Delving into the Latest Updates on Oprelvekin with Synapse

Overview

Basic Info

Drug Type

Interleukins

Synonyms

IL-11 (Pfizer), Interleukin-11 (Pfizer), Oprelvekin (USAN/INN)

+ [6]

Target

IL-11RA

Mechanism

IL-11RA stimulants(Interleukin 11 receptor alpha stimulants), Thrombopoiesis stimulants

Therapeutic Areas

Hemic and Lymphatic DiseasesImmune System DiseasesCongenital Disorders+ [3]

Active Indication-

Inactive Indication

Crohn DiseaseHemophilia AMenorrhagia+ [3]

Originator Organization

Pfizer Inc.

Active Organization-

Inactive Organization

Wyeth ABWyeth Pharmaceuticals LLC

University of Pittsburgh

Drug Highest PhaseWithdrawn

First Approval Date

US (25 Nov 1997),

Thrombocytopenia

RegulationOrphan Drug (US)

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Structure/Sequence

Sequence Code 13648

Source: *****

The purpose of this study is to learn more about what causes insulin resistance. It has been suggested that proper breakdown of fat into energy (oxidation) in the body is important to allow insulin to keep blood sugar in the normal range. The investigators want to know if having one of the fatty acid oxidation disorders could have an influence on insulin action. Fatty acid oxidation disorders are genetic disorders that inhibit one of the enzymes that converts fat into energy. The investigators will study both normal healthy people and people with a long-chain fatty acid oxidation disorder.

Start Date01 Feb 2016

Sponsor / Collaborator

Oregon Health & Science University

NCT02314273

/ CompletedPhase 4IIT

Effect of Treatment Using rhIL-11 in Patients With Thrombocytopenia After Chemotherapy for Childhood Acute Lymphoblastic Leukemia

The goal of this clinical research study is to find out if rhIL-11（Interleukin 11） may increase the platelet count in Childhood patients with acute lymphocytic leukemia (ALL) who develop low platelet counts while receiving standard CAT（cyclophosphamide+Cytosine arabinoside+mercaptopurine，7d） therapy.

Start Date01 Sep 2011

Sponsor / Collaborator

Shanghai Children's Medical Center

[+1]

NCT01317966

/ WithdrawnNot ApplicableIIT

A Multicentre Investigation of Recombinant Human Interleukin-11 (rhIL-11) Combination Low-dose Rituximab in Management of Steroid-Resistant/Relapsed Immune Thrombocytopenia (ITP)

The purpose of this study is to determine whether Recombinant Human Interleukin-11 (rhIL-11) Combination Low-dose Rituximab prednisone are effective and safe in the management of Steroid-Resistant/Relapsed Immune Thrombocytopenia (ITP).

Start Date01 Mar 2011

Sponsor / Collaborator

Shandong University

[+5]

100 Clinical Results associated with Oprelvekin

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100 Translational Medicine associated with Oprelvekin

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100 Patents (Medical) associated with Oprelvekin

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218

Literatures (Medical) associated with Oprelvekin

01 Feb 2024·Zhonghua wei zhong bing ji jiu yi xue

[Effect of recombinant human thrombopoietin on platelets in rats with D-galactosamine salt-induced acute liver failure].

Article

Author: Jing, Li ; Wang, Fengmei ; Tang, Fei ; Liang, Jing ; Liu, Gang

OBJECTIVETo evaluate the effects of recombinant human thrombopoietin (rhTPO) on platelet count (PLT) and liver function in acute liver failure (ALF) rats by observing the dynamic changes of PLT, thrombopoietin (TPO) and liver function during ALF.METHODSTwenty-four male Sprague-Dawley (SD) rats were divided into model group, TPO group and interleukin-11 (IL-11) group using a random number table method, with eight rats in each group. All rats were intraperitoneally injected with D-galactosamine (D-GalN, 1 500 mg/kg, dosed within 72 hours) to induce the ALF model. After modeling, rats in TPO group was received subcutaneous injection of 15 μg/kg of rhTPO for 5 days, and rats in IL-11 group was received subcutaneous injection of 0.45 mg/kg of IL-11 for 5 days. Venous blood samples were collected before and at 1, 3, 5, 7 and 12 days after molding for whole blood cell detection. The level of TPO in serum was detected by enzyme-linked immunosorbent assay (ELISA). Liver function indexes including serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBil) and albumin (ALB) were measured before and at 1, 3 and 5 days after modeling. The rats were sacrificed 12 days after the modeling, and the pathological changes of liver tissue were observed by hematoxylin-eosin (HE) staining.RESULTSTwo rats in each group died within 24-48 hours after modeling. HE staining showed that all three groups of ALF rats showed large flake necrosis of hepatocytes, disorder of hepatic lobular structure, mesh scaffold collapse, hepatic sinus congestion and hemorrhage, and flake infiltration of inflammatory cells on day 12 after modeling. The levels of serum ALT, AST and TBil of rats in each group were significantly increased 1 day after modeling and then decreased. The level of ALB decreased significantly on the first day after modeling and then increased, but there was no significant difference in the trend of liver function indexes among the three groups. PLT in the three groups decreased rapidly on day 1 after modeling, and then recovered gradually with the improvement of liver function. The PLT of the TPO group rose to the peak value 7 days after molding and was significantly higher than that of the model group [PLT (×10⁹/L): 1 673.3±347.5 vs. 855.3±447.0, P < 0.05], while there was no significant difference between the IL-11 group and the model group [PLT (×10⁹/L): 1 350.3±386.6 vs. 855.3±447.0, P > 0.05]. The level of serum TPO of the three groups increased significantly on day 1 after modeling, then decreased, and dropped to the lowest value on day 5, but there was no significant difference in the trend of serum TPO level among the three groups.CONCLUSIONSPLT in ALF rats decreased rapidly in the early stage and recovered gradually with the improvement of liver function, and the serum TPO level increased first and then decreased. Injection of rhTPO can significantly increase PLT in ALF rats, but has no significant effect on liver function and survival rate.

