedabad—380060,Gujarat,India

Sanmey Pradhan, Mahek Patel, Hit Ghodasara, Riddhi Trivedi, Pyrazole: A Promising Agent for The Ovarian and Prostate Cancer Therapy, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 2, 1433-1444. https://doi.org/10.5281/zenodo.18583384

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