2.1.2 Bendamustine:

Bendamustine (2) is a nitrogen mustard-containing benzimidazole derivative, that exerts cytotoxic effects through DNA alkylation and is clinically indicated for certain lymphoid cancers. Bendamustine represents a potent alkylating agent recognized, notable efficacy and acceptable tolerance in many blood cancers ³⁵. used to treat non-Hodgkin lymphoma and chronic lymphocytic leukemia.³⁶ In managing individuals with mantle cell lymphoma (NCT03834688) over 60, bendamustine is presently being studied further as a combined treatment with Venetoclax, a Bcl-2 inhibitor, and Rituximab.

2.1.3 Selumetinib:

On April 10, 2020, the USFDA (United States Food and Drug Administration) granted regulatory approval to selumetinib (3), a benzimidazole-derived small molecule. For managing pediatric patients with plexiform neurofibromas and neurofibromatosis type 1^37-38. The oral MEK1/2 kinase inhibitor and AstraZeneca-developed drug marketed as Koselugo was created by AstraZeneca. For its use as an additional treatment in specific thyroid cancer cases, It has also received orphan drug designation in the US ^{39- 40}.

2.1.4 Abemaciclib:

The benzimidazole-derived small molecule Abemaciclib (4), was approved by the USFDA on 2017, September 28,. It is therapeutically used in hormone receptor–positive and HER2-negative advanced or metastatic breast cancer, either as combination therapy/ treatment with fulvestrant or as a standalone treatment following chemotherapy failure. The drug, devised by Eli Lilly and sold under the name Verzenio, selectively blocks the cyclin-dependent kinase 6 and 4 (CDK6 and CDK4) ⁴¹. Abemaciclib is also being studied in several clinical trial stages for various cancers and mutation-related malignancies, assessed both alone and together with other treatment protocols^42-
43.

2.1.5 Veliparib

Veliparib (5), is an orally active PARP inhibitor belonging to the benzimidazole class. The compound has exhibited promising antitumor efficacy in both experimental models and clinical evaluations, with notable activity observed in BRCA-mutated ovarian cancer. Veliparib is an orally administered poly ADP-ribose polymerase (PARP) suppressor. Currently under study, it has shown favorable results in both preclinical and clinical evaluations, especially given for ovarian carcinoma including BRCA mutation instances⁴⁴. Further evaluation of Veliparib alone and combined with other treatments for other ovarian cancer forms is being investigated ^{45- 46}.

2.1.6 Dovitinib

Dovitinib (6) is a small-molecule benzimidazole derivative, that targets multiple tyrosine kinases and is undergoing evaluation as a potential anticancer therapeutic. Dovitinib is an orally administered and powerful pan-tyrosine kinase (pan-TKI) suppressor with action against, the Vascular Endothelial Growth Factor Receptor (VEGFR), Fibroblast Growth Factor Receptor (FGFR) and several different tyrosine kinases.⁴⁷ Currently in development, dovitinib is being investigated for managing metastatic breast cancer, gastrointestinal renal cell carcinoma and stromal tumors. A Premarket Approval (PMA) application was submitted to the U.S. FDA by Allarity Therapeutics on April 2, 2021 (as stated on the firm's official website). Additionally, dovitinib is under clinical study for mutation-associated cancers and is in Phase II evaluation for castration-resistant prostate cancer⁴⁸.

2.1.7 Pracinostat

The benzimidazole-derived compound Pracinostat (7), exhibits potent HDAC inhibitory activity and is undergoing clinical investigation for the management of various malignancies. It is an orally available next-generation histone deacetylase (HDAC) suppressor with high promise for antitumor effects^49-50and under investigation for managing acute myeloid leukemia (AML).⁵¹ Other investigations have suggested that Pracinostat also can slow the spread and proliferation of breast cancer through down regulation of the IL-6/STAT3 pathway ⁵².

