KIF18A - Indication Prioritization Report

1. Executive Summary

• Target snapshot: KIF18A is a kinesin-8 family microtubule-depolymerizing motor protein essential for chromosome congression during mitosis. It is selectively required by chromosomally unstable (CIN) tumor cells, establishing a synthetic lethal therapeutic window.

• Scope: 1,000 indications across 14 therapeutic areas were ranked by PandaOmics; this report analyzes the top 50 indications in oncology and aging-related disease areas (Oncology, Rare/genetic, Neurologic, Cardiovascular, Endocrine/metabolic). Oncology dominates (29/50 indications), with Rare and genetic disease contributing 14.

• Lead indications: Breast cancer (#3), hepatocellular carcinoma (#4), colorectal cancer (#5), ovarian carcinoma (#22), and non-small cell lung carcinoma (#24) are the highest-ranked specific indications. Six Phase 1/2 clinical trials are already active for KIF18A inhibitors in solid tumors, primarily ovarian cancer, breast cancer, and NSCLC. See verdict.

• Expansion opportunities: Hepatocellular carcinoma (#4), glioblastoma (#10), medulloblastoma (#46), gastric carcinoma (#74), papillary renal cell carcinoma (#19), and prostate carcinoma (#26) represent high-scoring untapped opportunities with no active KIF18A inhibitor trials. See untapped opportunities.

• Aging-related diseases: No published evidence links KIF18A directly to aging biology, cellular senescence, or neurodegeneration. The aging-related indications in the filtered set (neurodegenerative disease #40, diabetes mellitus #37) have low PandaOmics scores driven primarily by network co-embedding rather than direct evidence.

• Reliability: KIF18A is not a hub gene; scores are driven by specific omics signals (network, matrix factorization, heterogeneous graph walk) reflecting genuine biological connections to cell cycle and mitosis pathways. See confidence.

• Evidence character: The strongest independent evidence lines are: (1) functional studies demonstrating CIN-selective synthetic lethality (Marquis et al. 2021); (2) pharmacological validation with multiple chemical series (Payton et al. 2024, Phillips et al. 2025); (3) unfavorable prognostic association validated by TCGA/HPA in kidney RCC, HCC, pancreatic adenocarcinoma, and lung adenocarcinoma.

• Recommendation: Prioritize CIN-high solid tumors (ovarian HGSOC, TNBC, CRC, HCC) where KIF18A overexpression and CIN are well-documented. The key differentiator from prior kinesin inhibitor failures (Eg5/KSP) is biomarker-guided patient selection using CIN status. For expansion, hepatocellular carcinoma and glioblastoma have the strongest untapped PandaOmics signal with supporting expression and network evidence. Combination with immune checkpoint inhibitors (anti-PD-1) in CRC is a high-value strategy based on recent preclinical evidence (Liu et al. 2025).

2. Target Characterization

KIF18A is a kinesin superfamily motor protein (kinesin-8 family) that functions as a motile microtubule depolymerase. It suppresses kinetochore oscillations during mitosis, ensuring proper chromosome congression at the metaphase plate. The protein contains a kinesin motor domain (residues 11-355) and localizes to microtubules and the cytokinetic bridge.

KIF18A is classified as an essential protein and a predicted intracellular protein (HPA). It is cell-cycle-dependent (CCD) at both protein and transcript levels. The critical therapeutic insight is that KIF18A is dispensable for normal cell division but selectively required by CIN-high tumor cells, which depend on KIF18A to manage the consequences of elevated chromosome mis-segregation rates.

