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Nurix Therapeutics Presents New Preclinical and Phase 1 Translational Data Supporting Bexobrutideg (NX-5948) in Chronic Spontaneous Urticaria at the 2026 Society for Investigative Dermatology Annual Meeting

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Nurix Therapeutics (Nasdaq: NRIX) reported new preclinical and Phase 1 translational data for its oral BTK degrader bexobrutideg (NX-5948) in chronic spontaneous urticaria (CSU). Data show potent, highly selective BTK degradation across key immune cells and rapid, robust BTK loss in blood and skin of healthy volunteers.

According to Nurix, bexobrutideg achieved ~25-fold greater potency than remibrutinib in preclinical FcεRI-driven models and produced larger reductions in ear swelling and vascular permeability in a mouse anaphylaxis model, supporting further clinical development in CSU and broader inflammation and immunology indications.

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AI-generated analysis. Not financial advice.

Positive

  • Preclinical data show ~25-fold greater potency vs remibrutinib in FcεRI-driven CSU models
  • Robust, rapid BTK degradation in blood and skin in Phase 1 healthy volunteers
  • Highly selective BTK degradation across >8,700 proteins in broad proteomic analysis
  • Oral tablet formulation achieves virtually complete BTK degradation in key tissues
  • Safety, pharmacokinetic and pharmacodynamic profile to date supports continued development in CSU
  • Preclinical models show greater reductions in ear swelling and vascular permeability vs remibrutinib

Negative

  • Data are limited to preclinical studies and Phase 1 healthy volunteers, not CSU patients
  • Bexobrutideg remains in early clinical development, with efficacy in target indications unproven
  • Comparisons with remibrutinib are based on preclinical models rather than head-to-head clinical trials

News Market Reaction – NRIX

-0.91%
3 alerts
-0.91% News Effect
+5.0% Peak Tracked
-10.7% Trough Tracked
-$15M Valuation Impact
$1.65B Market Cap
0.0x Rel. Volume

On the day this news was published, NRIX declined 0.91%, reflecting a mild negative market reaction. Argus tracked a peak move of +5.0% during that session. Argus tracked a trough of -10.7% from its starting point during tracking. Our momentum scanner triggered 3 alerts that day, indicating moderate trading interest and price volatility. This price movement removed approximately $15M from the company's valuation, bringing the market cap to $1.65B at that time.

Data tracked by StockTitan Argus on the day of publication.

Key Figures

Potency vs remibrutinib: ~25-fold greater potency Proteomic coverage: more than 8,700 proteins ORR in CLL: 83% +5 more
8 metrics
Potency vs remibrutinib ~25-fold greater potency Preclinical CSU FcεRI-driven mast cell and basophil degranulation
Proteomic coverage more than 8,700 proteins Global proteomic selectivity analysis for BTK degradation
ORR in CLL 83% Phase 1a CLL/SLL bexobrutideg, 47 evaluable patients
Median PFS 22.1 months Phase 1a CLL/SLL bexobrutideg
ORR in WM 75.0% Phase 1 Waldenström macroglobulinemia bexobrutideg, 28 evaluable pts
Revenue $6.3M Q1 2026 reported revenue
R&D expense $84.1M Q1 2026 research and development spending
Net loss $87.2M Q1 2026 net loss

Market Reality Check

Price: $15.28 Vol: Volume 0.98M is 18% above...
normal vol
$15.28 Last Close
Volume Volume 0.98M is 18% above 20-day average 0.83M (relative volume 1.18x). normal
Technical Trading about 13% above 200-day MA of $14.30, at $16.18 and 28% below 52-week high.

Peers on Argus

NRIX was up 1.38% with modestly elevated volume. Peers were mixed: RIGL up 6.32%...

NRIX was up 1.38% with modestly elevated volume. Peers were mixed: RIGL up 6.32%, RLAY up 3.12%, PRME and DAWN slightly positive, while AVBP was slightly negative. No broad momentum signal appeared in the scanner.

