Revolution Medicines Announces Closing of Concurrent Upsized Public Offerings with Aggregate Gross Proceeds of Approximately $2.2 Billion, Including Full Exercise of Underwriters’ Option to Purchase Additional Shares

On April 17, 2026 Revolution Medicines, Inc. (Nasdaq: RVMD), a late-stage clinical oncology company developing targeted therapies for patients with RAS-addicted cancers, reported the closing of its concurrent upsized public offerings of 12,147,887 shares of its common stock at a public offering price of $142.00 per share and $500.0 million aggregate principal amount of 0.50% convertible senior notes due 2033 (the "notes"). The shares of common stock issued and sold in the common stock offering include 1,584,506 shares issued upon exercise in full by the underwriters of their option to purchase additional shares of common stock at the public offering price, less underwriting discounts and commissions. The gross proceeds from the offerings, before deducting underwriting discounts and commissions and other offering expenses payable by Revolution Medicines, were approximately $2,225.0 million.

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J.P. Morgan, TD Cowen and Guggenheim Securities acted as book-running managers for the note offering and the common stock offering. LifeSci Capital acted as lead manager for the note offering and the common stock offering.

The notes are senior, unsecured obligations of Revolution Medicines and will accrue interest at a rate of 0.50% per annum, payable semi-annually in arrears on May 1 and November 1 of each year, beginning on November 1, 2026. The notes will mature on May 1, 2033, unless earlier repurchased, redeemed or converted. Before February 1, 2033, noteholders will have the right to convert their notes only upon the occurrence of certain events. From, and including, February 1, 2033, noteholders may convert their notes at any time at their election until the close of business on the second scheduled trading day immediately before the maturity date. Revolution Medicines will settle conversions by paying or delivering, as applicable, cash, shares of its common stock or a combination of cash and shares of its common stock, at Revolution Medicines’ election. The initial conversion rate is 5.0302 shares of common stock per $1,000 principal amount of notes, which represents an initial conversion price of approximately $198.80 per share of common stock. The initial conversion price represents a premium of approximately 40.0% over the public offering price per share of common stock in the common stock offering. The conversion rate and conversion price will be subject to adjustment upon the occurrence of certain events.

The notes will be redeemable, in whole or in part (subject to certain limitations), for cash at Revolution Medicines’ option at any time, and from time to time, on or after May 6, 2030 and on or before the 31st scheduled trading day immediately before the maturity date, but only if the last reported sale price per share of Revolution Medicines’ common stock exceeds 130% of the conversion price for a specified period of time and certain other conditions are satisfied. The redemption price will be equal to the principal amount of the notes to be redeemed, plus accrued and unpaid interest, if any, to, but excluding, the redemption date.

If a "fundamental change" (as defined in the indenture for the notes) occurs, then, subject to a limited exception, noteholders may require Revolution Medicines to repurchase their notes for cash. The repurchase price will be equal to the principal amount of the notes to be repurchased, plus accrued and unpaid interest, if any, to, but excluding, the fundamental change repurchase date.

Revolution Medicines estimates that the aggregate net proceeds from the offerings were approximately $2,137.2 million, after deducting the underwriting discounts and commissions and estimated offering expenses. Revolution Medicines intends to use the net proceeds from the offerings for general corporate purposes, including research and development expenses, expenses relating to the potential commercialization of one or more of its product candidates, general and administrative expenses and capital expenditures.

The offerings were made pursuant to an effective shelf registration statement on file with the Securities and Exchange Commission (the "SEC"). Each offering was made only by means of a prospectus supplement relating to that offering and an accompanying prospectus. Copies of the final prospectus supplement and the accompanying prospectus relating to each offering may be obtained for free by visiting EDGAR on the SEC’s website at www.sec.gov. Alternatively, copies of these documents may be obtained by contacting: J.P. Morgan Securities LLC, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717 or by email at [email protected] and [email protected]; TD Securities (USA) LLC, c/o Broadridge Financial Solutions, 1155 Long Island Avenue, Edgewood, NY 11717, or by email at [email protected]; and Guggenheim Securities, LLC, Attention: Equity Syndicate Department, 330 Madison Avenue, 8th Floor, New York, NY 10017, by telephone at (212) 518-9544, or by email at [email protected].