Target summary:

• Function: Microtubule-depolymerizing kinesin that suppresses kinetochore oscillations during mitosis; essential for chromosome alignment at the metaphase plate.
• Baseline expression: Expressed predominantly in mitotic/proliferating cells; tissue-level expression highest in testis (12.8 nTPM), lymphoid tissue (8.9 nTPM), and bone marrow (7.8 nTPM). Cell-type enrichment in mitotic cells across multiple tissues (HPA). Detail in Sec 5.1.
• Differential expression: Significantly upregulated in hepatocellular carcinoma (logFC=0.52, p=7.1e-71), gastric carcinoma (logFC=0.49, p=4.6e-86), invasive breast ductal carcinoma (logFC=0.43, p=2.6e-19), and NSCLC (logFC=0.39, p=3.0e-75). Detail in Sec 5.2.
• Associated drugs: No approved drugs. Clinical-stage KIF18A inhibitors: sovilnesib/AMG-650 (Ph1, Volastra/Amgen), VLS-1488 (Ph1/2, Volastra), ATX-295 (Ph1, Accent Therapeutics), GenSci122 (Ph1, GenSci), GH2616 (Ph1, Genhouse), MEN2501 (Ph1, Stemline/Menarini).
• Modality fit: Intracellular target; small molecule is the validated modality (all 6 clinical candidates are oral small molecules). Required direction: inhibition.
• 3D structures: 7 experimental PDB structures; best resolution 2.2 Å (X-ray, 3LRE). Detail in Sec 2.1.
• Constraint & tractability: ClinVar: 152 total variants, 20 pathogenic. KIF18A is a mitotic gene — inhibition is tolerated by normal cells but lethal to CIN-high tumors (synthetic lethal window). Detail in Sec 7.
• Safety concerns: KIF18A inhibition is predicted to be well-tolerated in normal cells based on preclinical data; Kif18a-null mice show male infertility (germinal cell aplasia) but are otherwise viable. No dose-limiting toxicities observed up to 800 mg in VLS-1488 Phase 1 data (ASCO 2025). Bone marrow toxicity is the theoretical risk given expression in proliferating hematopoietic cells.
• Genetics (trait associations): No GWAS Catalog associations found for KIF18A. ClinVar: 152 variants, 20 pathogenic.
• Paralog cross-reactivity: Closest paralog is KIF18B (36.4% identity) — moderate cross-reactivity risk; other kinesin family members (KIF25 27.6%, KIF3B 27.2%) are more distant.
• Species homology: Mouse 76.2%, rat 71.9%, dog 85.4%, macaque 96.8% identity. Rodent models are informative but identity is below the >80% high-confidence threshold for mouse/rat; dog and macaque models are preferred for translational studies.
• IP landscape: Active patent space with ~693 patent documents. Key assignees include Volastra Therapeutics (composition-of-matter for VLS-1488 and sovilnesib), Accent Therapeutics (ATX-295), Amgen (AMG-650), and Chinese biotechs (GenSci, Genhouse). Recent filings include indication-specific use patents for ovarian cancer, colorectal cancer, and breast cancer. The space is competitive but not yet crowded with approved composition-of-matter patents.

Overall verdict. KIF18A is a structurally tractable (2.2 Å X-ray, oral small molecule validated), CIN-selective target with 6 active Phase 1/2 clinical trials and robust preclinical validation across multiple solid tumors. The synthetic lethal mechanism differentiates it from failed Eg5/KSP kinesin inhibitors. The main risk is the competitive landscape (5+ companies, same mechanism) and the early clinical stage (no Phase 2 efficacy data yet). The untapped whitespace lies in CIN-high solid tumors beyond ovarian/breast (HCC, GBM, CRC, gastric, prostate), where strong PandaOmics omics signals and expression data support expansion. Aging-related indications lack direct evidence and are not recommended for pursuit.

2.1 3D structures (PDB)

7 experimental structures are available for KIF18A:

The 2.2 Å X-ray structure (3LRE) covers the motor domain and is suitable for structure-based drug design. The 2.41 Å structure (9YMG) captures KIF18A bound to a non-hydrolyzable ATP analog and tubulin, providing mechanistic insight.

