Orabase-formulated Gentian Violet Effectively Improved Oral Potentially Malignant Disorder in vitro and in vivo.

Biochem Pharmacol. 2019 Nov 13;:113713

Authors: Wang YY, Xiao LY, Wu PC, Chen YK, Lo S, Hu SCS, Chen YH, Chiu CCC, Yuan SSF

Abstract
Oral cancer is a prevalent cancer in male worldwide. Oral potentially malignant disorders (OMPDs) are the oral mucosa lesions that have high malignant transformation rate to oral cancer. The mainstay for OMPDs treatment includes carbon dioxide (CO2) laser and surgery, which may lead to the side effects of scarring and impaired function of oral cavity in the patients and reduced their willingness to receive curative therapy. Therefore, developing a non-invasive and function-preserving therapy is clinically important. Since development of a novel chemotherapeutic drug requires a lot of time and cost, we applied the high-throughput screening (HTS) approach to identify new bioactivities for FDA-approved drugs, known as drug repurposing. Through this drug repurposing approach, we discovered that gentian violet (GV), which is well known for its antibacterial, antifungal, antihelminthic, antitrypanosomal and antiviral activities, was able to induce significant cell death in DOK oral precancerous cells through ROS production. Moreover, decreased phosphorylation of p53(Ser15) and NFκB(Ser536) was required for GV-induced cell death. In vivo, 3% GV orabase effectively suppressed the progression of DMBA-induced oral precancerous lesions. In conclusion, this new formulation of GV through drug repurposing has the potential to be further developed as a therapeutic drug for OPMD clinically.

PMID: 31733192 [PubMed - as supplied by publisher]

Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.

Eur J Med Chem. 2019 Nov 04;:111848

Authors: Ni S, Chen X, Yu Q, Xu Y, Hu Z, Zhang J, Zhang W, Li B, Yang X, Mao F, Huang J, Sun Y, Li J, Jia L

Abstract
Protein neddylation is a posttranslational modification of conjugating the neuronal precursor cell-expressed developmentally down-regulated protein 8 (Nedd8) to substrates. Our previous work revealed that neddylation pathway is overactivated in various human lung cancers and correlates with the disease progression, whereas pharmacologically targeting this pathway has emerged as an attractive therapeutic strategy. As a follow-up research, 1331 approved drugs were investigated the inhibitory activities of cullin1 neddylation for screening the hit compounds via an improved enzyme-based assay. An antihypertensive agent, candesartan cilexetic (CDC), was identified as a novel neddylation inhibitor that ATP-competitively suppressing Nedd8-activating enzyme (NAE, E1) in mechanism, which inhibited the cullins neddylation superior than two representative non-covalent NAE inhibitors, M22 and mitoxantrone. Following with the findings such as apoptotic induction and tumor growth suppression in human lung cancer A549 in vitro and in vivo, CDC represents a potential anticancer lead compound with promising neddylation inhibitory activity.

PMID: 31732254 [PubMed - as supplied by publisher]

Inhibition of the Formation In Vitro of Putatively Carcinogenic Metabolites Derived from S. haematobium and O. viverrini by Combination of Drugs with Antioxidants.

Molecules. 2019 Oct 25;24(21):

Authors: Gouveia MJ, Nogueira V, Araújo B, Gärtner F, Vale N

Abstract
Infections caused by Schistosoma haematobium and Opisthorchis viverrini are classified as carcinogenic. Although carcinogenesis might be a multifactorial process, it has been postulated that these helminth produce/excrete oxysterols and estrogen-like metabolites that might act as initiators of their infection-associated carcinogenesis. Current treatment and control of these infections rely on a single drug, praziquantel, that mainly targets the parasites and not the pathologies related to the infection including cancer. Thus, there is a need to search for novel therapeutic alternatives that might include combinations of drugs and drug repurposing. Based on these concepts, we propose a novel therapeutic strategy that combines drugs with molecule antioxidants. We evaluate the efficacy of a novel therapeutic strategy to prevent the formation of putative carcinogenic metabolites precursors and DNA adducts. Firstly, we used a methodology previously established to synthesize metabolites precursors and DNA adducts in the presence of CYP450. Then, we evaluated the inhibition of their formation induced by drugs and antioxidants alone or in combination. Drugs and resveratrol alone did not show a significant inhibitory effect while N-acetylcysteine inhibited the formation of most metabolite precursors and DNA adducts. Moreover, the combinations of classical drugs with antioxidants were more effective rather than compounds alone. This strategy might be a valuable tool to prevent the initiation of helminth infection-associated carcinogenesis.

