World Health Day is a good moment to call attention to a silent emergency that’s putting the health of everyone on our planet at risk: Antimicrobial resistance (AMR) is quietly eroding the foundations of modern medicine.
On a day when we talk about equity and prevention, it’s worth pausing to consider a threat that often only makes headlines once people are already sick — when routine infections fail to respond, surgeries become riskier, and chemotherapy patients lose their safety net. AMR isn’t an abstract lab problem; it is already causing preventable deaths, lengthening hospital stays, driving up medical bills, and forcing clinicians to choose older, more toxic, or intravenous treatments because simple oral antibiotics no longer work. For families, this looks like longer recoveries, infertility after an untreated infection, or tragic neonatal losses from preventable diseases — real human consequences that ripple through communities and strain health systems. If we want better health for everyone, addressing AMR must move from technical briefing rooms into everyday public health action.
The scale is sobering. The World Health Organization’s (WHO) 2020 estimate of roughly 374 million new cases of four curable STIs still frames the global burden, but since then, many regions have reported rebounds in gonorrhea and syphilis as testing and clinic access resumed after pandemic disruptions.1 In the U.S. and parts of Europe, public health authorities documented rising syphilis and gonorrhea case counts and a worrying resurgence of congenital syphilis. Making matters worse, AMR—particularly in Neisseria gonorrhoeae—has progressed, narrowing oral treatment options and pushing clinicians toward more complex, often costlier regimens. The net effect is more severe outcomes, higher health‑system costs, and growing urgency for new diagnostics, stewardship, and oral therapeutics.
This threat is why we must broaden the playbook: Rather than only discovering new antibiotics, we need strategies that protect and restore the utility of previously effective oral drugs, and we need to produce new oral agents with mechanisms that pathogens have not yet overcome.
Following are three complementary scientific approaches TAXIS is currently researching to combat AMR—efflux pump inhibitors, DHFR inhibitors, and FtsZ inhibitors.
Efflux Pump Inhibitors (EPIs) — helping antibiotics stay inside bacteria.
Bacteria use efflux pumps to push antibiotics out before the drugs can take effect. When those pumps are active, even a highly effective antibiotic can be rendered ineffective. Efflux pump inhibitors are designed to block that export machinery, allowing antibiotics to accumulate inside bacterial cells and exert their effects. This approach may restore the activity of drugs that are currently ineffective against resistant strains.
Why it matters: EPIs may revive well-known, orally available antibiotics—drugs clinicians already know how to prescribe and health systems know how to deliver—potentially shifting care from hospital infusions back to outpatient treatment and lowering costs.
DHFR Inhibitors — precise targeting of a vital bacterial enzyme.
Dihydrofolate reductase (DHFR) is essential for producing the nucleotides bacteria need to replicate, so blocking it halts bacterial growth. The challenge is designing molecules that inhibit bacterial DHFR without affecting the human version, which would cause toxicity. New tricyclic DHFR compounds are engineered to be highly selective for the bacterial enzyme, orally absorbable, and less likely to drive resistance.
Why it matters: A safe, oral DHFR inhibitor would provide clinicians with a new, practical outpatient option for infections increasingly resistant to current therapies—reducing hospital burden and improving access to timely treatment.
FtsZ Inhibitors — disrupting bacterial cell division at its source.
FtsZ is a protein that orchestrates bacterial cell division. Inhibitors targeting FtsZ prevent the assembly or function of the division ring, causing bacteria to fail to divide. This represents a fundamentally different mechanism from traditional antibiotics and is therefore less likely to encounter existing resistance pathways.
Why it matters: Targeting cell division offers a novel route to broad antibacterial activity and can complement other drug classes in combination therapy, reducing the likelihood that resistance to one agent undermines treatment.
A Layered Defense
No single approach is a silver bullet. EPIs may revive existing drugs, DHFR inhibitors may introduce new selective oral agents, and FtsZ inhibitors may provide novel mechanisms that bypass current resistance patterns. Together, these approaches are intended to create a layered defense: restore what works where possible, develop new options where needed, and diversify the pharmacologic toolkit so clinicians have choices that match patient needs and local resistance patterns.
But turning these ideas into real medicines takes more than strong chemistry. Candidates must be safe, as effective as oral therapies, scalable to manufacture, and resilient against the emergence of new resistance. That means planning early for absorption and clearance, defining a clear safety window, and ensuring manufacturability at scale. It also requires collaboration with clinicians, public health experts, and regulators so new treatments fit into real-world care pathways.
World Health Day is a call to action. AMR demands a coordinated global effort—stronger surveillance, better stewardship to preserve existing therapies, and sustained investment in scalable drug development that prioritizes oral, accessible medicines. Scientific progress gives us reason for cautious optimism, but only coordinated action and thoughtful translation will change outcomes.
Recognition of a problem without action won’t save lives; this World Health Day, let’s commit to both.
References
- Centers For Disease Control & Prevention. Sexually Transmitted Infections Surveillance, 2024 (Provisional), September, 2025. Center For Disease Control. https://www.cdc.gov/sti-statistics/annual/index.html