3. Indication Prioritization Overview

PandaOmics scored KIF18A across 1,000 indications in 14 therapeutic areas. This analysis focuses on the top 50 indications in oncology and aging-related therapeutic areas (Oncology, Rare/genetic disease, Neurologic disease, Cardiovascular disease, Endocrine/metabolic disease).

3.1 Therapeutic-area landscape

Where the signal concentrates.

Oncology dominates, accounting for 58% of the top 50 filtered indications. Rare and genetic disease (28%) includes several pediatric brain tumors (glioblastoma, medulloblastoma) and chromosomal instability syndromes. Aging-related areas (neurologic, cardiovascular, endocrine) contribute only 7 indications with lower scores.

3.2 Leading indications

The top-ranked specific diseases and the clinical compounds targeting KIF18A for each. Ordered by PandaOmics rank; the 23 scores are shown in the heatmap below.

Figure 1. Top 10 leading indications for KIF18A (23 PandaOmics scores). The 23 scores for the 10 top-ranked specific indications, ordered by composite rank. Network (PPI) and matrix factorization scores are consistently high across oncology indications, reflecting KIF18A's integration into mitotic and cell-cycle networks dysregulated in cancer.

3.3 Untapped opportunities

The same ranking with indications that already have active KIF18A inhibitor trials removed — where to expand.

3.2 vs 3.3: Section 3.2 lists the strongest associations, including indications with active clinical trials. Section 3.3 is that ranking filtered to indications with no active KIF18A inhibitor trial — the actionable whitespace.

Since KIF18A has no approved drugs, all indications are technically untapped. However, active clinical trials exist for ovarian cancer, breast cancer (TNBC), and NSCLC. The table below excludes those:

The untapped whitespace is dominated by CIN-high solid tumors — hepatocellular carcinoma, glioblastoma, gastric carcinoma, and papillary renal cell carcinoma — where the biological rationale (CIN dependence + KIF18A overexpression) is strong but no clinical programs exist.

Supplementary (NOT embedded in the body): The full grouped heatmap (all therapeutic areas x 23 scores) is at visualizations/indication_heatmap.png (+ interactive visualizations/indication_heatmap.html); the complete per-indication score matrix is outputs/indication_scores_full.csv.

4. Drug, Competitive & Trial Landscape

4.1 Drugs against KIF18A & tiers

KIF18A has no approved drugs (ChEMBL). All compounds are in early clinical development (Phase 1/2):

Tiers: Since no drugs are approved for any indication, all indications are Tier 2 (development-phase drugs exist) or Tier 3 (no drug against target for that specific indication). Tier 1 (approved drug) does not apply.

4.2 Modality fit

KIF18A is an intracellular motor protein (microtubule/cytokinetic bridge localization). The required therapeutic direction is inhibition (blocking ATPase/motor activity).

The clinically validated modality is oral small molecule inhibition of the kinesin motor domain. All 6 clinical programs use this approach.

4.3 Competitive landscape

KIF18A is a novel target with no approved drugs. The competitive landscape consists of:

KIF18A inhibitor programs (5 companies):

Kinesin inhibitor class history (cautionary context): Eg5/KSP (KIF11) inhibitors were the first mitotic kinesin inhibitor class to reach clinical trials. Ispinesib (SB-715992) failed in Phase 2 across melanoma (Lee et al. 2008), HNSCC (Tang et al. 2008), HCC (Knox et al. 2008), RCC (Lee et al. 2008), and prostate cancer (Beer et al. 2008) — with no objective responses in any trial. The failure was attributed to: (1) no patient selection biomarker; (2) narrow therapeutic window (bone marrow toxicity); and (3) resistance via allosteric mechanisms (Talapatra et al. 2013). KIF18A inhibitors are fundamentally differentiated by CIN-selective synthetic lethality — normal cells tolerate KIF18A loss while CIN-high tumors die.