This press release shall not constitute an offer to sell or a solicitation of an offer to buy any securities referred to in this press release, nor shall there be any sale of any such securities in any state or other jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or other jurisdiction.

(Press release, Revolution Medicines, APR 17, 2026, View Source [SID1234664474])

Precision Biologics to Reveal New AML Target for CAR-NK at American Association for Cancer Research (AACR) Annual Meeting on April 19th, 2026

On April 17, 2026 Precision Biologics, Inc. reported a new target in Acute Myeloid Leukemia (AML) for CAR-NK therapy. Recent data for several human AML subtypes expressing truncated core 1 O-glycans will be presented in a poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting on April 19th, 2026, in San Diego, CA, USA.

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Poster title: NEO-201-recognized truncated Core 1 O-glycans represent a new target for CAR-NK therapy in AML

Presentation of the poster will be made in person on the following date and location:

Sunday, April 19th, 2:00pm – 5:00pm PT

San Diego Convention Center, San Diego, CA, USA

Exhibit Hall

Session Category: Immunology

Session Title: Alternative Cell Type and in Situ Cell Therapies

Location: Poster Section 7

Poster Board Number: 7

Poster Number: 133

Abstract Number: 7933 (published in Cancer Research: View Source)

BACKGROUND:

Acute myeloid leukemia (AML) continues to have poor long-term outcomes, particularly in high-risk and relapsed/refractory disease. Progress in AML immunotherapy has been hindered by the scarcity of antigens selectively expressed on leukemic cells while sparing hematopoietic stem/progenitor cells (HSPCs).

Recent data to be presented for the first time at AACR (Free AACR Whitepaper), clearly identifies truncated Core 1 O-glycans recognized by NEO-201 as a novel AML-associated antigen present across multiple subtypes and largely absent from early hematopoietic progenitors. The potent antileukemic activity of NEO-201CAR NK cells in preclinical systems highlights the promise of this approach and sets the stage for advancing truncated Core 1 O-glycan-directed Cellular therapies into translational and clinical development.

"What was surprising to us was this novel target originally was discovered in solid tumors not healthy tissue, but its expression is also found in hematologic cancers. This provides the basis of targeting this specific glycan when developing cellular therapies for the treatment of refractory leukemias" said Dr. Philip M. Arlen, of Precision Biologics, Inc.

With a 5-year relative survival of only 32.9% from 2015 – 2021, it’s estimated that in the US in 2025 AML claimed about 22,000 new cases, with over 11,000 deaths. (seer.cancer.gov)

(Press release, Precision Biologics, APR 17, 2026, View Source [SID1234664490])

Boundless Bio Presents Preclinical Breast Cancer Data from its Oral Kinesin Degrader Program at 2026 AACR Annual Meeting

On April 17, 2026 Boundless Bio (Nasdaq: BOLD), a clinical-stage oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, reported preclinical data supporting its lead ecDNA-directed therapy (ecDTx), BBI-940, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026. Boundless has identified a novel kinesin target ("Kinesin") essential to ecDNA segregation and inheritance in cancer cells, but non-essential in healthy cells. BBI-940, a potentially first-in-class, oral, and selective Kinesin degrader, is currently being evaluated in the Phase 1 KOMODO-1 trial (NCT07408089) in patients with advanced or metastatic ER+/HER2- breast cancer and TNBC-LAR.

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"Extrachromosomal DNA is well established as a distinct enabler of chromosomal instability associated with oncogene amplification, therapeutic resistance, and poor outcomes for patients," said Chris Hassig, Ph.D., Chief Scientific Officer of Boundless Bio. "We have discovered and validated a novel kinesin target that plays a critical role in ecDNA segregation during cell division, thereby affording tumors with a high degree of genomic plasticity. Our data demonstrate that selective degradation of this target delivered potent antitumor activity in validated breast cancer models, particularly those with ecDNA. Our genetic, in vitro, in vivo, and toxicity profile of BBI-940 supports our recently initiated, first-in-human KOMODO-1 clinical trial evaluating BBI-940 in ER+/HER2- and TNBC-LAR breast cancer patients."

