Target intelligence / Profile preview

Melanoma antigen family C1 (MAGE-C1) (MAGE-C1)

Target
MAGE-C1
Molecular classification
Cancer-testis antigen, Melanoma antigen (MAGE) family, Other
01

Overview

Melanoma antigen family C1 (MAGE-C1), also known as CT7, is a prominent member of the cancer-testis antigen (CTA) family, characterized by its restricted expression in the immune-privileged testis and aberrant overexpression in various malignancies [1, 2]. It is most notably expressed in multiple myeloma, where it serves as a critical driver of malignant plasma cell survival and a marker of poor prognosis [1, 9]. Biologically, MAGE-C1 functions as an anti-apoptotic factor and a regulator of the cell cycle, specifically promoting the G2/M phase transition to support rapid tumor cell proliferation [3, 5]. Due to its high tumor specificity and strong immunogenicity, it is a major target for cancer immunotherapies, including mRNA vaccines and T-cell receptor (TCR) engineered T-cell therapies [20, 23]. Clinical strategies often utilize MAGE-C1 to elicit a robust cytotoxic T-lymphocyte response against cancer cells while sparing normal tissues [11, 22]. Furthermore, research indicates that silencing MAGE-C1 can significantly enhance the sensitivity of tumor cells to chemotherapy and proteasome inhibitors like bortezomib [3, 6]. As a result, MAGE-C1 remains a high-priority target for developing personalized and targeted treatments for hematological and solid tumors [7, 27].

Other names
CT7CT7.1Cancer/testis antigen 7.1Melanoma-associated antigen C1Melanoma antigen family C, 1Cancer/testis antigen family 7, member 1
02

Mechanism of action

MAGE-C1 is targeted primarily through immunotherapy, where mRNA-based vaccines or T-cell receptor (TCR) engineered T-cells are used to induce a tumor-specific cytotoxic T-lymphocyte response against cells expressing the antigen [20, 23]. Additionally, silencing MAGE-C1 expression can sensitize malignant cells to proteasome inhibitors like bortezomib by promoting apoptosis and disrupting cell cycle progression [3, 6].

03

Biological functions

Cell cycleApoptosisCell proliferationImmune response
04

Disease associations

Cancer
05

Safety considerations

Off-target toxicity due to potential cross-reactivity with other MAGE family membersTumor heterogeneity and antigen loss leading to immune evasionCytokine release syndrome (CRS) associated with T-cell therapiesTherapeutic resistance in tumors with low HLA expression
06

Interacting drugs

BNT116

4 more in the full profile.

07

Biomarkers

MAGE-C1 protein expression (IHC)MAGE-C1 mRNA expression (RT-PCR)Serum anti-MAGE-C1 IgG antibodiesNuclear vs. cytoplasmic protein localization

Beyond the preview

Go deeper on Melanoma antigen family C1 (MAGE-C1) (MAGE-C1).

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 Melanoma antigen family C1 (MAGE-C1) (MAGE-C1).

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