A Phase 2b, Randomized, Double-Blind, Parallel Group, Placebo-Controlled 60-Week Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin in the Treatment of Severe to Very Severe Alopecia Areata in Adult Patients (Rezolve AA)

This is an interventional, randomized, double blind, parallel group, placebo-controlled, Phase 2b, 3-arm study to assess the effect of pegylated-recombinant-human interleukin-2 (rezpegaldesleukin) in adult participants with severe to very severe alopecia areata.
The estimated duration includes a screening period of up to 35 days, a 36-week treatment period, and a 24-week follow-up period. The maximum study duration is approximately 65 weeks for all participants.

Start Date02 Apr 2024

Sponsor / Collaborator

Nektar Therapeutics

NCT06136741 / RecruitingPhase 2

A Phase 2b, Randomized, Double-Blind, Parallel-Group, Placebo-Controlled 54-Week Study to Evaluate the Efficacy and Safety of Rezpegaldesleukin in the Treatment of Adult Patients With Moderate-to-Severe Atopic Dermatitis

This is an interventional, randomized, parallel group, treatment, Phase IIb, double blind, 4-arm study to assess the effect of pegylated-recombinant-human interleukin-2 (rezpegaldesleukin) in adult participants with moderate to severe atopic dermatitis.
The estimated duration is 15-35 days for screening and then up to approximately day 378 (last dose on day 280 + 98 days safety follow-up) for all patients. Patients with a response at Week 16 (end of induction therapy) will be re-randomized for the maintenance therapy period.

Start Date23 Oct 2023

Sponsor / Collaborator

Nektar Therapeutics

NCT05565729 / CompletedPhase 1

A Phase 1, Randomized, Placebo-controlled, Participant- and Investigator-blind, Single-dose Study of the Pharmacokinetics of LY3471851 Following Subcutaneous Dosing of LY3471851 in Healthy Participants

The purpose of this study is to compare two different formulations (test & reference) of LY3471851 in healthy participants. This study will compare how much of each formulation gets into the blood stream and how long it takes the body to remove it. Information about any side effects that may occur will also be collected. Participants will remain in the study for about 12 weeks, after receiving the study drug that is LY3471851.

Start Date05 Oct 2022

Sponsor / Collaborator

Nektar Therapeutics

[+1]

100 Clinical Results associated with Rezpegaldesleukin

100 Translational Medicine associated with Rezpegaldesleukin

100 Patents (Medical) associated with Rezpegaldesleukin

Literatures (Medical) associated with Rezpegaldesleukin

01 Jan 2022·Journal of translational autoimmunity

Selective expansion of regulatory T cells by NKTR-358 in healthy volunteers and patients with systemic lupus erythematosus

Article

Author: Levin, Robert ; Furie, Richard ; Diab, Isam ; Fanton, Christie ; Hanan, Nathan ; Chindalore, Vishala ; Zalevsky, Jonathan ; Dickerson, Daniel ; Dixit, Neha ; Haglund, Cat ; Kotzin, Brian L ; Gibbons, Jacqueline

Objective:

To evaluate NKTR-358, a polyethylene glycol-interleukin-2 conjugate composition designed to selectively induce regulatory T cells (Tregs), in first-in-human studies.

Methods:

Healthy volunteers and patients with systemic lupus erythematosus (SLE) received single- or multiple-dose (biweekly) NKTR-358 or placebo in two sequential, randomized, phase 1 studies (single ascending dose [SAD; NCT04133116] and multiple ascending dose [MAD; NCT03556007]). Primary objectives were safety and tolerability; secondary objectives included pharmacokinetics (PK) and immune effects of NKTR-358; exploratory objectives included effects on SLE disease activity.