2.1.8 Galeterone

Galeterone (8), is a benzimidazole-linked small molecule, that is currently under investigation as an orally delivered therapeutic candidate. Galeterone, a powerful androgen receptor antagonist developed by Tokai Pharmaceuticals, is mainly under study for the therapy and control of prostate carcinoma ^53. Also, in-vivo investigations have documented that galeterone alone has displayed the ability to hinder breast cancer growth, and that when used together with cisplatin, the result was markedly better compared to cisplatin alone. ⁵⁴

2.1.9 Nazartinib

Napartinib (9) is a small-molecule benzimidazole derivative, that is currently undergoing development for the management of non–small cells lung cancer, particularly EGFR mutation–positive tumors.⁵⁵ Nazartinib has shown encouraging effectiveness and was generally well tolerated in adult patients with EGFR-mutant lung cancer in a Phase I clinical study trial ⁵⁶. Its role alone and in combination treatment plans for various types of mutated carcinoma continues to be evaluated in ongoing clinical trials ^57-58.

2.2 BENZIMIDAZOLE SCAFFOLDS SERVE AS POWERFUL INHIBITORS OF KINASES

Anticancer agents usually work by inhibiting transcription and DNA synthesis, regulating gene expression, disrupting microtubules, DNA intercalation, and enzyme blockade. Targeted therapy has become more well-known as a crucial cancer treatment strategy in recent years. Tyrosine kinases, structural proteins, phosphoinositide 3-kinase (PI3K), and other protein kinases are the specific targets of many modern anticancer medications. One such medication is binimetinib, which, as was previously mentioned, inhibits mitogen-activated protein kinases. Here, we highlight a few recent instances of enzyme inhibitors based on benzimidazoles that exhibit strong anticancer properties.

2.2.1 Inhibitors of EGFR

Akhter and colleagues synthesized a novel series of benzimidazole scaffolds -based oxadiazole derivatives and evaluated their activity and potential as EGFR inhibitors. Among these, compounds 10 and 11 exhibited remarkable EGFR binding, with IC₅₀ values of 0.081 μM and 0.098 μM, respectively. Both derivatives also showed significant cytotoxicity across multiple human cancer cell lines, including HepG2, A549, MDA-MB-231, and MCF7. Specifically, compound 10 inhibited cell viability with IC₅₀ values of 12.5 μM, 15.2 μM, 14.5 μM, and 5.0 μM against HepG2, A549, MDA-MB-231, and MCF7 cells, respectively. In comparison, compound 11 demonstrated IC₅₀ values of 15.6 μM, 13.2 μM, 0.131 μM, and 2.5 μM in the same respective cell lines. Further mechanistic studies revealed that compound 10 induced a concentration-dependent arrest or inhibit of the MCF7 cell cycle at the G2/M phase, highlighting its potential to interfere with cell proliferation. Docking studies indicated that both molecules engaged effectively within the protein kinase active site and showed binding modes similar to those of the known EGFR inhibitor erlotinib. Following the OECD guidelines, the oral LD50 values for compounds 10 and 11 are between 500 and 2000 mg/kg, suggesting that they are non-toxic and safe, as indicated by acute toxicity tests⁵⁹.

In a separate study, Srour and colleagues designed a novel series of compounds integrating thiazole and benzimidazole scaffolds, aiming to target and inhibit EGFR tyrosine kinase activity. Compounds 12 & 13 demonstrated powerful inhibitory action, with IC₅₀ values of 71.67 nM and 109.71 nM, correspondingly. Compound 12 had an IC50 of 11.91 μM against MCF7 cancer cells, whereas compound 13 displayed better suppression with an IC50 of 6.30 μM. With 65% and 11.9% inhibition, respectively, both molecules showed moderate inhibition of healthy hTERT-RPE1 cells. Compound 13 was also tested for cell cycle activity in MCF7 cells due to its balanced bioactivity, and it induced G2/M phase arrest. Additionally, it considerably lowered PARP-1 enzyme levels while raising the level of apoptosis indicators such as p53, caspase-3 and the Bax/Bcl-2 ratio. Based on molecular docking, 12 and 13 form hydrogen bonds with residues Lys-721 and Phe-699, respectively, and bind effectively at the EGFR active site ^60.

