INTRODUCTION:

Uncontrolled proliferation and spread of aberrant cells throughout the body characterizes the complicated disorders known as cancer^1,2,3. This disease can originate in almost any organ or tissue within the body. It remains to be one of the most serious medical issues in the world, contributing to around Ten million fatalities in 2020—nearly one out of every six deaths (WHO 2025). The complexity of cancer is highlighted by its epidemiology, which includes a number of risk variables such as genetic changes, workplace exposures, lifestyle decisions, social circumstances, and infectious agentsas shown in Fig.1^4,5.

Received on 10.07.2025 Revised on 25.07.2025

Accepted on 06.08.2025 Published on 12.08.2025

Available online from August 18, 2025

Asian J. Research Chem.2025; 18(4):228-234.

DOI: 10.52711/0974-4150.2025.00035

This work is licensed under a Creative Commons Attribution-Non Commercial-Share Alike 4.0 International License. Creative Commons License.

Fig. 1: Risk factors, Type of Cancer, Current Strategies, Future Directions

The statistics are stark: in the US alone, cancer incidence is projected to increase by 49% from 2015 to 2050⁶. After the United States of America and China, India came in at number three in cancer population. Global Cancer Observatory predicted that cancer cases across India would rise to 2 million in 2040⁷. The development of resistance to low levels of success in tumors, drug therapy, toxicity, cancer recurrence, and drug development to conduct clinical testing are limiting factors that exacerbate cancer treatment problems. Cancer can be prevented by raising awareness of the fundamental causes of the disease and its risk factors. Benzimidazole is a bicyclic heteroaromatic compound consists of two rings: one ring is six membered and other is five membered rings connected at the 4^th& 5^th positions⁸. This compound was called glyoxalin created by using glyoxal, formaldehyde, and ammonia in 1858 by Heinrich Debus⁹. It is considered a derivative of imidazole. Its other name is 1H-Benzimidazole. In 1872, Hobrecker first synthesized derivative of benzaimidazole¹⁰.

Benzimidazole:

Benzimidazole Derivatives Mechanism of Action as an Anticancer:

Anticancer activity: It activates pro-apoptotic proteins (p53-mediated pathway) promoting programmed cell death. It also binds to tubulin, preventing microtubule formation and disrupting cell division, leading to cell cycle arrest and apoptosis. Furthermore, Benzimidazole also act as topoisomerase inhibitor or alkylating agent, causing DNA damage and disrupting replication as shown in Fig. 2¹¹.

Fig. 2: Mechanism of Action of Benzimidazole as an Anticancer

Pharmacological Profile:

Benzimidazole derivatives are used in various approaches such as anticancer, antiviral, antimicrobial, antiinflammatory, antibacterial activity as show in Fig. 3¹².

Fig. 3: Pharmacological Activities of Benzimidazole

Tahlan et al., designed a benzimidazole benzamide substances and assessed against HCT116 (colon) cancer cell line using the SRB assay. They found two specific derivatives, compounds 1&2 drug, exhibited notable anticancer activity when compared with standard 5-fluorouracil (5-FU). The found IC₅₀ value of compound 1&2 and 5-FU were 5.85µM, 4.53µM and 9.99 µM respectively¹³.

Gu W et al., created compounds 3& 4, a new group of 1H-benzo[d]imidazole derivative of dehydroabietic acid, with anticancer properties. They further found, most of these substances were highly toxic to cancer cell line (SMMC-7721 and HepG2) and less harm to healthy liver cells (LO2)¹⁴.

Mook Jr RA et al., found that compound 5(4-chloro-2-(5-trifluoromethyl)-1H-benzo[d]imidazole-2-yl) phenol was block the canonical Wnt pathway while minimizing affects on equilibrium cellular ATP levels. Similarly, Niclosamide's also show the inhibitory action on Wnt signaling from its broader effects on ATP regulation¹⁵.

Shao KP et al., created pyrimidine-benzimidazole hybrid compounds 6 and 7 which were examined for moderate to strong antitumor activities against the gastric cancer cell and human breast cancer cell¹⁶.

Kim JS et al., Compound 8 was highly selective for the Breast cancer cell, with an inhibitory concentration value of 3.55µg/ml. whereas the compound 9 had the potential anticancer activities with IC₅₀values of 4.47µg/ml, 4.68µg/ml & 5.50µg/ml against lung adenocarcinoma cancer cell type, Breast cancer and prostate cancer. This suggests that compound 9 has potency as a new drug for treatment of multiple types of cancer^17,18,19,20.

