Target intelligence / Profile preview

Solute carrier family 30 member 10 (SLC30A10)

Target
SLC30A10
Molecular classification
Transporter, Cation diffusion facilitator (CDF) superfamily, Membrane protein
01

Overview

Solute carrier family 30 member 10 (SLC30A10) is a transmembrane protein that belongs to the cation diffusion facilitator (CDF) superfamily of metal transporters[1][5]. Unlike most SLC30 family members, which typically transport zinc, SLC30A10 is specialized for exporting manganese and plays a critical role in manganese homeostasis. It is highly expressed in the liver, brain, small intestine, and testis, where it helps to excrete excess manganese into the bile and maintain safe intracellular concentrations[1][3]. Loss-of-function mutations in the SLC30A10 gene are the cause of inherited hypermanganesemia with dystonia, polycythemia, and cirrhosis—characterized by increased manganese in neurological and hepatic tissues, leading to movement disorders (dystonia, parkinsonism), liver disease, and hematological abnormalities[3][4][6]. SLC30A10 is essential for protecting cells, especially neurons and hepatocytes, from manganese toxicity, and is regulated by cellular manganese levels and potentially by hypoxia signaling pathways (HIF)[2]. There is active research into pharmacological modulation of SLC30A10 as a strategy for treating manganese toxicity[6].

Other names
Zinc transporter 10ZnT-10manganese transporter SLC30A10ZNT10ZNT8ZRC1DKFZp547M236zinc resistance conferring homolog (S. cerevisiae)HMNDYT1HMDPC
02

Mechanism of action

Drugs or interventions targeting SLC30A10 would primarily work by modulating manganese transport/efflux to reduce intracellular manganese and prevent toxicity[6][2].

03

Biological functions

Manganese efflux/transportMetal ion homeostasisNeuroprotectionHepatic and intestinal manganese excretion
04

Disease associations

Neurodegenerative disease (e.g. parkinsonism, dystonia)Inherited metabolic disease (hypermanganesemia with dystonia, polycythemia, cirrhosis)Liver disease
05

Safety considerations

Risk of manganese deficiency if efflux is excessively increasedrisk of neurotoxicity and hepatic dysfunction with impaired activityinherited mutations may lead to severe movement disorders and liver disease[3][4][6].
06

Interacting drugs

None currently approved or directly reported in clinical use; compounds under research may include metal chelators or small molecules affecting metal homeostasis, but no named drugs in current indexed literature[6][1].
07

Biomarkers

Elevated blood manganesegenetic testing for SLC30A10 mutations

Beyond the preview

Go deeper on Solute carrier family 30 member 10 (SLC30A10).

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 Solute carrier family 30 member 10 (SLC30A10).

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