Last update 01 Nov 2024

HMOX2

Last update 01 Nov 2024

Basic Info

Synonyms

heme oxygenase (decycling) 2, Heme oxygenase 2, Heme oxygenase 2 soluble form

+ [3]

Introduction

Catalyzes the oxidative cleavage of heme at the alpha-methene bridge carbon, released as carbon monoxide (CO), to generate biliverdin IXalpha, while releasing the central heme iron chelate as ferrous iron. Catalyzes the oxidative cleavage of heme at the alpha-methene bridge carbon, released as carbon monoxide (CO), to generate biliverdin IXalpha, while releasing the central heme iron chelate as ferrous iron.

Drugs associated with HMOX2

Stannsoporfin

Target

HMOX1 x HMOX2

Mechanism

HMOX1 inhibitors [+1]

Active Org.-

Originator Org.

Shire Development LLC

Active Indication-

Inactive Indication

Hyperbilirubinemia [+4]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with HMOX2

NCT02000830 / CompletedNot Applicable

A Four-Year Blinded Outcomes Follow-up Study of Patients Who Received Stannsoporfin or Placebo in Clinical Trial 64,185-204

The objectives of this follow up study are to evaluate the long-term effects of stannsoporfin (Stanate) on the health, growth, and development of patients who received a single dose of stannsoporfin with PT used to treat hyperbilirubinemia compared with patients in the control (placebo plus PT) group in clinical trial 64,185-204.

Start Date17 Oct 2013

Sponsor / Collaborator

InfaCare Pharmaceutical Corp.

NCT01887327 / CompletedPhase 2

A Phase 2b Multicenter, Single Dose, Randomized, Double Blind, Placebo-Controlled, Parallel-Group Study Evaluating the Safety and Efficacy of Two Doses of Stannsoporfin in Combination With Phototherapy in Neonates

It is normal for red blood cells to die, even in newborn babies. The waste from that is called bilirubin. The liver clears bilirubin out of the body.
Some babies are born with illness that makes red blood cells die too fast, so the liver is not strong enough to keep up with it.
The yellowish color in eyes or skin means there is too much bilirubin in the body. It can be dangerous if a baby's bilirubin gets too high.
Special lights are put on jaundiced babies (called phototherapy) to help the liver get rid of bilirubin.
This study tests an experimental drug to see if it can help the liver even more, by safely cutting down the amount of bilirubin the body is making in the first place.

Start Date16 Oct 2013

Sponsor / Collaborator

InfaCare Pharmaceutical Corp.

EUCTR2009-018267-27-ES / Not yet recruitingNot Applicable

A 5-Year, Extension, Follow-up, Blinded-Outcomes Trial of Subjects Having Received Stannsoporfin or Placebo in Clinical Trial 64,185-202Un estudio ciego de seguimiento y ampliación de 5 años de duración de pacientes que recibieron estansoporfina o placebo en el ensayo clínico 64.185-202

Start Date08 Jun 2010

Sponsor / Collaborator

InfaCare Pharmaceutical Corp.

100 Clinical Results associated with HMOX2

100 Translational Medicine associated with HMOX2

0 Patents (Medical) associated with HMOX2

1,160

Literatures (Medical) associated with HMOX2

01 Dec 2024·Molecular and Cellular Neuroscience

Inhibition of phosphodiesterase 10A mitigates neuronal injury by modulating apoptotic pathways in cold-induced traumatic brain injury

Article

Author: Dogan, Enes ; Kilic, Ertugrul ; Altintas, Mehmet O ; Beker, Mustafa C ; Balaban, Buse ; Beker, Mustafa C. ; Ozpinar, Aysenur ; Sengun, Nursena ; Bayraktaroglu, Cigdem ; Altunay, Serdar ; Altintas, Mehmet O.

Brain injury develops from a complex series of pathophysiological phases, resulting in acute necrotic or delayed apoptotic cell death after traumatic brain injury (TBI). Inhibition of apoptotic cell death is critical for the treatment of acute neurodegenerative disorders, such as TBI. Here, we investigated the role of phosphodiesterase 10A (PDE10A) in the development of neuronal injury, particularly in apoptotic cell death. Using the PDE10A inhibitor TAK-063, we found that PDE10A inhibition is associated with decreased brain injury, brain swelling, and blood brain barrier disruption 48 h after cold-induced TBI. Furthermore, a particularly notable result was observed with 3 mg/kg TAK-063, which reduced disseminated neuronal injury. Protein abundance analysis revealed that PDE10A inhibition activates survival kinases AKT and ERK-1/-2, which were associated with the decreased activation of MMP-9 and PTEN. Additionally, iNOS and nNOS levels significantly reduced in the TAK-063 group, playing roles in inflammation and apoptosis. A planar surface immunoassay was performed for in-depth analyses of the apoptotic signaling pathways. We observed that inhibition of PDE10A resulted in the decreased expression of TNFRSF1A, TNFRSF10B, and TNFRSF6 receptors, particularly inducing apoptotic cell death. Moreover, these findings correlated with reduced levels of pro-apoptotic proteins, including PTEN, p27, Cytochrome-c, cleaved Caspase-3, Bad, and p53. Interestingly, TAK-063 treatment reduced levels of anti-apoptotic proteins or enzymes, including XIAP, Claspin, and HIF1α, without affecting Bcl-x, MCL-1, SMAC, HO-1, HO-2, HSP27, HSP60, and HSP70. The findings suggest that PDE10A regulates cellular signaling predominantly pro-apoptotic pathways, and inhibition of this protein is a promising approach for the treatment of acute brain injury.