Details of the presentation are as follows:

Title: Selective degradation of a novel kinesin as a potential therapeutic strategy addressing high-risk extrachromosomal DNA (ecDNA) positive cancers, including breast cancer
Abstract Number: LB361
Session Title: Late-Breaking Research: Experimental and Molecular Therapeutics 3
Session Date and Time: Tuesday April 21, 2026, 2:00 PM – 5:00 PM PT
Location: Poster Section 53
Poster Board Number: 18

Genetic and pharmacologic degradation of Kinesin caused ecDNA mis-segregation, ecDNA depletion, and reduced viability of ecDNA+ cancer cells. Selective degradation of Kinesin in a panel of tumor cell lines demonstrated sensitivity across multiple tumor types and 32% sensitivity in breast cancer cell lines, including those positive for ecDNA and FGFR1 gain. This molecularly defined subgroup for Kinesin degradation was further validated in vivo with demonstrated monotherapy tumor regressions in an ecDNA+ TNBC-LAR model, and significant antitumor activity as monotherapy and combination in an ecDNA+/FGFR1+ ER+ breast cancer model.

About BBI-940
Our lead ecDTx, BBI-940, is a novel, oral, and selective kinesin degrader being evaluated in the ongoing, first-in-human Phase 1 KOMODO-1 (Kinesin Oral Molecular Degrader for Oncology) clinical trial (NCT07408089) in patients with advanced or metastatic estrogen receptor-positive, HER2-negative (ER+/HER2-) breast cancer or triple-negative breast cancer of the luminal androgen receptor subtype (TNBC-LAR). BBI-940 targets a specific kinesin protein, "Kinesin", essential for ecDNA segregation and inheritance in cancer cells, but non-essential in healthy cells. BBI-940 is designed to exploit the heightened dependence of ecDNA-positive tumors on mitotic machinery by degrading Kinesin to induce mitotic catastrophe and cell death.

(Press release, Boundless Bio, APR 17, 2026, View Source [SID1234664506])

Mount Sinai Health System and SOPHiA GENETICS Announce Collaboration to Advance Precision Cancer Care from AACR 2026

On April 16, 2026 SOPHiA GENETICS (NASDAQ: SOPH), a global leader in AI-driven precision medicine, reported that the Mount Sinai Health System, one of the leading academic health systems in the United States, will adopt the AI-powered SOPHiA DDM Platform to advance cancer research and enhance genomic testing capabilities.

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Mount Sinai, a National Cancer Institute-designated Comprehensive Cancer Center in New York City, supports care for more than 4,000 oncology patients annually. Mount Sinai’s Molecular Pathology team will leverage SOPHiA DDM to strengthen next-generation sequencing (NGS) capabilities for blood cancers and solid tumors. The Platform is designed to enable detection and interpretation of a wide range of complex genomic variants while improving operational efficiency by consolidating critical steps in the analysis pipeline and reducing manual interpretation time.

By combining Mount Sinai’s clinical excellence with SOPHiA DDM’s advanced AI-powered analytics, the hospital will be equipped to interpret complex genomic datasets at scale and optimize laboratory resources, enabling teams to focus on direct patient care.

Jane Houldsworth, Ph.D., Director of Molecular Oncology Pathology of the Mount Sinai Health System, said: "The collaboration between Mount Sinai and SOPHiA GENETICS reinforces our commitment to scientific innovation by integrating powerful digital tools into our workflows to support high-quality, data-driven cancer care. Leveraging SOPHiA DDM has enabled us to reduce hands-on analysis time and improve our testing turnaround times, enabling our clinicians to provide better patient care."

John Carey, Managing Director, North America, SOPHiA GENETICS, said: "Mount Sinai is widely regarded as one of the world’s leading centers for cancer research and was recently ranked No. 1 globally among health care institutions in the Nature AI Index, underscoring its leadership in artificial intelligence and data-driven innovation. We are honored to support their teams with an AI-native platform and global network designed to deliver faster results, greater operational efficiency, and deeper genomic understanding to help shape the future of precision oncology."

