Verdinexor (Laverdia) for Canine Lymphoma: Mechanism and Evidence

Bottom line

• Verdinexor (marketed as Laverdia-CA1 by Dechra Veterinary Products) is an oral selective inhibitor of nuclear export that has been used for non-Hodgkin T-cell lymphoma in dogs.[1]
• Its target is exportin 1 (XPO1, also called KPT-335's target); XPO1 overexpression exports tumor-suppressor proteins out of the nucleus, and verdinexor blocks that export to restore tumor-suppressor function, inducing cell-cycle arrest and apoptosis.[2][3]
• In an open-label pilot study of eight dogs with cutaneous epitheliotropic T-cell lymphoma, 75% achieved complete response, partial response, or stable disease, and the authors concluded verdinexor could be considered a safe palliative option for that disease.[1]
• The most common adverse effects reported in that pilot were weight loss, inappetence, vomiting, and lethargy; verdinexor did not significantly reduce pruritus.[1]
• This page summarizes published evidence for licensed veterinary professionals; it is not a dosing guide, and all dosing must follow the current label and formulary.

Drug facts

• Class: Selective inhibitor of nuclear export (SINE); exportin 1 (XPO1) inhibitor
• Mechanism: Blocks XPO1-mediated nuclear export of tumor-suppressor proteins, restoring their function and driving cell-cycle arrest and apoptosis in lymphoma cells[2][3]
• Route: Oral
• Indication context: Used for non-Hodgkin (T-cell) lymphoma in dogs; marketed as Laverdia-CA1 (Dechra Veterinary Products)[1]
• Dosing: Not specified here; follow the current label and formulary for the individual patient

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What the evidence shows

Mechanism: blocking nuclear export to restore tumor suppression

Lymphoma is the most common neoplasm of lymphoid tissue in dogs, and exportin 1 (XPO1) is a major nuclear receptor that exports proteins and RNA out of the nucleus. When XPO1 is upregulated, it can strip tumor-suppressor proteins of their function by exporting them from the nucleus into the cytoplasm. Verdinexor (the compound KPT-335) is a selective XPO1 inhibitor that blocks this translocation, restoring tumor-suppressor function and inducing cell-cycle arrest and apoptosis.[2]

In vitro work in canine lymphoma cell lines has shown that XPO1 messenger RNA and protein are expressed across multiple canine lymphoma lines, and that those lines respond to verdinexor with dose-dependent growth inhibition and reduced viability, with half-maximal inhibitory concentrations in the high-nanomolar range.[2] A related study found that verdinexor reduces XPO1 protein in a dose-dependent manner through proteasome-mediated degradation.[3]

Clinical signal: an open-label pilot in cutaneous T-cell lymphoma

The most direct clinical evidence in the published literature is an open-label pilot study evaluating verdinexor in eight client-owned dogs with cutaneous epitheliotropic T-cell lymphoma — a presentation for which verdinexor efficacy had not previously been characterized. Dogs were treated with oral verdinexor on a twice-weekly schedule with a minimum interval between doses, and adjunctive therapy was permitted after Day 14.[1]

Seventy-five percent of patients achieved complete response, partial response, or stable disease, and the mean time to disease progression was approximately 56 days. There was a statistically significant reduction in the study's disease-extent score (the Canine Epitheliotropic Lymphoma Extent and Severity Index) when each dog's lowest score was compared with baseline. Notably, verdinexor did not significantly reduce pruritus at any time point, whether given as monotherapy or alongside lokivetmab with or without glucocorticoids. The authors concluded verdinexor could be considered a safe, palliative treatment for canine cutaneous epitheliotropic T-cell lymphoma.[1]

Combination with conventional chemotherapy: preclinical evidence

Because single-agent activity is partial, there is interest in combining verdinexor with conventional cytotoxic drugs. In four canine lymphoma cell lines, combining verdinexor with doxorubicin or vincristine significantly suppressed cell proliferation compared with either single agent, and the verdinexor-driven reduction in XPO1 protein was reversed by proteasome inhibition.[3] This is preclinical, cell-line evidence — it supports the biological rationale for combination strategies but does not establish a clinical protocol.

How this fits clinical practice

This section summarizes the published evidence base for licensed practitioners and is not clinical guidance. Verdinexor is an orally administered option with a distinct mechanism from conventional cytotoxic chemotherapy, which makes it of interest where an at-home oral agent is preferred or where conventional protocols are not feasible. The strongest clinical evidence is a small, open-label pilot in a specific disease presentation (cutaneous epitheliotropic T-cell lymphoma), so the efficacy signal should be read as preliminary rather than definitive, and the partial single-agent activity is consistent with the preclinical rationale for combination approaches.

Dosing for an individual patient must follow the current label and formulary; this page does not provide dose recommendations. As with any antineoplastic agent, appropriate client communication about gastrointestinal and constitutional adverse effects, monitoring, and safe-handling precautions applies.

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References

1. Vlodaver EM, Keating MK, Bidot WA, Bruyette DS, Rosenkrantz WS. Efficacy of verdinexor for the treatment of naive canine epitheliotropic cutaneous T-cell lymphoma: an open-label pilot study. Vet Dermatol. 2024;35(5):536-546. https://pubmed.ncbi.nlm.nih.gov/39074816/
2. Primarizky H, Kambayashi S, Baba K, Tani K, Okuda M. Exportin 1 (XPO1) expression and effectiveness of XPO1 inhibitor against canine lymphoma cell lines. Vet Sci. 2025;12(8):700. https://pubmed.ncbi.nlm.nih.gov/40872651/
3. Primarizky H, Kambayashi S, Baba K, Tani K, Okuda M. Combination effect of exportin 1 inhibitor (KPT-335) with doxorubicin or vincristine in canine lymphoma cell lines. J Vet Med Sci. 2026;88(1):119-125. https://pubmed.ncbi.nlm.nih.gov/41285475/

Changelog

• 2026-06-05: First published.