4.4 Clinical-trial landscape (ClinicalTrials.gov)

6 active clinical trials for KIF18A inhibitors:

The most advanced program is VLS-1488 (Phase 1/2), with initial data presented at ASCO 2025 showing no dose-limiting toxicities up to 800 mg in 52 patients. CIN-high solid tumors are the primary focus across all programs, with ovarian cancer (HGSOC) as the lead indication for most developers.

5. Expression

Two different reads:

• Baseline expression (5.1): where KIF18A is normally expressed — a constitutive pattern.
• Differential expression (5.2): in which diseases KIF18A is dysregulated vs normal tissue — a disease signal.

5.1 Baseline expression (where the target is expressed)

KIF18A is a cell-cycle-dependent protein (CCD) expressed predominantly in mitotic/proliferating cells. Cell-type enrichment: mitotic cells in adrenal gland, minor salivary gland, skin, spleen, stomach, and early spermatids in testis. Tissue-level expression is highest in testis (12.8 nTPM), lymphoid tissue (8.9 nTPM), and bone marrow (7.8 nTPM) (Human Protein Atlas, proteinatlas.org, CC-BY-SA 4.0). Full table in outputs/celltype_expression.csv.

Figure 3. KIF18A baseline tissue expression. Top tissues by RNA expression (nTPM). KIF18A expression is enriched in tissues with high proliferative activity (testis, lymphoid tissue, bone marrow), consistent with its role as a mitotic kinesin. Source: Human Protein Atlas (proteinatlas.org, CC-BY-SA 4.0).

5.2 Differential expression (disease dysregulation - PandaOmics)

KIF18A differential expression across the top diseases (real logFC and p-value), from PandaOmics' pre-computed expression meta-analysis:

KIF18A is significantly upregulated in multiple solid tumors, with the strongest signals in hepatocellular carcinoma (logFC=0.52), gastric carcinoma (logFC=0.49), and invasive breast ductal carcinoma (logFC=0.43). All solid tumor indications show upregulation, consistent with the known biology of increased mitotic activity in cancer. The Alzheimer's disease signal (logFC=0.12) is weak and likely driven by glial proliferation rather than a direct KIF18A-disease mechanism.

6. Pathways & Network Interactions

6.1 Reactome pathways

KIF18A participates in mitotic cell cycle pathways:

- Cell Cycle, Mitotic (R-HSA-69278)

- Mitotic Prometaphase (R-HSA-68877)

- Resolution of Sister Chromatid Cohesion (R-HSA-2500257)

- Chromosome Maintenance (R-HSA-73886)

The pathway profile is consistent with KIF18A's role as a mitotic kinesin — all pathways relate to cell division, chromosome segregation, and kinetochore function.

6.2 STRING interactors

Direct protein interactors and confidence scores:

Figure 4. KIF18A STRING interaction network. Nodes = proteins; edges = functional associations (thicker = higher confidence); edge colour = evidence type. KIF18A's interactors are overwhelmingly mitotic regulators — kinetochore motors (CENPE), checkpoint proteins (CDC20, BUB1B), and other kinesins (KIF11, KIF2C). Source: STRING v12.0.

KIF18A PandaOmics interactome community score is consistently HIGH (>0.90) across the top oncology indications, reflecting KIF18A's central position in the mitotic/cell-cycle network that is dysregulated in cancer.

6.3 Target knowledge graph

KIF18A's interaction network connects it to key mitotic regulators (CENPE, CDC20, KIF11) that are themselves established cancer biology nodes. The drug-disease edges are limited to clinical-stage compounds since no KIF18A drugs are approved. The STRING partners create a coherent mitotic network, and the PandaOmics disease nodes cluster in solid tumors where cell-cycle dysregulation is a hallmark.

7. Genetic Evidence & Target Validation

7.1 Human genetic associations

GWAS Catalog: No GWAS associations found for KIF18A. This is consistent with KIF18A being an essential mitotic gene — loss-of-function variants would be strongly selected against, limiting common-variant associations.

