Search

In the current investigation, new monomers of myrrhanone B and lupeolic acid were prepared via reaction of triterpenic acids with linkers in the presence of K 2 CO 3 . In addition, new bis-myrrhanone B homodimers, myrrhanone B-myrrhanol B heterodimers, and bis-myrrhanone β-boswellic acids heterodimer were prepared. Evaluation of these compounds on the proliferation of four different human cancer cell lines, viz., FaDu (pharynx carcinoma), A2780 (ovarian carcinoma), HT29 (colon adenocarcinoma) and A375 (malignant melanoma) has been performed. It is worth mentioning that compounds 4 , 7 , 8 , 10 , and 11 possess potent antiproliferative effect towards HT29 cancer cells with IC 50 values of 8.1 μM, 5.4 μM, 8.8 μM, 6.8 μM, and 8.2 μM, respectively. In addition, these compounds display good to moderate antiproliferative activities towards A2780 and A375 with IC 50 values ranging from 10.4 to 24.2 μM. Moreover, the molecular docking studies of most active compounds ( 4, 7, 8, 10 and 11 ) with six anti-cancer drug targets DHFR, VEGFR2, HER-2/neu, CDK6, hCA-IX and LOX also carried, in order to know the mode of binding interaction and energy of this class of compounds. [ABSTRACT FROM AUTHOR]

Catechins, the dietary phytochemicals present in green tea and other beverages, are considered to be potent inducers of apoptosis and cytotoxicity to cancer cells. While it is believed that the antioxidant properties of catechins and related dietary agents may contribute to lowering the risk of cancer induction by impeding oxidative injury to DNA, these properties cannot account for apoptosis induction and chemotherapeutic observations. Catechin (C), epicatechin (EC), epigallocatechin (EGC) and epigallocatechin-3-gallate (EGCG) are the four major constituents of green tea. In this article, using human peripheral lymphocytes and comet assay, we show that C, EC, EGC and EGCG cause cellular DNA breakage and can alternatively switch to a prooxidant action in the presence of transition metals such as copper. The cellular DNA breakage was found to be significantly enhanced in the presence of copper ions. Catechins were found to be effective in providing protection against oxidative stress induced by tertbutylhydroperoxide, as measured by oxidative DNA breakage in lymphocytes. The prooxidant action of catechins involved production of hydroxyl radicals through redox recycling of copper ions. We also determined that catechins, particularly EGCG, inhibit proliferation of breast cancer cell line MDA-MB-231 leading to a prooxidant cell death. Since it is well established that tissue, cellular and serum copper levels are considerably elevated in various malignancies, cancer cells would be more subject to redox cycling between copper ions and catechins to generate reactive oxygen species (ROS) responsible for DNA breakage. Such a copper dependent prooxidant cytotoxic mechanism better explains the anticancer activity and preferential cytotoxicity of dietary phytochemicals against cancer cells. [ABSTRACT FROM AUTHOR]

Background: The majority of pancreatic ductal adenocarcinoma (PDAC) patients experience disease progression while on treatment with gemcitabine and nanoparticle albumin‐bound (nab)‐paclitaxel (GemPac) necessitating the need for a more effective treatment strategy for this refractory disease. Previously, we have demonstrated that nuclear exporter protein exportin 1 (XPO1) is a valid therapeutic target in PDAC, and the selective inhibitor of nuclear export selinexor (Sel) synergistically enhances the efficacy of GemPac in pancreatic cancer cells, spheroids and patient‐derived tumours, and had promising activity in a phase I study. Methods: Here, we investigated the impact of selinexor–gemcitabine–nab‐paclitaxel (Sel‐GemPac) combination on LSL‐KrasG12D/+; LSL‐Trp53R172H/+; Pdx1‐Cre (KPC) mouse model utilising digital spatial profiling (DSP) and single nuclear RNA sequencing (snRNAseq). Results: Sel‐GemPac synergistically inhibited the growth of the KPC tumour‐derived cell line. The Sel‐GemPac combination reduced the 2D colony formation and 3D spheroid formation. In the KPC mouse model, at a sub‐maximum tolerated dose (sub‐MTD) , Sel‐GemPac enhanced the survival of treated mice compared to controls (p <.05). Immunohistochemical analysis of residual KPC tumours showed re‐organisation of tumour stromal architecture, suppression of proliferation and nuclear retention of tumour suppressors, such as Forkhead Box O3a (FOXO3a). DSP revealed the downregulation of tumour promoting genes such as chitinase‐like protein 3 (CHIL3/CHI3L3/YM1) and multiple pathways including phosphatidylinositol 3'‐kinase‐Akt (PI3K‐AKT) signalling. The snRNAseq demonstrated a significant loss of cellular clusters in the Sel‐GemPac‐treated mice tumours including the CD44+ stem cell population. Conclusion: Taken together, these results demonstrate that the Sel‐GemPac treatment caused broad perturbation of PDAC‐supporting signalling networks in the KPC mouse model. Highlights: The majority of pancreatic ductal adenocarcinoma (PDAC) patients experience disease progression while on treatment with gemcitabine and nanoparticle albumin‐bound (nab)‐paclitaxel (GemPac).Exporter protein exportin 1 (XPO1) inhibitor selinexor (Sel) with GemPac synergistically inhibited the growth of LSL‐KrasG12D/+; LSL‐Trp53R172H/+; Pdx1‐Cre (KPC) mouse derived cell line and enhanced the survival of mice.Digital spatial profiling shows that Sel‐GemPac causes broad perturbation of PDAC‐supporting signalling in the KPC model. [ABSTRACT FROM AUTHOR]