PMID: 31731402 [PubMed - in process]

Old wine in new bottles: Drug repurposing in oncology.

Eur J Pharmacol. 2019 Nov 12;:172784

Authors: Antoszczak M, Markowska A, Markowska J, Huczyński A

Abstract
Increasing costs, much time consumption and high risk of failure associated with the process of de novo development of new anticancer drugs have prompted the pharmaceutical industry to seek alternative strategies that may facilitate and accelerate the whole process. In particular, the repurposing strategy, known also as repositioning or reprofiling strategy, is a potential source of new treatment options for cancer patients with high unmet medical needs. However, it should be noted that the repurposing strategy, being still a new trend in drug development, should only complement the process of discovering new anticancer drugs, and should not be its alternative. The best repurposable oncological drug candidates are the agents whose original patent protection has already expired, and for which there is a possibility to create a formulation enabling, together with a new therapeutic indication, new patent protection. In this review article we discuss the advantages of the repurposing strategy, and provide an overview of a number of promising candidates, such as aspirin, artesunate, cimetidine, doxycycline, ivermectin, metformin, rapamycin (sirolimus), and thalidomide, that have the potential to be repurposed as anticancer drugs both in cancer prevention and therapy. In addition, we highlight some of the studies regarding the signalling pathways and molecular targets altered by these drugs, and describe the biological mechanisms underlying their anticancer effects.

PMID: 31730760 [PubMed - as supplied by publisher]

A Novel Drug Repositioning Approach Based on Integrative Multiple Similarity Measures.

Curr Mol Med. 2019 Nov 14;:

Authors: Yan C, Feng L, Wang W, Wang J, Zhang G, Luo J

Abstract
BACKGROUND: Drug repositioning refers to discovering new indications for the existing drugs, which can improve the efficiency of drug research and development.
METHODS: In this work, a novel drug repositioning approach based on integrative multiple similarity measure, called DR_IMSM, is proposed. The process of integrative similarity measure contains three steps. First, a heterogeneous network can be constructed based on known drug-disease association, shared entities information for drug pairwise and diseases pairwise. Second, a deep learning method, DeepWalk, is used to capture the topology similarity for drug and disease. Third, a similarity integration and adjusting process are further conducted to obtain more comprehensive drug and disease similarity measure,respectively.
RESULTS: On this basis, an Bi-random walk algorithm is implemented in the constructed heterogeneous network to rank diseases for each drug. Compared with other approaches, the proposed DR_IMSM can achieve superior performance in terms of AUC on the gold standard datasets. Case studies further confirm the practical significance of DR_IMSM.

PMID: 31729291 [PubMed - as supplied by publisher]

The assessment of efficient representation of drug features using deep learning for drug repositioning.

BMC Bioinformatics. 2019 Nov 14;20(1):577

Authors: Moridi M, Ghadirinia M, Sharifi-Zarchi A, Zare-Mirakabad F

Abstract
BACKGROUND: De novo drug discovery is a time-consuming and expensive process. Nowadays, drug repositioning is utilized as a common strategy to discover a new drug indication for existing drugs. This strategy is mostly used in cases with a limited number of candidate pairs of drugs and diseases. In other words, they are not scalable to a large number of drugs and diseases. Most of the in-silico methods mainly focus on linear approaches while non-linear models are still scarce for new indication predictions. Therefore, applying non-linear computational approaches can offer an opportunity to predict possible drug repositioning candidates.
RESULTS: In this study, we present a non-linear method for drug repositioning. We extract four drug features and two disease features to find the semantic relations between drugs and diseases. We utilize deep learning to extract an efficient representation for each feature. These representations reduce the dimension and heterogeneity of biological data. Then, we assess the performance of different combinations of drug features to introduce a pipeline for drug repositioning. In the available database, there are different numbers of known drug-disease associations corresponding to each combination of drug features. Our assessment shows that as the numbers of drug features increase, the numbers of available drugs decrease. Thus, the proposed method with large numbers of drug features is as accurate as small numbers.
CONCLUSION: Our pipeline predicts new indications for existing drugs systematically, in a more cost-effective way and shorter timeline. We assess the pipeline to discover the potential drug-disease associations based on cross-validation experiments and some clinical trial studies.