By utilizing the SOPHiA DDM for Blood Cancers and SOPHiA DDM for Solid Tumors applications, Mount Sinai joins a growing network of more than 990 global institutions using SOPHiA GENETICS’ decentralized platform to accelerate precision medicine. This collaboration underscores SOPHiA GENETICS’ mission to democratize data-driven medicine, delivering scalable, cloud-native solutions that empower healthcare institutions to expand access to advanced genomic testing and improve patient outcomes worldwide.

The collaboration was announced from the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting in San Diego. Learn more by connecting with SOPHiA GENETICS at AACR (Free AACR Whitepaper) booth #4248 from April 17 – 22, 2026.

(Press release, Mount Sinai Hospital, APR 16, 2026, View Source [SID1234664442])

INmune Bio Inc. Announces New Preclinical Data at AACR 2026 Demonstrating INB03 (XPro1595) Overcomes Resistance and Reduces Metastases in HER2-Positive Breast Cancer Models

On April 16, 2026 INmune Bio Inc. (NASDAQ: INMB) (the "Company"), a clinical-stage biotechnology company focused on developing therapies that harness the patient’s innate immune system, reported new preclinical data for INB03 (XPro1595 for oncology). The data will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 in San Diego on April 17-22.

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The poster, titled, "Soluble TNF blockade overcomes tyrosine kinase inhibitors resistance in HER2-positive breast cancer," details how INB03 ("XPro"), a first-in-class dominant-negative soluble TNF (sTNF) inhibitor, significantly enhances the anti-tumor activity of the tyrosine kinase inhibitors (TKIs) lapatinib and tucatinib while reducing metastatic spread to the brain, lungs, and liver in HER2-positive breast cancer models. It was authored by collaborators from the Instituto de Biología y Medicina Experimental (IBYME-CONICET) in Buenos Aires, Argentina.

Key Scientific Findings:

Overcoming Resistance in Vitro: The combination of INB03 (10 µg/mL) with either lapatinib (1 µM) or tucatinib (10 µM) produced statistically superior inhibition of cell proliferation and migration in both HER2+ JIMT-1 and brain-metastatic JIMT-1 Br3-luc cell lines compared to TKIs alone (p < 0.05 to p < 0.0001).
Enhanced Tumor Control In Vivo: In female nude mice bearing JIMT-1 or JIMT-1 Br3-luc tumors, INB03 + TKI combinations markedly slowed tumor growth compared to TKIs alone.
Reduction of Metastatic Spread: The addition of INB03 significantly reduced the incidence of metastases to brain, lung, and liver (quantified by ex-vivo IVIS luminescence imaging). Notably, it further enhanced tucatinib’s effect on lung metastases (p < 0.05 to p < 0.0001).
Mechanism of Action: These results support prior research showing that selective sTNF neutralization with INB03 down-regulates MUC4, a protein that shields the HER2 molecule and prevents therapies from binding effectively.
"These results build on our prior work showing that selective sTNF neutralization with INB03 down-regulates MUC4, restoring sensitivity to HER2-targeted therapies," said Roxana Schillaci, Ph.D., lead investigator. "The ability of INB03 to overcome TKI resistance and limit metastatic dissemination, including to the brain, highlights its potential to address key unmet needs in advanced HER2-positive breast cancer."

David Moss, CEO of INmune Bio, added, "INB03 continues to demonstrate broad therapeutic potential across solid tumors by targeting the soluble TNF pathway. These AACR (Free AACR Whitepaper) data reinforce our confidence in advancing INB03 combinations in the clinic for patients who have developed resistance to standard TKIs or who are at high risk for brain metastases."

The poster will be available for viewing during the AACR (Free AACR Whitepaper) 2026 meeting on April 21st.

About XPro (INB03)

XPro is a next-generation inhibitor of tumor necrosis factor (TNF) that is currently in clinical trial and acts differently than currently available TNF inhibitors in that it neutralizes soluble TNF (sTNF), without affecting trans-membrane TNF (tmTNF) or TNF receptors. XPro could have potential substantial beneficial effects in patients with neurologic disease by decreasing neuroinflammation. For more information about the importance of targeting neuroinflammation in the brain to improve cognitive function and restore neuronal communication visit this section of INmune Bio’s website.

(Press release, INmune Bio, APR 16, 2026, View Source [SID1234664458])