Last update 19 Sep 2024

BMPR1B

Last update 19 Sep 2024

Basic Info

Synonyms

ALK6, BMP type-1B receptor, BMPR-1B

+ [5]

Introduction

On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP7/OP-1 and GDF5. Positively regulates chondrocyte differentiation through GDF5 interaction.

Drugs associated with BMPR1B

DWP-431

Target

BMPR1A x BMPR1B

Mechanism

BMPR1A stimulants [+1]

Active Org.

Daewoong Pharmaceutical Co., Ltd.

Originator Org.

Daewoong Pharmaceutical Co., Ltd.

Active Indication

Alveolar Bone Loss [+1]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date25 Jun 2014

Eptotermin alfa

Target

BMPR1A x BMPR1B x BMPR2

Mechanism

BMPR1A stimulants [+2]

Active Org.-

Originator Org.

Curis, Inc.

Active Indication-

Inactive Indication

Amyotrophic Lateral Sclerosis [+3]

Drug Highest PhaseWithdrawn

First Approval Ctry. / Loc.

EU [+3]

First Approval Date17 May 2001

UK-383367

Target

BMPR1A x BMPR1B

Mechanism

BMPR1A antagonists [+1]

Active Org.-

Originator Org.

Pfizer Inc.

Active Indication-

Inactive Indication

Cicatrix

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with BMPR1B

NCT04670965 / Not yet recruitingNot ApplicableIIT

Release Kinetics of rhBMP-2 Using E-PRF as an Autologous Carrier: An in Vitro Analysis

This study is seeking to evaluate the binding of a commercially-available, recombinant human osteoinductive growth factor, rhBMP-2, to a human blood derived product scaffold, enhanced Platelet-rich fibrin (E-PRF), and the release of such a growth factor over time in an in vitro (laboratory) environment. The investigators will compare these release kinetics to those of the FDA approved carrier for rhBMP-2, an absorbable collagen sponge (ACS), a combination of E-PRF and ACS, and E-PRF alone.

Start Date01 Aug 2024

Sponsor / Collaborator

The University of Alabama at Birmingham

CTRI/2024/05/067147 / Not yet recruitingPhase 4IIT

Evaluation of the effect of Recombinant Human Bone Morphogenic Protein-2 on crestal bone height and osseointegration around endosseous implants - nil

Start Date10 Jun 2024

Sponsor / Collaborator-

NCT05719181 / RecruitingPhase 1IIT

Effect of Recombinant Human Bone Morphogenetic Protein-2 With an Absorbable Collagen Sponge on Stability of Dental Implant: (Split Mouth Randomized Clinical Trial Study of 6\12\2021 to20\4\2023

Effect of Recombinant Human Bone Morphogenetic Protein-2 with an Absorbable Collagen Sponge on Stability of Dental Implant: (Split Mouth Randomized Clinical Trial Study.

Start Date06 Dec 2021

Sponsor / Collaborator

University of Baghdad

100 Clinical Results associated with BMPR1B

100 Translational Medicine associated with BMPR1B

0 Patents (Medical) associated with BMPR1B

580

Literatures (Medical) associated with BMPR1B

01 Jun 2024·Neoplasia

Cell communication pathway prognostic model identified detrimental neurodevelopmental pathways in neuroblastoma

Article

Author: Xue, Yao ; Zhang, Yixuan ; Li, Huimin ; Fang, Yongjun ; Zhou, Chunlei ; Ma, Xiaopeng ; Wang, Yaping ; Zhang, Yidan ; Wang, Jiali ; Rong, Liucheng

Neurodevelopmental cell communication plays a crucial role in neuroblastoma prognosis. However, determining the impact of these communication pathways on prognosis is challenging due to limited sample sizes and patchy clinical survival information of single cell RNA-seq data. To address this, we have developed the cell communication pathway prognostic model (CCPPM) in this study. CCPPM involves the identification of communication pathways through single-cell RNA-seq data, screening of prognosis-significant pathways using bulk RNA-seq data, conducting functional and attribute analysis of these pathways, and analyzing the post-effects of communication within these pathways. By employing the CCPPM, we have identified ten communication pathways significantly influencing neuroblastoma, all related to axongenesis and neural projection development, especially the BMP7-(BMPR1B-ACVR2B) communication pathway was found to promote tumor cell migration by activating the transcription factor SMAD1 and regulating UNK and MYCBP2. Notably, BMP7 expression was higher in neuroblastoma samples with distant metastases. In summary, CCPPM offers a novel approach to studying the influence of cell communication pathways on disease prognosis and identified detrimental communication pathways related to neurodevelopment.

