Interaction Analysis of the Spike Protein of Delta and Omicron Variants of SARS-CoV-2 with hACE2 and Eight Monoclonal Antibodies Using the Fragment Molecular Orbital Method.

In the past 2 years, since the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), multiple SARS-CoV-2 variants have emerged. Whenever a new variant emerges, considerable time is required to analyze the binding affinity of the viral surface proteins to human angiotensin-converting enzyme 2 (hACE2) and monoclonal antibodies. To efficiently predict the binding affinities associated with hACE2 and monoclonal antibodies in a short time, herein, we propose a method applying statistical analysis to simulations performed using molecular and quantum mechanics. This method efficiently predicted the trend of binding affinity for the binding of the spike protein of each variant of SARS-CoV-2 to hACE2 and individually to eight commercial monoclonal antibodies. Additionally, this method accurately predicted interaction energy changes in the crystal structure for 10 of 13 mutated residues in the Omicron variant, showing a significant change in the interaction energy of hACE2. S375F was found to be a mutation that majorly changed the binding affinity of the spike protein to hACE2 and the eight monoclonal antibodies. Our proposed analysis method enables the prediction of the binding affinity of new variants to hACE2 or to monoclonal antibodies in a shorter time compared to that utilized by the experimental method.

Evaluation of Selective COX-2 Inhibition and In Silico Study of Kuwanon Derivatives Isolated from Morus alba.

Six kuwanon derivatives (A/B/C/E/H/J) extracted from the roots of Morus alba L. were evaluated to determine their cyclooxygenase (COX)-1 and 2 inhibitory effects. Cyclooxygenase (COX) is known as the target enzyme of nonsteroidal anti-inflammatory drugs (NSAIDs), which are the most widely used therapeutic agents for pain and inflammation. Among six kuwanon derivatives, kuwanon A showed selective COX-2 inhibitory activity, almost equivalent to that of celecoxib, a known COX inhibitor. Kuwanon A showed high COX-2 inhibitory activity (IC50 = 14 µM) and a selectivity index (SI) range of >7.1, comparable to celecoxib (SI > 6.3). To understand the mechanisms underlying this effect, we performed docking simulations, fragment molecular orbital (FMO) calculations, and pair interaction energy decomposition analysis (PIEDA) at the quantum-mechanical level. As a result, kuwanon A had the strongest interaction with Arg120 and Tyr355 at the gate of the COX active site (-7.044 kcal/mol) and with Val89 in the membrane-binding domain (-6.599 kcal/mol). In addition, kuwanon A closely bound to Val89, His90, and Ser119, which are residues at the entrance and exit routes of the COX active site (4.329 Å). FMO calculations and PIEDA well supported the COX-2 selective inhibitory action of kuwanon A. It showed that the simulation and modeling results and experimental evidence were consistent.

The Effect of Hyaluronidase on the Fat Graft.

BACKGROUND: Fat grafting has been widely used for facial rejuvenation and soft tissue reconstruction. However, it is associated with a lower retention rate than expected and complications such as fat necrosis or calcification. Several techniques that may increase the survival rate of fat grafts have been proposed. The techniques that promote the recipient sites vascularity to increase the survival rate of fat grafts include administration of growth factors, platelet- rich plasma, and adipose derived-stem cells or preconditioning of the recipient fat graft site. METHODS: In this study, the authors evaluated the effect of hyaluronidase on autologous fat graft survival by pretreatment with hyaluronidase at the recipient site by using an animal model. In the experimental group, the recipient site of the fat graft was pretreated with hyaluronidase before fat grafting, whereas the control group was pretreated with normal saline. RESULTS: After 8 weeks of fat grafting, the average volume retention was 78.2% in the experimental group and 68.6% in control group. Considerable fibrosis between the fat globules in the control group was confirmed with Masson trichrome staining. CD31 immunofluorescence staining was performed and stained vessels were counted. Counted vessel number was significantly greater in the experimental group than in the control group. CONCLUSIONS: Pretreatment of hyaluronidase on the fat graft recipient site is a good option to enhance the outcome of the fat graft in the clinical setting.

Anti-Inflammatory Activity and ROS Regulation Effect of Sinapaldehyde in LPS-Stimulated RAW 264.7 Macrophages.