PMID: 31726977 [PubMed - in process]

Decoding the similarities and specific differences between latent and active tuberculosis infections based on consistently differential expression networks.

Brief Bioinform. 2019 Nov 13;:

Authors: Sun J, Shi Q, Chen X, Liu R

Abstract
Although intensive efforts have been devoted to investigating latent tuberculosis (LTB) and active tuberculosis (PTB) infections, the similarities and differences in the host responses to these two closely associated stages remain elusive, probably due to the difficulty in identifying informative genes related to LTB using traditional methods. Herein, we developed a framework known as the consistently differential expression network to identify tuberculosis (TB)-related gene pairs by combining microarray profiles and protein-protein interactions. We thus obtained 774 and 693 pairs corresponding to the PTB and LTB stages, respectively. The PTB-specific genes showed higher expression values and fold-changes than the LTB-specific genes. Furthermore, the PTB-related pairs generally had higher expression correlations and would be more activated compared to their LTB-related counterparts. The module analysis implied that the detected gene pairs tended to cluster in the topological and functional modules. Functional analysis indicated that the LTB- and PTB-specific genes were enriched in different pathways and had remarkably different locations in the NF-κB signaling pathway. Finally, we showed that the identified genes and gene pairs had the potential to distinguish TB patients in different disease stages and could be considered as drug targets for the specific treatment of patients with LTB or PTB.

PMID: 31724702 [PubMed - as supplied by publisher]

A Prospective Overview of Drug Repurposing in Drug Discovery and Development.

Curr Med Chem. 2019;26(28):5338-5339

Authors: Olgen S

PMID: 31721690 [PubMed - in process]

Integrative analysis of clinical and bioinformatics databases to identify anticancer properties of digoxin.

Sci Rep. 2019 Nov 12;9(1):16597

Authors: Yokoyama S, Sugimoto Y, Nakagawa C, Hosomi K, Takada M

Abstract
Cardiac glycosides, such as digoxin, inhibit Na+/K+-ATPases and cause secondary activation of Na+/Ca2+ exchangers. Preclinical investigations have suggested that digoxin may have anticancer properties. In order to clarify the functional mechanisms of digoxin in cancer, we performed an integrative analysis of clinical and bioinformatics databases. The US Food and Drug Administration Adverse Event Reporting System and the Japan Medical Data Center claims database were used as clinical databases to evaluate reporting odds ratios and adjusted sequence ratios, respectively. The BaseSpace Correlation Engine and Connectivity Map bioinformatics databases were used to investigate molecular pathways related to digoxin anticancer mechanisms. Clinical database analyses suggested an inverse association between digoxin and four cancers: gastric, colon, prostate and haematological malignancy. The bioinformatics database analysis suggested digoxin may exert an anticancer effect via peroxisome proliferator-activated receptor α and apoptotic caspase cascade pathways. Our integrative analysis revealed the possibility of digoxin as a drug repositioning candidate for cancers.

PMID: 31719612 [PubMed - in process]

Identification of relevant hub genes for early intervention at gene coexpression modules with altered predicted expression in schizophrenia.

Prog Neuropsychopharmacol Biol Psychiatry. 2019 Nov 09;:109815

Authors: Rodriguez-López J, Arrojo M, Paz E, Páramo M, Costas J

Abstract
Genetic risk for schizophrenia is due to the joint effect of multiple genes acting mainly at two different processes, prenatal/perinatal neurodevelopment and adolescence/early adulthood synapse maturation. Identification of important genes at the second process is of relevance for early intervention. The aim of this work was to identify gene co-expression modules with altered expression in schizophrenia during adolescence/early adulthood. To this goal, we predicted frontal cortex gene expression in one discovery sample, the largest GWAS of schizophrenia from the Psychiatric Genomics Consortium, using S-prediXcan, and in one target sample, consisting of 625 schizophrenic patients and 819 controls from Spain, using prediXcan. Prediction models were trained on GTEx frontal cortex expression dataset. In parallel, we identified brain co-expression modules from BrainSpan using WGCNA. Then, we estimated polygenic risk scores based on predicted expression (PE-PRS) for each co-expression module in the target sample, based on PE-PRS model from the discovery sample. This analysis led to the identification of a module with mainly adolescence/adulthood expression whose PE-PRS was significantly associated with schizophrenia. The module was significantly enriched in synaptic processes. Several hub genes at this module are drugabble, according to the drug-gene interaction database, and/or involved in synaptic transmission, such as the voltage-gated ion channels SCN2B and KCNAB2, the calcium calmodulin kinases CAMK2A and CAMK1G, or genes involved in synaptic vesicle cycle, such as DNM1, or SYNGR1. Therefore, identification of this module may be the first step in patient stratification based on biology, as well as in drug design and drug repurposing efforts.