Pyrazole-benzimidazole compounds were also discovered by Akhter et al. to be potent EGFR inhibitors. Among these, compounds 14 and 15 displayed potent suppression of EGFR kinase, with IC₅₀ values of 0.97 μM and 1.7 μM, respectively. In the cytotoxicity assays confirmed their efficacy across multiple cancer cell lines: compound 14 inhibited MCF7, A549, and MDA-MB-231 cells with IC₅₀ values of 0.98 μM, 2.20 μM, and 11.90 μM, respectively, while compound 15 demonstrated IC₅₀ values of 1.70 μM, 2.80 μM, and 15.20 μM against the same lines. Mechanistic studies indicated that compound 14 induced apoptosis by arresting the MCF7 G2/M phase of cell cycle. Molecular docking studies further revealed, compound 14 establishes stable hydrogen bonds and hydrophobic interactions within the EGFR active site (H- EGFR) , supporting its inhibitory potential (Figure 3). ⁶¹.

Figure 3. Benzimidazole derivatives identified as potent EGFR inhibitors.

2.2.2 VEGFR 2 inhibitors

Abdullaziz and colleagues devised a novel category of 2-furylbenzimidazole compounds showing potent VEGFR 2 kinase inhibitory activities. Compounds 16 and 17 demonstrated notable suppression, achieving total inhibition rates of 94.0% and 96.0% with IC₅₀ values of 0.63 μM and 1.25 μM, respectively, compared to the reference drug Sorafenib, which exhibited an IC₅₀ of 0.10 μM. In vitro cytotoxicity studies further confirmed their anti-proliferative potential, with IC₅₀ values ranging from 8.3 to 9.8 μM against HepG2 and MCF7 cell lines. In-silico molecular docking investigations revealed that the 2-furylbenzimidazole scaffold engages in critical hydrogen bonding interactions with key residues Glu-885 and Asp-1046 within the VEGFR-2 active site, providing a structural rationale for the observed kinase inhibition. ^62.

Compound 18, a novel 2-aminobenzimidazole derivative, was reported by Lien and associates to be a potent VEGFR-2 inhibitor. The compound 18 showed 30% suppression of the kinase mechanism and effectively hindered VEGF-A-induced angiogenesis at 10 μM. It also hindered MDA-MB-231 cell growth in vivo and reduced lung metastasis of B16F10 melanoma in mouse models. Based on the docking analysis, compound 18 forms a favorable interaction with VEGFR-2, particularly through the creation of a H-bond (hydrogen bond) between residue His1026 and the benzimidazole nitrogen ⁶³.

Several benzimidazole derivatives with good and selective-vascular endothelial growth factor receptor -2 (VEGFR-2) inhibition were more recently produced by Yuan and colleagues. The compound 19 showed significant anti-angiogenic activity and IC₅₀ of 0.054 μM against VEGFR-2 kinase. Compound 19 revealed promising cytotoxicity against A549 and HepG2 cancer cells in vitro, with IC₅₀ of 73.81 μM and 2.57 μM respectively. Compound 19 induced G0/G1 phase cell cycle arrest in HepG2 cells in a dose/concentration-dependent manner, as determined by cell cycle analysis. The findings were corroborated by molecular docking experiments, where strong interactions and binding inside the ATP-binding pocket of VEGFR-2 kinase were observed ⁶⁴(Figure 4).

Figure 4. Benzimidazole derivatives identified as potent VEGFR-2 inhibitors.