Simple Summary: Non-Hodgkin's lymphomas (NHL) are cancers of the white blood cells. While some NHL subtypes, such as Diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL), grow and spread aggressively, others, like follicular lymphoma (FL), are indolent in nature. Irrespective of how fast they grow, all NHL subtypes can spread to other organs in the body if not treated. In this study, we have demonstrated that the targeted inhibition of p21-activated kinase 4 (PAK4) and nicotinamide phosphoribosyl transferase (NAMPT) in different NHL subtypes by a novel, orally bioavailable, dual inhibitor KPT-9274 can lead to energy depletion, inhibition of cell proliferation, and ultimately apoptosis. KPT-9274 treatment shows potent anti-tumor effects in DLBCL and MCL subcutaneous xenograft models and enhances mice survival in a systemic FL model. Therefore, this study demonstrates the potential of targeting PAK4 and NAMPT by a small molecule inhibitor KPT-9274 for NHL therapy. Diffuse large B-cell lymphoma (DLBCL), grade 3b follicular lymphoma (FL), and mantle cell lymphoma (MCL) are aggressive non-Hodgkin's lymphomas (NHL). Cure rates are suboptimal and novel treatment strategies are needed to improve outcomes. Here, we show that p21-activated kinase 4 (PAK4) and nicotinamide phosphoribosyl transferase (NAMPT) is critical for lymphoma subsistence. Dual targeting of PAK4-NAMPT by the Phase I small molecule KPT-9274 suppressed cell proliferation in DLBCL, FL, and MCL. Growth inhibition was concurrent with apoptosis induction alongside activation of pro-apoptotic proteins and reduced pro-survival markers. We observed NAD suppression, ATP reduction, and consequent cellular metabolic collapse in lymphoma cells due to KPT-9274 treatment. KPT-9274 in combination with standard-of-care chemotherapeutics led to superior inhibition of cell proliferation. In vivo, KPT-9274 could markedly suppress the growth of WSU-DLCL2 (DLBCL), Z-138, and JeKo-1 (MCL) sub-cutaneous xenografts, and a remarkable increase in host life span was shown, with a 50% cure of a systemic WSU-FSCCL (FL) model. Residual tumor analysis confirmed a reduction in total and phosphorylated PAK4 and activation of the pro-apoptotic cascade. This study, using various preclinical experimental models, demonstrates the therapeutic potential of targeting PAK4-NAMPT in DLBCL, FL, and MCL. The orally bioavailable, safe, and efficacious PAK4-NAMPT dual inhibitor KPT-9274 warrants further clinical investigation. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy, with limited therapeutic options. Here, we evaluated the role of regulator of chromosome condensation 1 (RCC1) in PDAC. RCC1 functions as a guanine exchange factor for GTP-binding nuclear protein Ran (Ran) GTPase and is involved in nucleocytoplasmic transport. RCC1 RNA expression is elevated in PDAC tissues compared to normal pancreatic tissues and correlates with poor prognosis. RCC1 silencing by RNAi and CRISPR-Cas9 knockout (KO) results in reduced proliferation in 2-D and 3-D cell cultures. RCC1 knockdown (KD) reduced migration and clonogenicity, enhanced apoptosis, and altered cell cycle progression in human PDAC and murine cells from LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx1-Cre (KPC) tumors. Mechanistically, RCC1 KO shows widespread transcriptomic alterations including regulation of PTK7, a co-receptor of the Wnt signaling pathway. RCC1 KD disrupted subcellular Ran localization and the Ran gradient. Nuclear and cytosolic proteomics revealed altered subcellular proteome localization in Rcc1 KD KPC-tumor-derived cells and several altered metabolic biosynthesis pathways. In vivo, RCC1 KO cells show reduced tumor growth potential when injected as sub-cutaneous xenografts. Finally, RCC1 KD sensitized PDAC cells to gemcitabine chemotherapy treatment. This study reveals the role of RCC1 in pancreatic cancer as a novel molecular vulnerability that could be exploited to enhance therapeutic response. • RCC1 is overexpressed in PDAC thus driving proliferation and progression. • Silencing of RCC1 reduced viability and enhanced apoptosis of PDAC cells. • Ran is regulated by RCC1 which is essential for subcellular proteome organization. • Tumor growth was arrested in RCC1 knockout PDAC xenograft mouse models. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) remains an unmet clinical problem in urgent need of newer molecularly driven treatment modalities. Calcium signals, particularly those associated with calcium release-activated calcium (CRAC) channels, are known to influence the development, growth, and metastasis of many cancers. This is the first study investigating the impact of CRAC channel inhibition on PDAC cell lines and patient-derived tumor models. PDAC cell lines were exposed to a novel CRAC channel inhibitor, RP4010, in the presence or absence of standard of care drugs such as gemcitabine and nab-paclitaxel. The in vivo efficacy of RP4010 was evaluated in a hyaluronan-positive PDAC patient-derived xenograft (PDx) in the presence or absence of chemotherapeutic agents. Treatment of PDAC cell lines with single-agent RP4010 decreased cell growth, while the combination with gemcitabine/nab-paclitaxel exhibited synergy at certain dose combinations. Molecular analysis showed that RP4010 modulated the levels of markers associated with CRAC channel signaling pathways. Further, the combination treatment was observed to accentuate the effect of RP4010 on molecular markers of CRAC signaling. Anti-tumor activity of RP4010 was enhanced in the presence of gemcitabine/nab-paclitaxel in a PDAC PDx model. Our study indicates that targeting CRAC channel could be a viable therapeutic option in PDAC that warrants further clinical evaluation. [ABSTRACT FROM AUTHOR]