ClinVar: 152 total variants, 20 classified as pathogenic. The pathogenic variants are associated with chromosome instability and infertility phenotypes.

The absence of GWAS hits does not weaken the cancer indication case — KIF18A's cancer role is driven by somatic overexpression and CIN dependence, not germline variation. PandaOmics GWAS sub-module scores (0.74-0.91 across top indications) reflect network-level co-association rather than direct KIF18A GWAS hits.

7.2 Constraint, tractability & essentiality

gnomAD: KIF18A shows evidence of LoF intolerance (LOEUF < 0.6), consistent with its essential role in cell division. This supports the biological reality of the target but also signals that complete inhibition in normal tissues could carry risk — hence the importance of the CIN-selective therapeutic window.

Essentiality: KIF18A is classified as an essential protein (HPA). DepMap data shows KIF18A dependency is enriched in CIN-high cell lines, consistent with the synthetic lethal mechanism. Normal/CIN-low cells are not KIF18A-dependent.

Genetic-support verdict: Moderate/indirect genetic support. No GWAS hits, but strong somatic overexpression data (Section 5.2), CIN-selective dependency (DepMap/functional studies), and ClinVar pathogenic variants collectively validate KIF18A as a real target. The evidence character is functional/somatic rather than germline-genetic.

8. Species Homology & Paralogs

Orthologs (Ensembl Compara):

Paralogs:

• Translational read: Mouse (76.2%) and rat (71.9%) identity is moderate, below the >80% high-confidence threshold. Kif18a-null mice are viable (with male infertility), supporting the safety window, but efficacy studies should be interpreted with caution. Macaque (96.8%) and dog (85.4%) are preferred translational models.

• Paralog / off-target read: KIF18B is the closest paralog at 36.4% identity. While the motor domain is conserved across the kinesin family, the overall sequence divergence (all paralogs <37%) suggests selectivity is achievable. All clinical KIF18A inhibitors report selectivity over KIF18B and other kinesin family members. The key selectivity concern is KIF11 (Eg5), the other mitotic kinesin with clinical-stage inhibitors; KIF18A inhibitors must avoid KIF11 inhibition to prevent the bone marrow toxicity that limited Eg5/KSP inhibitors.

9. Biological Rationale (Published Evidence)

CIN-selective synthetic lethality (foundational mechanism) — KIF18A is dispensable for normal cell division but selectively required by CIN-high tumor cells. Marquis et al. (2021) demonstrated that CIN tumor cells specifically require KIF18A for proliferation. Payton et al. (2024) provided pharmacological proof-of-concept with AMG-650, showing selective killing of CIN-high cancer cell lines.

Breast cancer — KIF18A overexpression correlates with higher tumor grade and proliferative index in invasive breast cancer (Kasahara et al. 2016). KIF18A is a predictive biomarker of poor benefit from endocrine therapy in early ER+ breast cancer (Alfarsi et al. 2019), suggesting patients with high KIF18A tumors may benefit from KIF18A inhibition as an alternative strategy.

Hepatocellular carcinoma — KIF18A promotes cell proliferation and metastasis in HCC through functional assays (Ren et al. 2024). Additionally, KIF18A induces EMT in hepatoma cells through the 5-LOX-dependent arachidonic acid pathway, providing a non-mitotic oncogenic mechanism (Wang et al. 2025). HPA validates KIF18A as an unfavorable prognostic marker in HCC (TCGA + validation cohort, p=8.1e-7).

Colorectal cancer — Targeted deletion of Kif18a protects from colitis-associated colorectal tumors in mice through impairing Akt phosphorylation (Zhu et al. 2013). Critically, targeting KIF18A triggers antitumor immunity and enhances PD-1 blockade in CRC with CIN phenotype (Liu et al. 2025), supporting a combination strategy.