Hranjec et al., found benzimidazo[1,2-α] quinoline compound 10 which can fit between DNA base pairs and leads to DNA damage. Its IC₅₀ value range from 0.7-2.5µM against all tested cell lines, with preference against HeLa cell line ²¹.

Yoon et al., designed a new benzimidazole compounds with three different substitutions (1,2,5-trisubstitued), against SIRT1 and SIRT2 enzyme. Among these, compound 11 had showed IC₅₀value of 54.21µM & 26.85µM against SIRT1 and SIRT2, respectively. Further, they revealed that compound 11 had strong anticancer activity against MD Anderson-Metastatic Breast-468, Human Colorectal tumor 116, and Columbia Country Research Foundation-Cancer Experimental Model (human T- lymphoblastic leukemia cell line)²².

Singh and Tandon., developed 2-aryl-5-substituted-2,5-bis-benzimidazole topoisomerase inhibitors. The IC₅₀value of compounds 12 and 13 were 0.6 to 5.5µM against U87, MCF7 and HeLa cancer cell lines. Further, addition of halogen atoms (especially fluorine and chlorine) to the phenyl ring of these compounds improved affinity to DNA with strong activity against cancer cell lines²³.

Wang et al., developed 1,2-disubstituted benzimidazole compounds, inhibitors of microtubule elongation. They found compound 14 was most effective, with an IC₅₀ of 1.5µM, against human cancer cell lines²⁴.

Zhang et al., developed 1,2-diarylbenzimidazole based compounds and showed compound 15 had IC₅₀ value of 8.47µM and GI₅₀values ranges 0.71 to 2.41µM against cervical cancer, liver cancer, lung adenocarcinoma cancer, and breast cancer²⁵.

Baig et al., designed a imidazo[2,1-b] thiazole-benzimidazole nucleus against cervical cancer cell, lung adenocarcinoma cancer, breast cancer, and prostate cancer. They found cytotoxic potency of compound 16 against lung adenocarcinoma cancer, with an IC₅₀ value of 1.08µM²⁶.

Panchal et al., developed a 1H-benzimidazole substances by adding 2-chloroquinolone to the 2^ndposition which was assessed by anticancer activity against breast cancer-7 cell and lung adenocarcinoma cell type. They found compound 17 was more potent counter to the Michigan Cancer Foundation-7 cell, with half maximal inhibitory concentration of 197µM, while the compound 18 had showed greater activity against the lung adenocarcinoma cancer, with an IC₅₀ of 89µM ²⁷.

Akhtar et al., investigated group of 1H-benzimidazole-linked pyrazole substances against MCF-7 cancer cell types, Immortalized keratinocyte cancer cell type, MD Anderson-Metastatic Breast-231, Pulmonary adenocarcinoma cancer, and hepatic cancer. Among these, compound 19 had a notable effect on A549 lung cancer cells, by arrest cell division in the G2 (growth 2) phase to the M (mitosis) phase and triggering cell death, with an IC₅₀ of 2.2 µM. Additionally, compound 19 inhibited the EGFR activity, with an IC₅₀ of 0.97µM ²⁸.

Delaney S et al., found that the complexes compounds 20, 21, and 22 were the more effective than the chemotherapy cisplatin against Human lung adenocarcinoma cancer, with an IC₅₀ value of 8.9µM, 8.7µM& 5.8µM and cisplatin with IC₅₀ of 16.5µM. Additionally, investigated against MD Anderson- Metastatic Breast-231 cell line, the inhibitory concentration value of molecule 20, 21 & 22 were all below 10µM, while cisplatin had an IC₅₀ value of 19.4µM²⁹.

Demirayak et al., developed a benzo [4,5] imidzo[1,2-a] pyrazine derivatives against blood cancer, pulmonary, colon, ovarian, kidney, and breast tumor cell line. They were evaluated by thesulforhodamine (SRB) protein assay and melphalan and cisplatin were used as standard chemotherapy agents. The compounds 23&24 were demonstrated the most significant cytotoxic effects specifically against leukemia cell lines³⁰.

Rajendar et al., developed aryl quinolon-benzimidazole-1,2,3-triazole substance. Compound 25 possess exceptional cytotoxicity activity with IC₅₀ values of malignant cervix neoplasm (0.012 µM), pulmonary adenocarcinoma cancer (0.043 µM), breast tumor (0.19 µM), and colon tumor cell (0.11 µM) indicate its potential as anticancer when compared to Etoposide which was used as a standard drug³¹.