We evaluated the anti-inflammatory effects of SNAH in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages by performing nitric oxide (NO) assays, cytokine enzyme-linked immunosorbent assays, Western blotting, and real-time reverse transcription-polymerase chain reaction analysis. SNAH inhibited the production of NO (nitric oxide), reactive oxygen species (ROS), tumor necrosis factor (TNF)-α, and interleukin (IL)-6. Additionally, 100 µM SNAH significantly inhibited total NO and ROS inhibitory activity by 93% (p < 0.001) and 34% (p < 0.05), respectively. Protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) stimulated by LPS were also decreased by SNAH. Moreover, SNAH significantly (p < 0.001) downregulated the TNF-α, IL-6, and iNOS mRNA expression upon LPS stimulation. In addition, 3-100 µM SNAH was not cytotoxic. Docking simulations and enzyme inhibitory assays with COX-2 revealed binding scores of -6.4 kcal/mol (IC50 = 47.8 µM) with SNAH compared to -11.1 kcal/mol (IC50 = 0.45 µM) with celecoxib, a known selective COX-2 inhibitor. Our results demonstrate that SNAH exerts anti-inflammatory effects via suppression of ROS and NO by COX-2 inhibition. Thus, SNAH may be useful as a pharmacological agent for treating inflammation-related diseases.

The Effect of Nefopam Infusion during Laparascopic Cholecystectomy on Postoperative Pain.

Background: While recovery from remifentanil is fast due to its rapid metabolism, it can induce hyperalgesia by activation of N-methyl-D-aspartic acid (NMDA) receptors. Therefore, administration of NMDA receptor antagonists such as ketamine is effective in relieving hyperalgesia caused by remifentanil. A previous study showed that nefopam administration before anesthesia combined with low-dose remifentanil reduced pain and analgesic consumption during the immediate postoperative period. We hypothesized that intraoperative infusion of nefopam during laparoscopic cholecystectomy would be as effective as ketamine in controlling pain during the acute postoperative period after sevoflurane and remifentanil based anesthesia. Methods: Sixty patients scheduled to undergo laparoscopic cholecystectomy were randomly divided into three groups. General anesthesia was maintained with sevoflurane and effect-site target concentration of remifentanil (4 ng/ml) in all patients. An intravenous bolus of nefopam (0.3 mg/kg) was given, followed by continuous infusion (65 µg/kg/h) in Group N (n=20). An intravenous bolus of ketamine (0.3 mg/kg) was administered, followed by continuous infusion (180 µg/kg/h) in Group K (n=20), and Group C received a bolus and subsequent infusion of normal saline equal to the infusion received by Group K (n=20). We compared postoperative Visual Analogue Scale (VAS) scores and analgesic requirements over the first 8 postoperative hours between groups. Results: The pain scores (VAS) and fentanyl requirements for 1 h after surgery were significantly lower in the nefopam and ketamine groups compared with the control group (p<0.05). There were no differences between the nefopam and ketamine groups. The three groups showed no differences in VAS scores and number of analgesic injections from 1 to 8 h after surgery. Conclusion: Intraoperative nefopam infusion during laparoscopic cholecystectomy reduced opioid requirements and pain scores (VAS) during the early postoperative period after remifentanil-based anesthesia.

Soy-Leaf Extract Exerts Atheroprotective Effects via Modulation of Krüppel-Like Factor 2 and Adhesion Molecules.

Soy-leaf extracts exert their cardioprotective effects by inducing endothelium-dependent vasodilation in the arteries, and they favorably modulate the serum lipid profile. In this study, we investigated the atheroprotective effects of an ethanol extract of soy leaf (ESL) in human umbilical vein endothelial cells (HUVECs) and high-cholesterol diet (HCD)-fed low-density lipoprotein receptor deficient (LDLR-/-) mice. ESL induced the expression of Krüppel-like factor 2 (KLF2), an endothelial transcription factor, and endothelial nitric oxide synthase (eNOS), and suppressed the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) through moderate inflammatory signal activation, not only in tumor necrosis factor-α (TNF-α)-stimulated HUVECs but also in 7-ketocholesterol (7-KC)-stimulated HUVECs. ESL supplementation reduced aortic lesion formation in Western diet-fed LDLR-/- mice by 46% (p < 0.01) compared to the HCD group. ESL also markedly decreased the aortic expression levels of VCAM-1, ICAM-1, monocyte chemotactic protein-1 (MCP-1), TNF-α, IL-6, IL-1ß, matrix metallopeptidase 9 (MMP-9), and fractalkine, while the expression of KLF2 was significantly increased. These results suggest that ESL supplementation has potential for preventing HCD-induced atherosclerosis effectively.

