Target intelligence / Profile preview

Mitotic spindle assembly checkpoint protein MAD1 (MAD1)

Target
MAD1
Molecular classification
Cell cycle regulator, Spindle assembly checkpoint protein, Tumor suppressor, Other (not an enzyme, receptor, ion channel, or transporter)
01

Overview

Mitotic spindle assembly checkpoint protein MAD1 (commonly called MAD1, encoded by MAD1L1) is a highly conserved cell cycle protein essential for the mitotic spindle assembly checkpoint. MAD1 acts at unattached kinetochores, recruiting MAD2 and facilitating assembly of the mitotic checkpoint complex (MCC), which delays anaphase onset until all chromosomes achieve proper spindle attachment. This prevents aneuploidy and genomic instability. MAD1 functions as a homodimer and interacts physically with MAD2L1 and other spindle checkpoint proteins. Mutations or altered regulation of MAD1 have been implicated in multiple cancers (due to loss of checkpoint control and induction of aneuploidy) and some psychiatric and neurodevelopmental disorders. While MAD1 is a pivotal node in mitotic control and a potential biomarker, it is not currently a direct therapeutic target for any drug, and modulation of its function carries significant safety concerns due to its role in chromosome segregation fidelity[1][2][3][4][5][7].

Other names
Mitotic arrest deficient 1 like 1MAD1L1MAD1PIG9TP53I9TXBP181
02

Mechanism of action

Not applicable (No established drugs directly target MAD1; its pathway can be indirectly affected by microtubule inhibitors and agents affecting mitotic checkpoint regulation)

03

Biological functions

Cell cycle checkpoint controlPrevention of anaphase onset until chromosomes are properly alignedSpindle assembly checkpoint signalingTumor suppressionRegulation of neuronal migration and differentiation[2][4][5][7]
04

Disease associations

Cancer (gene mutations or altered expression contribute to cancer risk and aneuploidy)[4][5]Psychiatric disorders (schizophrenia, bipolar disorder, depression)[2][4][6]Neurodevelopmental disorders[4]Other (general chromosomal instability/aneuploidy)
05

Safety considerations

Direct inhibition or loss of MAD1 function can cause chromosomal instability (aneuploidy), tumorigenesis, and defective cell division; thus, targeting MAD1 is likely to have significant adverse cytogenetic effects[4][5]
06

Interacting drugs

None established or approved (MAD1 is not a current direct drug target; no drugs are directly known to interact with or modulate MAD1 in clinical use)[7]
07

Biomarkers

Altered expression, SNPs, and methylation of MAD1L1 are associated with cancer and some psychiatric disorders and may serve as biomarkers for risk or disease severity[4][6]

Beyond the preview

Go deeper on Mitotic spindle assembly checkpoint protein MAD1 (MAD1).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Mitotic spindle assembly checkpoint protein MAD1 (MAD1).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call