2.2.3 Dual inhibitors - Targeting EGFR and VEGFR-2

Meguid and colleagues reported a novel series of benzimidazole derivatives functioning as dual inhibitors of both EGFR and VEGFR-2 kinases. Compounds 20 and 21 exhibited strong inhibition of EGFR, while their activity against VEGFR-2 was moderate. Specifically, compound 20 displayed IC₅₀ values of 0.157 μM for EGFR and 123.27 μM for VEGFR-2, whereas compound 21 showed greater potency with IC₅₀ values of 0.109 μM and 69.62 μM for the same kinases, respectively. In cytotoxicity assays against HeLa cells, compounds 20 and 21 recorded IC₅₀ values of 1.62 μM and 1.44 μM, outperforming the standard chemotherapeutic agent doxorubicin (IC₅₀ = 2.05 μM). Cell cycle investigations further demonstrated that both derivatives induced G0/G1 phase arrest in HeLa cells. Molecular docking aalysis revealed favorable binding energies of −9.4 and −9.7 kcal/mol for compounds 20 and 21, with both molecules fitting efficiently into the active site of HER2 kinase.⁶⁵

Quinazoline-containing benzimidazole analogues were reported by Kassab and colleagues. in a related study as potential VEGFR-2 and EGFR kinase inhibitors. Compound 22 exhibited strong inhibitory action toward EGFR kinase with an IC₅₀ of 127.4 μM, while its action against VEGFR-2 kinase was relatively lower, with an IC₅₀ of 185.7 μM. n addition, compound 22 demonstrated promising cytotoxic effects, inhibiting the proliferation of MCF7 cells with an IC₅₀ value of 13.0 μM. ⁶⁶ (Figure 5).

Figure 5. Examples of benzimidazole derivatives as effective EGFR/VEGFR twin inhibitors

2.2.4 PI3K (Phosphoinositide 3-kinase) inhibitors

The compound 23 - also known as GSK2636771, is a novel, potent, and orally available benzimidazole derivative that displays significant antitumor activity as a selective PI3K beta inhibitor. Preclinical studies showed that GSK2636771 effectively suppresses protein kinase B activity and halts the proliferation of PTEN deficient cancer cells in both time and dose-dependent fashion. Oral formulation GSK2636771 as a monotherapy in patients with advanced solid cancer produced a promising safety profile, significant drug exposure and effective target inhibition in a first-in-human clinical trial ^{67- 68}.

A novel benzimidazole derivative class was reported by Jin et al. as potent PI3K inhibitors. The compound 24 showed the greatest activity against PI3Kα, with inhibition levels of 36% and 86%, whereas the reference drug Alpelisib produced 110% and 109% inhibition at 50 nM and 500 nM. Compound 24 forms six favorable hydrogen bonds with important residues VAL-851, GLN-859, and SER-854 according to molecular docking studies. Additionally, the thiazole core and amide groups in compound 24 are critical to its bioactivity, as per HOMO LUMO calculations performed using Gaussian 09 software^.69

Recently, Yang et al. revealed a completely new group of dehydroabietic acid derivatives based on benzimidazoles with selective PI3Kα inhibitors. Compound 25 displayed potent inhibitory action against PI3Kα with an IC₅₀ of 0.012 μM, showing seventeen (17)-fold selectivity over PI3Kβ (IC₅₀ = 0.21 μM). As a selective PI3Kα inhibitor, it dose dependently lowered phosphorylated Akt levels in HCT-116 cancer cells. The in-vitro cytotoxicity assays indicated that compound 25 significantly suppressed a variety of cancer cell lines, including HCT-116, HeLa, MCF-7, Ges-1 and HepG2 with IC₅₀ values of 0.62μM, 0.17 μM, 0.72 μM, 21.94 μM and 0.42 μM, and respectively. Moreover, the apoptosis studies indicated that compound 25 induces dose dependent programmed cell death in HCT-116 cells and may therefore be a potent lead for anticancer drug design and development ⁷⁰.