PMID: 31715283 [PubMed - as supplied by publisher]

A botanical drug composed of three herbal materials attenuates the sensorimotor gating deficit and cognitive impairment induced by MK-801 in mice.

J Pharm Pharmacol. 2019 Nov 12;:

Authors: Koo B, Bae HJ, Goo N, Kim J, Kim J, Cai M, Jung IH, Cho K, Jung SY, Chang SW, Jang DS, Ryu JH

Abstract
OBJECTIVES: A botanical drug derived from the ethanolic extract composed of Clematis chinensis Osbeck (Ranunculaceae), Trichosanthes kirilowii Maximowicz (Cucurbitaceae) and Prunella vulgaris Linné (Lamiaceae) has been used to ameliorate rheumatoid arthritis as an ethical drug in Korea. In our study, we investigated the effect of this herbal complex extract (HCE) on schizophrenia-like behaviours induced by MK-801.
METHODS: HCE (30, 100 or 300 mg/kg, p.o) was orally administered to male ICR mice to a schizophrenia-like animal model induced by MK-801. We conducted an acoustic startle response task, an open-field task, a novel object recognition task and a social novelty preference task.
KEY FINDINGS: We found that a single administration of HCE (100 or 300 mg/kg) ameliorated MK-801-induced abnormal behaviours including sensorimotor gating deficits and social or object recognition memory deficits. In addition, MK-801-induced increases in phosphorylated Akt and GSK-3β expression levels in the prefrontal cortex were reversed by HCE (30, 100 or 300 mg/kg).
CONCLUSIONS: These results imply that HCE ameliorates MK-801-induced dysfunctions in prepulse inhibition, social interactions and cognitive function, partly by regulating the Akt and GSK-3β signalling pathways.

PMID: 31713882 [PubMed - as supplied by publisher]

Repurposing of drugs as STAT3 inhibitors for cancer therapy.

Semin Cancer Biol. 2019 Nov 08;:

Authors: Thilakasiri PS, DMello RS, Nero TL, Parker MW, Ernst M, Chand AL

Abstract
Drug repurposing is a valuable approach in delivering new cancer therapeutics rapidly into the clinic. Existing safety and patient tolerability data for drugs already in clinical use represent an untapped resource in terms of identifying therapeutic agents for off-label protein targets. The multicellular effects of STAT3 mediated by a range of various upstream signaling pathways make it an attractive therapeutic target with utility in a range of diseases including cancer, and has led to the development of a variety of STAT3 inhibitors. Moreover, heightened STAT3 transcriptional activation in tumor cells and within the cells of the tumor microenvironment contribute to disease progression. Consequently, there are many STAT3 inhibitors in preclinical development or under evaluation in clinical trials for their therapeutic efficacy predominantly in inflammatory diseases and cancer. Despite these advances, many challenges remain in ultimately providing STAT3 inhibitors to patients as cancer treatments, highlighting the need not only for a better understanding of the mechanisms associated with STAT3 activation, but also how various pharmaceutical agents suppress STAT3 activity in various cancers. In this review we discuss the importance of STAT3-dependent functions in cancer, review the status of compounds designed as direct-acting STAT3 inhibitors, and describe some of the strategies for repurposing of drugs as STAT3 inhibitors for cancer therapy.

PMID: 31711994 [PubMed - as supplied by publisher]

Synergistic Microbicidal Effect of Auranofin and Antibiotics Against Planktonic and Biofilm-Encased S. aureus and E. faecalis.