29 May 2024·Science Translational Medicine

An ALK2 inhibitor, BLU-782, prevents heterotopic ossification in a mouse model of fibrodysplasia ossificans progressiva

Article

Author: LaBranche, Timothy P ; Zhu, Xing Julia ; Dorsch, Marion ; Lengauer, Christoph ; Davis, Alison J ; Palmer, Michael ; Stevison, Faith ; Garner, Andrew P ; Stewart, Rachel ; Albayya, Faris ; Vassiliadis, John ; Hodous, Brian L ; Xu, Lan ; Brubaker, Jason D ; Fleming, Paul ; Wang, Ruduan ; Guzi, Timothy J ; Lobbardi, Riadh ; Wilson, Douglas ; Sheets, Michael P ; Hunter, Jeffrey W ; Brooijmans, Natasja ; Williams, Brett D ; Kim, Joseph L ; Kim, Sean ; Bouchard, Keith ; Kadambi, Vivek ; Russo, Joelle ; Graul, Chris ; Greenblatt, Elliot ; Hussein, Amira ; Lyon, Morgan

Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease driven by gain-of-function variants in activin receptor–like kinase 2 (ALK2), the most common variant being ALK2 R206H . In FOP, ALK2 variants display increased and dysregulated signaling through the bone morphogenetic protein (BMP) pathway resulting in progressive and permanent replacement of skeletal muscle and connective tissues with heterotopic bone, ultimately leading to severe debilitation and premature death. Here, we describe the discovery of BLU-782 (IPN60130), a small-molecule ALK2 R206H inhibitor developed for the treatment of FOP. A small-molecule library was screened in a biochemical ALK2 binding assay to identify potent ALK2 binding compounds. Iterative rounds of structure-guided drug design were used to optimize compounds for ALK2 R206H binding, ALK2 selectivity, and other desirable pharmacokinetic properties. BLU-782 preferentially bound to ALK2 R206H with high affinity, inhibiting signaling from ALK2 R206H and other rare FOP variants in cells in vitro without affecting signaling of closely related homologs ALK1, ALK3, and ALK6. In vivo efficacy of BLU-782 was demonstrated using a conditional knock-in ALK2 R206H mouse model, where prophylactic oral dosing reduced edema and prevented cartilage and heterotopic ossification (HO) in both muscle and bone injury models. BLU-782 treatment preserved the normal muscle-healing response in ALK2 R206H mice. Delayed dosing revealed a short 2-day window after injury when BLU-782 treatment prevented HO in ALK2 R206H mice, but dosing delays of 4 days or longer abrogated HO prevention. Together, these data suggest that BLU-782 may be a candidate for prevention of HO in FOP.

01 Apr 2024·Biochemical Genetics

Bioinformatics Analysis of the Genetic and Epigenetic Alterations of Bone Morphogenetic Protein Receptors in Metastatic Breast Cancer

Review

Author: Putri, Herwandhani ; Hermawan, Adam

The leading cause of mortality in patients with breast cancer is metastasis, and bone morphogenetic protein (BMP) signaling activation regulates metastasis in breast cancer. This study explored the genetic and epigenetic modification of BMP receptor genes associated with metastatic breast cancer cells using bioinformatics. The genetic and epigenetic alterations of BMP receptors (BMPR1A, BMPR1B, BMPR2, ACVR2A, ACVR1, ACVR2B, ACVR1B, HJV, and ENG) were examined using cBioportal and methSurv, respectively. mRNA expression was analyzed using TNM plot and bcgenex, and protein expression was studied using Human Protein Atlas. Prognostic value and ROC were investigated using Kaplan-Meier (KM) and ROC plot, respectively. Finally, mutant function was predicted using several databases, including PolyPhen-2, FATHMM, Mutation Assessor, and PredictSNP. Oncoprint analysis showed genetic alterations in BMPR1A (39%), BMPR1B (13%), BMPR2 (34%), ACVR2A (14%), ACVR1 (7%), ACVR2B (13), ACVR1B (35%), HJV (40%), and ENG (33%) across the patients with breast cancer in The Metastatic Breast Cancer Project. The mRNA and protein levels of BMPR2 were increased in metastatic breast tumor tissues compared with those in normal and breast tumor tissues. BMPR1A and BMPR2 showed the highest and lowest levels of epigenetic alterations among the BMP receptors, respectively. The patients with breast cancer who had low levels of BMPR2 had a better overall survival (OS) than those with high levels of BMPR2. Functional mutation prediction showed that mutants in BMPR2 (R272L, E274K, and L685F), ACVR2A (S127L), and ACVR1B (R484H), are deleterious, probably damaging, and possess a cancer phenotype. ROC plot revealed no BMP receptors correlated with endocrine therapy sensitivity. BMPR1B, BMPR2, and ACVR2A levels were significantly linked as moderate prediction of anti-HER2, BMPR2, and ACVR1B demonstrated moderate predictive potential for chemotherapy sensitivity. This study contributed in fully comprehending the significance of genetic and epigenetic alterations in BMP receptors and BMP signaling in metastatic breast cancer cells for the development of breast cancer treatment plans.

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BMPR1B

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