Lenvatinib is a multitargeted tyrosine kinase inhibitor (TKI) that shows improved median progression-free survival (PFS) in patients with thyroid carcinomas. However, virtually all patients ultimately progress, indicating the need for a better understanding of the mechanisms of resistance. Here, we examined the molecular profile of anaplastic thyroid cancer cells (8505C) exposed to lenvatinib and found that long-term exposure to lenvatinib caused phenotypic changes. Consistent with change toward mesenchymal morphology, activation of pro-survival signaling, nuclear exporter protein exportin 1 (XPO1) and Rho GTPase effector p21 activated kinases (PAK) was also observed. RNA-seq analysis showed that prolonged lenvatinib treatment caused alterations in numerous cellular pathways and several oncogenes such as CEACAM (carcinoembryonic antigen-related cell adhesion molecule) and NUPR1 (Nuclear protein 1) were also upregulated. Further, we evaluated the impact of XPO1 and PAK4 inhibition in the presence or absence of lenvatinib. Targeted inhibition of XPO1 and PAK4 could sensitize the 8505C cells to lenvatinib. Both XPO1 and PAK4 inhibitors, when combined with lenvatinib, showed superior anti-tumor activity in 8505C sub-cutaneous xenograft. These studies bring forward novel drug combinations to complement lenvatinib for treating anaplastic thyroid cancer. Such combinations may possibly reduce the chances of lenvatinib resistance in thyroid cancer patients. [ABSTRACT FROM AUTHOR]