Gao et al., developed benzimidazole acridine derivatives against immortalized human leukemia cancer and hepatic adenocarcinoma. The colchicine and imatinib were used as standard. They concluded that the compound 26 had potential against both immortalized blood cell and hepatic tumor cell. Aditionally, they found using immortalized human leukemia cell type that the compound 26 effectively bind to DNA and inhibits topoisomerase-׀, and induces apoptosis in a DNA topoisomerase-׀ inhibition test³².

Sharma et al., developed benzimidazole-thiazolidine-dione hybrids and investigated against human cancer cell line. They had showed that compound 27 had more potency than 5-fluorouracil against pulmonary tumor with IC₅₀ of 11.46µM and 30.47µM, respectively. Additionally, compound 27 showed no toxicity to normal MCF10A cells³³.

Goud et al., reported that compound 28 had showed more potency than 5-fluorouracil counter to breast tumor, with IC₅₀ of 3.20µM. They proposed the compound 28 induce apoptosis and cell cycle disruption at the G2 (Growth 2) phase and M (Mitosis phase) and DNA synthesis phase. Further, apoptosis was confirmed by cell shrinkage, increased Reactive oxygen species levels, and changes in the mitochondrial membrane potential. Additionally, this derivative strongly inhibited galectin-1³⁴.

Acar Cevik et al., concluded the compound 29 had showed antitumor activities against breast cancer and hepatic carcinoma cell, with IC₅₀ value of 5.17µM & 5.99µM, respectively. Whereas, the standard doxorubicin had IC₅₀ of 10.53µM and 14.28 µM. Additionally, compound 29 and letrozole inhibited the aromatase enzyme with IC₅₀ value of 2.31µM & 0.032 µM, respectively³⁵.

Husain et al., showed that two benzimidazole/furanone hybrids, compounds 30 and 31, had anticancer activity. Further, found IC₅₀ value from 9.1 micrometer to 12.7 micrometer against the pulmonary adenocarcinoma cancer, breast tumor, and prostate tumor cell type. Doxorubicin, as standard drug with lower inhibitory concentration of 0.8 µM³⁶.

Marketed drugs having Benzimidazole scaffolds: Commercial available drugs possess benzimidazole skeleton as shown in Fig. 4 Veliparib is an anticancer drug designed to target and block PARP proteins, which are crucial for repairing DNA damage in cancer cells. The drug has demonstrated promising results in several cancer types particularly: ovarian cancer, breast cancer, and lung cancer. It inhibits both PARP1 and PARP2 enzymes, induces synthetic lethality in cancer cells, can potentiate the effects of various chemotherapeutic treatments ³⁷.

Nocodazole is a specialized drug used in cancer treatment that works by interfering with cell division. It is an antineoplastic agent that disrupts microtubule dynamics in cells. By preventing microtubule polymerization, it effectively stops cancer cells from completing mitosis. It arrests cell cycle at G2 (Gap 2 phase) to the M (mitosis) phase, binds with high affinity to tubulin proteins, induces cancer cell death³⁸.

CONCLUSION:

Benzimidazole and its derivatives have emerged as a highly versatile group of heterocyclic molecules with wide ranging biological functions and significant therapeutic potential. Over the years, extensive research has demonstrated their efficacy in antimicrobial, antiviral, anticancer, anti-inflammatory, and antiparasitic applications, among others. Structural modifications of the benzimidazole core have led to the discovery of numerous potent compounds with improved pharmacological profiles and target specificity. The continued interest in benzimidazole derivatives underscores their relevance in drug discovery and development. Future efforts should focus on optimizing their pharmacokinetic properties, reducing toxicity, and exploring novel targets through rational drug design and advanced synthetic methodologies. This study provides a valuable foundation for the systematic design of improved 1H-benzimidazole scaffolds with elevated and biogenic anticancer activities, ultimately leading to higher specificity in targeting cancer cells. Overall, benzimidazole scaffolds remain a cornerstone in medicinal chemistry, offering promising avenues for the development of new therapeutic agents. This review ultimately positions benzimidazoles not merely as chemical entities, but as versatile platforms for engineering the next generation of cancer cures – adaptable, affordable, and aligned with the evolving understanding of cancer biology. The challenge now lies in translating this immense potential into therapies that extend both the quality and quantity of life for patients worldwide.

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Received on 03.07.2025 Revised on 21.07.2025

Accepted on 05.08.2025 Published on 12.08.2025

Available online from August 18, 2025

Asian J. Research Chem.2025; 18(4):217-227.

DOI: 10.52711/0974-4150.2025.00034

This work is licensed under a Creative Commons Attribution-Non Commercial-Share Alike 4.0 International License. Creative Commons License.