Ovarian cancer — The KIF18A inhibitor ATX020 induces mitotic arrest and DNA damage in CIN-unstable HGSOC cells (Nair et al. 2025). Novel cyclohexenyl KIF18A inhibitors show activity in ovarian cancer models (Zhang et al. 2024). Ovarian HGSOC has the highest CIN burden of any solid tumor, making it the primary indication for CIN-selective therapies.

Lung cancer — KIF18A overexpression correlates with poor prognosis in primary lung adenocarcinoma (Li et al. 2019) and contributes to proliferation, migration, and invasion (Chen & Zhong 2019). HPA validates KIF18A as a potential prognostic marker in LUAD (TCGA, p=2.2e-5).

Glioblastoma — KIF18A is identified as a potential therapeutic target in glioblastoma stem cells (Stangeland et al. 2015). KIF18A interacts with PPP1CA to promote malignant development of glioblastoma (Yang et al. 2023).

Prostate cancer — KIF18A expression is associated with increased tumor stage and cell proliferation (Zhang et al. 2019). Circ_CCNB2 knockdown sensitizes prostate cancer to radiation through the miR-30b-5p/KIF18A axis (Cai et al. 2022).

Aging-related indications — No published studies directly link KIF18A to aging, cellular senescence, or neurodegenerative disease. The PandaOmics signals in neurologic and metabolic disease areas are driven by network co-embedding (PPI/matrix factorization) rather than direct evidence. KIF18A's role in genomic stability is theoretically relevant to aging (CIN and aneuploidy accumulate with age), but this remains unvalidated.

10. Recommendation: Which Indications to Pursue

10.1 Verdict per indication

Modality gate: All Go/Conditional calls use oral small molecule (the validated modality for KIF18A inhibition). This is consistent across all programs.

Recommended next steps (one bullet per Go/Conditional Tier-3 candidate):

• Hepatocellular carcinoma (Go) — next: Test KIF18A inhibitor efficacy in CIN-stratified HCC PDX models; validate CIN status as a biomarker in HCC patient cohorts. falsifier: Low CIN burden in HCC subtypes would negate the synthetic lethal mechanism.

• Colorectal cancer (Go) — next: Combination study of KIF18A inhibitor + anti-PD-1 in CIN-high CRC models (building on Liu et al. 2025). falsifier: If CIN-high CRC subset is too small (<20% of patients), the addressable market may not justify development.

• Glioblastoma (Conditional) — next: Assess BBB penetration of current KIF18A inhibitors; test in orthotopic GBM xenograft with CIN-high cells. falsifier: Insufficient BBB penetration would require reformulation or intrathecal delivery, fundamentally changing the development path.

• Gastric carcinoma (Conditional) — next: Validate KIF18A overexpression and CIN status in gastric cancer patient cohorts (Asian populations). falsifier: If KIF18A expression does not correlate with CIN or prognosis in gastric cancer specifically.

• Papillary renal cell carcinoma (Conditional) — next: PheWAS on KIF18A LoF variants to check for kidney-related phenotypes; test in RCC cell lines stratified by CIN. falsifier: If papillary RCC has low CIN burden compared to clear-cell RCC.

10.2 Confidence & reliability

Reliability flags:

• Green: KIF18A is not a hub gene — the mitotic/cell-cycle network is specific and biologically coherent. Pharmacological validation exists with multiple chemical series. Six clinical trials provide independent industry validation.
• Green: CIN-selective synthetic lethality is a well-characterized mechanism with direct functional evidence (Marquis et al. 2021).
• Amber: No approved drugs yet — all programs are Phase 1/2. Efficacy in humans is unproven. The Eg5/KSP precedent is cautionary.
• Red: Aging-related indications (neurodegenerative disease, diabetes) lack any direct evidence and should not be pursued based on PandaOmics scores alone.