Front Microbiol. 2019;10:2453

Authors: She P, Zhou L, Li S, Liu Y, Xu L, Chen L, Luo Z, Wu Y

Abstract
Methicillin-resistant/susceptible Staphylococcus aureus (MRSA/MSSA) and Enterococcus faecalis strains are often found in community- and hospital-acquired infections. The single use of conventional antibiotics hardly completely kills the bacterial cells of interest, especially in the form of biofilms. Thus, drug repurposing and antimicrobial combination are promising ways to solve this problem. Antimicrobial susceptibility assays against cocci in a suspension and in a biofilm mode of growth were performed with broth microdilution methods. Checkerboard assays and the cutaneous mouse infection model were used to examine the activity of auranofin and conventional antibiotics alone and in combination. In the present study, auranofin possesses potent antimicrobial activities against both planktonic cells and biofilms with minimum inhibitory concentrations ranging 0.125-0.5 mg/L. Auranofin in combination with linezolid or fosfomycin showed synergistic antimicrobial activities against S. aureus MSSA and MRSA both in vitro and in vivo. Similarly, auranofin also behaved synergistic effect with chloramphenicol against E. faecalis. Additionally, auranofin improved the antibiofilm efficacy of chloramphenicol and linezolid, even on the biofilms grown on a catheter surface. Though, S. epidermidis showed significant susceptibility to AF treatment, no synergistic antimicrobial effects were observed with antibiotics we tested. In all, the use of a combination of auranofin with linezolid, fosfomycin, and chloramphenicol can provide a synergistic microbicidal effect in vitro and in vivo, which rapidly enhances antimicrobial activity and may help prevent or delay the emergence of resistance.

PMID: 31708908 [PubMed]

Drug Discovery and Repurposing Inhibits a Major Gut Pathogen-Derived Oncogenic Toxin.

Front Cell Infect Microbiol. 2019;9:364

Authors: Metz P, Tjan MJH, Wu S, Pervaiz M, Hermans S, Shettigar A, Sears CL, Ritschel T, Dutilh BE, Boleij A

Abstract
Objective: The human intestinal microbiome plays an important role in inflammatory bowel disease (IBD) and colorectal cancer (CRC) development. One of the first discovered bacterial mediators involves Bacteroides fragilis toxin (BFT, also named as fragilysin), a metalloprotease encoded by enterotoxigenic Bacteroides fragilis (ETBF) that causes barrier disruption and inflammation of the colon, leads to tumorigenesis in susceptible mice, and is enriched in the mucosa of IBD and CRC patients. Thus, targeted inhibition of BFT may benefit ETBF carrying patients. Design: By applying two complementary in silico drug design techniques, drug repositioning and molecular docking, we predicted potential BFT inhibitory compounds. Top candidates were tested in vitro on the CRC epithelial cell line HT29/c1 for their potential to inhibit key aspects of BFT activity, being epithelial morphology changes, E-cadherin cleavage (a marker for barrier function) and increased IL-8 secretion. Results: The primary bile acid and existing drug chenodeoxycholic acid (CDCA), currently used for treating gallstones, cerebrotendinous xanthomatosis, and constipation, was found to significantly inhibit all evaluated cell responses to BFT exposure. The inhibition of BFT resulted from a direct interaction between CDCA and BFT, as confirmed by an increase in the melting temperature of the BFT protein in the presence of CDCA. Conclusion: Together, our results show the potential of in silico drug discovery to combat harmful human and microbiome-derived proteins and more specifically suggests a potential for retargeting CDCA to inhibit the pro-oncogenic toxin BFT.

PMID: 31709196 [PubMed - in process]

Towards Better Drug Repositioning: Targeted Immunoinflammatory Therapy for Diabetic Nephropathy.

Curr Med Chem. 2019 Nov 08;:

Authors: Zhang Q, Yang M, Xiao Y, Han Y, Yang S, Sun L

Abstract
Diabetic nephropathy (DN) is one of the most common and important microvascular complications of diabetes mellitus (DM). The main clinical features of DN are proteinuria and a progressive decline in renal function , which are associated with structural and functional changes in the kidney. The pathogenesis of DN is multifactorial, including genetic, metabolic and haemodynamic factors, which can trigger a sequence of events. Controlling metabolic risks such as hyperglycaemia, hypertension and dyslipidaemia is not enough to slow the progression of DN. Recent studies have emphasized immunoinflammation as a critical pathogenic factor in the progression of DN. Therefore, targeting inflammation is considered a potential and novel treatment strategy for DN. In this review, we will briefly introduce the inflammatory process of DN and discuss the anti-inflammatory effects of antidiabetic drugs when treating DN.

