Pritelivir: 93% Healing Rate and FDA Goal Set for 2026 — Mechanism and Target Explained
German biotech company AiCuris Anti-infective Cures AG has announced new clinical data for its two lead antiviral candidates, Pritelivir and AIC468, during the ID Week 2025 infectious disease conference held in Atlanta, Georgia.
According to the presentation, Pritelivir, an investigational treatment for refractory herpes simplex virus (HSV) infections, demonstrated strong efficacy and safety in Phase 2, achieving 93% lesion healing within 28 days compared with 57% for foscarnet, the current standard therapy for resistant HSV cases.
These results, along with data from the pivotal Phase 3 trial—which has already met its primary endpoint with statistical superiority—have reinforced Pritelivir’s potential as a breakthrough therapy. The drug has already received FDA Breakthrough Therapy Designation, and AiCuris plans to submit a New Drug Application (NDA) in 2026, preparing for commercial launch in the United States.
The company also presented Phase 1 safety and pharmacokinetic data for AIC468, a novel antisense oligonucleotide (ASO) therapy targeting BK virus (BKV) infections in kidney transplant recipients. The study showed no dose-related toxicity or severe adverse events, supporting advancement into Phase 2 trials in early 2026.
Why Pritelivir Matters
Herpes simplex virus (HSV-1 and HSV-2) remains one of the most persistent viral infections in humans.
While most people experience mild or episodic symptoms, immunocompromised patients—such as transplant recipients or cancer patients—often suffer from chronic or drug-resistant infections that are difficult to control.
Conventional antivirals such as acyclovir, valacyclovir, and foscarnet work by inhibiting viral DNA polymerase, but they require activation by a viral enzyme called thymidine kinase (TK).
When the virus mutates this TK gene, the drug can no longer function—creating acyclovir-resistant HSV.
That’s where Pritelivir is different.
Instead of depending on the TK enzyme, it targets the helicase–primase complex, an earlier and essential step in viral DNA replication.
By shuttingeven against
Clinical Comparison: Pritelivir vs. Acyclovir / Foscarnet
| Parameter | Pritelivir | Acyclovir |
|---|---|---|
| Mechanism | Helicase–Primase inhibitor (TK-independent) | DNA polymerase inhibitor (TK-dependent) |
| Activity vs. resistant HSV | ✅ Effective | ❌ Ineffective |
| Lesion healing (Phase 2) | 93 % (within 28 days) | 57–70 % |
| Treatment discontinuation (side effects) | 0 % | ~40 % |
| Dosing frequency | Once daily (oral) | 3–5 times per day (oral / IV) |
| Recurrence rate / year | 1–2 outbreaks | 4–6 outbreaks |
| Viral DNA shedding reduction | ↓ 80–90 % | ↓ 40–50 % |
The Science Behind the Advantage
To put it simply:
Acyclovir stops the virus after it starts copying its DNA.
Pritelivir prevents the virus from starting replication at all.
This difference in timing explains why Pritelivir shows such strong results—
it attacks the replication process at its very origin.
Because it bypasses the viral TK enzyme, Pritelivir remains active against resistant HSV strains,
a feature that makes it especially valuable for patients with compromised immune systems or chronic recurrences.
Conclusion: Toward a New Era in HSV Treatment
With Pritelivir achieving a 93% healing rate in resistant herpes,
AiCuris is rapidly emerging as a key innovator in antiviral therapy.
For patients with acyclovir-resistant HSV,
Pritelivir may represent the first truly effective oral treatment—
and potentially the most important advance in herpes management in decades.
Mechanism and Target of Pritelivir
Pritelivir is not a drug designed exclusively for patients with drug-resistant HSV infections.
However, it has shown particularly strong efficacy in patients who do not respond to existing antivirals such as acyclovir or valacyclovir.
This compound works by inhibiting the helicase–primase complex, a key enzyme system involved in the early stages of viral DNA unwinding and replication.
As a result, the virus is prevented from initiating DNA synthesis altogether.
In most drug-resistant HSV strains, mutations occur in the thymidine kinase (TK) or DNA polymerase genes, which renders traditional antivirals ineffective.
Because Pritelivir targets a completely different viral protein (the helicase–primase complex),
it remains active even against HSV strains that have developed resistance to standard treatments.
In other words, Pritelivir is not only effective for resistant HSV patients,
but also for all HSV infections, while being especially beneficial for those with acyclovir-resistant or immunocompromised conditions.
The clinical trials were initially focused on immunocompromised and resistant patient populations, as these are the groups where Pritelivir’s therapeutic potential can be most clearly demonstrated.
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