Delving into the Latest Updates on Stannsoporfin with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Sn Mesoporphyrin, Sn-mesoporphyrin, SnMP

+ [6]

Target

HMOX1 x HMOX2

Mechanism

HMOX1 inhibitors(Heme oxygenase 1 inhibitors), HMOX2 inhibitors(Heme oxygenase 2 inhibitors)

Therapeutic Areas

Other DiseasesEndocrinology and Metabolic DiseaseCongenital Disorders

Active Indication-

Inactive Indication

HyperbilirubinemiaHyperbilirubinemia, NeonatalJaundice+ [2]

Originator Organization

Shire Development LLC

Active Organization-

Inactive Organization

InfaCare Pharmaceutical Corp.InfacareShire Pharmaceuticals Services Ltd.

+ [2]

Drug Highest PhaseDiscontinuedNDA/BLA

First Approval Date-

Regulation-

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Structure

Molecular FormulaC34H36Cl2N4O4Sn

InChIKeyODRRBSYZKPDLOV-UHFFFAOYSA-N

CAS Registry106344-20-1

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 Stannsoporfin

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100 Translational Medicine associated with Stannsoporfin

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100 Patents (Medical) associated with Stannsoporfin

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251

Literatures (Medical) associated with Stannsoporfin

06 Mar 2024·The Journal of Maternal-Fetal & Neonatal MedicineQ4 · MEDICINE

Neonatal hyperbilirubinemia and the role of unbound bilirubin

Q4 · MEDICINE

Review

Author: Hegyi, Thomas ; Kleinfeld, Alan

BACKGROUNDNeonatal jaundice occurs in more than 80% of newborn infants. Although mild jaundice is physiologic and possibly neuroprotective, severe hyperbilirubinemia can lead to neurologic dysfunction and death. Hyperbilirubinemia is due to an imbalance between bilirubin production and the developing excretory capacity in the first days of life. Management utilizes total serum bilirubin (TSB) levels, although recent advances suggest a role for unbound bilirubin.GOALSThe goal of this review is to examine bilirubin biology, toxicology, and clinical effects, discuss preventive and therapeutic measures, describe neurodevelopmental consequences, and propose that, with the advent of new technology, unbound bilirubin is the optimal measurement for the management.METHODSComprehensive review on neonatal hyperbilirubinemia.RESULTSNeonatal hyperbilirubinemia can be prevented by tin mesoporphyrin to limit heme oxygenase activity, a key enzyme in bilirubin production, or restricting bilirubin's absorption from the gastrointestinal tract. Treatment modalities include removing bilirubin from the body by exchange transfusion, binding to immunoglobulin, or converting it to a water-soluble isomer with phototherapy. While these approaches have evolved during the past decades, the diagnosis, intervention indications, and prognosis have consistently relied on TSB concentration despite its poor ability to predict an outcome.CONCLUSIONSTotal serum bilirubin is inadequate to optimize care of the term and preterm infant with hyperbilirubinemia. A rapid, accurate, and more effective indicator of bilirubin neurotoxicity is needed to manage jaundiced infants and for the universal screening of newborn infants. Future measurements of free bilirubin unattached to albumin will improve the management of neonatal hyperbilirubinemia.

07 Feb 2024·Antimicrobial Agents and Chemotherapy

The heme oxygenase-1 metalloporphyrin inhibitor stannsoporfin enhances the bactericidal activity of a novel regimen for multidrug-resistant tuberculosis in a murine model

Article

Author: Fotouhi, Nader ; Ayeh, Samuel ; Yilma, Addis ; Karanika, Styliani ; Ruelas Castillo, Jennie ; Krug, Stefanie ; Costa, Diego L. ; Garcia, Andrew ; Karakousis, Petros C. ; Sher, Alan ; Serbina, Natalya ; Quijada, Darla ; Neupane, Pranita

ABSTRACT Multidrug-resistant (MDR) Mycobacterium tuberculosis (Mtb) poses significant challenges to global tuberculosis (TB) control efforts. Host-directed therapies (HDTs) offer a novel approach to TB treatment by enhancing immune-mediated clearance of Mtb. Prior preclinical studies found that the inhibition of heme oxygenase-1 (HO-1), an enzyme involved in heme metabolism, with tin-protoporphyrin IX (SnPP) significantly reduced mouse lung bacillary burden when co-administered with the first-line antitubercular regimen. Here, we evaluated the adjunctive HDT activity of a novel HO-1 inhibitor, stannsoporfin (SnMP), in combination with a novel MDR-TB regimen comprising a next-generation diarylquinoline, TBAJ-876 (S), pretomanid (Pa), and a new oxazolidinone, TBI-223 (O) (collectively, SPaO), in Mtb-infected BALB/c mice. After 4 weeks of treatment, SPaO + SnMP 5mg/kg reduced mean lung bacillary burden by an additional 0.69 log 10 ( P = 0.01) relative to SPaO alone. As early as 2 weeks post-treatment initiation, SnMP adjunctive therapy differentially altered the expression of pro-inflammatory cytokine genes and CD38, a marker of M1 macrophages. Next, we evaluated the sterilizing potential of SnMP adjunctive therapy in a mouse model of microbiological relapse. After 6 weeks of treatment, SPaO + SnMP 10mg/kg reduced lung bacterial burdens to 0.71 ± 0.23 log 10 colony-forming units (CFUs), a 0.78 log-fold greater decrease in lung CFU compared to SpaO alone ( P = 0.005). However, adjunctive SnMP did not reduce microbiological relapse rates after 5 or 6 weeks of treatment. SnMP was well tolerated and did not significantly alter gross or histological lung pathology. SnMP is a promising HDT candidate requiring further study in combination with regimens for drug-resistant TB.