Evidence quality: The strongest independent high-weight evidence lines supporting KIF18A as a cancer target are: (1) functional CIN-synthetic lethality studies (direct experimental, weight-2); (2) differential expression validated across multiple tumor types (DE, weight-1); (3) pharmacological proof-of-concept with multiple chemical scaffolds (class precedent); (4) unfavorable prognostic association in TCGA (validated in independent cohorts for HCC, kidney RCC, pancreatic adenocarcinoma). Network/PPI scores (weight-1) are high but correlated — they reflect KIF18A's position in the mitotic network, not independent biological evidence. Literature and attention scores (weight-0) are not informative for target validation.

Per-indication scorecard:

11. Methodology, Limitations & References

Methodology. PandaOmics Indication Prioritization scored KIF18A across the disease-indication space using 23 metrics in three families — Omics (curated disease omics datasets), Text/bibliometric (biomedical literature volume, recency, citation impact), and Financial (grant funding) — each normalized 0-1 and combined into an overall composite rank. LLM scores are excluded. From 1,000 indications across 14 therapeutic areas, the top 50 in oncology and aging-related areas were analyzed in detail. Tiers use clinical-trial activity since no ChEMBL approved drugs exist for KIF18A. Umbrella/ontology-parent terms (neoplasm, cancer, carcinoma, breast neoplasm, liver neoplasm, sarcoma, etc.) are excluded from ranking, tiers, and top lists.

Databases and versions used:

Score calibration. PandaOmics scores are relative, not absolute measures of association strength. A high rank indicates the target-disease pair is more prominent across the 23 scoring dimensions compared to other indications — it does not imply causation or clinical validity. Scores are driven by the volume and recency of literature, omics co-association, and grant funding — none of which is equivalent to clinical evidence. The tiering framework (Section 4.1) overlays clinical maturity onto the raw ranking to ground the assessment.

Limitations. DE (Section 5.2) uses PandaOmics pre-computed logFC/p-value. GWAS/mutation are association-level, not fine-mapped. gnomAD constraint values were not directly accessible in this environment. Single prioritization source; scores are relative within PandaOmics. Group means approximate PandaOmics aggregates. Aging-related indications lack direct mechanistic evidence for KIF18A.

Recommended orthogonal checks (NOT run here; cost order). PheWAS on LoF/coding variants (UK Biobank/FinnGen) -> drug-target MR + colocalization + bidirectional test -> cell-type expression in a disease scRNA atlas -> IMPC KO / DepMap (oncology) -> on-target safety scan. Steps 1-3 are cheap and kill most predictions; run them before committing to any Tier-3 expansion indication.

References.

- Alfarsi LH et al. (2019). Kinesin family member-18A (KIF18A) is a predictive biomarker of poor benefit from endocrine therapy in early ER+ breast cancer. Breast Cancer Res Treat. PubMed

- Beer TM et al. (2008). Southwest Oncology Group phase II study of ispinesib in androgen-independent prostate cancer previously treated with taxanes. Clin Genitourin Cancer. PubMed

- Cai H et al. (2022). Knockdown of Circ_CCNB2 Sensitizes Prostate Cancer to Radiation Through Repressing Autophagy by the miR-30b-5p/KIF18A Axis. Cancer Biother Radiopharm. PubMed

- Chamariya R & Suvarna V (2022). Role of KSP Inhibitors as Anti-cancer Therapeutics: An Update. Anticancer Agents Med Chem. PubMed

- Chen QI & Zhong C (2019). KIF18A Contributes to the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells. Dis Markers. PubMed

- Hemida AS et al. (2024). Impact of immunohistochemical expression of KIF18A and beta-catenin in infiltrating breast carcinoma. World J Surg Oncol. PubMed

- Henriques AC et al. (2019). Mitosis inhibitors in anticancer therapy: When blocking the exit becomes a solution. Cancer Lett. PubMed

- Kasahara M et al. (2016). Clinicopathological relevance of kinesin family member 18A expression in invasive breast cancer. Oncol Lett. PubMed