A new a bisflavan-3-ol, boerhavianane (1), was isolated from Boerhavia elegans L. The structure of the flavanol dimer was elucidated by detailed spectroscopic analysis including 1H, 13C NMR, COSY, HMQC, HMBC, and ESI-MS. Boerhavianane (1) was evaluated for its anticancer activity and demonstrated a significant reduction in the viability of breast cancer cells in a concentration-dependent manner with an IC50 value of 38.48 μg/mL. Moreover, boerhavianane (1) was also screened for DPPH antioxidant activity and acetyl cholinesterase, xanthine oxidase, urease, and α-glucosidase enzyme inhibition activities. Preliminary results showed that it exhibited significant inhibition (81.0 ± 2.0%) against urease enzyme, whereas for DPPH radical scavenging it showed moderate activity (75.0 ± 1.5%). [ABSTRACT FROM AUTHOR]

A new flavonoid glycoside, named desmiflavanoside (1), was isolated from the MeOH extract of Desmidorchis flava (N.E.Br.) Meve & Liede, and its structure was elucidated based on 1D and 2D NMR spectroscopic techniques as well as mass spectrometry. Preliminary studies demonstrated that although compound 1 is moderately cytotoxic at lower concentrations, its activity plateaus at higher concentrations. Notably, compound 1 demonstrated a significant dose-dependent response to lipid peroxidation and that its antilipid peroxidation was similar (89.6 ± 0.81%) to the known standard (BHT; 91.3 ± 0.49%; p < 0.051). On the other hand, the flavone glycoside 1 did not show inhibitory effects against urease and acetylcholinesterase enzymes. [ABSTRACT FROM AUTHOR]

Bio-guided fractionation of the guggul gum resin of Commiphora mukul HOOK using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay for the breast cancer cell line MDA-MB-231 led to the isolation of a new C17 norditerpene named myrrhanone C ( 1) along with two known polypodane-type triterpenes, namely, myrrhanone B ( 2) and myrrhanol B ( 3). The structures of the isolated compounds were elucidated by means of 1D (1H and 13C) and 2D (correlation spectroscopy, heteronuclear single-quantum coherence, heteronuclear multiple-bond correlation, and nuclear Overhauser effect spectroscopy) NMR spectroscopy as well as mass (electrospray ionization-mass spectroscopy) spectral analyses. Interestingly myrrhanone C ( 1) was able to induce a substantial decline in cell proliferation. It reduced the viability of cancer cells by almost 81% and 87% at concentrations of 50 and 100 μg mL−1, respectively. Myrrhanone B ( 2) and myrrhanol B ( 3) showed a concentration-dependent growth inhibitory effect on cancer cells, with the latter being slightly more cytotoxic than the former at both the concentrations tested. Furthermore, myrrhanone C ( 1) and myrrhanone B ( 2) showed good α-glucosidase and urease inhibition. [ABSTRACT FROM AUTHOR]

There is compelling evidence that serum, tissue and intracellular levels of copper are elevated in all types of cancer. Copper has been suggested as an important co-factor for angiogenesis. It is also a major metal ion present inside the nucleus, bound to DNA bases, particularly guanine. We have earlier proposed that the interaction of phenolic-antioxidants with intracellular copper leads to the generation of reactive oxygen species (ROS) that ultimately serve as DNA cleaving agents. To further validate our hypothesis we show here that the antioxidant gossypol and its semi-synthetic derivative apogossypolone induce copper-mediated apoptosis in breast MDA-MB-231, prostate PC3 and pancreatic BxPC-3 cancer cells, through the generation of ROS. MCF10A breast epithelial cells refractory to the cytotoxic property of these compounds become sensitized to treatment against gossypol, as well as apogossypolone, when pre-incubated with copper. Our present results confirm our earlier findings and strengthen our hypothesis that plant-derived antioxidants mobilize intracellular copper instigating ROS-mediated cellular DNA breakage. As cancer cells exist under significant oxidative stress, this increase in ROS-stress to cytotoxic levels could be a successful anticancer approach. [ABSTRACT FROM AUTHOR]