Previous Clinical trial Reports

5 past events · Latest: Dec 08 (Positive)
Same Type Pattern 5 events
Date Event Sentiment Move Catalyst
Dec 08 ASH WM data Positive +18.7% Phase 1 WM data showed 75% ORR with manageable safety profile.
Dec 06 ASH CLL data Positive +18.7% Phase 1a/1b CLL data with 83% ORR and strong PFS at RP2D.
Dec 01 CLL webcast preview Neutral -4.4% Announcement of webcast to review Phase 1 bexobrutideg data.
Nov 07 NX-1607 SITC data Positive -1.7% Phase 1 NX-1607 translational data showing immune activation signals.
Oct 18 NX-1607 ESMO data Positive +5.6% NX-1607 Phase 1a data with 49.3% DCR and tumor responses.
Pattern Detected

Clinical trial updates have often led to strong moves, with several double-digit gains but also occasional negative reactions despite similar-positive data.

Recent Company History

Across recent clinical trial communications, Nurix has repeatedly highlighted encouraging data from its degrader pipeline. December 2025 updates on bexobrutideg in CLL and Waldenström macroglobulinemia produced high response rates and drove double-digit gains around +18.68%. Other clinical updates on NX‑1607 showed immune activation but saw modestly negative to mixed price reactions. Today’s CSU translational data extend bexobrutideg from hematologic malignancies into immunology, reinforcing the asset’s versatility within Nurix’s broader targeted protein degradation strategy.

Historical Comparison

+7.4% avg move · Over the past year, NRIX’s clinical trial updates showed an average move of 7.38%, with several doub...
clinical trial
+7.4%
Average Historical Move clinical trial

Over the past year, NRIX’s clinical trial updates showed an average move of 7.38%, with several double‑digit gains. Today’s +1.38% reaction to new bexobrutideg CSU data sits at the lower end of this historical range.

Historical updates focused on hematologic malignancies (CLL, Waldenström) and CBL-B programs. The current release extends bexobrutideg’s Phase 1 translational story into chronic spontaneous urticaria, suggesting a progression from oncology-only use toward broader immunology indications.

Market Pulse Summary

This announcement highlights new preclinical and Phase 1 translational data for bexobrutideg in chro...
Analysis

This announcement highlights new preclinical and Phase 1 translational data for bexobrutideg in chronic spontaneous urticaria, emphasizing robust BTK degradation in blood and skin and roughly 25-fold greater potency versus remibrutinib in preclinical models. Historically, Nurix’s clinical trial updates have produced mixed market reactions, with some double-digit gains and some declines. Investors may watch for future CSU-specific trials, durability and safety readouts, and how these immunology efforts balance against ongoing oncology development and spending.