Results:

There were eight ascending dose cohorts in the SAD study (0.3-28.0 μg/kg: n = 76; placebo: n = 24) and four in the MAD study (3-24.0 μg/kg: n = 36; placebo: n = 12). Most adverse events (AEs) were grade 1-2 injection-site reactions, with no treatment-related serious or severe AEs, or deaths. PK data showed dose proportionality and prolonged exposure (mean half-life: 7.4-12.9 days). Dose-dependent, selective, and sustained increases in percentages and absolute numbers of total CD4⁺ Tregs and CD25^bright Tregs were observed, with no significant changes in conventional CD4⁺ and CD8⁺ T cells, and low-level increases in natural killer cells. At the highest doses tested, administration of NKTR-358 resulted in a 12-17-fold increase in CD25^bright Tregs over baseline that was sustained for 20-30 days.

Conclusion:

NKTR-358 was well tolerated, had a suitable PK profile for biweekly dosing, and led to marked and selective dose-dependent increases in CD25^bright Tregs, with no significant changes in conventional T cells. These results provide strong support for further testing in SLE and other inflammatory diseases.

01 Jan 2021·Journal of translational autoimmunity

NKTR-358: A novel regulatory T-cell stimulator that selectively stimulates expansion and suppressive function of regulatory T cells for the treatment of autoimmune and inflammatory diseases

Article

Author: Zhang, Ping ; Dixit, Neha ; Lee, Myong ; Kuo, Peiwen ; Doberstein, Stephen K ; Fanton, Christie ; Cetz, Janet ; Sweeney, Theresa D ; Kamihara, Yusuke ; VanderVeen, Laurie A ; Dixit, Vidula ; Chang, Thomas ; Rubas, Werner ; Langowski, John L ; Kirksey, Yolanda ; Ritz, Jerome ; Tang, Yinyan ; Zalevsky, Jonathan ; Maiti, Mekhala ; Ji, Chunmei ; Kim, Grace ; Kirk, Peter

Impaired interleukin-2 (IL-2) production and regulatory T-cell dysfunction have been implicated as immunological mechanisms central to the pathogenesis of multiple autoimmune and inflammatory diseases. NKTR-358, a novel regulatory T-cell stimulator, is an investigational therapeutic that selectively restores regulatory T-cell homeostasis in these diseases. We investigated NKTR-358's selectivity for regulatory T-cells, receptor-binding properties, ex vivo and in vivo pharmacodynamics, ability to suppress conventional T-cell proliferation in mice and non-human primates, and functional activity in a murine model of systemic lupus erythematosus. In vitro, NKTR-358 demonstrated decreased affinity for IL-2Rα, IL-2Rβ, and IL-2Rαβ compared with recombinant human IL-2 (rhIL-2). A single dose of NKTR-358 in cynomolgus monkeys produced a greater than 15-fold increase in regulatory T-cells, and the increase lasted until day 14, while daily rhIL-2 administration for 5 days only elicited a 3-fold increase, which lasted until day 7. Repeated dosing of NKTR-358 over 6 months in cynomolgus monkeys elicited cyclical, robust increases in regulatory T-cells with no loss in drug activity over the course of treatment. Regulatory T-cells isolated from NKTR-358-treated mice displayed a sustained, higher suppression of conventional T-cell proliferation than regulatory T-cells isolated from vehicle-treated mice. NKTR-358 treatment in a mouse model (MRL/MpJ-Fas^lpr) of systemic lupus erythematosus for 12 weeks maintained elevated regulatory T-cells for the treatment duration and ameliorated disease progression. Together, these results suggest that NKTR-358 has the ability to elicit sustained and preferential proliferation and activation of regulatory T-cells without corresponding effects on conventional T-cells, with improved pharmacokinetics compared with rhIL-2.

14 Jan 2019·ACS biomaterials science & engineeringQ3 · ENGINEERING & TECHNOLOGY

Folic-Acid-Adorned PEGylated Graphene Oxide Interferes with the Cell Migration of Triple Negative Breast Cancer Cell Line, MDAMB-231 by Targeting miR-21/PTEN Axis through NFκB

Q3 · ENGINEERING & TECHNOLOGY

Article

Author: Chattopadhyay, Dipankar ; Ghosh, Avijit ; Upadhyay, Priyanka ; Basu, Arijita ; Adhikary, Arghya