Chandrasekhar and associates reported the creation of a new series of benzimidazole derivatives that exhibited strong inhibitory activity against PI3K. Compound 26 exhibited potent inhibition of the PI3Kβ isoform, achieving an IC₅₀ value of 0.002 μM, while displaying high selectivity relative to the other class I PI3K isoforms. These results highlight its strong specificity and effectiveness as a PI3Kβ-targeted inhibitor.. With respect to hepatic blood flow, experimental pharmacokinetics of compound 26 revealed either low or intermediate clearance in a range of preclinical species, including Beagle dogs, Cynomolgus monkeys, Rhesus monkeys, and Spaghetti rats. Interestingly, the compound presented high permeability and bioavailability after oral administration in the rat. ⁷¹

Wu and colleagues reported a new series of triazine scaffold -functionalized benzimidazole derivatives exhibiting strong potent dual inhibition of PI3K and mTOR. Most compounds in this series showed IC₅₀ values below 33 nM, reflecting strong enzymatic suppression. Among them, compound 27 emerged as the most active, with IC₅₀ values of 5.60 μM and 5.1 μM against mTOR and PI3Kδ, respectively, and 7.30 nM and 21.30 nM for PI3Kα and PI3Kβ. The dual inhibitory potential of compound 27 was further validated by the Western blot study analysis, which confirmed the suppression of Akt and p70S6K phosphorylation. The substance also displayed durable antiproliferative effects on a number of cancer cell lines studies, with IC ₅₀ values of 0.9 μM (HCT116), 0.4 μM (MCF-7), 1.5 μM (MDA-MB-231), 7.3 μM (CNE2), and 7.7 μM (HeLa). According to these findings, compound 27 is a dual PI3K/mTOR inhibitor that shows promise for future advancement in cancer treatment ⁷².

A novel class of benzimidazole derivatives that target PI3Kδ was presented by Shin et al. The IC₅₀ of compound 28 was 1.78 μM against PI3Kβ and 0.016 μM against PI3Kδ, whereas compound 29 showed values of 2.33 μM and 0.019 μM against the same isoforms, respectively These compounds had good oral bioavailability, according to pharmacokinetic evaluation (45% for compound 28 and 41% for compound 29). Both substances successfully suppressed the production of KLH-specific antibodies, according to in vivo research studies⁷³.

He et al. disclosed benzimidazole fused with isoquinolinone derivatives, that target the PI3K/mTOR/Akt signaling pathway to suppress the development of cancer cells. Compound 30 showed strong inhibitory effect against HT29 and SW620 and cancer cells with GI 50 values of24.13 μM and 23.78 μM, respectively. Moreover, By downregulating cyclin B1 and CDK1 expression, the compound triggered cell cycle G2/M- phase inhibition or arrest in human colorectal type of cancer cells and simultaneously decreased the phosphorylation levels of Akt and mTOR ⁷⁴.

Wu et al. synthesized benzimidazole core containing triazine as potent PI3K and mTOR inhibitors.The IC values of compounds 31 and 32 against PI3Kδ were determined to be 2.3 nM and 13.0 nM, indicating strong inhibitory potency.Additionally, they markedly inhibited PI3Kβ (34.0 nM and 28.0 nM) and PI3Kα (14.6 nM and 20.1 nM). Both compounds also showed strong mTOR inhibition, with IC 50 50 42 values of 12.90 nM and 15.40 nM. Further evaluation of compound-32 revealed its moderate antiproliferative activity across multiple cancer cell lines, including HeLa, HepG2, HCT116, MCF7, and MDA-MB-231, with IC₅₀ values of 2.40 μM, 1.30 μM, 0.30 μM, 4.90 μM, and 4.80 μM, respectively. The western blot study analysis confirmed the dual inhibitory potential of compound 32 against PI3K and mTOR, demonstrating effective suppression of downstream signaling pathways⁷⁵.

Figure 6. Benzimidazole-based compounds acting as effective PI3K inhibitors.