Key Terms

btk, targeted protein degradation, e3 ligase, proteasomal degradation, +4 more
8 terms
btk medical
"Bexobrutideg demonstrates potent BTK degradation across key immune cell types"
Bruton's tyrosine kinase (BTK) is an enzyme that acts like a light switch inside certain immune and blood cells, helping them send signals that control growth, survival and activity. Investors care because medicines that block or modify BTK can change how cancers and autoimmune diseases are treated; clinical trial results, safety profiles and regulatory decisions for BTK-targeting drugs can materially alter a biotech or pharmaceutical company’s prospects and valuation.
targeted protein degradation medical
"focused on the discovery, development and commercialization of targeted protein degradation medicines"
Targeted protein degradation is a drug approach that uses small molecules to mark harmful or malfunctioning proteins inside cells so the cell’s own disposal system breaks them down, rather than simply blocking their activity. For investors, it matters because this method can potentially tackle diseases that traditional drugs cannot reach, offering a new class of therapies with broad commercial and patent potential—like switching from silencing a problem to removing it entirely.
e3 ligase medical
"through recruitment of the cereblon E3 ligase complex, which efficiently marks the BTK protein"
An E3 ligase is a cellular enzyme that attaches a tiny molecular tag to specific proteins, marking them for disposal by the cell’s cleanup machinery; think of it as the postal worker that stamps items for removal. Investors care because drugs that use or hijack E3 ligases can selectively destroy disease-causing proteins, creating a new class of targeted therapies and potentially boosting the value of companies developing such platforms or partnerships.
proteasomal degradation medical
"marks the BTK protein for proteasomal degradation, thereby eliminating both the kinase-dependent"
Proteasomal degradation is the cell’s process for recognizing and breaking down unwanted or damaged proteins using a molecular machine called the proteasome, like a cellular shredder that recycles parts. Investors should care because drugs or technologies that alter this disposal system can change how diseases are treated, affect drug effectiveness and safety, and create measurable biomarkers — all of which can materially impact a company’s pipeline and valuation.
fcεri medical
"enhanced suppression of FcεRI-driven pathology versus remibrutinib"
A high‑affinity IgE receptor found on certain immune cells that acts like an alarm sensor: when it binds the allergy antibody IgE it triggers release of chemicals that cause allergic reactions. Investors watch this protein because it is a common drug target and diagnostic marker—therapies that block or modulate it can prevent symptoms, affect clinical trial outcomes, regulatory approval prospects, and market potential for allergy and asthma treatments.
bcr signaling medical
"deeper suppression of BCR signaling than BTK inhibitors in preclinical assays"
BCR signaling is the chain of biochemical messages triggered when a B cell’s surface receptor recognizes a target, telling the cell to grow, survive or make antibodies. Investors care because when this pathway is overactive it can drive blood cancers or autoimmune disease, and many drugs in development aim to block specific steps—making BCR signaling a key indicator of potential therapeutic value and market opportunity.
pharmacokinetic medical
"Taken together, the safety, pharmacokinetic, and pharmacodynamic profile observed to date"
Pharmacokinetic describes how a drug moves through and leaves the body — how it is absorbed, spread to tissues, broken down and excreted — like tracking a package from pickup to delivery and disposal. For investors, these properties determine effective dose, safety risks, how often a medicine must be taken, and how reliably it works, which in turn influence clinical trial success, regulatory approval chances, production complexity and a drug’s commercial value.
pharmacodynamic medical
"Taken together, the safety, pharmacokinetic, and pharmacodynamic profile observed to date"
Pharmacodynamic describes how a drug acts on the body — the biological effects it produces, how strong those effects are, and how long they last. For investors, pharmacodynamic data show whether a treatment actually works and at what dose, shaping expectations about a drug’s safety, effectiveness, regulatory success and market potential; think of it like testing how well a key turns a lock and whether it reliably opens the door.

AI-generated analysis. Not financial advice.

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In preclinical studies of CSU, Bexobrutideg demonstrates potent BTK degradation across key immune cell types and enhanced suppression of FcεRI-driven pathology versus remibrutinib

In healthy volunteers, both single- and multiple-ascending-dose oral dosing of bexobrutideg led to rapid and robust BTK degradation in blood and skin

Phase 1 studies support continued exploration of new tablet formulation in inflammation and immunology indications

BRISBANE, Calif., May 14, 2026 (GLOBE NEWSWIRE) -- Nurix Therapeutics (Nasdaq: NRIX), a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines, today announced the presentation of new preclinical and Phase 1 translational data highlighting the potential of bexobrutideg (NX-5948), the company’s wholly owned Bruton’s tyrosine kinase (BTK) degrader, in chronic spontaneous urticaria (CSU). The data are being presented at the 2026 Society for Investigative Dermatology Annual Meeting, taking place May 13–16, 2026, in Chicago, Illinois.

The findings demonstrate that targeted degradation of BTK may provide broader and deeper suppression of pathogenic immune signaling than BTK inhibition alone, supporting the future clinical development of bexobrutideg in inflammation and immunology indications.

“These data reinforce the potential of targeted protein degradation to deliver a fundamentally different level of control over immune-mediated disease biology,” said Arthur T. Sands, M.D., Ph.D., president and chief executive officer of Nurix Therapeutics. “By catalytically eliminating BTK, rather than transiently inhibiting it, a single molecule of bexobrutideg can degrade thousands of BTK proteins per hour. Importantly, we have demonstrated virtually complete BTK degradation in both blood and skin of healthy volunteers utilizing our new tablet formulation. Bexobrutideg has the potential to provide deeper and more durable suppression of pathogenic signaling, with the goal of delivering meaningful new treatment options for patients with chronic inflammatory diseases.”

“The results highlight a categorical advantage of the degrader approach. While BTK inhibitors can only block kinase activity, complete protein removal by bexobrutideg eliminates both kinase and scaffolding functions simultaneously,” said Gwenn M. Hansen, Ph.D., chief scientific officer at Nurix Therapeutics. “In the context of controlling FcεRI-driven mast cell and basophil degranulation, the key drivers of CSU pathology, this translated in preclinical studies into a ~25-fold greater potency compared to remibrutinib while maintaining a highly BTK-selective profile based on global proteomic analyses of more than 8,700 proteins.”