Triple negative breast cancer (TNBC), characterized by its aggressive and highly metastatic nature, is difficult to cure by the currently available therapies. In our investigation, folic-acid-adorned PEGylated graphene oxide (FA-PEG-GO) was synthesized by modifying graphene oxide (GO) with folic acid-PEG conjugate (FA-PEG-NH₂) by EDC/NHS coupling reaction. FA-PEG-GO exhibited an exceptional potential to attenuate cell migration of TNBC cell line ,MDAMB-231 as compared to GO because of the adorned folic acid moiety, which rendered better targeting. FA-PEG-GO inhibited cell migration by actin depolymerization and perturbing lamellipodia formation. The immunocytochemistry and western blot data unraveled the fact that FA-PEG-GO inhibited cell migration by targeting miR-21 by restricting the nuclear translocation of NFκB. The downregulation of miR-21 resulted in the elevation of PTEN expression which sequentially downregulated pFAK resulting in inhibition of cell migration. Moreover, upregulation of PTEN in FA-PEG-GO treated cells led to the decrease in expression of the downstream regulators including pAkt(Ser473) and pERK1/2, which contributed to the retardation of cell migration. Interestingly, the overexpression of NFκB-p65 by the transfection of NFκB-p65 expression plasmid in TNBC cells reversed the inhibitory effect of FA-PEG-GO on the nuclear translocation of NFκB-p65 which stabilized miR-21 expression and successively downregulated PTEN expression in FA-PEG-GO treated cells. Furthermore, miR-21 overexpression by transfection of miR-21 mimic in turn downregulated PTEN expression and sequentially restored the expression of pFAK even upon FA-PEG-GO treatment. miR-21 overexpression also compensated the inhibitory effect of FA-PEG-GO on pAkt(Ser473) and pERK1/2 which was evident from their significant expression in FA-PEG-GO-treated cells. The studies on chick embryo model ratified the ex ovo antimigratory efficacy of FA-PEG-GO. Altogether, our study unveiled the enormous potential of FA-PEG-GO to attenuate migration of TNBC cell line, MDAMB-231 by targeting the miR-21/PTEN axis through NFκB and thereby providing insights on cancer treatment.

News (Medical) associated with Rezpegaldesleukin

12 Jun 2024

·www.prnewswire.com

Nektar Therapeutics Presents First Preclinical Data on NKTR-0165, a TNFR2 Agonist Antibody Being Developed for the Treatment of Inflammatory Diseases, at EULAR 2024