Sesamol decreases melanin biosynthesis in melanocyte cells and zebrafish: Possible involvement of MITF via the intracellular cAMP and p38/JNK signalling pathways.

The development of antimelanogenic agents is important for the prevention of serious aesthetic problems such as melasma, freckles, age spots and chloasma. The aim of this study was to investigate the antimelanogenic effect of sesamol, an active lignan isolated from Sesamum indicum, in melan-a cells. Sesamol strongly inhibited melanin biosynthesis and the activity of intracellular tyrosinase by decreasing cyclic adenosine monophosphate (cAMP) accumulation. Sesamol significantly decreased the expression of melanogenesis-related genes, such as tyrosinase, tyrosinase-related protein-1,2 (TRP-1,2), microphthalmia-associated transcription factor (MITF) and melanocortin 1 receptor (MC1R). In addition, sesamol also induces phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK). Moreover, sesamol dose-dependently decreased zebrafish pigment formation, tyrosinase activity and expression of melanogenesis-related genes. These findings indicate that sesamol inhibited melanin biosynthesis by down-regulating tyrosinase activity and melanin production via regulation of gene expression of melanogenesis-related proteins through modulation of MITF activity, which promoted phosphorylation of p38 and JNK in melan-a cells. Together, these results suggest that sesamol strongly inhibits melanin biosynthesis, and therefore, sesamol represents a new skin-whitening agent for use in cosmetics.

Cellular Anti-Melanogenic Effects of a Euryale ferox Seed Extract Ethyl Acetate Fraction via the Lysosomal Degradation Machinery.

The aim of this study was to investigate the effect of ethyl acetate fraction of Euryale ferox seed extracts (Efse-EA) on melanogenesis in immortalized mouse melanocyte cell line, melan-a. Efse-EA showed strong dose-dependent mushroom tyrosinase inhibitory activity. Treatment of melan-a cells with 30 µg/mL Efse-EA produced strong inhibition of cellular tyrosinase and melanin synthesis. Efse-EA significantly reduced the levels of melanogenesis-related proteins, such as tyrosinase, tyrosinase-related proteins 1 and 2, and microphthalmia-associated transcription factor. Because Efse-EA treatment reduced tyrosinase protein levels without changing its mRNA expression, we investigated whether this decrease was related to proteasomal or lysosomal degradation of tyrosinase. We found that chloroquine, a lysosomal proteolysis inhibitor, almost completely abolished both the down-regulation of tyrosinase and the inhibition of melanin synthesis induced by Efse-EA. These results suggested that Efse-EA may contribute to the inhibition of melanogenesis by altering lysosomal degradation of tyrosinase, and that this extract may provide a new cosmetic skin-whitening agent.

S-(-)-10,11-dihydroxyfarnesoic acid methyl ester inhibits melanin synthesis in murine melanocyte cells.

The development of antimelanogenic agents is important for the prevention of serious aesthetic problems such as melasmas, freckles, age spots, and chloasmas. In the course of screening for melanin synthesis inhibitors, we found that the culture broth from an insect morphopathogenic fungus, Beauveria bassiana CS1029, exhibits potent antimelanogenic activity. We isolated and purified an active metabolite and identified it as S-(-)-10,11-dihydroxyfarnesoic acid methyl ester (dhFAME), an insect juvenile hormone. To address whether dhFAME inhibits melanin synthesis, we first measured the size of the melanin biosynthesis inhibition zone caused by dhFAME. dhFAME also showed inhibitory activity against mushroom tyrosinase in Melan-a cells. Intracellular, dose-dependent tyrosinase inhibition activity was also confirmed by zymography. In addition, we showed that dhFAME strongly inhibits melanin synthesis in Melan-a cells. Furthermore, we compared levels of TYR, TRP-1, TRP-2, MITF, and MC1R mRNA expression by reverse-transcription polymerase chain reaction and showed that treatment of Melan-a cells with 35 µM dhFAME led to an 11-fold decrease in TYR expression, a 6-fold decrease in TRP-2 expression, and a 5-fold decrease in MITF expression. Together, these results indicate that dhFAME is a potent inhibitor of melanin synthesis that can potentially be used for cosmetic biomaterial(s).

