OnCo

Cell-cycle and DNA-damage checkpoints

Every dividing cell passes three gates and keeps a damage-response crew behind them. Tumours break the gates to grow and then depend on the ones they have left; the drugs here either hold a gate shut (CDK4/6 inhibitors) or force one open so the cell divides into death (WEE1, ATR, PARP, Aurora and MPS1 inhibitors). Pink means an approved drug exists.

16 members4 gates2 with an approved drug33 productsJSONThe other meaning: immune checkpoints

The cell-cycle ring

Hover or focus a node for where it acts and its drugs; click for its row.

G1SG2MG1/S gatecommit to copying DNAG2/M gatecommit to dividingSpindle assembly checkpointinside mitosisDNA-damage responsethe sensors behind every gateCDK4/6Cyclin D1RBp16 (CDKN2A)ATRCHK1WEE1PLK1ATMCHK2p53PARP1Aurora AAurora BMPS1 (TTK)BUB1

approved drug against it checkpoint member, no approval yet gate

Spindle assembly checkpoint

PLK1, Aurora A, Aurora B, MPS1 (TTK), BUB1
Checkpoint gate · 4 members

G1/S: the decision to copy DNA

The first gate. Cyclin D and CDK4/6 phosphorylate RB, which lets the cell commit to copying its DNA; p16 holds CDK4/6 back. Hormone-driven breast cancers lean on this gate, which is why CDK4/6 inhibitors work there.

Checkpoint gate · 4 members

G2/M: the decision to divide

The second gate, held shut by ATR, CHK1 and WEE1 until copied DNA is checked. Tumours that have lost p53 cannot stop at the first gate, so they rely on this one; drugs that force it open push them into a lethal mitosis.

“Tumour cells lacking functional p53 are defective in the G1/S checkpoint and become highly dependent on the G2/M checkpoint to maintain genomic stability, and are consequently vulnerable to WEE1 inhibitors, which override the G2/M checkpoint and induce cell death through mitotic catastrophe.” Chen et al. 2021, Front Med: WEE1 inhibitors and statins in cancers with p53 mutations

  • Member
    Works with
    Where it acts

    Ubiquitous, highest in testis; a sensor kinase that starts checkpoint signalling on replication stalling, ultraviolet light or ionising radiation. UniProt Q13535

    Best drug status
    Small molecule
    1 stopped
    • Ceralasertib (AZD6738) programme: The study terminated because the clinical development programme for ceralasertib has been discontinued (registry text, December 2025). ClinicalTrials.gov NCT06929260
    Approvals by cancer
    None
  • Member
    Works with
    Where it acts

    Ubiquitous, most abundant in thymus, testis, small intestine and colon; required for checkpoint arrest and repair activation when DNA is damaged or unreplicated. UniProt O14757

    Best drug status
    No product with a status
    1 stopped
    Approvals by cancer
    None
    Drugs
    No product in the corpus
    • Prexasertib (ACR-368, a CHK1/2 inhibitor) completed phase 2 in platinum-resistant ovarian cancer and is in phase 2 in endometrial cancer. ClinicalTrials.gov NCT03414047
  • Works with
    Where it acts

    A negative regulator of entry into mitosis that phosphorylates CDK1 on tyrosine 15, peaking in G2. UniProt P30291

    Best drug status
    Small molecule
    2 stopped
    • Adavosertib (AZD1775) programme: Study terminated because the clinical development programme for adavosertib has been discontinued. ClinicalTrials.gov NCT04949425
    • Azenosertib with carboplatin and pembrolizumab in triple-negative breast cancer: Terminated due to concern for toxicity from previously reported serious adverse events; never reached phase 2. ClinicalTrials.gov NCT06351332
    Approvals by cancer
    None
  • Member
    Works with
    Where it acts

    Placenta and colon (UniProt tissue); acts throughout M phase on centrosome maturation, spindle assembly, cohesin removal and mitotic exit. UniProt P53350

    Best drug status
    Small molecule
    1 stopped
    • Volasertib (Boehringer Ingelheim): Development programme of study drug volasertib was stopped by Boehringer Ingelheim due to manufacturing problems. ClinicalTrials.gov NCT02198482
    Approvals by cancer
    None
Checkpoint gate · 4 members

DNA-damage response

The sensors and repair crews behind both gates. ATM and ATR detect breaks and stalled forks, CHK1 and CHK2 relay the alarm, p53 decides between pause, repair and death, and PARP patches single-strand breaks. Cancers that have lost one route depend on the others.

Checkpoint gate · 4 members

Spindle assembly checkpoint

The last gate, inside mitosis. MPS1, BUB1 and Aurora B keep the cell from pulling its chromosomes apart until every one is attached; Aurora A and PLK1 build the spindle. Taxanes and vinca alkaloids kill by holding this gate shut for good.

“Vinca alkaloids and taxanes kill cancer cells through chronic arrest in mitosis as a consequence of chronic spindle assembly checkpoint activation.” Yuan et al. 2015: targeting the spindle assembly checkpoint for breast cancer treatment

  • Works with
    Where it acts

    High in testis, weak in skeletal muscle, thymus and spleen; high in colon, ovarian, prostate, neuroblastoma, breast and cervical cancer cell lines. Builds the spindle and separates centrosomes. UniProt O14965

    Best drug status
    Small molecule
    Approvals by cancer
    None
    Drugs
  • Works with
    Where it acts

    High in thymus; spleen, lung, testis, colon, placenta and fetal liver; up-regulated in cancer cells during M phase, absent from normal liver and high in metastatic liver. UniProt Q96GD4

    Best drug status
    No product with a status
    1 stopped
    Approvals by cancer
    None
    Drugs
    No product in the corpus
  • Works with
    Where it acts

    Present in rapidly proliferating cell lines; phosphorylates MAD1 to arm the spindle assembly checkpoint and repairs wrong kinetochore attachments. UniProt P33981

    Best drug status
    No product with a status
    Approvals by cancer
    None
    Drugs
    No product in the corpus
  • Works with
    Where it acts

    High in testis and thymus, less in colon, spleen, lung and small intestine; tissues with a high mitotic index. Assembles checkpoint proteins at the kinetochore. UniProt O43683

    Best drug status
    No product with a status
    Approvals by cancer
    None
    Drugs
    No product in the corpus

Sources. Identifiers from the HGNC REST API; where each protein acts from the UniProt function or tissue-specificity comment for the accession named; the p53-loss dependency and the taxane mechanism from the reviews quoted under their gates; drug statuses from the linked drug records; phases for agents without a record, and every stopped programme, from the ClinicalTrials.gov study cited. Taxonomy in src/data/checkpoint-map.ts.