– NKTR-0165 Demonstrates Selective Enhancement of Treg Cell Function Through Novel Agonistic Mechanism – – IND-Enabling Studies Underway for NKTR-0165 with First-in-Human Studies Planned in First Half of 2025 - SAN FRANCISCO, June 12, 2024 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) today announced the presentation of a poster highlighting new preclinical data on NKTR-0165 at the European Alliance of Associations for Rheumatology (EULAR) 2024 Congress. NKTR-0165 is a novel, first-in-class tumor necrosis factor receptor 2 (TNFR2) agonist and bivalent antibody designed to selectively stimulate TNFR2 receptor activity, without modulation of the TNFR1 signaling. TNFR2 signaling has been shown to be an important gatekeeper of inflammation and its absence or deficit is associated with a broad range of autoimmune diseases. TNFR2 is highly expressed on Tregs, neuronal cells and endothelial cells and has been shown to potentiate the suppressive effects and overall functional properties of regulatory T cells (Tregs). "The preclinical data presented at EULAR show that NKTR-0165 is a unique antibody that selectively binds to TNFR2 on Tregs to enhance its immunosuppressive activities, and could potentially become a first-in-class treatment for various autoimmune diseases, including ulcerative colitis and vitiligo," said Jonathan Zalevsky, Ph.D., Senior Vice President and Chief Research & Development Officer at Nektar. "By selectively binding to TNFR2, NKTR-0165 upregulates expression of proteins that are critical to Treg proliferation and function. Animal models show that NKTR-0165 reduces inflammation through the selective enhancement of Treg cell function via TNFR2 agonism. These data demonstrate a unique and differentiated profile for this bivalent antibody in the field of TNFR2 agonists." The poster presentation is available for download at . Key details and takeaways from the presentation are as follows: Abstract 3174: "A Novel Therapeutically Active Anti-TNFR2 Agonistic Antibody Promotes Treg Proliferation and Induction of Treg Functional Markers", Miyazaki, et al. NKTR-0165 shows selective TNFR2 binding and receptor agonism in human Tregs, with minimal binding and signaling activity in other TNFR2-expressing immune cells in vitro and in vivo. NKTR-0165 agonistic activity enhances Treg lineage stabilization and upregulates expression of proteins involved in Treg proliferation and function. NKTR-0165 demonstrates therapeutic efficacy in a KLH-induced delayed type hypersensitivity (DTH) model in human TNFR2 knock-in mice. About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in two Phase 2b clinical trials, one in atopic dermatitis and one in alopecia areata. Our pipeline also includes a preclinical candidate NKTR-0165, which is a bivalent tumor necrosis factor receptor type II agonist antibody. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements which can be identified by words such as: "could," "design," "develop," "potential" and similar references to future periods. Examples of forward-looking statements include, among others, statements we make regarding the therapeutic potential of NKTR-0165 and rezpegaldesleukin, observations from early data emerging from preclinical research of NKTR-0165, the potential of the technology incorporated into our drug candidates, and the future development plans for NKTR-0165 and rezpegaldesleukin. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, anticipated events and trends, the economy and other future conditions. Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Our actual results may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Important factors that could cause our actual results to differ materially from those indicated in the forward-looking statements include, among others: (i) our statements regarding the therapeutic potential of NKTR-0165 and rezpegaldesleukin are based on preclinical and clinical findings and observations and are subject to change as research and development continue; (ii) NKTR-0165 and rezpegaldesleukin are investigational agents and continued research and development for these drug candidates is subject to substantial risks, including negative safety and efficacy findings in future clinical studies (notwithstanding positive findings in earlier preclinical and clinical studies); (iii) rezpegaldesleukin is in clinical development and NTKR-0165 is in preclinical development, and the risk of failure is high and can unexpectedly occur at any stage prior to regulatory approval; (iv) the timing of the commencement or end of clinical trials and the availability of clinical data may be delayed or unsuccessful due to challenges caused by health epidemics, regulatory delays, slower than anticipated patient enrollment, manufacturing challenges, changing standards of care, evolving regulatory requirements, clinical trial design, clinical outcomes, competitive factors, or delay or failure in ultimately obtaining regulatory approval in one or more important markets; (v) we may not achieve the expected cost savings we expect from our 2022 corporate restructuring and reorganization plan or our 2023 cost restructuring plan and we may undertake additional restructuring and cost-saving activities in the future, (vi) patents may not issue from our patent applications for our drug candidates, patents that have issued may not be enforceable, or additional intellectual property licenses from third parties may be required; and (vii) certain other important risks and uncertainties set forth in our Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission on May 10, 2024. Any forward-looking statement made by us in this press release is based only on information currently available to us and speaks only as of the date on which it is made. We undertake no obligation to update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise. Contact: For Investors: Vivian Wu of Nektar Therapeutics 628-895-0661 For Media: David Rosen of Argot Partners (212) 600-1902 [email protected] SOURCE Nektar Therapeutics

Phase 2AACRImmunotherapy

30 May 2024

·www.prnewswire.com

Nektar Management to Present at Upcoming Investor Conferences

SAN FRANCISCO, May 30, 2024 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) management is scheduled to present at upcoming investor conferences: Jefferies Healthcare Conference in New York City on Thursday, June 6, 2024 at 3:30 p.m. Eastern Time / 12:30 p.m. Pacific Time Goldman Sachs 45th Annual Global Healthcare Conference in Miami on Monday, June 10, 2024 at 2:00 p.m. Eastern Time / 11:00 a.m. Pacific Time The presentations will be accessible via webcast through links posted on the Investor Events section of the Nektar website: . The webcasts will be available for replay until July 6, 2024 and July 10, 2024, respectively. About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in two Phase 2b clinical trials, one in atopic dermatitis and one in alopecia areata. Our pipeline also includes a preclinical candidate NKTR-0165, which is a bivalent tumor necrosis factor receptor type II agonist antibody. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. Contact: For Investors: Vivian Wu of Nektar Therapeutics 628-895-0661 For Media: David Rosen of Argot Partners (212) 600-1902 [email protected] SOURCE Nektar Therapeutics