Protective effects of Y-27632 against cisplatin-induced ototoxicity: A zebrafish model Y-27632 and cisplatin-induced ototoxicity.

Cisplatin is an effective chemotherapy agent against various solid malignancies; however, it is associated with irreversible bilateral sensorineural hearing loss, emphasizing the need for drug development to prevent this complication, with the current options being very limited. Rho-associated coiled-coil-containing protein kinase (ROCK) is a serine-threonine protein kinase involved in various cellular processes, including apoptosis regulation. In this study, we used a transgenic zebrafish model (Brn3C: EGFP) in which hair cells within neuromasts are observed in green under fluorescent microscopy without the need for staining. Zebrafish larvae were exposed to cisplatin alone or in combination with various concentrations of Y-27632, a potent ROCK inhibitor. Hair cell counts, apoptosis assessments using the terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling assay, FM1-43FX labeling assay and behavioral analyses (startle response and rheotaxis) were performed to evaluate the protective effects of Y-27632 against cisplatin-induced ototoxicity. Cisplatin treatment reduced the number of hair cells in neuromasts, induced apoptosis, and impaired zebrafish larval behaviors. Y-27632 demonstrated a dose-dependent protective effect against cisplatin-induced hair cell loss and apoptosis. These findings suggest that Y-27632, as a ROCK inhibitor, mitigates cisplatin-induced hair cell loss and associated ototoxicity in zebrafish.

Anti-androgen receptor activity of apoptotic CK2 inhibitor CX4945 in human prostate cancer LNCap cells.

Androgen receptor (AR) is crucial for transcriptional signaling in prostate cancers. The anti-cancer activity of protein kinase CK2 (formerly called casein kinase 2)-specific small molecule inhibitors have been reported in several cancers including prostate cancers. The orally available CX4945, a potent and selective small molecule inhibitor of CK2, has advanced into human clinical trials and has exhibited strong anti-tumor activity. The inhibition of CK2 leads to a down-regulation of the AR-dependent transcription, but the functional relevance of CX4945 to AR-dependent transcription in AR-positive LNCap cells has not been studied yet. Our observation of inhibitory effects of CX4945 on the expression or phosphorylation levels of CK2α, Akt and anti-apoptotic molecules including IAP family members agreed with a previous study showing the effect of CK2 inhibition in cancer cells. This study also provides novel information on the impact of CX4945 in the inhibition of AR-dependent transcriptional activation in LNCap cells via its down-regulation. Pharmacologic inhibition experiment revealed that CX4945 could exhibit its anti-cancer activity in LNCap cells via the independent inhibitions of AR and Akt-survivin signalings.

PFN1 Prevents Psoriasis Pathogenesis through IκBζ Regulation.

PFN1 is an actin-binding protein that regulates actin polymerization, cell proliferation, apoptosis, angiogenesis, and carcinogenesis. Its dysregulation has been reported in diverse pathologic diseases; however, the role of PFN1 in psoriasis has not yet been elucidated. In this study, we show that PFN1 expression is increased in both skin and serum of patients with psoriasis. PFN1 was markedly expressed in the epidermis of psoriatic lesions, and its expression positively correlated with psoriasis severity. IL-17A treatment of keratinocytes increased PFN1 expression, whereas TNF-α induced PFN1 expression and secretion. In addition, knockdown of PFN1 with short hairpin RNA resulted in an altered expression of psoriasis-associated inflammatory markers, HBD2, S100A7, S100A9, and Ki-67, and recombinant PFN1 suppressed the IL-17A‒induced inflammatory response in keratinocytes. Interestingly, recombinant PFN1 also suppressed IL-17A‒induced IκBζ, an important player in immune response in psoriasis. Collectively, our results show that PFN1 acts as a negative regulator of psoriatic inflammation through the suppression of IκBζ and that the balanced level of PFN1 is important for IκBζ regulation. Thus, the expression of PFN1 can be used as a biomarker for psoriasis severity, and it can be considered as a possible target for the treatment of psoriasis.

Fat Graft with Allograft Adipose Matrix and Magnesium Hydroxide-Incorporated PLGA Microspheres for Effective Soft Tissue Reconstruction.