Aberrant nuclear protein transport, often observed in cancer, causes mislocalization-dependent inactivation of critical cellular proteins. Earlier we showed that overexpression of exportin 1 is linked to higher grade and Gleason score in metastatic castration resistant prostate cancer (mCRPC). We also showed that a selective inhibitor of nuclear export (SINE) selinexor and second generation eltanexor (KPT-8602) could suppress mCRPC growth, reduce androgen receptor (AR), and re-sensitize to androgen deprivation therapy. Here we evaluated the combination of KPT-8602 with PARP inhibitors (PARPi) olaparib, veliparib and rucaparib in 22rv1 mCRPC cells. KPT-8602 synergized with PARPi (CI < 1) at pharmacologically relevant concentrations. KPT-8602-PARPi showed superior induction of apoptosis compared to single agent treatment and caused up-regulation of pro-apoptotic genes BAX, TP53 and CASPASE 9. Mechanistically, KPT-8602-PARPi suppressed AR, ARv7, PSA and AR targets FOXA1 and UBE2C. Western blot analysis revealed significant down-regulation of AR, ARv7, UBE2C, SAM68, FOXA1 and upregulation of cleaved PARP and cleaved CASPASE 3. KPT-8602 with or without olaparib was shown to reduce homologous recombination-regulated DNA damage response targets including BRCA1, BRCA2, CHEK1, EXO1, BLM, RAD51, LIG1, XRCC3 and RMI2. Taken together, this study revealed the therapeutic potential of a novel combination of KPT-8602 and PARP inhibitors for the treatment of mCRPC. [ABSTRACT FROM AUTHOR]

Abstract Elucidation of bioactive chemical compounds from rhizobacteria is highly utilized in pharmaceuticals and naturopathy, due to their health benefits to human and plants. In current study, four cyclopeptides along with one phenyl amide were isolated from the ethyl acetate extract of Bacillus velezensis sp. RA5401. Their structures were determined and characterized as cycle (L-prolyl-L-leucyl) 2 (1), cyclo (L-prolyl- l -valine) 2 (2), cycle (L-phenylanalyl-L-propyl) 2 (3), cyclo (D-pro-L-tyr-L-pro-L-tyr) 2 (4) and N-(2-phenylethyl)acetamide (5) on the basis of electron spray ionization mass spectrometry (ESI-MS), nuclear magnetic resonance (NMR) techniques and comparison with the literature data. The five compounds have been isolated for the first time from this species. The effect of various concentrations of these compounds on the proliferation of MDA-MB-231 breast cancer cells was examined. It was found that 1 and 2 induced concentration-independent anti-proliferative effects, while 3 , 4 and 5 inhibited cancer cell proliferation in a concentration-dependent manner. Furthermore, to determine the suitable binding targets of these compounds within cancer cell line, detailed target prediction and comparative molecular-docking studies were performed. The compounds 1 and 2 hit intracellular anti-cancer targets of proteases family, while compounds 3 , 4 and 5 interacted with different membrane receptors of G-Protein-Coupled Receptors (GPCRs). In conclusion, the Bacillus velezensis RA5401 can be an ideal strain to produce anti-proliferative constituents at industrial scale. Highlights • First report on the isolation of cyclotetrapetides from Bacillus velezensis strain. • Three compounds (3 , 4 and 5) inhibited cancer cell proliferation in a concentration-dependent manner. • Bacillus velezensis can be an ideal strain to produce anti-proliferative constituents at industrial scale. • In silico docking study of the compounds displayed possible mode of action in a hypothetical way. [ABSTRACT FROM AUTHOR]

Two new C-glucosyl chromones named aloeverasides A ( 1) and B ( 2) were isolated from the resin of Commiphora gileadensis (L.) C. Chr. The structures of the two new natural products were elucidated based on 1D- (1H- and 13C-NMR) and 2D-NMR (COSY, HSQC, and HMBC) spectroscopic techniques and mass spectrometry (ESI-MS). Aloeverasides A ( 1) and B ( 2) were evaluated for their anticancer activity, and both induced a 76.4 and 70.5% growth inhibition of the breast cancer cell line (MDA-MB-231) at a concentration of 100 μ m. Both compounds were also evaluated for their 1,1-diphenyl-2-picryl-hydrazyl antioxidant, urease enzyme, and α-glucosidase enzyme inhibition activities. Aloeverasides A ( 1) and B ( 2) displayed good urease enzyme inhibition activities (62 and 55%, resp.), as well as antioxidant activity in which aloeveraside A ( 1) had a value of 60% inhibition, while aloeveraside B ( 2) demonstrated a more potent antioxidant activity with 80% inhibition. [ABSTRACT FROM AUTHOR]