Bexobrutideg Demonstrates Differentiated Activity in Chronic Spontaneous Urticaria
CSU is an autoimmune condition driven by aberrant activation of mast cells and basophils through FcεRI signaling, leading to chronic itching and swelling. Both upstream autoantibody production and downstream effector signaling are dependent on BTK, making it a highly relevant therapeutic target.

Bexobrutideg is an orally bioavailable BTK degrader designed to eliminate the BTK protein through recruitment of the cereblon E3 ligase complex, which efficiently marks the BTK protein for proteasomal degradation, thereby eliminating both the kinase-dependent and scaffolding functions of BTK.

Key Findings

  • Bexobrutideg potently and selectively degrades BTK across primary human B cells, basophils, and mast cells in preclinical assays
  • Bexobrutideg demonstrates deeper suppression of BCR signaling than BTK inhibitors in preclinical assays by eliminating both enzymatic and scaffolding functions of BTK
  • Across a broad proteomic analysis of more than 8,700 proteins, bexobrutideg shows highly selective BTK degradation preclinically
  • Bexobrutideg produced greater reductions in ear swelling and vascular permeability than remibrutinib in a preclinical mouse model of passive cutaneous anaphylaxis model
  • In healthy volunteers, both single- and multiple-ascending-dose oral dosing of bexobrutideg led to rapid and robust BTK degradation in blood and skin, a key tissue of disease involvement in CSU

These data support the potential for bexobrutideg to deliver deep, tissue-level suppression of pathogenic immune signaling in CSU. Taken together, the safety, pharmacokinetic, and pharmacodynamic profile observed to date suggests bexobrutideg may offer meaningful advantages over BTK inhibitors across CSU and other IgE-mediated and autoimmune diseases.

About Bexobrutideg (NX-5948) in Inflammation and Immunology
Bexobrutideg is an investigational, oral, brain-penetrant, highly selective small-molecule degrader of BTK being developed within Nurix’s inflammation and immunology (I&I) portfolio. It is designed to remove BTK and thereby disrupt signaling pathways that drive abnormal B-cell activation and Fc receptor-mediated effector functions implicated in a range of autoimmune and allergic conditions. Bexobrutideg is currently being evaluated, with a new tablet formulation, in a first-in-human single-ascending-dose and multiple-ascending-dose (SAD/MAD) study in healthy volunteers (NCT06717269).

In oncology, bexobrutideg is currently being evaluated in the DAYBreak CLL-201 clinical trial (NCT07221500), a pivotal single-arm Phase 2 study of bexobrutideg in patients with relapsed or refractory CLL. Nurix also continues enrollment in the NX-5948-301 Phase 1a/1b clinical trial (NCT05131022) of bexobrutideg in patients with relapsed or refractory B cell malignancies.

About Nurix Therapeutics, Inc.
Nurix Therapeutics is a clinical stage biopharmaceutical company focused on the discovery, development and commercialization of targeted protein degradation medicines, the next frontier in innovative drug design aimed at improving treatment options for patients with cancer and autoimmune diseases. Nurix’s wholly owned, clinical stage pipeline includes degraders of Bruton’s tyrosine kinase (BTK), a B-cell signaling protein, and inhibitors of Casitas B-lineage lymphoma proto-oncogene B (CBL-B), an E3 ligase that regulates activation of multiple immune cell types including T cells and NK cells. Nurix also is advancing multiple potentially first-in-class or best-in-class degraders and degrader antibody conjugates (DACs) in its preclinical pipeline. Nurix’s partnered drug discovery pipeline consists of a preclinical stage degrader of STAT6, SAR448272/NX-3911, in collaboration with Sanofi, a clinical stage degrader of IRAK4, GS6791, in collaboration with Gilead, as well as multiple additional programs under collaboration agreements with Gilead Sciences, Inc., Sanofi S.A. and Pfizer Inc., within which Nurix retains certain options for co-development, co-commercialization and profit sharing in the United States for multiple drug candidates. Powered by an AI-integrated discovery engine capable of tackling virtually any protein class, and coupled with unparalleled ligase expertise, Nurix’s dedicated team has built a formidable advantage in translating the science of targeted protein degradation into clinical advancements. Nurix aims to establish degrader-based treatments at the forefront of patient care, writing medicine’s next chapter with a new script to outmatch disease. Nurix is headquartered in Brisbane, California. For additional information visit http://www.nurixtx.com.