01 Jan 2024·International Immunopharmacology

IL-11 ameliorates oxidative stress damage in neurons after spinal cord injury by activating the JAK/STAT signaling pathway

Article

Author: Zuo, Lugen ; Wang, Yueyue ; Chen, Yue ; Shi, Jinran ; Zhang, Xiaofeng ; Li, Bohan ; Sun, Yang ; Geng, Zhijun ; Li, Jing ; Lü, Hezuo ; Hu, Jianguo ; Xu, Yibo ; Xiao, Linyu ; Song, Xue ; Wang, Lian

OBJECTIVEExcess reactive oxygen species (ROS) generated by oxidative stress is a crucial factor affecting neuronal dysfunction after spinal cord injury (SCI). IL-11 has been reported to have antioxidative stress capacity. In the present study, we investigated the protective effect and mechanism of IL-11 against neuronal cell damage caused by oxidative imbalance.METHODSWe established a H₂O₂-induced oxidative stress injury model in PC12 cells and observed the effects of IL-11 on cellular activity, morphology, oxidase and antioxidant enzymes, and ROS release. Furthermore, the effect of IL-11 on apoptosis of PC12 cells was assessed by flow cytometry, a TUNEL assay and Western blotting. Transcriptome analysis and rescue experiments revealed the mechanism by which IL-11 protects neurons from oxidative stress damage. For the in vivo investigation, an adenovirus-mediated IL-11 overexpression SCI rat model was constructed to validate the beneficial effect of IL-11 against SCI.RESULTSIL-11 significantly improved the viability and enhanced the antioxidant activity of H₂O₂-treated PC12 cells while reducing ROS release. In addition, IL-11 reduced H₂O₂-induced PC12 cell apoptosis. Transcriptome analysis revealed that the JAK/STAT pathway may be related to the antioxidant activity of IL-11. Treatment with a JAK/STAT inhibitor (Stattic) exacerbated the oxidative damage induced by H₂O₂ and attenuated the protective effects of IL-11. The results of in vivo studies showed that IL-11 prevented neuronal apoptosis due to oxidative imbalance and promoted the restoration of motor function in SCI rats by activating the JAK/STAT signaling pathway.CONCLUSIONIL-11 inhibited oxidative stress-induced neuronal apoptosis at least in part by activating the JAK/STAT signaling pathway and further promoted the recovery of motor function. These findings suggest that IL-11 may be an effective target for the treatment for SCI.

01 Dec 2023·European Journal of Pharmacology

Cardioprotective effect of Interleukin-11 against warm ischemia-reperfusion injury in a rat heart donor model

Article

Author: Inui, Tomohiko ; Suzuki, Shota ; Fujio, Yasushi ; Tanaka, Shota ; Matsumiya, Goro ; Ishikawa, Kiyotake ; Obana, Masanori ; Ikeuchi, Hiroki ; Sakata, Tomoki ; Shiko, Yuki ; Kawasaki, Yohei ; Kohno, Hiroki