Phase 2

09 May 2024

·www.prnewswire.com

Nektar Therapeutics Reports First Quarter 2024 Financial Results

SAN FRANCISCO, May 9, 2024 /PRNewswire/ -- Nektar Therapeutics (Nasdaq: NKTR) today reported financial results for the first quarter ended March 31, 2024. Cash and investments in marketable securities at March 31, 2024 were $326.0 million as compared to $329.4 million at December 31, 2023. Nektar's cash and marketable securities are expected to support strategic development activities and operations into the third quarter of 2026. "In the first quarter, we made significant progress with our highly promising immunology and inflammation pipeline," said Howard W. Robin, President and CEO of Nektar. "REZPEG is advancing in the clinic in our Phase 2b study in patients with atopic dermatitis and in our Phase 2b study in patients with alopecia areata. Enrollment for both studies is on-track, and we expect to report topline data from these trials in the first half of 2025. Building out our Treg pipeline, our novel bivalent antibody targeting the TNFR2 receptor is progressing through IND-enabling studies to support entering the clinic next year." Summary of Financial Results Revenue in the first quarter of 2024 was $21.6 million as compared to the same $21.6 million in the first quarter of 2023. Total operating costs and expenses in the first quarter of 2024 were $57.1 million as compared to $156.3 million in the first quarter of 2023. Operating costs and expenses for the first quarter of 2023 included a one-time $76.5 million non-cash goodwill impairment charge. Operating costs and expenses for the first quarter of 2024 further decreased as compared to 2023 due to decreases in restructuring, impairment and costs of terminated program, as well as decreases in R&D and G&A expense. R&D expense in the first quarter of 2024 was $27.4 million as compared to $30.5 million for the first quarter of 2023. R&D expense for the first quarter of 2024 decreased primarily due to a decrease in employee costs and related facilities costs, partially offset by an increase in expense for the development of rezpegaldesleukin and NKTR-0165, our TNFR2 agonist antibody. G&A expense was $20.1 million in the first quarter of 2024 as compared to $21.1 million in the first quarter of 2023. Restructuring, impairment and other costs of the terminated program were $1.0 million in the first quarter of 2024 as compared to $21.2 million in the first quarter of 2023. Restructuring, impairment and other costs of terminated program decreased primarily due to $13.2 million in non-cash lease and equipment impairment charges and $5.5 million in severance expense recognized in the first quarter of 2023. Net loss for the first quarter of 2024 was $36.8 million or $0.19 basic and diluted loss per share as compared to a net loss of $137.0 million or $0.73 basic and diluted loss per share in the first quarter of 2023. First Quarter 2024 and Recent Business Highlights In March 2024, Nektar initiated a Phase 2b study of rezpegaldesleukin in patients with severe to very severe alopecia areata. The Company expects topline data from this study in the first half of 2025. Enrollment is ongoing in the Phase 2b study of rezpegaldesleukin in patients with moderate-to-severe atopic dermatitis. The Company expects topline data from the study in the first half of 2025. In March 2024, we entered into a securities purchase agreement with TCG Crossover Fund, an institutional accredited investor, to sell securities in a private placement financing for gross proceeds to the Company of approximately $30 million, before deducting expenses. Conference Call to Discuss First Quarter 2024 Financial Results Nektar management will host a conference call to review the results beginning at 5:00 p.m. Eastern Time/2:00 p.m. Pacific Time, May 9, 2024. This press release and live audio-only webcast of the conference call can be accessed through a link that is posted on the Home Page and Investors section of the Nektar website: . The web broadcast of the conference call will be available for replay through June 9, 2024. To access the conference