BACKGROUND: Autologous fat grafting is one of the most common procedures used in plastic surgery to correct soft tissue deficiency or depression deformity. However, its clinical outcomes are often suboptimal, and lack of metabolic and architectural support at recipient sites affect fat survival leading to complications such as cyst formation, calcification. Extracellular matrix-based scaffolds, such as allograft adipose matrix (AAM) and poly(lactic-co-glycolic) acid (PLGA), have shown exceptional clinical promise as regenerative scaffolds. Magnesium hydroxide (MH), an alkaline ceramic, has attracted attention as a potential additive to improve biocompatibility. We attempted to combine fat graft with regenerative scaffolds and analyzed the changes and viability of injected fat graft in relation to the effects of injectable natural, and synthetic (PLGA/MH microsphere) biomaterials. METHODS: In vitro cell cytotoxicity, angiogenesis of the scaffolds, and wound healing were evaluated using human dermal fibroblast cells. Subcutaneous soft-tissue integration of harvested fat tissue was investigated in vivo in nude mouse with random fat transfer protocol Fat integrity and angiogenesis were identified by qRT-PCR and immunohistochemistry. RESULTS: In vitro cell cytotoxicity was not observed both in AAM and PLGA/MH with human dermal fibroblast. PLGA/MH and AAM showed excellent wound healing effect. In vivo, the AAM and PLGA/MH retained volume compared to that in the only fat group. And the PLGA/MH showed the highest angiogenesis and anti-inflammation. CONCLUSION: In this study, a comparison of the volume retention effect and angiogenic ability between autologous fat grafting, injectable natural, and synthetic biomaterials will provide a reasonable basis for fat grafting.

Molecules and signaling pathways involved in the expression of OC-STAMP during osteoclastogenesis.

The receptor activator of nuclear factor-κB ligand (RANKL) is a key factor in regulating osteoclastogenesis and in maintaining the survival of mature osteoclasts. We screened differentially expressed genes in RAW264.7 cells in response to RANKL and found osteoclast stimulatory transmembrane protein (OC-STAMP) as one of the RANKL-induced genes of interest. Recently, OC-STAMP has been identified as the RANKL-induced protein that promotes osteoclast differentiation, but the mechanism that regulates its expression is not understood. Therefore, the tissue distribution of OC-STAMP and the signaling pathways that regulate its expression were studied here. Similar to osteoclasts, OC-STAMP was expressed in most tissues, suggesting its involvement in the function of other tissues. Interestingly, OC-STAMP was downregulated by 17ß-estradiol at high concentrations, suggesting the potential relationship between OC-STAMP and estrogen. Importantly, the knockdown of OC-STAMP at the transcript level resulted in the inhibition of multinucleated osteoclast formation and the decreased expression of genes including transcription factor (such as c-Jun), receptors (such as RANK and c-Fms), a signaling molecule (such as TRAF6), and a cell fusion-related molecule (such as meltrin-α), suggesting that the osteoclast differentiation needs the coordinated expression of OC-STAMP with several molecules required for transcription, signaling transduction, and cell fusion. Additionally, the treatment of its specific antibody inhibited the formation and bone resorptive activity of mature osteoclasts, suggesting its involvement in the function of mature osteoclasts. Furthermore, studies with pharmacological inhibitors suggested PKCß or Akt might be the major signaling molecules to regulate the expression of OC-STAMP during osteoclastogenesis.

Effects of fraction obtained from Korean Corni Fructus extracts causing anti-proliferation and p53-dependent apoptosis in A549 lung cancer cells.

Corni Fructus has traditionally been used as herbal medicine for the treatment of tuberculosis, asthma, hepatitis, and chronic nephritis in Korea, Japan, and China. This research was carried out to evaluate the proliferative-inhibitory effect of CF extracts against cancer cells and to identify the new pro-substance from medicinal plants. Among these herbal extracts extracted from KCF (Korean Corni Fructus), JCF (Japanese Corni Fructus) and CCF (Chinese Corni Fructus), KCF extracts strongly induced anti-proliferation of cancer cells in a dose-dependent manner compared with other extracts. Moreover, after treatment with CM/F3 (fraction 3 obtained from KCF extracts) for 24 h, A549 cells were evaluated by several indicators such as cell viability, LDH release, DNA fragmentation, nuclear condensation, and apoptotic proteins in vitro. CM/F3 showed the tumor-selective growth inhibitory activity in a dose- and time-dependent manner in A549 cells. Consistently, CM/F3 effectively induced the activation of bax, cytochrome-c, caspase-3, -8, -9, p53, and p21 causing apoptosis, and caused the suppression of Cdk2, pRb, and E2F1 related to cell arrest in A549 cells. These results demonstrate that CM/F3 caused not only anti-proliferation but also cell death involving cell arrest through interaction between apoptotic proteins and the upregulation of p53 in A549 cells.