01 Jan 2024·Journal of clinical and medical sciences

Dysregulation of HO-1-SIRT1 Axis is Associated with AngII-Induced Adipocyte Dysfunction.

Article

Author: Lakhani, Hari Vishal ; Sodhi, Komal ; Zehra, Mishghan ; Pillai, Sneha ; Shapiro, Joseph I

Angiotensin II (AngII), a component of the Renin-Angiotensin-Aldosterone System (RAAS), has been implicated in the dysregulation of adipose tissue function. Inhibition of AngII has been shown to improve adipose tissue function in mice with metabolic syndrome. It is well established that the Heme Oxygenase-1 (HO-1), an antioxidant improves oxidative stress and phenotypic change in adipocytes. Molecular effects of high oxidative stress include suppression of Sirtuin-1 (SIRT1), which is amenable to redox manipulations. However, the underlying mechanisms by which the Renin-Angiotensin-Aldosterone System (RAAS) exerts its metabolic effects are not fully understood. In this study, we propose that AngII-induced oxidative stress may suppress adipocyte SIRT1 through down-regulation of HO-1. Consequently, this suppression of SIRT1 may result in the up-regulation of the Mineralocorticoid Receptor (MR). We further hypothesize that the induction of HO-1 would rescue SIRT1, thereby improving oxidative stress and adipocyte phenotype. To establish this hypothesis, we conducted experiments using mouse preadipocytes treated with AngII, in the presence or absence of Cobalt Protoporphyrin (CoPP), an inducer of HO-1, and Tin Mesoporphyrin (SnMP), an inhibitor of HO-1. Our data demonstrate that treatment of mouse preadipocytes with AngII leads to increased lipid accumulation, elevated levels of superoxide and inflammatory cytokines (Interleukin-6 and Tumor necrosis factor alpha), and reduced levels of adiponectin. However, these effects were attenuated by the induction of HO-1, and this attenuation was reversed by SnMP, indicating that the beneficial effects on adipocyte phenotype are modulated by HO-1. Furthermore, our findings reveal that AngII-treated preadipocytes exhibit upregulated MR levels and suppressed SIRT1 expression, which are rescued by HO-1 induction. Following treatment with CoPP and SIRT1 siRNA in mouse preadipocytes resulted in increased lipid accumulation and elevated levels of fatty acid synthase, indicating that the beneficial effects of HO-1 are modulated through SIRT1. Our study provides evidence that HO-1 restores cellular redox balance, rescues SIRT1, and attenuates the detrimental effects of AngII on adipocytes and systemic metabolic profile.

100 Deals associated with Stannsoporfin

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External Link

KEGG	Wiki	ATC	Drug Bank
D05922	-	-	DB04912

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Hyperbilirubinemia	NDA/BLA	-	Wellspring Worldwide, Inc.	-
Hyperbilirubinemia	NDA/BLA	-	Infacare	-
Hyperbilirubinemia	NDA/BLA	US	InfaCare Pharmaceutical Corp.	-
Hyperbilirubinemia	NDA/BLA	-	Mallinckrodt Plc	-
Hyperbilirubinemia	NDA/BLA	-	Shire Pharmaceuticals Services Ltd.	-
Hyperbilirubinemia	Phase 2	-	Wellspring Worldwide, Inc.	-
Hyperbilirubinemia	Phase 2	US	InfaCare Pharmaceutical Corp.	-
Hyperbilirubinemia	Phase 2	-	Shire Pharmaceuticals Services Ltd.	-
Hyperbilirubinemia	Discovery	-	Infacare	-
Hyperbilirubinemia	Discovery	-	Mallinckrodt Plc	-

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01887327 (JASMINE_204, CTgov)	Phase 2	Jaundice \| Jaundice, Neonatal	91	Phototherapy	ixfavuafra(wonqsgarpn) = fvrgwrjeeq ieelzutlyq (inmbzuortb, smvrcgcrii - itvjlliguv) View more	-	13 Nov 2019