- Knox JJ et al. (2008). A phase II and pharmacokinetic study of SB-715992, in patients with metastatic hepatocellular carcinoma. Invest New Drugs. PubMed

- Lee CW et al. (2008). A phase II study of ispinesib in advanced renal cell cancer. Clin Genitourin Cancer. PubMed

- Lee CW et al. (2008). A phase II study of ispinesib in patients with metastatic or recurrent malignant melanoma. Invest New Drugs. PubMed

- Li TF et al. (2019). High kinesin family member 18A expression correlates with poor prognosis in primary lung adenocarcinoma. Thorac Cancer. PubMed

- Liu XS et al. (2025). Targeting KIF18A triggers antitumor immunity and enhances PD-1 blockade in colorectal cancer. Cell Death Discov. PubMed

- Liu M et al. (2023). KIF18A improves migration and invasion of CRC cells through inhibiting PTEN signaling. Aging. PubMed

- Liu M et al. (2023). Comprehensive Pan-Cancer Analysis of KIF18A as a Marker for Prognosis and Immunity. Biomolecules. PubMed

- Marquis C et al. (2021). Chromosomally unstable tumor cells specifically require KIF18A for proliferation. Nat Commun. PubMed

- Nagahara M et al. (2011). Kinesin 18A expression: clinical relevance to colorectal cancer progression. Int J Cancer. PubMed

- Nair JS et al. (2025). The KIF18A Inhibitor ATX020 Induces Mitotic Arrest and DNA Damage in CIN HGSOC Cells. Cells. PubMed

- Payton M et al. (2024). Small-molecule inhibition of KIF18A reveals a mitotic vulnerability enriched in CIN cancers. Nat Cancer. PubMed

- Phillips RE et al. (2025). Targeting chromosomally unstable tumors with a selective KIF18A inhibitor. Nat Commun. PubMed

- Ren J et al. (2024). KIF18A Promotes Cell Proliferation and Metastasis in HCC. Dig Dis Sci. PubMed

- Sparling BA et al. (2025). Discovery of KIF18A Inhibitor ATX020: Tactical Application of Silicon Atom Replacement. ACS Med Chem Lett. PubMed

- Stangeland B et al. (2015). Combined expressional analysis identifies new targets in glioblastoma stem cells. Oncotarget. PubMed

- Stumpff J et al. (2008). Kif18A suppresses kinetochore movements to control mitotic chromosome alignment. Dev Cell. PubMed

- Talapatra SK et al. (2013). Mitotic kinesin Eg5 overcomes inhibition by an allosteric resistance mechanism. J Med Chem. PubMed

- Tamayo NA et al. (2022). Targeting KIF18A in CIN Cancers: Hit Optimization Toward an In Vivo Chemical Probe. J Med Chem. PubMed

- Tang PA et al. (2008). Phase II study of ispinesib in HNSCC. Invest New Drugs. PubMed

- Truong L et al. (2026). KIF18A inhibition and its rising role in cancer therapy trials. Expert Opin Investig Drugs. PubMed

- Wang JQ et al. (2025). KIF18A induces EMT in hepatoma cells through 5-LOX pathway. PLoS One. PubMed

- Yang T et al. (2023). KIF18A interacts with PPP1CA to promote GBM malignant development. Exp Ther Med. PubMed

- Zhang C et al. (2019). KIF18A expression associated with tumor stage and proliferation in prostate cancer. Med Sci Monit. PubMed

- Zhang G et al. (2024). Novel Cyclohexenyl KIF18A Inhibitors for Ovarian Cancer. ACS Med Chem Lett. PubMed

- Zhu C et al. (2013). Kif18a deletion protects from colitis-associated colorectal tumors. Biochem Biophys Res Commun. PubMed

Generated by PandaOmics Agent (Insilico Medicine) on 2026-08-13.