PMID: 31701843 [PubMed - as supplied by publisher]

Genomic interrogation of familial short stature contributes to the discovery of the pathophysiological mechanisms and pharmaceutical drug repositioning.

J Biomed Sci. 2019 Nov 07;26(1):91

Authors: Wong HS, Lin YJ, Lu HF, Liao WL, Chen CH, Wu JY, Chang WC, Tsai FJ

Abstract
BACKGROUND: Genetic factors, dysregulation in the endocrine system, cytokine and paracrine factors are implicated in the pathogenesis of familial short stature (FSS). Nowadays, the treatment choice for FSS is limited, with only recombinant human growth hormone (rhGH) being available.
METHODS: Herein, starting from the identification of 122 genetic loci related to FSS, we adopted a genetic-driven drug discovery bioinformatics pipeline based on functional annotation to prioritize crucial biological FSS-related genes. These genes were suggested to be potential targets for therapeutics.
RESULTS: We discovered five druggable subnetworks, which contained seven FSS-related genes and 17 druggable targerts.
CONCLUSIONS: This study provides a valuable drug repositioning accompanied by corresponding targetable gene clusters for FSS therapy.

PMID: 31699087 [PubMed - in process]

Current progress and future perspectives of polypharmacology : From the view of non-small cell lung cancer.

Semin Cancer Biol. 2019 Nov 04;:

Authors: Ramanathan K, Shanthi V, Maiti S, Shin WH, Kihara D

Abstract
A pre-eminent subtype of lung carcinoma, Non-small cell lung cancer accounts for paramount causes of cancer-associated mortality worldwide. Undeterred by the endeavour in the treatment strategies, the overall cure and survival rates for NSCLC remain substandard, particularly in metastatic diseases. Moreover, the emergence of resistance to classic anticancer drugs further deteriorates the situation. These demanding circumstances culminate the need of extended and revamped research for the establishment of upcoming generation cancer therapeutics. Drug repositioning introduces an affordable and efficient strategy to discover novel drug action, especially when integrated with recent systems biology driven stratagem. This review illustrates the trendsetting approaches in repurposing along with their numerous success stories with an emphasize on the NSCLC therapeutics. Indeed, these novel hits, in combination with conventional anticancer agents, will ideally make their way the clinics and strengthen the therapeutic arsenal to combat drug resistance in the near future.

PMID: 31698087 [PubMed - as supplied by publisher]

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AMPK activation induced by promethazine increases NOXA expression and Beclin-1 phosphorylation and drives autophagy-associated apoptosis in chronic myeloid leukemia.

Chem Biol Interact. 2019 Nov 01;:108888

Authors: Medeiros HCD, Colturato-Kido C, Ferraz LS, Costa CA, Moraes VWR, Paredes-Gamero EJ, Tersariol ILS, Rodrigues T

Abstract
Relapse and drug resistance is still major challenges in the treatment of leukemia. Promethazine, an antihistaminic phenothiazine derivative, has been used to prevent chemotherapy-induced emesis, although there is no report about its antitumor potential. Thus, we evaluated the promethazine cytotoxicity against several leukemia cells and the underlying mechanisms were investigated. Promethazine exhibited potent and selective cytotoxicity against all leukemia cell types in vitro at clinically relevant concentrations. Philadelphia positive chronic myeloid leukemia (CML) K562 cells were the most sensitive cell line. The cytotoxicity of promethazine in these cells was triggered by the activation of AMPK and inhibition of PI3K/AKT/mTOR pathway. The subsequent downstream effects were NOXA increase, MCL-1 decrease, and Beclin-1 activation, resulting in autophagy-associated apoptosis. These data highlight targeting autophagy may represent an interesting strategy in CML therapy, and also the antitumor potential of promethazine by acting in AMPK and PI3K/AKT/mTOR signaling pathways. Since this drug is currently used with relative low side effects, its repurposing may represent a new therapeutic opportunity for leukemia treatment.

PMID: 31682805 [PubMed - as supplied by publisher]

Editorial: Beyond Antimicrobials: Non-traditional Approaches to Combating Multidrug-Resistant Bacteria.

Front Cell Infect Microbiol. 2019;9:343

Authors: Kirienko NV, Rahme L, Cho YH

PMID: 31681623 [PubMed - in process]