No escape for ESKAPE pathogens

The World Health Organization (WHO) recognises antimicrobial resistance as one of the three most important human health concerns of our time. With our depth of in-house chemistry and biology knowledge and world leading anti-infective development experience at Neem, we see this as a serious opportunity to apply our knowledge to a worthwhile global challenge.

Our antimicrobial know-how is grounded in a fundamental understanding of the concepts of the intrinsic resistome, described by Olivares, et al (2013) as being comprised of the elements of phenotypic - and acquired resistance. These concepts reflect the impact that the external environment has on bacteria’s internal physiological states and account for a gap in traditional understanding of how antimicrobial resistance works. This model holds that physiological changes within bacteria contribute to development of antimicrobial resistance alongside the genetic changes and traditionally understood determinants of resistance development by bacteria.

At Neem we have particular know-how and research interest in understanding bacterial virulence as a driver of disease burden and treatment cost for infections that are caused by multidrug resistant Gram negative and Gram positive bacteria. This incorporates the phenotypic resistance elements of biofilms, persister cells and phenomenon such as swimming and swarming.

Chemical signalling between cells (quorum sensing) is one part of these phenotypic resistance functions. Quorum sensing and its inhibition modulates virulence factor expression in and biofilm secretion by bacteria. These processes are both drivers of development and spread of infection. Disruption of quorum sensing signals inhibits the cascade of virulence effects that would normally generate host outcomes such as infection, bacterial colonisation, inflammation and reduced effectiveness of antibiotics, as well as a broader impact of further resistance generation by bacteria to these antibiotics.

We are developing a portfolio of first-in-class molecules that target quorum sensing, virulence and biofilms as novel alternatives to antibiotics. We have also developed a proprietary screening cascade for identifying novel compounds that decrease virulence factor production and modulate the planktonic to sessile phenotype of singular and multiple species critical or high priority pathogen biofilms.

No escape for ESKAPE pathogens

The World Health Organization (WHO) recognises antimicrobial resistance as one of the three most important human health concerns of our time. With our depth of in-house chemistry and biology knowledge and world leading anti-infective development experience at Neem, we see this as a serious opportunity to apply our knowledge to a worthwhile global challenge.

Our antimicrobial know-how is grounded in a fundamental understanding of the concepts of the intrinsic resistome, described by Olivares, et al (2013) as being comprised of the elements of phenotypic - and acquired resistance. These concepts reflect the impact that the external environment has on bacteria’s internal physiological states and account for a gap in traditional understanding of how antimicrobial resistance works. This model holds that physiological changes within bacteria contribute to development of antimicrobial resistance alongside the genetic changes and traditionally understood determinants of resistance development by bacteria.

At Neem we have particular know-how and research interest in understanding bacterial virulence as a driver of disease burden and treatment cost for infections that are caused by multidrug resistant Gram negative and Gram positive bacteria. This incorporates the phenotypic resistance elements of biofilms, persister cells and phenomenon such as swimming and swarming.

Chemical signalling between cells (quorum sensing) is one part of these phenotypic resistance functions. Quorum sensing and its inhibition modulates virulence factor expression in and biofilm secretion by bacteria. These processes are both drivers of development and spread of infection. Disruption of quorum sensing signals inhibits the cascade of virulence effects that would normally generate host outcomes such as infection, bacterial colonisation, inflammation and reduced effectiveness of antibiotics, as well as a broader impact of further resistance generation by bacteria to these antibiotics.

We are developing a portfolio of first-in-class molecules that target quorum sensing, virulence and biofilms as novel alternatives to antibiotics. We have also developed a proprietary screening cascade for identifying novel compounds that decrease virulence factor production and modulate the planktonic to sessile phenotype of singular and multiple species critical or high priority pathogen biofilms.