2.2.5 Cyclin-dependent kinase (CDK) inhibitors:

Ibrahim et al. introduced a new family of flavopiridol fused with benzimidazole-hybrids with high activities as CDK2 and CDK9 kinase inhibitors. Among the tested compounds, compound 33 demonstrated the highest potency, with IC₅₀ values of 0.06 μM against CDK2 and 1.72 μM against CDK9. In addition to its kinase inhibition, it exhibited notable antiproliferative effects across a panel of cancer cell lines, including K562, PC3, and SKOV3, with IC₅₀ values of 50.8 μM, 85.0 μM, and 94.0 μM, respectively. Cell cycle analysis further revealed (Figure 7) that compound 33 induces a dose-dependent arrest in K562 cells, affecting both the G1 and G2 phases.⁷⁶

Figure 7. Benzimidazole derivatives exhibiting potent CDK inhibitory activity

2.3 BENZIMIDAZOLE-BASED HYBRID COMPOUNDS AS EFFECTIVE ANTICANCER AGENTS:

Pankaj and colleagues created and produced a novel class of benzimidazole core fused with thiazolidinedione hybrid derivatives bearing promising cytotoxic activity. The compound 34 inhibited the PC-3, MDA-MB-231, DU-145 and A549 cancer cell lines with IC₅₀ values of 39.86 μM, 29.17 μM, 31.40 μM, and 11.45 μM, respectively. Additionally, it induced concentration-dependent cell cycle arrest in A549 cells at the G2/M phase. In treated A549 cells, morphological changes were characterized by horseshoe-shaped nuclei, condensed chromatin, and cell shrinkage ⁷⁷.

Sivaramakarthikeyan and colleagues reported novel benzimidazole core with pyrazole hybrid analogues as promising anticancer candidates. Compounds 35 and 36 showed strong anticancer activity against SW1990 and AsPC1 pancreatic type of cancer cells, with half-maximal Inhibitory Concentration (IC₅₀) values between 30.90 μM and 61.80 μM. Useful interactions within the B-cell lymphoma proteins' active site were confirmed by molecular docking studies⁷⁸.

A new class of benzimidazole- quinoline hybrids was developed by Mantu et al., showing promising antitumor properties. At inhibition rates of 56.54% and 52.92%, compound 37 showed significant inhibition of the growth of the breast (MDA-MB-468) and renal (A498) cancer cell lines. With growth inhibition rates of 35% in total, compound 37 inhibited the non-small cell type of lung cancer (NCI-H23) cell line and leukemia cell line (RPMI-8226). ⁷⁹

Potent anticancer benzimidazole--thiazolidinedione derivatives were revealed by Sharma et al. The compounds- 38 and 39 exhibited potent anticancer activity across multiple cancer cell lines, HT1080 (bone), HeLa (cervical), MDA-MB-231 (breast), A549 (lung) and PC-3 (prostate). Their IC₅₀ ranged from 0.13 to 10.24 μM. Both compounds increased intracellular ROS levels through impairment of mitochondrial membrane potential and significantly inhibited A549 cell migration through disruption of F-actin organization. ⁸⁰

Benzimidazole--1,2,3-triazole hybrids that Bistrovic et al. synthesized possess superior anticancer activities. IC50 values for compounds 40 and 41 of 17.53 μM and 8.80 μM against HeLa cells and 0.05 μM and 6.18 μM against A549 cells, respectively, exhibited strong cytotoxic activity. The annexin V assay of compound 40 revealed a 70.59% reduction in viable cells with an increase in late apoptosis (40%) and early necrosis (27.81%). Similarly, the compound 41 decreased cell viability by 49.77%. High binding interaction with very strong affinities of the both compounds to the p38 kinase active site were established using molecular docking ⁸¹ (Figure 8).

Figure 8. Examples of benzimidazole having hybrid derivatives as effective anticancer agents.