Chemical affinity matrix-based identification of prohibitin as a binding protein to anti-resorptive sulfonyl amidine compounds.

In order to identify the binding proteins to anti-resorptive 5-chloro-1-(2,6-dimethylpiperidin-1-yl)-N-tosylpentan-1-imine (1), the chemical affinity matrix for the compound 1 (2b) was designed and synthesized. Using 2b-based chemical proteomics, prohibitin was identified as one of strong binding proteins for 2b.

Comparison of Digital PCR and Quantitative PCR with Various SARS-CoV-2 Primer-Probe Sets.

The World Health Organization (WHO) has declared the coronavirus disease 2019 (COVID-19) as an international health emergency. Current diagnostic tests are based on the reverse transcription-quantitative polymerase chain reaction (RT-qPCR) method, which is the gold standard test that involves the amplification of viral RNA. However, the RT-qPCR assay has limitations in terms of sensitivity and quantification. In this study, we tested both qPCR and droplet digital PCR (ddPCR) to detect low amounts of viral RNA. The cycle threshold (CT) of the viral RNA by RT-PCR significantly varied according to the sequences of the primer and probe sets with in vitro transcript (IVT) RNA or viral RNA as templates, whereas the copy number of the viral RNA by ddPCR was effectively quantified with IVT RNA, cultured viral RNA, and RNA from clinical samples. Furthermore, the clinical samples were assayed via both methods, and the sensitivity of the ddPCR was determined to be equal to or more than that of the RT-qPCR. However, the ddPCR assay is more suitable for determining the copy number of reference materials. These findings suggest that the qPCR assay with the ddPCR defined reference materials could be used as a highly sensitive and compatible diagnostic method for viral RNA detection.

Anti-human rhinovirus activity of gallic acid possessing antioxidant capacity.

Human rhinoviruses (HRVs) are a major cause of the common cold and until now there is no registered clinically effective antiviral chemotherapeutic agent for treatment of diseases caused by HRVs. Our previous report showed that gallic acid from Woodfordia fruticosa flowers possessed antioxidant activity. Many studies reported that antioxidants possess antiviral activities against various viruses. Therefore, we examined antiviral activity of gallic acid against HRVs and mode of its actions by observing the effect of gallic acid on HRV-induced cytopathic effect (CPE) and the infectivity of HRV particles, and then carried out a time-addition study. As a result, gallic acid actively inhibited HRV2 and -3 replications with antiviral activity more than 55% without cytotoxicity in human epitheloid carcinoma cervix (HeLa) cells at a concentration of 100 mug/mL. Also, ribavirin showed lower anti-HRV3 activity than gallic acid and similar anti-HRV3 activity to it. The addition of gallic acid to HRV-infected HeLa cells directly reduced the formation of a visible CPE. Furthermore, gallic acid did directly interact or activate with HRV particles. Collectively, we concluded that the inhibition of HRV production by gallic acid is mainly due to a general action as an antioxidant and the mode of action derived from the inhibition of virus absorption.

Antiviral and anticancer activities of 13(E)-labd-13-ene-8alpha,15-diol isolated from Brachyglottis monroi.

The antiviral activity of 13(E)-labd-13-ene-8alpha,15-diol (1), isolated from Brachyglottis monroi, was examined against human rhinovirus 2 (HRV2) and 3 (HRV3), and the anticancer activity on human cancer cells (A549 and Hep2). Compound (1) showed strong anti-HRV2 and HRV3 activity with a 50% inhibitory concentration (IC(50)) of 2.68 and 0.87 microg/mL, respectively, and a 50% cytotoxicity concentration (CC(50)) of 59.45 microg/mL. Ribavirin only showed anti-HRV3 activity with an IC(50) of 30.48 microg/mL and a CC(50) > 100 microg/mL. The addition of compound (1) to HRV-infected HeLa cells directly reduced the formation of visible cytopathic effect (CPE) and it directly interacted with HRV particles. Furthermore, A549 and Hep2 cells incubated with 32 microg/mL of compound (1) for 48 h exhibited antilung and antilaryngeal cancer activities, with a viability of less than 50%. These results suggest that compound (1) may be used as a potential antiviral and anticancer agent.