call, follow these instructions: Dial: (800) 715-9871 (U.S & Canada) Conference ID: 4855448 About Nektar Therapeutics Nektar Therapeutics is a clinical-stage biotechnology company focused on developing treatments that address the underlying immunological dysfunction in autoimmune and chronic inflammatory diseases. Nektar's lead product candidate, rezpegaldesleukin (REZPEG, or NKTR-358), is a novel, first-in-class regulatory T cell stimulator being evaluated in two Phase 2b clinical trials, one in atopic dermatitis and one in alopecia areata. Our pipeline also includes a preclinical candidate NKTR-0165, which is a bivalent tumor necrosis factor receptor type II agonist antibody. Nektar, together with various partners, is also evaluating NKTR-255, an investigational IL-15 receptor agonist designed to boost the immune system's natural ability to fight cancer, in several ongoing clinical trials. Nektar is headquartered in San Francisco, California. For further information, visit and follow us on LinkedIn. Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements which can be identified by words such as: "will," "expect," "develop," "potential," "advance," "anticipate," and similar references to future periods. Examples of forward-looking statements include, among others, statements regarding the therapeutic potential of, and future development plans for, rezpegaldesleukin and NKTR-0165. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, anticipated events and trends, the economy and other future conditions. Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Our actual results may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Important factors that could cause our actual results to differ materially from those indicated in the forward-looking statements include, among others: (i) our statements regarding the therapeutic potential of rezpegaldesleukin and NKTR-0165 are based on preclinical and clinical findings and observations and are subject to change as research and development continue; (ii) rezpegaldesleukin and NKTR-0165 are investigational agents and continued research and development for these drug candidates is subject to substantial risks, including negative safety and efficacy findings in future clinical studies (notwithstanding positive findings in earlier preclinical and clinical studies); (iii) rezpegaldesleukin is in clinical development and NTKR-0165 is in preclinical development, and the risk of failure is high and can unexpectedly occur at any stage prior to regulatory approval; (iv) the timing of the commencement or end of clinical trials and the availability of clinical data may be delayed or unsuccessful due to challenges caused by health epidemics, including the recent COVID-19 pandemic, regulatory delays, slower than anticipated patient enrollment, manufacturing challenges, changing standards of care, evolving regulatory requirements, clinical trial design, clinical outcomes, competitive factors, or delay or failure in ultimately obtaining regulatory approval in one or more important markets; (v) we may not achieve the expected cost savings we expect from our 2022 corporate restructuring and reorganization plan or our 2023 cost restructuring plan and we may undertake additional restructuring and cost-saving activities in the future, (vi) patents may not issue from our patent applications for our drug candidates, patents that have issued may not be enforceable, or additional intellectual property licenses from third parties may be required; and (vii) certain other important risks and uncertainties set forth in our Quarterly Report on Form 10-K filed with the Securities and Exchange Commission on March 5, 2024. Any forward-looking statement made by us in this press release is based only on information currently available to us and speaks only as of the date on which it is made. We undertake no obligation to update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise. Contact: For Investors: Vivian Wu of Nektar Therapeutics 628-895-0661 For Media: David Rosen of Argot Partners (212) 600-1902 [email protected] SOURCE Nektar Therapeutics