Shortage of donor organs for heart transplantation is a worldwide problem. Donation after circulatory death (DCD) has been proposed to expand the donor pool. However, in contrast to the donation after brain death that undergoes immediate cold preservation, warm ischemia and subsequent reperfusion injury are inevitable in DCD. It has been reported that interleukin-11 (IL-11) mitigates ischemia-reperfusion injury in rodent models of myocardial infarction and donation after brain death heart transplantation. We hypothesized that IL-11 also offers benefit to warm ischemia in an experimental model of cardiac transplantation that resembles DCD. The hearts of naïve male Sprague Dawley rats (n = 15/group) were procured, subjected to 25-min warm ischemia, and reperfused for 60 min using Langendorff apparatus. IL-11 or saline was administered intravenously before the procurement, added to maintenance buffer, and infused via perfusion during reperfusion. IL-11 group exhibited significantly better cardiac function post-reperfusion. Severely damaged mitochondria was found in the electron microscopic analysis of control hearts whereas the mitochondrial structure was better preserved in the IL-11 treated hearts. Immunoblot analysis using neonatal rat cardiomyocytes revealed increased signal transducer and activator of transcription 3 (STAT3) phosphorylation at Ser727 after IL-11 treatment, suggesting its role in mitochondrial protection. Consistent with expected activation of mitochondrial respiration by mitochondrial STAT3, immunohistochemical staining demonstrated a higher mitochondrial cytochrome c oxidase subunit 2 expression. In summary, IL-11 protects the heart from warm ischemia reperfusion injury by alleviating mitochondrial injury and could be a viable therapeutic option for DCD heart transplantation.

100 Deals associated with Oprelvekin

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External Link

KEGG	Wiki	ATC	Drug Bank
D05266	Oprelvekin	L03AC02	DB00038

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Hemophilia A	Preclinical	US	University of Pittsburgh	01 Jan 2010
Von Willebrand Diseases	Preclinical	US	University of Pittsburgh	01 Jan 2010
Menorrhagia	Preclinical	US	Wyeth AB	01 Jan 2008
Von Willebrand Disease, Type 1	Preclinical	US	Wyeth AB	01 Jul 2004
Crohn Disease	Preclinical	US	Wyeth AB	01 Apr 2002

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT02517307 (CTgov)	Not Applicable	Trifunctional Protein Deficiency With Myopathy and Neuropathy \| Medium Chain Acyl CoA Dehydrogenase Deficiency \| Carnitine Palmitoyltransferase II Deficiency, Late-Onset \| Fatty acid oxidation disorder \| VLCAD Deficiency	41	Hyperinsulinemic euglycemic clamp+Glycerol/Saline (Glycerol/Saline FAOD)	cpggxqbaeo(plfhknktmc) = oovpdipnap unidbvkcqe (zsmddzqyzz, sqevvhzqer - qjwapdfugr) View more	-	30 Jan 2024
				Hyperinsulinemic euglycemic clamp+Heparin+Intralipid (Intralipid FAOD)	cpggxqbaeo(plfhknktmc) = btckyylngo unidbvkcqe (zsmddzqyzz, oextwtfbqd - dabjhuesuy) View more
ESMO 12023 \| ESMO 22023 Manual	Not Applicable	Thrombocytopenia	14	Hetrombopag + IL-11	(crfmlmmvcy) = gkrubgyrcz cgugmargqb (fiinspvvtd ) View more	Positive	21 Oct 2023
				Hetrombopag	(crfmlmmvcy) = hysdmfeorh cgugmargqb (fiinspvvtd ) View more
NCT00886743 (CTgov)	Phase 2	Thrombocytopenia	19	Oprelvekin	kflkltrkbc(vvljopyelz) = urtvbxtuhi jsaswktxhs (cfffbaheru, dctbfaxzuk - udvyioyohy) View more	-	19 Apr 2017
NCT00994929 (IL-11DDAVP, CTgov)	Phase 2	Von Willebrand Diseases \| Hemophilia A	9	Neumega (Oprelvekin, Interleukin 11, IL-11)	zmqaiwhjez(jsthtqtdpl) = fakozqlfwz pwkpuqfxnd (zipgorspwz, hkkowzigpo - shvrhtocka) View more	-	02 Mar 2016
NCT00524225 (CTgov)	Phase 2	Von Willebrand Disease, Type 1	3	Neumega (Oprelvekin, Interleukin 11, IL-11)	cvealoboky(lkbsizwqfd) = btverpqeuc aegijfnciw (ivwuqflmgv, ejvgcipkxg - hnuuttlqbw) View more	-	07 Nov 2014
ASCO2010	Phase 2	Thrombocytopenia	83	mIL-11	xhfrzbfrxe(gunptaxuay) = yndsqvdbls oywwcleezv (xefrqkmeqp )	-	20 May 2010
				rhIL-11	xhfrzbfrxe(gunptaxuay) = flrwpdwzak oywwcleezv (xefrqkmeqp )
ASCO2004	Not Applicable	Relapsed Solid Neoplasm	-	rhTPO	(hdfvcieqik) = fglbprujzt zawjofcknz (rqbpbzzosj ) View more	-	15 Jul 2004
				rhIL-11 + G-SCF	(hdfvcieqik) = obbfakipno zawjofcknz (rqbpbzzosj ) View more