Forward-Looking Statements
This press release contains forward-looking statements within the meaning of the U.S. Private Securities Litigation Reform Act of 1995 and other federal securities laws. Any statements contained herein that do not describe historical facts, including statements regarding the therapeutic potential of bexobrutideg in CSU or other inflammation and immunology indications, the potential advantages of bexobrutideg over BTK inhibitors, the potential of BTK degraders to suppress pathogenic immune signaling or deliver a differentiated level of control over immune-mediated disease biology, the anticipated clinical development of bexobrutideg, including plans for future studies in inflammation and immunology indications, and the potential of the bexobrutideg tablet formulation, are forward-looking statements that involve risks and uncertainties that could cause actual results to differ materially from those discussed in such forward-looking statements. Such risks and uncertainties include, among others, the risks described under the heading “Risk Factors” in Nurix’s Quarterly Report on Form 10-Q for the fiscal period ended February 28, 2026, and subsequent filings with the SEC. Any of these risks and uncertainties could materially and adversely affect Nurix’s business and results of operations, which could, in turn, have a significant and adverse impact on Nurix’s stock price. Nurix cautions you not to place undue reliance on any forward-looking statements, which speak only as of the date they are made. Nurix undertakes no obligation to update publicly any forward-looking statements to reflect new information, events or circumstances after the date they were made or to reflect the occurrence of unanticipated events.

Contacts:
Investors
Kris Fortner
Nurix Therapeutics, Inc.
kfortner@nurixtx.com

Sylvia Wheeler
Wheelhouse Life Science Advisors
swheeler@wheelhouselsa.com

Media
Aljanae Reynolds
Wheelhouse Life Science Advisors
areynolds@wheelhouselsa.com

Kris Fortner
Nurix Therapeutics, Inc.
Kfortner@nurixtx.com


FAQ

What did Nurix Therapeutics (NRIX) announce about bexobrutideg at the 2026 SID meeting?

Nurix announced new preclinical and Phase 1 translational data for bexobrutideg (NX-5948) in chronic spontaneous urticaria. According to Nurix, the BTK degrader showed potent, selective BTK degradation and deep suppression of FcεRI-driven immune signaling, supporting continued clinical development in inflammation and immunology.

How does bexobrutideg (NX-5948) compare to remibrutinib in CSU preclinical models?

In preclinical FcεRI-driven mast cell and basophil assays, bexobrutideg showed about 25-fold greater potency than remibrutinib. According to Nurix, bexobrutideg also produced greater reductions in ear swelling and vascular permeability in a mouse passive cutaneous anaphylaxis model while maintaining a highly BTK-selective profile.

What Phase 1 results did Nurix (NRIX) report for bexobrutideg in healthy volunteers?

Nurix reported that single- and multiple-ascending-dose oral bexobrutideg led to rapid, robust BTK degradation in blood and skin. According to Nurix, the new tablet formulation achieved virtually complete BTK degradation in these tissues, supporting further evaluation in CSU and other immune-mediated diseases.

Why is BTK degradation by bexobrutideg important for chronic spontaneous urticaria treatment?

BTK is involved in both upstream autoantibody production and downstream FcεRI effector signaling in CSU. According to Nurix, bexobrutideg eliminates BTK protein, removing kinase and scaffolding functions, which in preclinical studies translated into deeper suppression of pathogenic immune signaling than BTK inhibition alone.

What makes bexobrutideg (NX-5948) different from traditional BTK inhibitors for NRIX investors?

Bexobrutideg is a targeted BTK degrader, designed to catalytically eliminate BTK rather than transiently inhibit it. According to Nurix, this approach can degrade thousands of BTK proteins per hour, potentially enabling deeper and more durable suppression of immune signaling in chronic inflammatory diseases.

What are the next development steps for Nurix’s bexobrutideg in CSU and immunology?

The current preclinical and Phase 1 data support continued clinical exploration of bexobrutideg’s tablet formulation in CSU and other IgE-mediated or autoimmune diseases. According to Nurix, the safety, pharmacokinetic and pharmacodynamic profile observed so far underpins plans for further inflammation and immunology studies.