Two new pregnane glycosides named desmiflavasides C ( 1 ) and D ( 2 ) were isolated from the sap of Desmidorchis flava (N.E.Br.) Meve & Liede and have had their structures confirmed from 1D and 2D NMR spectroscopic techniques and mass spectrometry (ESIMS). Further, the effects of desmiflavasides C ( 1 ) and D ( 2 ) on the proliferation of breast and ovarian cancer cells as well as normal breast epithelial cells in culture were examined. Interestingly, desmiflavasides C ( 1 ) and D ( 2 ) were able to cause a substantial decline in the viability of cancer cells in a concentration-dependent manner. Moreover, treatment of normal cells with compound 2 resulted in no significant growth inhibition, indicating that its cytotoxicity was selective towards cancer cells. Furthermore, the activity of compound 2 against cancer as well as normal epithelial cells was found to be similar to that of a previously reported pregnane glycoside, nizwaside ( 3 ). Molecular docking studies of desmiflavasides C ( 1 ) and D ( 2 ) and nizwaside ( 3 ) were carried out to ascertain if it was possible to predict any important binding orientations required of small molecule drug candidates with suggested protein target molecules for the purposes of being able to predict the affinity and activity to an acceptable degree by such compounds. Desmiflavaside D ( 2 ) showed a relatively good binding affinity (−22.4449 kcal/mol) as compared to the other two compounds viz., nizwaside ( 3 ) (−20.0319 kcal/mol), and desmiflavaside C ( 1 ) (−19.4042 kcal/mol). Docking results of the three pregnane glycosides viz., 1–3 revealed that these ligand molecules can accurately interact with the target protein. [ABSTRACT FROM AUTHOR]

Epidemiological studies suggest that dietary consumption of plant polyphenols is related to a lower incidence of various cancers. Among these compounds catechins (present in green tea and other beverages) are considered to be potent inducers of apoptosis and cytotoxicity to cancer cells. Thus these compounds can be used as leads to synthesize novel anticancer drugs with greater bioavailability. In view of this in this paper we have examined the chemical basis of cytotoxicity of catechins by studying the structure–activity relationship between catechin (C), epicatechin (EC), epigallocatechin (EGC) and epigallocatechin-3-gallate (EGCG). Using single cell alkaline gel electrophoresis (comet assay) we have established the relative efficiency of cellular DNA breakage as EGCG > EGC > EC > C. We also show that cellular DNA breakage is the result of mobilization of copper ions bound to chromatin and the generation of reactive oxygen species. Further the relative DNA binding affinity order was confirmed using molecular docking and thermodynamic studies by studying the interaction of catechins with calf thymus DNA. The results suggest that the synthesis of any novel anti cancer molecule based on the structure of catechins should have as many galloyl moieties as possible resulting in an increased number of hydroxyl groups that may facilitate the binding of the molecule to cellular DNA. [ABSTRACT FROM AUTHOR]

The frankincense resin of botanically-certified Boswellia sacra was pyrolyzed and the smoke was trapped into water using self-developed assembly. Two compounds, namely 1,2,4a,9-tetramethyl-1,2,3,4,4a,5, 6,14b-octahydropicene ( 1 ) and 2,9-dimethylpicene ( 2 ) were isolated from n -hexane extract of the smoke-saturated water. Their structures were determined by means of spectroscopic data including ESIMS, 1 H NMR, 13 C NMR, and 2D NMR (COSY, HSQC, HMBC, and NOESY). Dehydration of C-3 alcohols in boswellic acids (BAs) lead to aromatization of ring A followed by dehydrogenation and demethylation to afford triaromatic derivative viz., 1,2,4a,9-tetramethyl-1,2,3,4,4a,5, 6,14b-octahydropicene ( 1 ) and finally penta-aromatic derivative viz., 2,9-dimethylpicene ( 2 ). Compounds 1 and 2 were screened for their antiproliferative effects on MDA-MB-231 breast cancer cells. It was found that these pyrolysate products were capable of inhibiting cancer cell growth. However, this growth inhibitory effect was less when compared to their precursor AKBA (3-acetyl-11-keto-β-boswellic acid). The antiproliferative activity is inversely proportional to loss of functional groups. [ABSTRACT FROM AUTHOR]

The title compounds (I) display good urease enzyme inhibition activities, significant growth inhibition of the breast cancer cell line MDA-MB-231 as well as good antioxidant activities. [ABSTRACT FROM AUTHOR]

The title compounds (I) display good urease enzyme inhibition activities, significant growth inhibition of the breast cancer cell line MDA-MB-231 as well as good antioxidant activities. [ABSTRACT FROM AUTHOR]