Phase 2Financial StatementPhase 1

100 Deals associated with Rezpegaldesleukin

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Alopecia Areata	Phase 2	US	Nektar Therapeutics	02 Apr 2024
Alopecia Areata	Phase 2	CA	Nektar Therapeutics	02 Apr 2024
Dermatitis, Atopic	Phase 2	US	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	AU	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	BG	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	CA	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	HR	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	CZ	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	DE	Nektar Therapeutics	23 Oct 2023
Dermatitis, Atopic	Phase 2	HU	Nektar Therapeutics	23 Oct 2023

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04433585 (CTgov)	Phase 2	Systemic Lupus Erythematosus	291	LY3471851 (LY3471851 High Dose)	pzfshqmezw(fmosbonuif) = zyjzpmpxkm dugdnygega (dtoywoenov, yprtzxdidy - gnmhhecdzi) View more	-	23 Apr 2024
				LY3471851 (LY3471851 Mid Dose)	pzfshqmezw(fmosbonuif) = xidtvcwugc dugdnygega (dtoywoenov, baiklhwmfa - zmqrcmngjt) View more
NCT04081350 (Phase 1b study, EADV2023)	Phase 1	Dermatitis, Atopic Treg	-	Rezpegaldesleukin 12 µg/kg	vkctqqdjlx(ytzbkqyqpj) = siwxvnqpne ikfpefgoaq (gjphmznlzc ) View more	Positive	11 Oct 2023
				Rezpegaldesleukin 24 µg/kg	vkctqqdjlx(ytzbkqyqpj) = kartsljpvr ikfpefgoaq (gjphmznlzc ) View more
NCT04677179 (CTgov)	Phase 2	Colitis, Ulcerative	81	Placebo (Placebo (Induction Treatment Period))	mdasqrexxn(xjlpepfwgs) = szzhqzkvjq jsklqcrnft (unvuxtlljt, evexusgghg - doctlrjvjm) View more	-	05 Sep 2023
				LY3471851 (Low Dose LY3471851 (Induction Treatment Period))	mdasqrexxn(xjlpepfwgs) = zmcelwnegl jsklqcrnft (unvuxtlljt, yqxcxipmsw - ejnsnuqqpg) View more
NCT04433585 (ISLAND-SLE, Corporate Publications) Manual	Phase 2	Systemic Lupus Erythematosus	291	rezpegaldesleukin 300mcg Q2W	pjimskxwlz(utomdwfhdl) = hffeptegae hytqlffyzz (tjwjqgsgkh ) View more	Negative	23 Feb 2023
				rezpegaldesleukin 900mcg Q2W	pjimskxwlz(utomdwfhdl) = boodrhlhal hytqlffyzz (tjwjqgsgkh ) View more
NCT04119557 (Corporate Publications) Manual	Phase 1	Psoriasis	26	LY3471851	nyxyuxivpk(xohtldifmd) = yecyukekqp bmgqlwzhgo (hspuulpyur ) View more	Positive	07 Sep 2022
				Placebo	nyxyuxivpk(xohtldifmd) = jmpfgjyjsu bmgqlwzhgo (hspuulpyur ) View more
NCT04119557 (Corporate Publications) Manual	Phase 1	Psoriasis	26	LY3471851 24 µg/kg	svlqewkyug(zzabmlhejf) = mzuntopfta dxcuwesbue (dekiadwmpm ) View more	Positive	07 Sep 2022
				placebo	svlqewkyug(zzabmlhejf) = rmowtobcmk dxcuwesbue (dekiadwmpm ) View more
NCT04081350 (Corporate Publications) Manual	Phase 1	Dermatitis, Atopic	43	LY3471851 12 µg/kg	lwurarhnry(wxblcsfkca) = rihvzprwun rkahwipkwq (yorfypsitr ) View more	Positive	07 Sep 2022
				LY3471851 24 µg/kg	lwurarhnry(wxblcsfkca) = rajlvquaqy rkahwipkwq (yorfypsitr ) View more
NCT03556007 (Corporate Publications) Manual	Phase 1	Systemic Lupus Erythematosus	48	NKTR-358	nulplpmluu(iiuwkzzfbz) = NKTR-358 was safe and well tolerated in patients with mild-to-moderate SLE ggnafqceba (ljwjlyukhp )	Positive	04 Jun 2020
				Placebo
ACR2019	Not Applicable	Autoimmune Diseases	-	NKTR-358 0.3 µg/kg	ydxnfttymr(ywvyxumppi) = increased at doses >20 μg/kg xkofuvkxjw (chhwflatgn ) View more	-	10 Nov 2019
				NKTR-358 3.0 µg/kg

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Rezpegaldesleukin

Overview

Basic Info

Gene Sequence

Related

R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

Regulation