01 Oct 2024·Theriogenology

Impact of the near-physiological temperature on the in vitro maturation of bovine oocytes: A comparative proteomic approach

Article

Author: Quirino, Celia Raquel ; Maretto, Vinicius ; Silveira, Vanildo ; Pinto, Vitor Batista ; Bustamante-Filho, Ivan Cunha ; Ortiz Vega, Wilder Hernando ; Tavares, Winny Caldas Moreno ; Caldas-Bussiere, Maria Clara

In vivo, the temperature inside preovulatory follicles of cows is approximately 1 °C lower than rectal temperature. However, standard bovine oocyte in vitro maturation (IVM) protocols use 38.5 °C based on rectal temperature. This study evaluated the effect of reducing IVM temperature to 37.5 °C on the proteomic profile of oocytes compared to the routine 38.5 °C. Nuclear maturation rate and cumulus cell (CC) expansion (30 COCs per group, 21 replicates) were assessed by observing the first polar body and using a subjective scoring method (0-4). Total nitrite concentrations in the culture medium were measured using the Griess method. Differential proteomics was performed using LC-MS/MS on pooled oocyte samples (500 matured oocytes per group, three replicates), followed by gene ontology enrichment, protein-protein interaction, and putative miRNA target analyses. No significant differences were observed between the groups in nuclear maturation, CC expansion, or nitrite concentration (P > 0.05). A total of 806 proteins were identified, with 7 up-regulated and 12 down-regulated in the treatment group compared to the control. Additionally, 12 proteins were unique to the control group, and 8 were unique to the treatment group. IVM at 37.5 °C resulted in the upregulation of proteins involved in protein folding and GTP binding, and the downregulation of enzymes with oxidoreductase activity and proteins involved in cytoskeletal fiber formation. Furthermore, 43 bovine miRNAs potentially regulating these genes (DES, HMOX2, KRT75, FARSA, IDH2, CARHSP1) were identified. We conclude that IVM of bovine oocytes at 37.5 °C induces significant proteomic changes without impacting nuclear maturation, cumulus cell expansion, or nitrite concentration in the IVM medium.

01 Oct 2024·American Journal of Respiratory Cell and Molecular Biology

Extracellular Vesicle ASC: A Novel Mediator for Lung–Brain Axis in Preterm Brain Injury

Article

Author: Duara, Jo ; Cabrera Ranaldi, Erika D.L.R.M. ; Khan, Aisha ; Claure, Nelson ; de Rivero Vaccari, Juan Pablo ; Duncan, Matthew R. ; Benny, Merline ; Young, Karen ; Lee, Yee-Shuan ; Bancalari, Eduardo ; Starke, Natalie ; Schmidt, Augusto F. ; Challa, Naga Venkata Divya ; Chen, Shaoyi ; Wu, Shu ; Aguilar, Ana Cecilia ; Yuan, Huijun ; Schott, Alini ; Tan, April

Bronchopulmonary dysplasia (BPD) and neurodevelopmental impairment are among the most common morbidities affecting preterm infants. Although BPD is a predictor of poor neurodevelopmental outcomes, it is currently uncertain how BPD contributes to brain injury in preterm infants. Extracellular vesicles (EVs) are involved in interorgan communication in diverse pathological processes. ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain) is pivotal in inflammasome assembly and activation of inflammatory response. We assessed expression profiles of the alveolar macrophage (AM) markers CD11b, CD11c, and CD206 as well as ASC in EVs isolated from the plasma of preterm infants at risk for BPD at 1 week of age. We found that infants on higher fraction of inspired oxygen therapy (HO₂⩾30%) had increased concentrations of AM-derived EV-ASC compared with infants on lower fraction of inspired oxygen (LO₂<30%). To assess the function of these EVs, we performed adoptive transfer experiments by injecting them into the circulation of newborn mice. We discovered that mice that received EVs from infants on HO₂ had increased lung inflammation, decreased alveolarization, and disrupted vascular development, the hallmarks of BPD. Importantly, these EVs crossed the blood-brain barrier, and the EVs from infants on HO₂ caused inflammation, reduced cell survival, and increased cell death, with features of pyroptosis and necroptosis in the hippocampus. These results highlight a novel role for AM-derived EV-ASC in mediating the lung-to-brain cross-talk that is critical in the pathogenesis of BPD and brain injury and identify potential novel targets for preventing and treating BPD and brain injury in preterm infants.

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HMOX2

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