STM 434

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Ligands
STM 434

GtoPdb Ligand ID: 8991

Comment: STM 434 is an investigational fusion protein containing the extracellular domain of the activin receptor type 2B (ACVR2B, a.k.a. ActRIIB) fused to the Fc domain of human IgG1. This is one of the inventions claimed in patent US8501678 B2 [1]. It is not entirely clear which construct is STM 434, but it is likely to be either vActRIIB-IgG1Fc E28W (E10W) mature polypeptide (which has SEQ ID: 62) or vActRIIB-IgG1Fc E28Y (E10Y) mature polypeptide (SEQ ID: 64).

No information available.

No information available.

Summary of Clinical Use
STM 434 is being evaluated in Phase 1 clinical trial (NCT02262455) for its potential antineoplastic activity against ovarian cancer and other solid tumours. In October 2015, the US FDA Office of Orphan Products Development (OOPD) granted this therapeutic orphan drug designation for the treatment of ovarian cancer.

Summary of Clinical Use

STM 434 is being evaluated in Phase 1 clinical trial (NCT02262455) for its potential antineoplastic activity against ovarian cancer and other solid tumours. In October 2015, the US FDA Office of Orphan Products Development (OOPD) granted this therapeutic orphan drug designation for the treatment of ovarian cancer.

Mechanism Of Action and Pharmacodynamic Effects
Activin A (a member of the transforming growth factor β superfamily; HGNC gene name inhibin beta A (INHBA)) , is overexpressed in a variety of cancers and plays a key role in promoting cancer cell proliferation, migration, and survival. STM 434 selectively binds to endogenous activin A, effectively neutralising its activity. As a result the activin A/ActRIIB-mediated signaling pathway is not activated and this results in reduced proliferation of activin A-overexpressing tumour cells.

Mechanism Of Action and Pharmacodynamic Effects

Activin A (a member of the transforming growth factor β superfamily; HGNC gene name inhibin beta A (INHBA)) , is overexpressed in a variety of cancers and plays a key role in promoting cancer cell proliferation, migration, and survival. STM 434 selectively binds to endogenous activin A, effectively neutralising its activity. As a result the activin A/ActRIIB-mediated signaling pathway is not activated and this results in reduced proliferation of activin A-overexpressing tumour cells.

Clinical Trials
Clinical Trial ID	Title	Type	Source	Comment	References
NCT02262455	Effects of STM 434 Alone or in Combination With Liposomal Doxorubicin in Patients With Ovarian Cancer or Other Advanced Solid Tumors	Phase 1 Interventional	Santa Maria Biotherapeutics