3. CONCLUSION:

Kinase inhibition is one of the most important tactics among the many different ways that benzimidazole-based compounds target mutated cancer cells, which has led to their investigation as anticancer agents. The potential of benzimidazole derivatives in targeted cancer therapies is still being thoroughly investigated. The quantity of clinically approved benzimidazole-based cancer treatments has been constrained by issues like attaining high target specificity and overcoming poor selectivity. However, to overcome these constraints, research is still being done to create next-generation kinase inhibitors derived from benzimidazoles.

Interestingly, there has been a growing interest in enzyme inhibitors based on benzimidazoles. The US FDA has recently approved medications that are effective against different types of mutated cancers, such as MEK inhibitors like Binimetinib and Selumetinib, and EGFR inhibitors like Abemaciclib. Furthermore, numerous benzimidazole-based derivatives are under investigation as potential inhibitors targeting key kinases, including EGFR, VEGFR-2, CDK, and PI3K.

Despite the remarkable kinase inhibition demonstrated by some of these experimental compounds, they have not yet met the necessary safety standards. Yet, these molecules are promising lead structures that could produce highly effective anticancer drugs with better safety profiles if they are modified strategically and used in logical drug design. The recent developments in benzimidazole-based kinase inhibitors are highlighted in this review, offering insightful information that could help medicinal chemists find and create safer, more effective targeted cancer treatments.

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Received on 04.01.2026 Revised on 09.02.2026

Accepted on 10.03.2026 Published on 10.04.2026

Available online from April 13, 2026

Asian J. Research Chem.2026; 19(2):126-136.

DOI: 10.52711/0974-4150.2026.00022

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

Name of the Drug	Trial-ID	Study Description
Binimetinib	NCT04965818	A Phase 1b/2 trial investigating Futibatinib with Binimetinib for the treatment of advanced KRAS-mutant tumor patients
	NCT03170206	Evaluation of Palbociclib (CDK4/6 -inhibitor) plus Binimetinib in KRAS-mutant NSCLC
Bendamustine	NCT04217317	Study on CPI-613 with Bendamustine in relapsed or refractory, T-cell Non-Hodgkin lymphoma
	NCT04510636	A drug Pembrolizumab and Bendamustine combination in Hodgkin lymphoma
Selumetinib	NCT02768766	Intermittent Selumetinib dosing in treating uveal melanoma
	NCT05101148	Study on the effect of food on Selumetinib absorption in adolescents with NF1-related tumors
Abemaciclib	NCT04003896	Use of Abemaciclib in biliary tract cancers after failure of first-line treatment
	NCT04040205	Abemaciclib for soft tissue and bone sarcomas with CDK pathway alterations
Veliparib	NCT02723864	Combination of Veliparib and VX-970 along with cisplatin in patients with refractory solid tumors
	NCT01434316	Combined therapy of Veliparib and Dinaciclib in advanced solid tumors
Dovitinib	NCT01635907	Evaluation of Dovitinib in patients with neuroendocrine tumors
Pracinostat	NCT03848754	Pracinostat in combination with gemtuzumab ozogamicin for relapsed or refractory acute myeloid leukemia.
Galeterone	NCT04098081	Study of drug galeterone combined with drug gemcitabine in metastatic pancreatic adenocarcinoma
Nazartinib	NCT02108964	Phase I/II trial of Nazartinib for treating EGFR-mutated solid tumors
	NCT02335944	Nazartinib combined with INC280 in NSCLC patients with EGFR mutations

INTRODUCTION:

Figure 1. Benzimidazole derivatives as clinical agents

2. ADVANCES OF ANTICANCER AGENTS DEVELOPED FROM BENZIMIDAZOLE SCAFFOLDS:

2.1. BENZIMIDAZOLE SCAFFOLDS - MARKETED ANTICANCER AGENTS:

2.1.1. Binimetinib:

Table 1. Benzimidazole core anticancer agents in clinical trials status.

2.1.2 Bendamustine:

2.1.3 Selumetinib: